PMID- 33001857
OWN - NLM
STAT- MEDLINE
DCOM- 20210401
LR  - 20210401
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 36
IP  - 1
DP  - 2021 Mar 26
TI  - Balancing incomplete COVID-19 evidence and local priorities: risk
      communication and stakeholder engagement strategies for school re-
      opening.
PG  - 27-37
LID - 10.1515/reveh-2020-0092 [doi]
AB  - In the midst of the COVID-19 pandemic, United States (U.S.) educational
      institutions must weigh incomplete scientific evidence to inform
      decisions about how best to re-open schools without sacrificing public
      health. While many communities face surging case numbers, others are
      experiencing case plateaus or even decreasing numbers. Simultaneously,
      some U.S. school systems face immense infrastructure challenges and
      resource constraints, while others are better positioned to resume face-
      to-face instruction. In this review, we first examine potential
      engineering controls to reduce SARS-CoV-2 exposures; we then present
      processes whereby local decision-makers can identify and partner with
      scientists, faculty, students, parents, public health officials, and
      others to determine the controls most appropriate for their communities.
      While no solution completely eliminates risks of SARS-CoV-2 exposure and
      illness, this mini-review discusses engaged decision and communication
      processes that incorporate current scientific knowledge, school district
      constraints, local tolerance for health risk, and community priorities to
      help guide schools in selecting and implementing re-opening strategies
      that are acceptable, feasible, and context-specific.
CI  - (c) 2020 Walter de Gruyter GmbH, Berlin/Boston.
FAU - Hoover, Anna G
AU  - Hoover AG
AD  - Department of Preventive Medicine and Environmental Health, University of
      Kentucky, College of Public Health, Lexington, KY40506, USA.
FAU - Heiger-Bernays, Wendy
AU  - Heiger-Bernays W
AD  - Department of Environmental Health, Boston University, School of Public
      Health, Boston, MA02118, USA.
FAU - Ojha, Sweta
AU  - Ojha S
AD  - Department of Civil Engineering, University of Kentucky, College of
      Engineering, Lexington, KY40506, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
AUID- ORCID: https://orcid.org/0000-0003-3423-9610
AD  - Department of Civil Engineering, University of Kentucky, College of
      Engineering, Lexington, KY40506, USA.
LA  - eng
GR  - G08 LM013185/LM/NLM NIH HHS/United States
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007381/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20201001
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
SB  - IM
MH  - COVID-19/*epidemiology/*prevention & control/transmission
MH  - Communicable Disease Control/methods/organization &
      administration/statistics & numerical data
MH  - *Communication
MH  - Humans
MH  - Public Health
MH  - *Return to School/organization & administration
MH  - Risk
MH  - SARS-CoV-2
MH  - *Stakeholder Participation
MH  - United States/epidemiology
PMC - PMC7933073
MID - NIHMS1645221
OTO - NOTNLM
OT  - COVID-19
OT  - airborne transmission
OT  - children health
OT  - indoor air
OT  - stakeholder engagement
EDAT- 2020/10/02 06:00
MHDA- 2021/04/02 06:00
CRDT- 2020/10/01 17:15
PMCR- 2022/03/26 00:00
PHST- 2020/07/27 00:00 [received]
PHST- 2020/09/08 00:00 [accepted]
PHST- 2022/03/26 00:00 [pmc-release]
PHST- 2020/10/02 06:00 [pubmed]
PHST- 2021/04/02 06:00 [medline]
PHST- 2020/10/01 17:15 [entrez]
AID - 10.1515/reveh-2020-0092 [doi]
AID - /j/reveh.ahead-of-print/reveh-2020-0092/reveh-2020-0092.xml [pii]
PST - epublish
SO  - Rev Environ Health. 2020 Oct 1;36(1):27-37. doi: 10.1515/reveh-2020-0092.
      Print 2021 Mar 26.

PMID- 32105967
OWN - NLM
STAT- MEDLINE
DCOM- 20200710
LR  - 20210602
IS  - 1873-6424 (Electronic)
IS  - 0269-7491 (Linking)
VI  - 261
DP  - 2020 Jun
TI  - Prebiotic inulin consumption reduces dioxin-like PCB 126-mediated
      hepatotoxicity and gut dysbiosis in hyperlipidemic Ldlr deficient mice.
PG  - 114183
LID - S0269-7491(19)37026-5 [pii]
LID - 10.1016/j.envpol.2020.114183 [doi]
AB  - Exposure to some environmental pollutants increases the risk of
      developing inflammatory disorders such as steatosis and cardiometabolic
      diseases. Diets high in fermentable fibers such as inulin can modulate
      the gut microbiota and lessen the severity of pro-inflammatory diseases,
      especially in individuals with elevated circulating cholesterol. Thus, we
      aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched
      with 8% inulin would be protected from the pro-inflammatory toxic effects
      of PCB 126. Four groups of male Ldlr(-/-) mice were fed a high
      cholesterol diet containing 8% inulin or 8% cellulose (control) for 12
      weeks. At weeks 2 and 4, mice were exposed to PCB 126 or vehicle
      (control). PCB 126 exposure induced wasting and impaired glucose
      tolerance, which were attenuated by inulin consumption. PCB 126 exposure
      induced hepatic lipid accumulation and increased inflammatory gene
      expression, which were both decreased by inulin consumption. In addition,
      inulin feeding decreased atherosclerotic lesion development in the aortic
      root and modulated the expression of enzymes related to glycolysis.
      Finally, 16S rRNA sequencing of gut microbial populations showed that PCB
      126 modulated multiple microbiota genera (e.g., 3-fold decrease in
      Allobaculum and 3-fold increase in Coprococcus) which were normalized in
      inulin fed mice. Overall our data support the hypothesis that a dietary
      intervention that targets the gut microbiota may be an effective means of
      attenuating dioxin-like pollutant-mediated diseases.
CI  - Copyright (c) 2020 Elsevier Ltd. All rights reserved.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, USA; Lexington Veterans Affairs Medical Center,
      Lexington, KY, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, USA; Lexington Veterans Affairs Medical Center,
      Lexington, KY, USA.
FAU - Mottaleb, M Abdul
AU  - Mottaleb MA
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, USA; Lexington Veterans Affairs Medical Center,
      Lexington, KY, USA.
FAU - Sui, Yipeng
AU  - Sui Y
AD  - Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, USA.
FAU - Zhou, Changcheng
AU  - Zhou C
AD  - Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, USA.
FAU - Deng, Pan
AU  - Deng P
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA.
FAU - Wang, Chunyan
AU  - Wang C
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA. Electronic
      address: bhennig@uky.edu.
LA  - eng
GR  - S10 OD021753/OD/NIH HHS/United States
GR  - R01 HL123358/HL/NHLBI NIH HHS/United States
GR  - K99 ES028734/ES/NIEHS NIH HHS/United States
GR  - R00 ES028734/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 ES023470/ES/NIEHS NIH HHS/United States
GR  - R01 HL131925/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20200220
PL  - England
TA  - Environ Pollut
JT  - Environmental pollution (Barking, Essex : 1987)
JID - 8804476
RN  - 0 (Dioxins)
RN  - 0 (Prebiotics)
RN  - 0 (RNA, Ribosomal, 16S)
RN  - 9005-80-5 (Inulin)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - *Chemical and Drug Induced Liver Injury
MH  - *Dioxins
MH  - Dysbiosis
MH  - *Gastrointestinal Microbiome
MH  - Inulin
MH  - Male
MH  - Mice
MH  - Polychlorinated Biphenyls
MH  - Prebiotics
MH  - RNA, Ribosomal, 16S
PMC - PMC7220843
MID - NIHMS1566895
OTO - NOTNLM
OT  - Dioxin
OT  - Fiber
OT  - Gut microbiota
OT  - Inulin
OT  - Polychlorinated biphenyls
COIS- Declaration of competing interest The authors declare that there are no
      competing financial interests.
EDAT- 2020/02/28 06:00
MHDA- 2020/07/11 06:00
CRDT- 2020/02/28 06:00
PHST- 2019/11/25 00:00 [received]
PHST- 2020/01/25 00:00 [revised]
PHST- 2020/02/11 00:00 [accepted]
PHST- 2020/02/28 06:00 [pubmed]
PHST- 2020/07/11 06:00 [medline]
PHST- 2020/02/28 06:00 [entrez]
AID - S0269-7491(19)37026-5 [pii]
AID - 10.1016/j.envpol.2020.114183 [doi]
PST - ppublish
SO  - Environ Pollut. 2020 Jun;261:114183. doi: 10.1016/j.envpol.2020.114183.
      Epub 2020 Feb 20.

PMID- 31776573
OWN - NLM
STAT- MEDLINE
DCOM- 20200916
LR  - 20210121
IS  - 1945-2403 (Electronic)
IS  - 0146-4760 (Linking)
VI  - 44
IP  - 4
DP  - 2020 May 18
TI  - High-Throughput UHPLC-MS/MS Measurement of Per- and Poly-Fluorinated
      Alkyl Substances in Human Serum.
PG  - 339-347
LID - 10.1093/jat/bkz097 [doi]
AB  - Per- and poly-fluorinated alkyl substances (PFASs) are a large group of
      synthetic surfactant chemicals with widespread uses in food packaging and
      textile manufacturing and as the main constituent of aqueous film-forming
      firefighting foams. PFASs are highly persistent in the environment, and
      human exposures are extensive with these chemicals detectable in the
      blood of almost all adult Americans. PFASs exhibit a range of toxic
      effects in preclinical models. In humans, PFAS exposure has been
      associated with lower birth weights, decreased immune responses, cancer
      and impaired fertility and elevated circulating cholesterol levels. We
      have developed a sensitive high-throughput method for quantification of
      representative PFAS in human serum and plasma for biomonitoring and
      epidemiological studies of human health effects of PFAS exposure. The
      method combines robust and reproducible 96-well plate format sample
      preparation with ultra-performance liquid chromatography-tandem mass
      spectrometry. The method was developed, validated and used for targeted
      measurements of eight short-/long-chain PFAS analytes in human serum.
      Targeted analytes were measured in 50 microliters of sample using mass-
      labeled internal standards. Mean spiked recoveries (n = 10) of target
      analytes for three tiers quality control (QC-low, QC-medium, QC-high)
      samples ranged from 70 to 127% with 2-14% relative standard deviation
      (RSD). The average spiked recoveries (n = 10) of surrogates were 79-115%
      with 8-12% RSD for QC-low, 90-123% with 7-12% RSD for QC-medium and
      82-114% with 9-15% RSD for QC-high. The limit of detection for the target
      compounds was 0.05-0.04 ng/mL. The method was used to reveal regional
      differences in PFAS exposures in Kentucky residents receiving care at the
      University of Kentucky Hospitals.
CI  - (c) The Author(s) 2020. Published by Oxford University Press. All rights
      reserved. For permissions, please email: journals.permissions@oup.com.
FAU - Mottaleb, M Abdul
AU  - Mottaleb MA
AD  - Division of Cardiovascular Medicine, The Gill Heart and Vascular
      Institute, Superfund Research Center and Center for Appalachian Research
      in Environmental Sciences, University of Kentucky College of Medicine,
      Lexington Veterans Affairs Medical Center, Lexington, KY 40536, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Division of Cardiovascular Medicine, The Gill Heart and Vascular
      Institute, Superfund Research Center and Center for Appalachian Research
      in Environmental Sciences, University of Kentucky College of Medicine,
      Lexington Veterans Affairs Medical Center, Lexington, KY 40536, USA.
AD  - Institute of Environmental Health Sciences and Department of
      Pharmacology, Wayne State University, Detroit, MI 48202, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Division of Cardiovascular Medicine, The Gill Heart and Vascular
      Institute, Superfund Research Center and Center for Appalachian Research
      in Environmental Sciences, University of Kentucky College of Medicine,
      Lexington Veterans Affairs Medical Center, Lexington, KY 40536, USA.
LA  - eng
GR  - IS1 BX003153/BX/BLRD VA/United States
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 OD021753/OD/NIH HHS/United States
PT  - Journal Article
PL  - England
TA  - J Anal Toxicol
JT  - Journal of analytical toxicology
JID - 7705085
RN  - 0 (Environmental Pollutants)
RN  - 0 (Fluorocarbons)
SB  - IM
MH  - Chromatography, High Pressure Liquid
MH  - Chromatography, Liquid
MH  - Environmental Pollutants/*blood
MH  - Fluorocarbons/*blood
MH  - Humans
MH  - Plasma
MH  - Solid Phase Extraction
MH  - Tandem Mass Spectrometry
PMC - PMC7299301
EDAT- 2019/11/30 06:00
MHDA- 2020/09/17 06:00
CRDT- 2019/11/29 06:00
PHST- 2019/07/19 00:00 [received]
PHST- 2019/09/04 00:00 [revised]
PHST- 2019/10/06 00:00 [accepted]
PHST- 2019/11/30 06:00 [pubmed]
PHST- 2020/09/17 06:00 [medline]
PHST- 2019/11/29 06:00 [entrez]
AID - 5644223 [pii]
AID - 10.1093/jat/bkz097 [doi]
PST - ppublish
SO  - J Anal Toxicol. 2020 May 18;44(4):339-347. doi: 10.1093/jat/bkz097.

PMID- 32973372
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2328-8612 (Electronic)
IS  - 1082-7161 (Linking)
VI  - 26
IP  - 1
DP  - 2020 Spring
TI  - Mountains of Abundance: A Fruit and Vegetable Walking Program in Central
      Appalachia.
PG  - 106-127
LID - 10.5406/jappastud.26.1.0106 [doi]
FAU - Koempel, Annie
AU  - Koempel A
AD  - Registered Dietitian, PhD student in Anthropology, and program manager
      for UK's Superfund Research Community Engagement Core.
FAU - Brewer, Dawn
AU  - Brewer D
AD  - Registered Dietitian and Assistant Professor in the Department of
      Dietetics and Human Nutrition at the University of Kentucky.
FAU - Mudd-Martin, Gia
AU  - Mudd-Martin G
AD  - Associate Professor in the College of Nursing at the University of
      Kentucky.
FAU - Stephenson, Tammy
AU  - Stephenson T
AD  - Associate Professor in the Department of Dietetics and Human Nutrition at
      the University of Kentucky.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - J Appalach Stud
JT  - Journal of Appalachian studies
JID - 101760648
PMC - PMC7511086
MID - NIHMS1066518
EDAT- 2020/09/26 06:00
MHDA- 2020/09/26 06:01
CRDT- 2020/09/25 06:00
PHST- 2020/09/25 06:00 [entrez]
PHST- 2020/09/26 06:00 [pubmed]
PHST- 2020/09/26 06:01 [medline]
AID - 10.5406/jappastud.26.1.0106 [doi]
PST - ppublish
SO  - J Appalach Stud. 2020 Spring;26(1):106-127. doi:
      10.5406/jappastud.26.1.0106.

PMID- 33073239
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210302
IS  - 2643-8429 (Electronic)
IS  - 2643-8429 (Linking)
VI  - 1
IP  - 1
DP  - 2020 Mar
TI  - Healthful nutrition as a prevention and intervention paradigm to decrease
      the vulnerability to environmental toxicity or stressors and associated
      inflammatory disease risks.
PG  - 13-14
LID - 10.1002/fft2.6 [doi]
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      Lexington, KY, USA.
FAU - Deng, Pan
AU  - Deng P
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      Lexington, KY, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20200326
PL  - United States
TA  - Food Front
JT  - Food frontiers
JID - 101762101
PMC - PMC7566652
MID - NIHMS1577676
EDAT- 2020/10/20 06:00
MHDA- 2020/10/20 06:01
CRDT- 2020/10/19 06:01
PHST- 2020/10/19 06:01 [entrez]
PHST- 2020/10/20 06:00 [pubmed]
PHST- 2020/10/20 06:01 [medline]
AID - 10.1002/fft2.6 [doi]
PST - ppublish
SO  - Food Front. 2020 Mar;1(1):13-14. doi: 10.1002/fft2.6. Epub 2020 Mar 26.

PMID- 33208988
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210325
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 59
IP  - 12
DP  - 2020 Mar 25
TI  - Thiol-Functionalized Membranes for Mercury Capture from Water.
PG  - 5287-5295
LID - 10.1021/acs.iecr.9b03761 [doi]
AB  - Pore functionalized membranes with appropriate ion exchange/chelate
      groups allow toxic metal sorption under convective flow conditions. This
      study explores the sorption capacity of ionic mercury in a polyvinylidene
      fluoride-poly(acrylic acid) (PVDFs-PAA) functionalized membrane
      immobilized with cysteamine (MEA). Two methods of MEA immobilization to
      the PVDF-PAA membrane have been assessed: (i) ion exchange (IE) and (ii)
      carbodiimide cross-linker chemistry using
      1-(3-dimethylaminopropyl)-3-ethyl carbodiimide hydrochloride (EDC) and
      N-hydroxysuccinimide (NHS), known as EDC/NHS coupling. The ion exchange
      method demonstrates that cysteamine (MEA) can be immobilized effectively
      on PVDF-PAA membranes without covalent attachment. The effectiveness of
      the MEA immobilized membranes to remove ionic mercury from the water was
      evaluated by passing a dissolved mercury(II) nitrate solution through the
      membranes. The sorption capacity of mercury for MEA immobilized membrane
      prepared by the IE method is 1015 mg/g PAA. On the other hand, the
      sorption capacity of mercury for MEA immobilized membrane prepared by
      EDC/NHS chemistry is 2446 mg/g PAA, indicating that membrane
      functionalization by EDC/NHS coupling enhanced mercury sorption 2.4 times
      compared to the IE method. The efficiencies of Hg removal are 94.1 +/-
      1.1 and 99.1 +/- 0.1% for the MEA immobilized membranes prepared by IE
      and EDC/NHS coupling methods, respectively. These results show potential
      applications of MEA immobilized PVDF-PAA membranes for industrial
      wastewater treatment specifically from energy and mining industries to
      remove mercury and other toxic metals.
FAU - Hernandez, Sebastian
AU  - Hernandez S
AUID- ORCID: 0000-0002-7513-5511
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046, United States.
FAU - Islam, Md Saiful
AU  - Islam MS
AUID- ORCID: 0000-0001-6234-953X
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046, United States.
FAU - Thompson, Samuel
AU  - Thompson S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046, United States.
FAU - Kearschner, Madison
AU  - Kearschner M
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046, United States.
FAU - Hatakeyama, Evan
AU  - Hatakeyama E
AD  - Chevron Energy Technology Company, Richmond, California 94801, United
      States.
FAU - Malekzadeh, Nga
AU  - Malekzadeh N
AD  - Chevron Energy Technology Company, Richmond, California 94801, United
      States.
FAU - Hoelen, Thomas
AU  - Hoelen T
AD  - Chevron Energy Technology Company, Richmond, California 94801, United
      States.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AUID- ORCID: 0000-0001-9948-9085
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046, United States.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20190822
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC7668402
MID - NIHMS1063732
EDAT- 2020/11/20 06:00
MHDA- 2020/11/20 06:01
CRDT- 2020/11/19 05:40
PHST- 2020/11/19 05:40 [entrez]
PHST- 2020/11/20 06:00 [pubmed]
PHST- 2020/11/20 06:01 [medline]
AID - 10.1021/acs.iecr.9b03761 [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2020 Mar 25;59(12):5287-5295. doi:
      10.1021/acs.iecr.9b03761. Epub 2019 Aug 22.

PMID- 32129346
OWN - NLM
STAT- MEDLINE
DCOM- 20200731
LR  - 20210305
IS  - 2050-7895 (Electronic)
IS  - 2050-7887 (Linking)
VI  - 22
IP  - 3
DP  - 2020 Mar 1
TI  - Comparison of modeled and measured indoor air trichloroethene (TCE)
      concentrations at a vapor intrusion site: influence of wind, temperature,
      and building characteristics.
PG  - 802-811
LID - 10.1039/c9em00567f [doi]
AB  - There is a lack of vapor intrusion (VI) models that reliably account for
      weather conditions and building characteristics, especially at sites
      where active alternative pathways, such as sewer connections and other
      preferential pathways, are present. Here, a method is presented to
      incorporate freely-available models, CONTAM, and CFD0, to estimate site-
      specific building air exchange rates (AERs) and indoor air contaminant
      concentrations by accounting for weather conditions and building
      characteristics at a well-known VI site with a land drain preferential
      pathway. To account for uncertainty in model input parameters that
      influence indoor air chlorinated volatile organic compound (CVOC)
      concentration variability, this research incorporated Monte Carlo
      simulations and compared model results with retrospective field data
      collected over approximately 1.5 years from the study site. The results
      of this research show that mass entry rates for TCE are likely influenced
      by indoor air pressures that can be modeled as a function of weather
      conditions (over seasons) and building characteristics. In addition, the
      results suggest that temporal variability in indoor air TCE
      concentrations is greatest (modeled and measured) due to the existence of
      a land drain, which acts as a preferential pathway, from the subsurface
      to the granular fill beneath the floor slab. The field data and modeling
      results are in good agreement and provide a rare comparison of field data
      and modeling results for a VI site. The modeling approach presented here
      offers a useful tool for decision makers and VI practitioners as they
      assess these complex and variable processes that have not been
      incorporated within other VI models.
FAU - Shirazi, Elham
AU  - Shirazi E
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, USA. kellypennell@uky.edu.
FAU - Hawk, Gregory S
AU  - Hawk GS
FAU - Holton, Chase W
AU  - Holton CW
FAU - Stromberg, Arnold J
AU  - Stromberg AJ
FAU - Pennell, Kelly G
AU  - Pennell KG
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20200304
PL  - England
TA  - Environ Sci Process Impacts
JT  - Environmental science. Processes & impacts
JID - 101601576
RN  - 0 (Air Pollutants)
RN  - 290YE8AR51 (Trichloroethylene)
SB  - IM
MH  - *Air Pollutants
MH  - *Air Pollution, Indoor
MH  - Retrospective Studies
MH  - Temperature
MH  - *Trichloroethylene
MH  - Wind
PMC - PMC7153494
MID - NIHMS1564885
EDAT- 2020/03/05 06:00
MHDA- 2020/08/01 06:00
CRDT- 2020/03/05 06:00
PHST- 2020/03/05 06:00 [pubmed]
PHST- 2020/08/01 06:00 [medline]
PHST- 2020/03/05 06:00 [entrez]
AID - 10.1039/c9em00567f [doi]
PST - ppublish
SO  - Environ Sci Process Impacts. 2020 Mar 1;22(3):802-811. doi:
      10.1039/c9em00567f. Epub 2020 Mar 4.

PMID- 31929677
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200117
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 594
DP  - 2020 Jan 15
TI  - Pd/Fe nanoparticle integrated PMAA-PVDF membranes for chloro-organic
      remediation from synthetic and site groundwater.
LID - 117454 [pii]
LID - 10.1016/j.memsci.2019.117454 [doi]
AB  - The poly(methacrylic acid) (PMAA) was synthesized in the pores of
      commercial microfiltration PVDF membranes to allow incorporation of
      catalytic palladium/iron (Pd/Fe) nanoparticles for groundwater
      remediation. Particles of 17.1 +/- 4.9 nm size were observed throughout
      the pores of membranes using a focused ion beam. To understand the role
      of Pd fractions and particle compositions, 2-chlorobiphenyl was used as a
      model compound in solution phase studies. Results show H2 production
      (Fe(0) corrosion in water) is a function of Pd coverage on the Fe.
      Insufficient H2 production caused by higher coverage (> 10.4% for 5.5
      wt%) hindered dechlorination rate. With 0.5 wt% Pd, palladized-Fe
      reaction rate (surface area normalized reaction rate, ksa = 0.12
      L/(m(2)-h) was considerably higher than isolated Pd and Fe particles. For
      groundwater, in a single pass of Pd/Fe-PMAA-PVDF membranes (0.5 wt% Pd),
      chlorinated organics, such as trichloroethylene (177 ppb) and carbon
      tetrachloride (35 ppb), were degraded to 16 and 0.3 ppb, respectively, at
      2.2 seconds of residence time. The degradation rate (observed ksa)
      followed the order of carbon tetrachloride > trichloroethylene >
      tetrachloroethylene > chloroform. A 36 h continuous flow study with
      organic mixture and the regeneration process show the potential for on-
      site remediation.
FAU - Wan, Hongyi
AU  - Wan H
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506-0046, USA.
FAU - Islam, Md Saiful
AU  - Islam MS
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506-0046, USA.
FAU - Briot, Nicolas J
AU  - Briot NJ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506-0046, USA.
FAU - Schnobrich, Matthew
AU  - Schnobrich M
AD  - Arcadis, Lexington, KY, 40509, USA.
FAU - Pacholik, Lucy
AU  - Pacholik L
AD  - Department of Civil Engineering University of Kentucky, Lexington, KY,
      40506-0046, USA.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - Department of Civil Engineering University of Kentucky, Lexington, KY,
      40506-0046, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506-0046, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20190907
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC6953629
MID - NIHMS1063721
OTO - NOTNLM
OT  - Chloro-organics removal
OT  - Focused ion beam
OT  - Groundwater remediation
OT  - H2 production
OT  - Pd/Fe membrane reactor
COIS- Conflicts of interest The authors declare no conflict of interest.
EDAT- 2020/01/14 06:00
MHDA- 2020/01/14 06:01
CRDT- 2020/01/14 06:00
PMCR- 2020/01/15 00:00
PHST- 2020/01/15 00:00 [pmc-release]
PHST- 2020/01/14 06:00 [entrez]
PHST- 2020/01/14 06:00 [pubmed]
PHST- 2020/01/14 06:01 [medline]
AID - 10.1016/j.memsci.2019.117454 [doi]
PST - ppublish
SO  - J Memb Sci. 2020 Jan 15;594. doi: 10.1016/j.memsci.2019.117454. Epub 2019
      Sep 7.

PMID- 31903045
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210102
IS  - 1383-5866 (Print)
IS  - 1383-5866 (Linking)
VI  - 230
DP  - 2020 Jan 2
TI  - Selective molecular separation of lignin model compounds by reduced
      graphene oxide membranes from solvent-water mixture.
LID - 115865 [pii]
LID - 10.1016/j.seppur.2019.115865 [doi]
AB  - Selective separation of lignin depolymerization products is key to
      fractionating and isolating high-value aromatic compounds from the
      depolymerization process. The primary aim of this study was to synthesis
      graphene oxide (GO) membranes for selective separations of lignin
      oligomeric units from polar organic solvent-water media. GO membranes
      were synthesized on a polymeric substrate by a shear assisted casting of
      aqueous GO dispersion using a wire-wound rod. Deposited GO was then
      reduced to different extents by controlled thermal incubation, and the
      impact on membrane performance was investigated. The extent of reduction
      of GO was established by extensive characterization with FTIR, XPS, Raman
      Spectroscopy, XRD, and contact angle measurements. Impressive performance
      with the rejection of over 70% for the model compound trimer BMP
      (2,6-bis[(2-hydroxy-5-methyl phenyl) methyl]-4-methylphenol) was achieved
      compared to only 20% rejection for the dimer GGE (guaiacylglycerol-beta-
      guaiacylether) with isopropanol-water (90-10% by volume) as a solvent.
      This corresponds to an encouraging selective separation with selective
      permeation of dimer (GGE) 3.5 times higher compared to trimer (BMP). rGO
      membranes exhibited a stable performance over 84 h of operation at a
      shear rate of 1.1 Pa in a cross-flow mode of operation. Selective
      separation of GO can be effectively modulated by controlling the O/C
      ratio by the extent of reduction of GO; indeed, the retention of trimeric
      compounds increased with increasing GO reduction. The remarkable
      performance of GO membranes could enable energy-efficient fractionation
      of lignin oligomeric compounds from polar organic solvents.
FAU - Aher, Ashish
AU  - Aher A
AD  - Dept. Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Sarma, Rupam
AU  - Sarma R
AD  - Dept. Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Crocker, Mark
AU  - Crocker M
AD  - Center for Applied Energy Research, Lexington, KY 40511, USA.
AD  - Dept. of Chemistry, University of Kentucky, Lexington, KY 40506, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Dept. Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20190727
PL  - Netherlands
TA  - Sep Purif Technol
JT  - Separation and purification technology
JID - 101526757
PMC - PMC6941755
MID - NIHMS1063724
EDAT- 2020/01/07 06:00
MHDA- 2020/01/07 06:01
CRDT- 2020/01/07 06:00
PHST- 2020/01/07 06:00 [entrez]
PHST- 2020/01/07 06:00 [pubmed]
PHST- 2020/01/07 06:01 [medline]
AID - 10.1016/j.seppur.2019.115865 [doi]
PST - ppublish
SO  - Sep Purif Technol. 2020 Jan 2;230. doi: 10.1016/j.seppur.2019.115865.
      Epub 2019 Jul 27.

PMID- 32973411
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1533-015X (Print)
IS  - 1533-0389 (Linking)
VI  - 19
IP  - 2
DP  - 2020
TI  - Community Forum Identifies Opportunities to Engage with Eastern Kentucky
      Community Leaders about Chronic Disease and Environmental Pollution.
PG  - 187-204
LID - 10.1080/1533015X.2019.1597660 [doi]
AB  - The NIEHS-sponsored Appalachian Health & Well-Being Community Forum held
      in Eastern Kentucky brought various community members together to
      communicate and establish better coordination of efforts to improve
      health and address regional environmental issues. The two-hour forum
      discussion provided bi-directional feedback about the needs and interests
      of community members. Top concerns of community members included obesity
      and obesity-related diseases and environmental pollution. Healthful
      lifestyles were identified as part of the remedy to protect health from
      potential adverse health effects associated with environmental pollution.
      This study highlights opportunities to engage with Appalachian
      communities around topics related to health and environmental pollution.
FAU - Brewer, Dawn
AU  - Brewer D
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
FAU - Travis, Elizabeth
AU  - Travis E
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
FAU - Koempel, Annie
AU  - Koempel A
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506.
FAU - Pennell, Kelly
AU  - Pennell K
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20190423
PL  - England
TA  - Appl Environ Educ Commun
JT  - Applied environmental education and communication (Print)
JID - 101528525
PMC - PMC7510481
MID - NIHMS1065192
OTO - NOTNLM
OT  - community engagement
OT  - environmental pollution
OT  - nutrition
COIS- Disclosure statement The authors do not have conflicts of interests to
      report.
EDAT- 2020/09/26 06:00
MHDA- 2020/09/26 06:01
CRDT- 2020/09/25 06:00
PHST- 2020/09/25 06:00 [entrez]
PHST- 2020/09/26 06:00 [pubmed]
PHST- 2020/09/26 06:01 [medline]
AID - 10.1080/1533015X.2019.1597660 [doi]
PST - ppublish
SO  - Appl Environ Educ Commun. 2020;19(2):187-204. doi:
      10.1080/1533015X.2019.1597660. Epub 2019 Apr 23.

PMID- 32095233
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2046-2069 (Print)
IS  - 2046-2069 (Linking)
VI  - 9
IP  - 66
DP  - 2019
TI  - Reduced graphene oxide-metal nanoparticle composite membranes for
      environmental separation and chloro-organic remediation.
PG  - 38547-38557
LID - 10.1039/c9ra08178j [doi]
AB  - This study explores the integration of separation performance of rGO
      membrane with heterogeneous oxidation reactions for remediation of
      organic contaminants from water. Herein, an approach was introduced based
      on layer-by-layer assembly for functionalizing rGO membranes with
      polyacrylic acid and then by in situ synthesis of Fe based reactive
      nanoparticles. TEM characterization of the cross-section lamella of the
      membranes showed a high density of nanoparticles (12% Fe) in the
      functionalized domain, signifying the importance of polyacrylic acid for
      in situ synthesis of nanoparticles. The membranes exhibited a pure water
      permeability of 1.9 LMH bar(-1). The membranes had low to moderate salt
      retention, and more than 90% neutral red retention (organic probe
      molecule, size: 1.2 nm). The membranes also exhibited high retention of
      humic acids (80%), preventing these organics from entering the reactive
      domain, and thus potentially reducing the formation of undesired by-
      products. A persulfate mediated oxidative pathway was employed to
      demonstrate the reactive removal of organic contaminants. The membranes
      achieved >95% conversion by convectively passing 2 mM persulfate feed at
      a transmembrane pressure of 0.4 bar. Successful degradation of TCE (up to
      61%) was achieved in a single pass by convective flowing of the feed
      solution through the membrane, generating up to 80% of the theoretical
      maximum chloride as one of the byproducts. Elevated temperatures
      significantly enhanced persulfate mediated TCE oxidation extent from 24%
      at 23 oC to 54% at 40 o C under batch operating conditions.
FAU - Aher, Ashish
AU  - Aher A
AD  - Chemicals and Materials Engineering Department, University of Kentucky,
      177 FPAT Bldg, Lexington, KY, 40506, USA.
FAU - Thompson, Samuel
AU  - Thompson S
AD  - Chemicals and Materials Engineering Department, University of Kentucky,
      177 FPAT Bldg, Lexington, KY, 40506, USA.
FAU - Nickerson, Trisha
AU  - Nickerson T
AD  - Chemicals and Materials Engineering Department, University of Kentucky,
      177 FPAT Bldg, Lexington, KY, 40506, USA.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - Civil Engineering Department, University of Kentucky, Lexington, KY,
      40506, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AUID- ORCID: 0000-0001-9948-9085
AD  - Chemicals and Materials Engineering Department, University of Kentucky,
      177 FPAT Bldg, Lexington, KY, 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20191126
PL  - England
TA  - RSC Adv
JT  - RSC advances
JID - 101581657
PMC - PMC7039523
MID - NIHMS1063727
COIS- Conflicts of interest The authors declare no conflict of interest.
EDAT- 2020/02/26 06:00
MHDA- 2020/02/26 06:01
CRDT- 2020/02/26 06:00
PHST- 2020/02/26 06:00 [entrez]
PHST- 2020/02/26 06:00 [pubmed]
PHST- 2020/02/26 06:01 [medline]
AID - 10.1039/c9ra08178j [doi]
PST - ppublish
SO  - RSC Adv. 2019;9(66):38547-38557. doi: 10.1039/c9ra08178j. Epub 2019 Nov
      26.

PMID- 31494643
OWN - NLM
STAT- MEDLINE
DCOM- 20191210
LR  - 20210214
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 34
IP  - 3
DP  - 2019 Sep 25
TI  - Building science approaches for vapor intrusion studies.
PG  - 245-250
LID - 10.1515/reveh-2019-0015 [doi]
AB  - Indoor air concentrations are susceptible to temporal and spatial
      variations and have long posed a challenge to characterize for vapor
      intrusion scientists, in part, because there was a lack of evidence to
      draw conclusions about the role that building and weather conditions
      played in altering vapor intrusion exposure risks. Importantly, a large
      body of evidence is available within the building science discipline that
      provides information to support vapor intrusion scientists in drawing
      connections about fate and transport processes that influence exposure
      risks. Modeling tools developed within the building sciences provide
      evidence of reported temporal and spatial variation of indoor air
      contaminant concentrations. In addition, these modeling tools can be
      useful by calculating building air exchange rates (AERs) using building
      specific features. Combining building science models with vapor intrusion
      models, new insight to facilitate decision-making by estimating indoor
      air concentrations and building ventilation conditions under various
      conditions can be gained. This review highlights existing building
      science research and summarizes the utility of building science models to
      improve vapor intrusion exposure risk assessments.
FAU - Shirazi, Elham
AU  - Shirazi E
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506, USA.
FAU - Ojha, Sweta
AU  - Ojha S
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506, USA, Phone: +1 (859) 218-2540, Fax: +1 (859) 257-4404.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Air Pollutants)
RN  - 0 (Gases)
SB  - IM
MH  - Air Pollutants/*analysis
MH  - Air Pollution, Indoor/*analysis
MH  - Environmental Exposure/*analysis
MH  - Environmental Monitoring/*methods
MH  - Gases/*analysis
MH  - Models, Theoretical
MH  - Risk Assessment/methods
PMC - PMC6944199
MID - NIHMS1064831
OTO - NOTNLM
OT  - building science
OT  - indoor air quality
OT  - modeling
OT  - volatile organic compounds
EDAT- 2019/09/09 06:00
MHDA- 2019/12/18 06:00
CRDT- 2019/09/09 06:00
PHST- 2019/03/15 00:00 [received]
PHST- 2019/06/17 00:00 [accepted]
PHST- 2019/09/09 06:00 [entrez]
PHST- 2019/09/09 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
AID - 10.1515/reveh-2019-0015 [doi]
AID - reveh-2019-0015 [pii]
PST - ppublish
SO  - Rev Environ Health. 2019 Sep 25;34(3):245-250. doi:
      10.1515/reveh-2019-0015.

PMID- 31408434
OWN - NLM
STAT- MEDLINE
DCOM- 20191210
LR  - 20210214
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 34
IP  - 3
DP  - 2019 Sep 25
TI  - Application of metabolomics to characterize environmental pollutant
      toxicity and disease risks.
PG  - 251-259
LID - 10.1515/reveh-2019-0030 [doi]
AB  - The increased incidence of non-communicable human diseases may be
      attributed, at least partially, to exposures to toxic chemicals such as
      persistent organic pollutants (POPs), air pollutants and heavy metals.
      Given the high mortality and morbidity of pollutant exposure associated
      diseases, a better understanding of the related mechanisms of toxicity
      and impacts on the endogenous host metabolism are needed. The metabolome
      represents the collection of the intermediates and end products of
      cellular processes, and is the most proximal reporter of the body's
      response to environmental exposures and pathological processes.
      Metabolomics is a powerful tool for studying how organisms interact with
      their environment and how these interactions shape diseases related to
      pollutant exposure. This mini review discusses potential biological
      mechanisms that link pollutant exposure to metabolic disturbances and
      chronic human diseases, with a focus on recent studies that demonstrate
      the application of metabolomics as a tool to elucidate biochemical modes
      of actions of various environmental pollutants. In addition, classes of
      metabolites that have been shown to be modulated by multiple
      environmental pollutants will be discussed with an emphasis on their use
      as potential early biomarkers of disease risks. Taken together,
      metabolomics is a useful and versatile tool for characterizing the
      disease risks and mechanisms associated with various environmental
      pollutants.
FAU - Deng, Pan
AU  - Deng P
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA.
FAU - Li, Xusheng
AU  - Li X
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA.
AD  - Department of Food Science and Engineering, Institute of Food Safety and
      Nutrition, College of Science and Engineering, Jinan University,
      Guangzhou, PR China.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA.
AD  - Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, and Lexington Veterans Affairs Medical Center, Lexington, KY,
      USA.
FAU - Wang, Chunyan
AU  - Wang C
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA.
AD  - Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, and Lexington Veterans Affairs Medical Center, Lexington, KY,
      USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA.
LA  - eng
GR  - K99 ES028734/ES/NIEHS NIH HHS/United States
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - Environmental Exposure/*adverse effects
MH  - Environmental Pollutants/*toxicity
MH  - Humans
MH  - Metabolomics/*methods
MH  - Noncommunicable Diseases/*epidemiology
PMC - PMC6915040
MID - NIHMS1062296
OTO - NOTNLM
OT  - POP
OT  - disease
OT  - heavy metal
OT  - metabolomics
OT  - pollutant
OT  - toxicity
EDAT- 2019/08/14 06:00
MHDA- 2019/12/18 06:00
CRDT- 2019/08/14 06:00
PHST- 2019/04/22 00:00 [received]
PHST- 2019/07/23 00:00 [accepted]
PHST- 2019/08/14 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2019/08/14 06:00 [entrez]
AID - 10.1515/reveh-2019-0030 [doi]
AID - reveh-2019-0030 [pii]
PST - ppublish
SO  - Rev Environ Health. 2019 Sep 25;34(3):251-259. doi:
      10.1515/reveh-2019-0030.

PMID- 31430256
OWN - NLM
STAT- MEDLINE
DCOM- 20200114
LR  - 20210214
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 34
IP  - 3
DP  - 2019 Sep 25
TI  - International scientists seek solutions for environmental problems.
PG  - 225
LID - 10.1515/reveh-2019-0058 [doi]
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, KY 40536, USA.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY 40536, USA, Phone: +1
      859-218-1387.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Editorial
PT  - Introductory Journal Article
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
SB  - IM
MH  - Environment
MH  - *Environmental Health
MH  - Europe
MH  - Humans
PMC - PMC6920627
MID - NIHMS1062294
EDAT- 2019/08/21 06:00
MHDA- 2020/01/15 06:00
CRDT- 2019/08/21 06:00
PHST- 2019/08/21 06:00 [pubmed]
PHST- 2020/01/15 06:00 [medline]
PHST- 2019/08/21 06:00 [entrez]
AID - 10.1515/reveh-2019-0058 [doi]
AID - reveh-2019-0058 [pii]
PST - ppublish
SO  - Rev Environ Health. 2019 Sep 25;34(3):225. doi: 10.1515/reveh-2019-0058.

PMID- 31078726
OWN - NLM
STAT- MEDLINE
DCOM- 20190729
LR  - 20200801
IS  - 1873-6351 (Electronic)
IS  - 0278-6915 (Linking)
VI  - 130
DP  - 2019 Aug
TI  - Pseudomonas aeruginosa-derived pyocyanin reduces adipocyte
      differentiation, body weight, and fat mass as mechanisms contributing to
      septic cachexia.
PG  - 219-230
LID - S0278-6915(19)30279-0 [pii]
LID - 10.1016/j.fct.2019.05.012 [doi]
AB  - Pseudomonas aeruginosa, a leading cause of sepsis, produces pyocyanin, a
      blue-pigmented virulence factor. Sepsis is associated with cachexia, but
      mechanisms are unknown and conventional nutrition approaches are not
      effective treatments. Pyocyanin has affinity for the aryl hydrocarbon
      receptor (AhR), which is expressed on adipocytes and regulates adipocyte
      differentiation. The purpose of this study was to define in vitro and in
      vivo effects of pyocyanin on adipocyte differentiation and body weight
      regulation as relates to septic cachexia. In 3T3-L1 preadipocytes,
      pyocyanin activated AhR and its downstream marker CYP1a1, and reduced
      differentiation. Administration of pyocyanin to male C57BL/6J mice
      acutely reduced body temperature with altered locomotion, but caused
      sustained weight loss. Chronic pyocyanin administration to male and
      female C57BL/6J mice resulted in sustained reductions in body weight and
      fat mass, with adipose-specific AhR activation. Pyocyanin-treated male
      mice had decreased energy expenditure and physical activity, and
      increased adipose explant lipolysis. In females, pyocyanin caused robust
      reductions in body weight, adipose-specific AhR activation, and increased
      expression of inflammatory cytokines in differentiated adipocytes. These
      results demonstrate that pyocyanin reduces adipocyte differentiation and
      decreases body weight and fat mass in male and female mice, suggesting
      that pyocyanin may play a role in septic cachexia.
CI  - Copyright (c) 2019. Published by Elsevier Ltd.
FAU - Larian, Nika
AU  - Larian N
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, KY, USA.
FAU - Ensor, Mark
AU  - Ensor M
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, KY, USA.
FAU - Thatcher, Sean E
AU  - Thatcher SE
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, KY, USA.
FAU - English, Victoria
AU  - English V
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, KY, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Department of Internal Medicine,University of Kentucky, Lexington, KY,
      USA.
FAU - Stromberg, Arnold
AU  - Stromberg A
AD  - Department of Statistics, University of Kentucky, Lexington, KY, USA.
FAU - Cassis, Lisa A
AU  - Cassis LA
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, KY, USA. Electronic address: lcassis@uky.edu.
LA  - eng
GR  - S10 OD021753/OD/NIH HHS/United States
GR  - P30 GM127211/GM/NIGMS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20190509
PL  - England
TA  - Food Chem Toxicol
JT  - Food and chemical toxicology : an international journal published for the
      British Industrial Biological Research Association
JID - 8207483
RN  - 0 (RNA, Messenger)
RN  - 9OQM399341 (Pyocyanine)
MH  - 3T3-L1 Cells
MH  - Adipocytes/*drug effects
MH  - Adiposity/*drug effects
MH  - Animals
MH  - Body Weight/*drug effects
MH  - Cachexia
MH  - Cell Differentiation/drug effects
MH  - Female
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Pilot Projects
MH  - *Pseudomonas aeruginosa
MH  - Pyocyanine/*pharmacology
MH  - RNA, Messenger
MH  - Sepsis
PMC - PMC6557674
MID - NIHMS1031728
OTO - NOTNLM
OT  - Adipocyte
OT  - Aryl hydrocarbon receptor
OT  - Cachexia
OT  - Pseudomonas aeruginosa
OT  - Pyocyanin
OT  - Sepsis
EDAT- 2019/05/13 06:00
MHDA- 2019/07/30 06:00
CRDT- 2019/05/13 06:00
PHST- 2019/03/25 00:00 [received]
PHST- 2019/05/07 00:00 [revised]
PHST- 2019/05/08 00:00 [accepted]
PHST- 2019/05/13 06:00 [pubmed]
PHST- 2019/07/30 06:00 [medline]
PHST- 2019/05/13 06:00 [entrez]
AID - S0278-6915(19)30279-0 [pii]
AID - 10.1016/j.fct.2019.05.012 [doi]
PST - ppublish
SO  - Food Chem Toxicol. 2019 Aug;130:219-230. doi: 10.1016/j.fct.2019.05.012.
      Epub 2019 May 9.

PMID- 30807179
OWN - NLM
STAT- MEDLINE
DCOM- 20200601
LR  - 20200601
IS  - 1535-3907 (Electronic)
IS  - 1535-3893 (Linking)
VI  - 18
IP  - 4
DP  - 2019 Apr 5
TI  - Proteomic Analysis Reveals Novel Mechanisms by Which Polychlorinated
      Biphenyls Compromise the Liver Promoting Diet-Induced Steatohepatitis.
PG  - 1582-1594
LID - 10.1021/acs.jproteome.8b00886 [doi]
AB  - Environmental pollution contributes to fatty liver disease pathogenesis.
      Polychlorinated biphenyl (PCB) exposures have been associated with liver
      enzyme elevation and suspected steatohepatitis in cohort studies. Male
      mice treated with the commercial PCB mixture, Aroclor 1260 (20 mg/kg),
      and fed high fat diet (HFD) for 12 weeks developed steatohepatitis.
      Receptor-based modes of action including inhibition of the epidermal
      growth factor (EGF) receptor were previously proposed, but other
      mechanisms likely exist. Objectives were to identify and validate the
      pathways, transcription factors, and mechanisms responsible for the
      steatohepatitis associated with PCB and HFD coexposures. Comparative
      proteomics analysis was performed in archived mouse liver samples from
      the aforementioned chronic exposure study. Pathway and transcription
      factor analysis (TFA) was performed, and selected results were validated.
      Liver proteomics detected 1103 unique proteins. Aroclor 1260 upregulated
      154 and downregulated 93 of these. Aroclor 1260 + HFD coexposures
      affected 55 pathways including glutathione metabolism, intermediary
      metabolism, and cytoskeletal remodeling. TFA of Aroclor 1260 treatment
      demonstrated alterations in the function of 42 transcription factors
      including downregulation of NRF2 and key nuclear receptors previously
      demonstrated to protect against steatohepatitis (e.g., HNF4alpha, FXR,
      PPARalpha/delta/gamma, etc.). Validation studies demonstrated that
      Aroclor 1260 significantly reduced HNF4alpha protein levels, while
      Aroclor 1260 + HFD reduced expression of the HNF4alpha target gene,
      albumin, in vivo. Aroclor 1260 attenuated EGF-dependent HNF4alpha
      phosphorylation and target gene activation in vitro. Aroclor 1260 reduced
      levels of NRF2, its target genes, and glutathione in vivo. Aroclor 1260
      attenuated EGF-dependent NRF2 upregulation, in vitro. Aroclor 1260
      indirectly activated hepatic stellate cells in vitro via induction of
      hepatocyte-derived TGFbeta. PCB exposures adversely impacted
      transcription factors regulating liver protection, function, and
      fibrosis. PCBs, thus, compromised the liver by reducing its protective
      responses against nutritional stress to promote diet-induced
      steatohepatitis. The identified mechanisms by which environmental
      pollutants influence fatty liver disease pathogenesis require
      confirmation in humans.
FAU - Hardesty, Josiah E
AU  - Hardesty JE
AUID- ORCID: 0000-0003-1955-3046
FAU - Wahlang, Banrida
AU  - Wahlang B
FAU - Falkner, K Cameron
AU  - Falkner KC
FAU - Shi, Hongxue
AU  - Shi H
FAU - Jin, Jian
AU  - Jin J
FAU - Zhou, Yun
AU  - Zhou Y
FAU - Wilkey, Daniel W
AU  - Wilkey DW
FAU - Merchant, Michael L
AU  - Merchant ML
FAU - Watson, Corey T
AU  - Watson CT
FAU - Feng, Wenke
AU  - Feng W
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center , University of Kentucky , Lexington , Kentucky
      40536 , United States.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center , University of Kentucky , Lexington , Kentucky
      40536 , United States.
FAU - Prough, Russell A
AU  - Prough RA
FAU - Cave, Matthew C
AU  - Cave MC
AD  - The Robley Rex Veterans Affairs Medical Center , Louisville , Kentucky
      40206 , United States.
AD  - The Jewish Hospital Liver Transplant Program , Louisville , Kentucky
      40202 , United States.
LA  - eng
GR  - S10 OD021753/OD/NIH HHS/United States
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P20 GM113226/GM/NIGMS NIH HHS/United States
GR  - P50 AA024337/AA/NIAAA NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 ES021375/ES/NIEHS NIH HHS/United States
GR  - F31 ES028982/ES/NIEHS NIH HHS/United States
GR  - R35 ES028373/ES/NIEHS NIH HHS/United States
GR  - P42 ES023716/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20190315
PL  - United States
TA  - J Proteome Res
JT  - Journal of proteome research
JID - 101128775
RN  - 0 (Proteome)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - *Diet, High-Fat
MH  - *Liver/chemistry/drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - *Non-alcoholic Fatty Liver Disease/chemically induced/metabolism
MH  - Polychlorinated Biphenyls/*toxicity
MH  - *Proteome/analysis/drug effects/metabolism
MH  - Proteomics
PMC - PMC7059562
MID - NIHMS1064832
OTO - NOTNLM
OT  - *Aroclor 1260
OT  - *EGFR
OT  - *HNF4alpha
OT  - *TASH
OT  - *liver
OT  - *metabolism
OT  - *polychlorinated biphenyl
OT  - *steatohepatitis
EDAT- 2019/02/27 06:00
MHDA- 2020/06/02 06:00
CRDT- 2019/02/27 06:00
PHST- 2019/02/27 06:00 [pubmed]
PHST- 2020/06/02 06:00 [medline]
PHST- 2019/02/27 06:00 [entrez]
AID - 10.1021/acs.jproteome.8b00886 [doi]
PST - ppublish
SO  - J Proteome Res. 2019 Apr 5;18(4):1582-1594. doi:
      10.1021/acs.jproteome.8b00886. Epub 2019 Mar 15.

PMID- 30768972
OWN - NLM
STAT- MEDLINE
DCOM- 20191219
LR  - 20200315
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 367
DP  - 2019 Mar 15
TI  - PCB 126 induces monocyte/macrophage polarization and inflammation through
      AhR and NF-kappaB pathways.
PG  - 71-81
LID - S0041-008X(19)30055-9 [pii]
LID - 10.1016/j.taap.2019.02.006 [doi]
AB  - Polychlorinated biphenyls (PCBs) are persistent organic pollutants that
      contribute to inflammatory diseases such as atherosclerosis, and
      macrophages play a key role in the overall inflammatory response.
      Depending on specific environmental stimuli, macrophages can be polarized
      either to pro-inflammatory (e.g., M1) or anti-inflammatory (e.g., M2)
      phenotypes. We hypothesize that dioxin-like PCBs can contribute to
      macrophage polarization associated with inflammation. To test this
      hypothesis, human monocytes (THP-1) were differentiated to macrophages
      and subsequently exposed to PCB 126. Exposure to PCB 126, but not to PCB
      153 or 118, significantly induced the expression of inflammatory
      cytokines, including TNFalpha and IL-1beta, suggesting polarization to
      the pro-inflammatory M1 phenotype. Additionally, monocyte chemoattractant
      protein-1 (MCP-1) was increased in PCB 126-activated macrophages,
      suggesting induction of chemokines which regulate immune cell recruitment
      and infiltration of monocytes/macrophages into vascular tissues. In
      addition, oxidative stress sensitive markers including nuclear factor
      (erythroid-derived 2)-like 2 (NFE2L2; Nrf2) and down-stream genes, such
      as heme oxygenase 1 (HMOX1) and NAD(P)H quinone oxidoreductase 1 (NQO1),
      were induced following PCB 126 exposure. Since dioxin-like PCBs may
      elicit inflammatory cascades through multiple mechanisms, we then
      pretreated macrophages with both aryl hydrocarbon receptor (AhR) and NF-
      kappaB antagonists prior to PCB treatment. The NF-kappaB antagonist
      BMS-345541 significantly decreased mRNA and protein levels of multiple
      cytokines by approximately 50% compared to PCB treatment alone, but the
      AhR antagonist CH-223191 was protective to a lesser degree. Our data
      demonstrate the involvement of PCB 126 in macrophage polarization and
      inflammation, indicating another important role of dioxin-like PCBs in
      the pathology of atherosclerosis.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Wang, Chunyan
AU  - Wang C
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      Lexington, KY, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      Lexington, KY, USA; Cardiovascular Medicine, University of Kentucky,
      Lexington, KY, USA.
FAU - Zhu, Beibei
AU  - Zhu B
AD  - Department of Internal Medicine, Division of Endocrinology, Barnstable
      Brown Diabetes and Obesity Center, University of Kentucky, Lexington, KY,
      USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      Lexington, KY, USA; Department of Animal and Food Sciences, University of
      Kentucky, Lexington, KY, USA. Electronic address: bhennig@uky.edu.
LA  - eng
GR  - K99 ES028734/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20190213
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (AHR protein, human)
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 2B2AQE8U50 (2,3',4,4',5-pentachlorobiphenyl)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
RN  - ZRU0C9E32O (2,4,5,2',4',5'-hexachlorobiphenyl)
SB  - IM
MH  - Basic Helix-Loop-Helix Transcription Factors/*agonists/metabolism
MH  - Cell Differentiation/*drug effects
MH  - Cytokines/*metabolism
MH  - Humans
MH  - Inflammation/*chemically induced/metabolism/pathology
MH  - Inflammation Mediators/*metabolism
MH  - Macrophages/*drug effects/metabolism/pathology
MH  - NF-kappa B/*metabolism
MH  - Phenotype
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Receptors, Aryl Hydrocarbon/*agonists/metabolism
MH  - Signal Transduction/drug effects
MH  - THP-1 Cells
PMC - PMC6402591
MID - NIHMS1521951
OTO - NOTNLM
OT  - *Atherosclerosis
OT  - *Cardiovascular disease
OT  - *Dioxins
OT  - *Inflammation
OT  - *Monocyte macrophage polarization
OT  - *PCB 126
EDAT- 2019/02/16 06:00
MHDA- 2019/12/20 06:00
CRDT- 2019/02/16 06:00
PHST- 2018/09/28 00:00 [received]
PHST- 2019/01/25 00:00 [revised]
PHST- 2019/02/11 00:00 [accepted]
PHST- 2019/02/16 06:00 [pubmed]
PHST- 2019/12/20 06:00 [medline]
PHST- 2019/02/16 06:00 [entrez]
AID - S0041-008X(19)30055-9 [pii]
AID - 10.1016/j.taap.2019.02.006 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2019 Mar 15;367:71-81. doi:
      10.1016/j.taap.2019.02.006. Epub 2019 Feb 13.

PMID- 30415113
OWN - NLM
STAT- MEDLINE
DCOM- 20190204
LR  - 20200225
IS  - 1879-1298 (Electronic)
IS  - 0045-6535 (Linking)
VI  - 217
DP  - 2019 Feb
TI  - Hepatic metabolomics reveals that liver injury increases PCB 126-induced
      oxidative stress and metabolic dysfunction.
PG  - 140-149
LID - S0045-6535(18)32067-8 [pii]
LID - 10.1016/j.chemosphere.2018.10.196 [doi]
AB  - The deleterious effects of PCB 126 are complex, and the role of the liver
      in modifying toxic insult is not well understood. We utilized
      metabolomics approaches to compare liver metabolites significantly
      affected by PCB 126 in control mice and a diet induced liver injury mouse
      model. In this 14-week study, mice were fed either an amino acid
      supplemented control diet (CD) or a methionine-choline deficient diet
      (MCD) which promoted nonalcoholic steatohepatitis (NASH) and were
      subsequently exposed to PCB 126. The liver metabolome was profiled by a
      global metabolomic analysis using LC-MS. There were clear differences
      between PCB 126 exposed and control mice in the hepatic metabolomic
      profiles (216 and 266 metabolites were altered in CD-fed and MCD-fed mice
      respectively after PCB 126 exposure). PCB 126 modulated
      glycerophospholipid metabolism, glutathione metabolism, and CoA
      biosynthesis pathways irrespective of diet; indicating that the
      disturbance in lipid metabolism and thiol metabolites are general markers
      of PCB 126 exposure irrespective of liver health. Additionally,
      metabolites associated with oxidative stress and mitochondrial
      dysfunction were greatly elevated in PCB 126 exposed mice with
      compromised livers (e.g., 4-hydroxy-nonenal glutathione, oxylipids, uric
      acid, and acylcarnitines). Moreover, PCB 126 exposure downregulated redox
      genes, and the effect was more pronounced in liver injury mice. In
      conclusion, this study demonstrates that PCB 126 could induce oxidative
      stress and metabolic dysfunction, and pre-existing liver injury can
      markedly modify PCB 126-induced metabolic changes. Using metabolic
      profiling, this study suggests mechanism of enhanced PCB 126 toxicity
      under liver injury settings.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Deng, Pan
AU  - Deng P
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY 40536, USA.
FAU - Barney, Jazmyne
AU  - Barney J
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Toxicology and Cancer Biology, College of Medicine,
      University of Kentucky, Lexington, KY 40536, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Division of Cardiovascular Medicine, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Division of Cardiovascular Medicine, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA.
FAU - Wahlang, Banrida
AU  - Wahlang B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY 40536, USA;
      Superfund Research Center, University of Louisville, Louisville, KY
      40202, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY 40536, USA.
      Electronic address: bhennig@uky.edu.
LA  - eng
GR  - S10 OD021753/OD/NIH HHS/United States
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - I01 CX001550/CX/CSRD VA/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P30 GM127211/GM/NIGMS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
DEP - 20181030
PL  - England
TA  - Chemosphere
JT  - Chemosphere
JID - 0320657
RN  - AE28F7PNPL (Methionine)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Diet/adverse effects
MH  - Lipid Metabolism/drug effects
MH  - Liver/drug effects/*metabolism
MH  - Metabolomics/*methods
MH  - Methionine/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Non-alcoholic Fatty Liver Disease/chemically induced
MH  - Oxidative Stress/*drug effects
MH  - Polychlorinated Biphenyls/pharmacology/*toxicity
PMC - PMC6626632
MID - NIHMS1030191
OTO - NOTNLM
OT  - Mass spectrometry
OT  - Metabolomics
OT  - Methionine-choline deficient diet
OT  - NASH
OT  - PCB 126
OT  - ROS
EDAT- 2018/11/12 06:00
MHDA- 2019/02/05 06:00
CRDT- 2018/11/12 06:00
PHST- 2018/07/11 00:00 [received]
PHST- 2018/10/26 00:00 [revised]
PHST- 2018/10/29 00:00 [accepted]
PHST- 2018/11/12 06:00 [pubmed]
PHST- 2019/02/05 06:00 [medline]
PHST- 2018/11/12 06:00 [entrez]
AID - S0045-6535(18)32067-8 [pii]
AID - 10.1016/j.chemosphere.2018.10.196 [doi]
PST - ppublish
SO  - Chemosphere. 2019 Feb;217:140-149. doi:
      10.1016/j.chemosphere.2018.10.196. Epub 2018 Oct 30.

PMID- 30447394
OWN - NLM
STAT- MEDLINE
DCOM- 20190527
LR  - 20200225
IS  - 1095-8274 (Electronic)
IS  - 1075-9964 (Linking)
VI  - 55
DP  - 2019 Feb
TI  - Environmental pollutant-mediated disruption of gut microbial metabolism
      of the prebiotic inulin.
PG  - 96-102
LID - S1075-9964(18)30199-9 [pii]
LID - 10.1016/j.anaerobe.2018.11.008 [doi]
AB  - Exposure to environmental pollutants is associated with a greater risk
      for metabolic diseases including cardiovascular disease. Pollutant
      exposure can also alter gut microbial populations that may contribute to
      metabolic effects and progression of inflammatory diseases. Short-chain
      fatty acids (SCFAs), produced from gut fermentation of dietary
      carbohydrates, such as inulin, exert numerous effects on host energy
      metabolism and are linked to a reduced risk of diseases. The hypothesis
      was that exposure to dioxin-like pollutants modulate gut microbial
      viability and/or fermentation processes. An inulin-utilizing isolate was
      collected from murine feces, characterized and used in subsequent
      experiments. Exposure to polychlorinated biphenyl, PCB 126 impeded
      bacterial viability of the isolate at concentrations of 20 and 200muM.
      PCB 126 exposure also resulted in a significant loss of intracellular
      potassium following exposure, indicating cell membrane disruption of the
      isolate. Furthermore, total fecal microbe samples from mice were
      harvested, resuspended and incubated for 24h in anaerobic media
      containing inulin with or without PCB 126. HPLC analysis of supernatants
      revealed that PCB 126 exposure reduced succinic acid production, but
      increased propionate production, both of which can influence host glucose
      and lipid metabolism. Overall, the presented evidence supports the idea
      that pollutant exposure may contribute to alterations in host metabolism
      through gut microbiota-dependent mechanisms, specifically through
      bacterial fermentation processes or membrane disruption.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, KY, USA.
FAU - Flythe, Michael D
AU  - Flythe MD
AD  - USDA Agricultural Research Service Forage-Animal Production Research
      Unit, Lexington, KY, USA; Department of Animal and Food Sciences, College
      of Agriculture, Food and Environment, University of Kentucky, Lexington,
      KY, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA. Electronic
      address: bhennig@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20181115
PL  - England
TA  - Anaerobe
JT  - Anaerobe
JID - 9505216
RN  - 0 (Anti-Infective Agents)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Fatty Acids, Volatile)
RN  - 0 (Prebiotics)
RN  - 9005-80-5 (Inulin)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Aerobiosis
MH  - Anaerobiosis
MH  - Animals
MH  - Anti-Infective Agents/*pharmacology
MH  - Bacteria, Anaerobic/drug effects
MH  - Environmental Pollutants/*pharmacology
MH  - Fatty Acids, Volatile/metabolism
MH  - Gastrointestinal Microbiome/*drug effects
MH  - Inulin/*metabolism
MH  - Male
MH  - Metabolism/*drug effects
MH  - Mice, Inbred C57BL
MH  - Polychlorinated Biphenyls/pharmacology
MH  - *Prebiotics
PMC - PMC6481639
MID - NIHMS1526875
OTO - NOTNLM
OT  - Dioxin
OT  - Fiber
OT  - Gut microbiota
OT  - Inulin
OT  - Polychlorinated biphenyls
EDAT- 2018/11/18 06:00
MHDA- 2019/05/28 06:00
CRDT- 2018/11/18 06:00
PHST- 2018/08/14 00:00 [received]
PHST- 2018/11/12 00:00 [revised]
PHST- 2018/11/14 00:00 [accepted]
PHST- 2018/11/18 06:00 [pubmed]
PHST- 2019/05/28 06:00 [medline]
PHST- 2018/11/18 06:00 [entrez]
AID - S1075-9964(18)30199-9 [pii]
AID - 10.1016/j.anaerobe.2018.11.008 [doi]
PST - ppublish
SO  - Anaerobe. 2019 Feb;55:96-102. doi: 10.1016/j.anaerobe.2018.11.008. Epub
      2018 Nov 15.

PMID- 31452560
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 0254-0584 (Print)
IS  - 0254-0584 (Linking)
VI  - 223
DP  - 2019 Feb 1
TI  - Novel magnetic core-shell nanoparticles for the removal of
      polychlorinated biphenyls from contaminated water sources.
PG  - 68-74
LID - 10.1016/j.matchemphys.2018.10.045 [doi]
AB  - In this work, we developed novel core-shell nanoparticle systems with
      magnetic core and polymer shell via atom transfer radical polymerization
      for use as high affinity nanoadsorbents for organic contaminants in water
      and wastewater treatment. Polyphenolic-based moieties, curcumin
      multiacrylate (CMA) and quercetin multiacrylate (QMA), were incorporated
      into poly(ethylene glycol) (PEG) based polymeric shells to create high
      affinity binding sites for the capture of polychlorinated biphenyls
      (PCBs) as a model pollutant. The resulting magnetic nanoparticles (MNPs)
      were characterized by Fourier transform infrared spectroscopy (FTIR),
      thermogravimetric analysis (TGA), transmission electron microscopy (TEM),
      X-ray diffraction (XRD), dynamic light scattering (DLS), and UV-visible
      spectroscopy. The affinity of these novel materials for PCB 126 was
      evaluated and fitted to the nonlinear Langmuir model to determine binding
      affinities (KD). The KD values obtained were: PEG MNPs (8.42 nM) < IO
      MNPs (8.23nM) < QMA MNPs (5.88 nM) < CMA MNPs (2.72 nM), demonstrating
      that the presence of polyphenolic-based moieties enhanced PCB 126 binding
      affinity, which is hypothesized to be a result of pi - pi stacking
      interactions. These values are lower that KD values for activated carbon,
      providing strong evidence that these novel core-shell nanoparticles have
      a promising application as nanoadsorbents for specific organic
      contaminants offering a cost effective alternative to current remediation
      approaches.
FAU - Gutierrez, Angela M
AU  - Gutierrez AM
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40506,
      USA.
FAU - Bhandari, Rohit
AU  - Bhandari R
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40506,
      USA.
FAU - Weng, Jiaying
AU  - Weng J
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40506,
      USA.
AD  - Department of Statistics, University of Kentucky, Lexington, KY, 40506,
      USA.
FAU - Stromberg, Arnold
AU  - Stromberg A
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40506,
      USA.
AD  - Department of Statistics, University of Kentucky, Lexington, KY, 40506,
      USA.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40506,
      USA.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40506,
      USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20181022
PL  - Netherlands
TA  - Mater Chem Phys
JT  - Materials chemistry and physics
JID - 101530424
PMC - PMC6710019
MID - NIHMS1511224
OTO - NOTNLM
OT  - Core-shell nanoparticles
OT  - Environmental remediation
OT  - Iron oxide
EDAT- 2019/08/28 06:00
MHDA- 2019/08/28 06:01
CRDT- 2019/08/28 06:00
PHST- 2019/08/28 06:00 [entrez]
PHST- 2019/08/28 06:00 [pubmed]
PHST- 2019/08/28 06:01 [medline]
AID - 10.1016/j.matchemphys.2018.10.045 [doi]
PST - ppublish
SO  - Mater Chem Phys. 2019 Feb 1;223:68-74. doi:
      10.1016/j.matchemphys.2018.10.045. Epub 2018 Oct 22.

PMID- 30511719
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20190128
LR  - 20200225
IS  - 1364-5528 (Electronic)
IS  - 0003-2654 (Linking)
VI  - 144
IP  - 2
DP  - 2019 Jan 14
TI  - Fluorescence based detection of polychlorinated biphenyls (PCBs) in water
      using hydrophobic interactions.
PG  - 677-684
LID - 10.1039/c8an00867a [doi]
AB  - Despite increasing controls in their production and disposal, persistent
      organic pollutants in water, even at concentrations below parts per
      million, represent an ongoing environmental health risk. Despite this
      concern, the detection of these compounds in water sources rely upon
      expensive, time consuming approaches that do not permit frequent
      monitoring and evaluation. In this work, a new fluorescence-based
      technique is presented for the detection of polychlorinated biphenyls
      (PCBs) in water. Benzopyrene (BaP) fluorescence was shown to increase
      with trace concentrations of aromatic organic pollutants. BaP forms a
      hydrophobic complex with PCBs, which has allowed for the successful
      detection of pollutants including PCB-126, PCB-153 and PCB-118. To
      determine the selectivity and robustness of this response, the impact of
      pH, ionic strength and humic acid to mimic surface water conditions is
      explored. While suppression of the signal was seen, these factors' impact
      on the detection of PCBs was minor, suggesting that a potential sensing
      strategy can be developed through this interaction. It is seen that the
      number and location of chlorine atoms are important along with the
      geometric orientation of molecule's structure.
FAU - Ahmad, Irfan
AU  - Ahmad I
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, USA. thomas.Dziubla@uky.edu.
FAU - Weng, Jiaying
AU  - Weng J
FAU - Stromberg, A J
AU  - Stromberg AJ
FAU - Hilt, J Z
AU  - Hilt JZ
FAU - Dziubla, T D
AU  - Dziubla TD
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - England
TA  - Analyst
JT  - The Analyst
JID - 0372652
PMC - PMC6331228
MID - NIHMS1000771
EDAT- 2018/12/05 06:00
MHDA- 2018/12/05 06:01
CRDT- 2018/12/05 06:00
PHST- 2018/12/05 06:00 [pubmed]
PHST- 2018/12/05 06:01 [medline]
PHST- 2018/12/05 06:00 [entrez]
AID - 10.1039/c8an00867a [doi]
PST - ppublish
SO  - Analyst. 2019 Jan 14;144(2):677-684. doi: 10.1039/c8an00867a.

PMID- 30547452
OWN - NLM
STAT- MEDLINE
DCOM- 20190610
LR  - 20200128
IS  - 1940-6029 (Electronic)
IS  - 1064-3745 (Linking)
VI  - 1894
DP  - 2019
TI  - In Vitro Methods for Assessing Nanoparticle Toxicity.
PG  - 1-29
LID - 10.1007/978-1-4939-8916-4_1 [doi]
AB  - As a consequence of their increase in annual production and widespread
      distribution in the environment, nanoparticles potentially pose a
      significant public health risk. The sought-after catalytic activity
      granted by their physiochemical properties doubles as a hazard to
      physiological processes following exposure through inhalation, oral,
      transdermal, subcutaneous, and intravenous uptake. Upon uptake into the
      body, their size, morphology, surface charge, coating, and chemical
      composition augment the response of biological systems to the materials
      and enhance their toxicity. Identification of each property is necessary
      to predict the harm imposed by foreign nanomaterials in the body. Assay
      methods ranging from endotoxin and lactate dehydrogenase (LDH) signaling
      to apoptosis and oxidative stress detection supply valuable techniques
      for exposing biomarkers of nanoparticle-induced cellular damage.
      Spectroscopic investigation of epithelial barrier permeation and
      distribution within living cells reveals the proclivity of nanoparticles
      to penetrate the body's natural defensive boundaries and deposit
      themselves in cytotoxic locations. Combination of the various
      characterization methodologies and assays is required for every new
      nanoparticulate system despite preexisting data for similar systems due
      to the lack of deterministic trends among investigated nanoparticles. The
      propensity of nanomaterials to denature proteins and oxidize substrates
      in their local environment generates significant concern for the
      applicability of several traditional in vitro assays, and the
      modification of susceptible approaches into novel methods suitable for
      the evaluation of nanoparticles comprises the focus of future work
      centered on nanoparticle toxicity analysis.
FAU - Savage, Dustin T
AU  - Savage DT
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, USA.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, USA.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY, USA. thomas.dziubla@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Methods Mol Biol
JT  - Methods in molecular biology (Clifton, N.J.)
JID - 9214969
SB  - IM
MH  - Animals
MH  - Biological Assay/*methods
MH  - Humans
MH  - In Vitro Techniques/*methods
MH  - Nanoparticles/chemistry/*toxicity
MH  - Spectrum Analysis/methods
MH  - Toxicity Tests/*methods
PMC - PMC6984383
MID - NIHMS1063812
OTO - NOTNLM
OT  - *Biocompatibility
OT  - *In vitro assays
OT  - *Mechanisms of toxicity
OT  - *Nanomaterials
OT  - *Nanoparticle characterization
OT  - *Nanoparticle toxicity
OT  - *Nanoparticle-cell interaction
OT  - *Reactive oxygen species
EDAT- 2018/12/14 06:00
MHDA- 2019/06/14 06:00
CRDT- 2018/12/15 06:00
PHST- 2018/12/15 06:00 [entrez]
PHST- 2018/12/14 06:00 [pubmed]
PHST- 2019/06/14 06:00 [medline]
AID - 10.1007/978-1-4939-8916-4_1 [doi]
PST - ppublish
SO  - Methods Mol Biol. 2019;1894:1-29. doi: 10.1007/978-1-4939-8916-4_1.

PMID- 30373033
OWN - NLM
STAT- MEDLINE
DCOM- 20181123
LR  - 20210109
IS  - 1873-6424 (Electronic)
IS  - 0269-7491 (Linking)
VI  - 242
IP  - Pt A
DP  - 2018 Nov
TI  - Dioxin-like PCB 126 increases intestinal inflammation and disrupts gut
      microbiota and metabolic homeostasis.
PG  - 1022-1032
LID - S0269-7491(18)31950-X [pii]
LID - 10.1016/j.envpol.2018.07.039 [doi]
AB  - The gut microbiome is sensitive to diet and environmental exposures and
      is involved in the regulation of host metabolism. Additionally, gut
      inflammation is an independent risk factor for the development of
      metabolic diseases, specifically atherosclerosis and diabetes. Exposures
      to dioxin-like pollutants occur primarily via ingestion of contaminated
      foods and are linked to increased risk of developing cardiometabolic
      diseases. We aimed to elucidate the detrimental impacts of dioxin-like
      pollutant exposure on gut microbiota and host gut health and metabolism
      in a mouse model of cardiometabolic disease. We utilized 16S rRNA
      sequencing, metabolomics, and regression modeling to examine the impact
      of PCB 126 on the microbiome and host metabolism and gut health. 16S rRNA
      sequencing showed that gut microbiota populations shifted at the phylum
      and genus levels in ways that mimic observations seen in chronic
      inflammatory diseases. PCB 126 reduced cecum alpha diversity (0.60 fold
      change; p=0.001) and significantly increased the Firmicutes to
      Bacteroidetes ratio (1.63 fold change; p=0.044). Toxicant exposed mice
      exhibited quantifiable concentrations of PCB 126 in the colon,
      upregulation of Cyp1a1 gene expression, and increased markers of
      intestinal inflammation. Also, a significant correlation between
      circulating Glucagon-like peptide-1 (GLP-1) and Bifidobacterium was
      evident and dependent on toxicant exposure. PCB 126 exposure disrupted
      the gut microbiota and host metabolism and increased intestinal and
      systemic inflammation. These data imply that the deleterious effects of
      dioxin-like pollutants may be initiated in the gut, and the modulation of
      gut microbiota may be a sensitive marker of pollutant exposures.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, USA; Lexington Veterans Affairs Medical Center,
      Lexington, KY, USA; Department of Pharmacology and Nutritional Sciences,
      College of Medicine, University of Kentucky, USA.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, USA.
FAU - Vsevolozhskaya, Olga
AU  - Vsevolozhskaya O
AD  - Department of Biostatistics, College of Public Health, University of
      Kentucky, Lexington, KY, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, USA; Lexington Veterans Affairs Medical Center,
      Lexington, KY, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, USA;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, USA. Electronic
      address: bhennig@uky.edu.
LA  - eng
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 OD021753/OD/NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20180717
PL  - England
TA  - Environ Pollut
JT  - Environmental pollution (Barking, Essex : 1987)
JID - 8804476
RN  - 0 (Dioxins)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0 (RNA, Ribosomal, 16S)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Dioxins/*toxicity
MH  - Gastrointestinal Microbiome/*drug effects
MH  - Homeostasis/*drug effects
MH  - Inflammation/chemically induced
MH  - Intestines
MH  - Male
MH  - Metabolomics
MH  - Mice
MH  - Microbiota/drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Polychlorinated Dibenzodioxins
MH  - RNA, Ribosomal, 16S/genetics
MH  - Toxicity Tests
PMC - PMC6211811
MID - NIHMS986674
OTO - NOTNLM
OT  - Diabetes
OT  - Dioxin
OT  - Gut microbiota
OT  - Inflammation
OT  - PCB 126
EDAT- 2018/10/31 06:00
MHDA- 2018/11/24 06:00
CRDT- 2018/10/31 06:00
PHST- 2018/05/01 00:00 [received]
PHST- 2018/07/02 00:00 [revised]
PHST- 2018/07/10 00:00 [accepted]
PHST- 2018/10/31 06:00 [entrez]
PHST- 2018/10/31 06:00 [pubmed]
PHST- 2018/11/24 06:00 [medline]
AID - S0269-7491(18)31950-X [pii]
AID - 10.1016/j.envpol.2018.07.039 [doi]
PST - ppublish
SO  - Environ Pollut. 2018 Nov;242(Pt A):1022-1032. doi:
      10.1016/j.envpol.2018.07.039. Epub 2018 Jul 17.

PMID- 32095034
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200229
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 556
DP  - 2018 Jun 15
TI  - Cellulose-graphene quantum dot composite membranes using ionic liquid.
PG  - 293-302
LID - 10.1016/j.memsci.2018.04.009 [doi]
AB  - Selective separation of small molecules by membranes is inhibited by the
      performance gap between nanofiltration and ultrafiltration membranes. In
      this work, a membrane that can efficiently remove small molecules (> 300
      Da) was created by incorporating graphene oxide quantum dots (GQDs) into
      a cellulose membrane using an ionic liquid (1-ethyl-3-methylimidazolium
      acetate). Incorporation of GQD into cellulose membranes using an ionic
      liquid brings several advantages over traditional mixed matrix membranes:
      1) GQDs are abundant in peripheral hydroxyl and carboxyl groups, thus
      GQDs have strong binding with cellulose through hydrogen bonding and
      forms a stable composite membrane. 2) Negative surface charge of GQDs
      helps prevent aggregation. 3) The size (5 nm) of GQD is smaller than most
      nanoparticles used in membranes, allowing for interesting pore forming
      properties. GQD-cellulose membranes were prepared by non-solvent induced
      phase separation in water. It was determined that about 45% of GQDs are
      incorporated from solution to membrane. GQDs were determined to be
      located on the membrane surface, giving the membrane negative surface
      charge and improved hydrophilicity. GQDs showed no leaching after
      convective flow through the membrane. Impact of GQD on membrane
      permeability and rejection was studied through convective flow
      experiments, and through longer term permeability studies.
FAU - Colburn, A
AU  - Colburn A
AD  - Department of Chemical and Materials Engineering, 177F. Paul Anderson
      Tower, University of Kentucky, Lexington, KY 40506, USA.
FAU - Wanninayake, N
AU  - Wanninayake N
AD  - Department of Chemistry, University of Kentucky, Lexington, KY 40506,
      USA.
FAU - Kim, D Y
AU  - Kim DY
AD  - Department of Chemistry, University of Kentucky, Lexington, KY 40506,
      USA.
FAU - Bhattacharyya, D
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, 177F. Paul Anderson
      Tower, University of Kentucky, Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20180408
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC7039517
MID - NIHMS1064661
OTO - NOTNLM
OT  - Composite membrane
OT  - GQD
OT  - Permeability
OT  - Phase inversion
OT  - Zeta potential
EDAT- 2018/06/15 00:00
MHDA- 2018/06/15 00:01
CRDT- 2020/02/26 06:00
PHST- 2020/02/26 06:00 [entrez]
PHST- 2018/06/15 00:00 [pubmed]
PHST- 2018/06/15 00:01 [medline]
AID - 10.1016/j.memsci.2018.04.009 [doi]
PST - ppublish
SO  - J Memb Sci. 2018 Jun 15;556:293-302. doi: 10.1016/j.memsci.2018.04.009.
      Epub 2018 Apr 8.

PMID- 28975503
OWN - NLM
STAT- MEDLINE
DCOM- 20181015
LR  - 20210117
IS  - 2190-3948 (Electronic)
IS  - 2190-393X (Linking)
VI  - 8
IP  - 3
DP  - 2018 Jun
TI  - The environmental pollutant, polychlorinated biphenyls, and
      cardiovascular disease: a potential target for antioxidant
      nanotherapeutics.
PG  - 740-759
LID - 10.1007/s13346-017-0429-9 [doi]
AB  - Despite production having stopped in the 1970s, polychlorinated biphenyls
      (PCBs) represent persistent organic pollutants that continue to pose a
      serious human health risk. Exposure to PCBs has been linked to chronic
      inflammatory diseases, such as cardiovascular disease, type 2 diabetes,
      obesity, as well as hepatic disorders, endocrine dysfunction,
      neurological deficits, and many others. This is further complicated by
      the PCB's strong hydrophobicity, resulting in their ability to accumulate
      up the food chain and to be stored in fat deposits. This means that
      completely avoiding exposure is not possible, thus requiring the need to
      develop intervention strategies that can mitigate disease risks
      associated with exposure to PCBs. Currently, there is excitement in the
      use of nutritional compounds as a way of inhibiting the inflammation
      associated with PCBs, yet the suboptimal delivery and pharmacology of
      these compounds may not be sufficient in more acute exposures. In this
      review, we discuss the current state of knowledge of PCB toxicity and
      some of the antioxidant and anti-inflammatory nanocarrier systems that
      may be useful as an enhanced treatment modality for reducing PCB
      toxicity.
FAU - Gupta, Prachi
AU  - Gupta P
AD  - Piramal Pharma Solutions, Lexington, KY, 40511, USA.
FAU - Thompson, Brendan L
AU  - Thompson BL
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA.
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA.
FAU - Wahlang, Banrida
AU  - Wahlang B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA.
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA.
FAU - Jordan, Carolyn T
AU  - Jordan CT
AD  - Department of Chemical and Materials Engineering, College of Engineering,
      University of Kentucky, Lexington, KY, 40506, USA.
FAU - Zach Hilt, J
AU  - Zach Hilt J
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA.
AD  - Department of Chemical and Materials Engineering, College of Engineering,
      University of Kentucky, Lexington, KY, 40506, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA.
AD  - Department of Animal and Food Sciences, College of Agriculture Food and
      Environment, University of Kentucky, Lexington, KY, 40546, USA.
FAU - Dziubla, Thomas
AU  - Dziubla T
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA. dziubla@engr.uky.edu.
AD  - Department of Chemical and Materials Engineering, College of Engineering,
      University of Kentucky, Lexington, KY, 40506, USA. dziubla@engr.uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Drug Deliv Transl Res
JT  - Drug delivery and translational research
JID - 101540061
RN  - 0 (Antioxidants)
RN  - 0 (Environmental Pollutants)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Antioxidants/*therapeutic use
MH  - Cardiovascular Diseases/*prevention & control
MH  - Environmental Exposure
MH  - Environmental Pollutants/chemistry/*toxicity
MH  - Humans
MH  - Nanomedicine
MH  - Oxidative Stress
MH  - Polychlorinated Biphenyls/chemistry/*toxicity
PMC - PMC5882597
MID - NIHMS910761
OTO - NOTNLM
OT  - *Antioxidant
OT  - *Nanocarriers
OT  - *PCBs
OT  - *Toxicity
EDAT- 2017/10/05 06:00
MHDA- 2018/10/16 06:00
CRDT- 2017/10/05 06:00
PHST- 2017/10/05 06:00 [pubmed]
PHST- 2018/10/16 06:00 [medline]
PHST- 2017/10/05 06:00 [entrez]
AID - 10.1007/s13346-017-0429-9 [doi]
AID - 10.1007/s13346-017-0429-9 [pii]
PST - ppublish
SO  - Drug Deliv Transl Res. 2018 Jun;8(3):740-759. doi:
      10.1007/s13346-017-0429-9.

PMID- 30718939
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 555
DP  - 2018 Jun
TI  - Role of membrane pore polymerization conditions for pH responsive
      behavior, catalytic metal nanoparticle synthesis, and PCB degradation.
PG  - 348-361
LID - 10.1016/j.memsci.2018.03.060 [doi]
AB  - This article describes the effects of changing monomer and cross-linker
      concentrations on the mass gain, water permeability, Pd-Fe nanoparticle
      (NP) loading, and the rate of degradation of
      3,3',4,4',5-pentachlorobiphenyl (PCB 126) of pore functionalized
      polyvinylidene fluoride (PVDF) membranes. In this study, monomer (acrylic
      acid (AA)) and cross-linker (N, N'- methylene-bis (acrylamide))
      concentrations were varied from 10 to 20 wt% of polymer solution and
      0.5-2 mol% of monomer concentration, respectively. Results showed that
      responsive behavior of membrane could be tuned in terms of water
      permeability over a range of 270-1 L m(-2) h(-1) bar(-1), which is a
      function of water pH. The NP size on the membrane surface was found in
      the range of 16-23 nm. With increasing cross-linker density the
      percentage of smaller NPs (< 10 nm) increases due to smaller mesh size
      formation during in-situ polymerization of membrane. NP loading was found
      to vary from 0.21 to 0.94 mg per cm(2) of membrane area depending on the
      variation of available carboxyl groups in membrane pore domain. The NPs
      functionalized membranes were then tested for use as a platform for the
      degradation of PCB 126. The observed batch reaction rate (Kobs) for PCB
      126 degradation for per mg of catalyst loading was found 0.08-0.1 h(-1).
      Degradation study in convective flow mode shows 98.6% PCB 126 is degraded
      at a residence time of 46.2 s. The corresponding surface area normalized
      reaction rate (K sa ) is found about two times higher than K sa of batch
      degradation; suggesting elimination of the effect of diffusion resistance
      for degradation of PCB 126 in convective flow mode operation. These Pd-
      Fe-PAA-PVDF membranes and nanoparticles are characterized by TGA, contact
      angle measurement, surface zeta potential, XRD, SEM, XPS, FIB, TEM and
      other techniques reveal the details about the membrane surface, pores and
      nanoparticles size, shape and size-distribution. Statistical analysis
      based on experimental results allows us to depict responsive behavior of
      functionalized membrane. In our best knowledge this paper first time
      reports detail study on responsive behavior of pore functionalized
      membrane in terms of permeability, NPs size, metal loading and its effect
      on PCB 126 degradation in a quantified approach.
FAU - Islam, Md Saiful
AU  - Islam MS
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower Building, Lexington, KY 40506, USA.
FAU - Hernandez, Sebastian
AU  - Hernandez S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower Building, Lexington, KY 40506, USA.
FAU - Wan, Hongyi
AU  - Wan H
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower Building, Lexington, KY 40506, USA.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower Building, Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20180323
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC6358284
MID - NIHMS995062
EDAT- 2019/02/06 06:00
MHDA- 2019/02/06 06:01
CRDT- 2019/02/06 06:00
PHST- 2019/02/06 06:00 [entrez]
PHST- 2019/02/06 06:00 [pubmed]
PHST- 2019/02/06 06:01 [medline]
AID - 10.1016/j.memsci.2018.03.060 [doi]
PST - ppublish
SO  - J Memb Sci. 2018 Jun;555:348-361. doi: 10.1016/j.memsci.2018.03.060. Epub
      2018 Mar 23.

PMID- 30719335
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2073-4360 (Electronic)
IS  - 2073-4360 (Linking)
VI  - 10
IP  - 4
DP  - 2018 Apr
TI  - Multienzyme immobilized polymeric membrane reactor for transformation of
      lignin model compound.
LID - 463 [pii]
LID - 10.3390/polym10040463 [doi]
AB  - We have developed a multienzyme functionalized membrane reactor for
      bioconversion of lignin model compound involving enzymatic catalysis.
      Layer-by-layer approach was used to immobilize three different enzymes
      (glucose oxidase, peroxidase and laccase) into pH-responsive membranes.
      This novel membrane reactor couples the in situ generation of hydrogen
      peroxide (by glucose oxidase) to oxidative conversion of a lignin model
      compound, guaiacylglycerol-B-guaiacylether (GGE). Preliminary
      investigation of the efficacy of these functional membranes towards GGE
      degradation is demonstrated under convective flow mode. Over 90% of the
      initial feed could be degraded with the multienzyme immobilized membranes
      at a residence time of approximately 22 seconds. GGE conversion product
      analysis revealed formation of oligomeric oxidation products with
      peroxidase, which might be potential hazard to membrane bioreactors.
      These oxidation products could be further degraded by laccase enzymes in
      the multienzymatic membranes explaining the potential of multienzyme
      membrane reactors. The multienzyme incorporated membrane reactors were
      active for about a month time of storage at 4 degrees C, and retention of
      activity was demonstrated after repetitive use.
FAU - Sarma, Rupam
AU  - Sarma R
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Islam, Md Saiful
AU  - Islam MS
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Running, Mark P
AU  - Running MP
AD  - Department of Biology, University of Louisville, Louisville, KY 40292.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20180423
PL  - Switzerland
TA  - Polymers (Basel)
JT  - Polymers
JID - 101545357
PMC - PMC6358281
MID - NIHMS995775
OTO - NOTNLM
OT  - layer-by-layer assembly
OT  - lignin
OT  - multienzyme
OT  - polymer membrane reactor
COIS- Conflicts of Interest: There are no conflicts to declare.
EDAT- 2019/02/06 06:00
MHDA- 2019/02/06 06:01
CRDT- 2019/02/06 06:00
PHST- 2019/02/06 06:00 [entrez]
PHST- 2019/02/06 06:00 [pubmed]
PHST- 2019/02/06 06:01 [medline]
AID - 10.3390/polym10040463 [doi]
PST - ppublish
SO  - Polymers (Basel). 2018 Apr;10(4). doi: 10.3390/polym10040463. Epub 2018
      Apr 23.

PMID- 29353125
OWN - NLM
STAT- MEDLINE
DCOM- 20190828
LR  - 20190828
IS  - 1096-0953 (Electronic)
IS  - 0013-9351 (Linking)
VI  - 162
DP  - 2018 Apr
TI  - Relationship between serum trimethylamine N-oxide and exposure to dioxin-
      like pollutants.
PG  - 211-218
LID - S0013-9351(18)30009-4 [pii]
LID - 10.1016/j.envres.2018.01.007 [doi]
AB  - Trimethylamine N-oxide (TMAO) is a diet and gut microbiota-derived
      metabolite that has been linked to cardiovascular disease risk in human
      studies and animal models. TMAO levels show wide inter and intra
      individual variability in humans that can likely be accounted for by
      multiple factors including diet, the gut microbiota, levels of the TMAO
      generating liver enzyme Flavin-containing monooxygenase 3 (FMO3) and
      kidney function. We recently found that dioxin-like (DL) environmental
      pollutants increased FMO3 expression to elevate circulating diet-derived
      TMAO in mice, suggesting that exposure to this class of pollutants might
      also contribute to inter-individual variability in circulating TMAO
      levels in humans. To begin to explore this possibility we examined the
      relationship between body burden of DL pollutants (reported by serum
      lipid concentrations) and serum TMAO levels (n = 340) in the Anniston, AL
      cohort, which was highly exposed to polychlorinated biphenyls (PCBs).
      TMAO concentrations in archived serum samples from the Anniston Community
      Health Survey (ACHS-II) were measured, and associations of TMAO with 28
      indices of pollutant body burden, including total dioxins toxic
      equivalent (TEQ), were quantified. Twenty-three (22 after adjustment for
      multiple comparisons) of the 28 indices were significantly positively
      associated with TMAO. Although the design of ACHS-II does not enable
      quantitative assessment of the contributions of previously known
      determinants of TMAO variability to this relationship, limited
      multivariate modeling revealed that total dioxins TEQ was significantly
      associated with TMAO among females (except at high BMIs) but not among
      males. Our results from this cross-sectional study indicate that exposure
      to DL pollutants may contribute to elevated serum TMAO levels.
      Prospective longitudinal studies will be required to assess the joint
      relationship between DL pollutant exposures, other determinants of TMAO,
      and health outcomes.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY 40536, USA;
      Lexington Veterans Affairs Medical Center, Lexington, Kentucky, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA.
FAU - Charnigo, Richard
AU  - Charnigo R
AD  - Department of Biostatistics, College of Public Health, University of
      Kentucky, Lexington, KY, USA.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Division of Cardiovascular Medicine, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA.
FAU - Soman, Sony
AU  - Soman S
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Division of Cardiovascular Medicine, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA.
FAU - Pavuk, Marian
AU  - Pavuk M
AD  - CDC Agency for Toxic Substances and Disease Registry, Atlanta, GA, USA.
FAU - Birnbaum, Linda
AU  - Birnbaum L
AD  - NCI at NIEHS, Research Triangle Park, NC 27709, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Lexington Veterans Affairs Medical Center, Lexington, Kentucky, USA;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY 40536, USA.
      Electronic address: bhennig@uky.edu.
LA  - eng
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 HL091812/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20180130
PL  - Netherlands
TA  - Environ Res
JT  - Environmental research
JID - 0147621
RN  - 0 (Dioxins)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Methylamines)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - FLD0K1SJ1A (trimethyloxamine)
SB  - IM
MH  - Animals
MH  - Cross-Sectional Studies
MH  - *Dioxins/toxicity
MH  - *Environmental Pollutants
MH  - Female
MH  - Humans
MH  - Male
MH  - *Methylamines/blood
MH  - Mice
MH  - *Obesity, Morbid
MH  - *Polychlorinated Biphenyls/toxicity
MH  - *Polychlorinated Dibenzodioxins/toxicity
MH  - Prospective Studies
PMC - PMC5811317
MID - NIHMS935282
OTO - NOTNLM
OT  - *Anniston
OT  - *Cardiovascular disease
OT  - *Dioxin
OT  - *FMO3
OT  - *TMAO
EDAT- 2018/01/22 06:00
MHDA- 2019/08/29 06:00
CRDT- 2018/01/22 06:00
PHST- 2017/10/16 00:00 [received]
PHST- 2018/01/08 00:00 [revised]
PHST- 2018/01/09 00:00 [accepted]
PHST- 2018/01/22 06:00 [pubmed]
PHST- 2019/08/29 06:00 [medline]
PHST- 2018/01/22 06:00 [entrez]
AID - S0013-9351(18)30009-4 [pii]
AID - 10.1016/j.envres.2018.01.007 [doi]
PST - ppublish
SO  - Environ Res. 2018 Apr;162:211-218. doi: 10.1016/j.envres.2018.01.007.
      Epub 2018 Jan 30.

PMID- 30718940
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 57
IP  - 12
DP  - 2018 Mar 28
TI  - Synthesis of Catalytic Nanoporous Metallic Thin Films on Polymer
      Membranes.
PG  - 4420-4429
LID - 10.1021/acs.iecr.8b00053 [doi]
AB  - Composite membranes were produced with a metallic thin film forming the
      upper layer of the composite on a porous polymer support. Commercially
      available membranes were used as supports with both micron and nanometer
      scale pores. Alloy films of ~110 nm thickness were deposited via
      magnetron sputtering to produce the top layer of the composite.
      Dealloying the film with sulfuric acid allowed the creation of a
      nanoporous film structure with a ligament size of 7.7 +/- 2.5 nm.
      Resulting composite membranes were permeable to water at all stages of
      production, and a UF PSf membrane with 90 nm of nanoporous Fe/Pd on top
      showed a flux of 183 LHM/bar. The films were evaluated for dechlorination
      of toxic polychlorinated biphenyls from water. At a loading of 6.6 mg/L
      of Pd attached to 13.2 cm(2) support in a 2.5 ppm PCB-1 solution with 1.5
      ppm dissolved H2, over 90% of PCB-1 was removed from solution in 30
      minutes, which produced the expected product biphenyl from the
      dechlorination reaction.
FAU - Detisch, Michael J
AU  - Detisch MJ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Balk, T John
AU  - Balk TJ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20180305
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC6358282
MID - NIHMS995061
OTO - NOTNLM
OT  - composite membranes
OT  - dealloying
OT  - dechlorination
OT  - nanoporous metals
EDAT- 2019/02/06 06:00
MHDA- 2019/02/06 06:01
CRDT- 2019/02/06 06:00
PHST- 2019/02/06 06:00 [entrez]
PHST- 2019/02/06 06:00 [pubmed]
PHST- 2019/02/06 06:01 [medline]
AID - 10.1021/acs.iecr.8b00053 [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2018 Mar 28;57(12):4420-4429. doi:
      10.1021/acs.iecr.8b00053. Epub 2018 Mar 5.

PMID- 29146079
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20180309
LR  - 20210109
IS  - 1879-1026 (Electronic)
IS  - 0048-9697 (Linking)
VI  - 616-617
DP  - 2018 Mar
TI  - Occurrence of chlorinated volatile organic compounds (VOCs) in a sanitary
      sewer system: Implications for assessing vapor intrusion alternative
      pathways.
PG  - 1149-1162
LID - S0048-9697(17)32923-6 [pii]
LID - 10.1016/j.scitotenv.2017.10.205 [doi]
AB  - Sewer systems have been recently recognized as potentially important
      exposure pathways to consider during vapor intrusion assessments;
      however, this pathway has not been well-characterized and there is need
      for additional information about the occurrence of volatile organic
      compounds (VOCs) in sewer systems. This paper reports the results of
      sewer gas sampling conducted in a sanitary sewer over the years of
      2014-2017. Sewer gas samples were collected and analyzed using several
      different techniques, including TO-15 (grab), TO-17 (passive),
      Radiello(R) (passive) and a novel continuous monitoring technique, the
      Autonomous Rugged Optical Multigas Analyzer (AROMA). The applicability of
      each of the different approaches used in this study is discussed in the
      context of investigating sanitary sewers as a vapor intrusion alternative
      pathway. The data confirmed that trichloroethylene (TCE) concentrations
      in sewer gas were detected adjacent to and extending hundreds of feet
      away from a previously defined vapor intrusion area, where TCE was a
      primary contaminant. TCE concentrations detected in sewer gas ranged from
      non-detect to 1600mug/m(3). Temporal variability was observed in TCE
      concentrations over timescales that ranged from minutes to months to
      years at discrete sampling locations. Spatial variability in sewer gas
      concentrations was also observed throughout the study area. Temporal and
      spatial variability may be caused by groundwater contamination sources in
      the study area, as well as sewer gas transport mechanisms.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Roghani, Mohammadyousef
AU  - Roghani M
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, United States.
FAU - Jacobs, Olivia P
AU  - Jacobs OP
AD  - Clearwater Group, 229 Tewksbury Avenue, Point Richmond, CA 94801, United
      States.
FAU - Miller, Anthony
AU  - Miller A
AD  - Entanglement Technologies, 42 Adrian Court, Burlingame, CA 94010, United
      States.
FAU - Willett, Evan J
AU  - Willett EJ
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, United States.
FAU - Jacobs, James A
AU  - Jacobs JA
AD  - Clearwater Group, 229 Tewksbury Avenue, Point Richmond, CA 94801, United
      States.
FAU - Viteri, C Ricardo
AU  - Viteri CR
AD  - Entanglement Technologies, 42 Adrian Court, Burlingame, CA 94010, United
      States.
FAU - Shirazi, Elham
AU  - Shirazi E
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, United States.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, United States. Electronic address: kellypennell@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R44 ES022538/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20171114
PL  - Netherlands
TA  - Sci Total Environ
JT  - The Science of the total environment
JID - 0330500
PMC - PMC5752621
MID - NIHMS920112
OTO - NOTNLM
OT  - Sampling methods
OT  - Sewer systems
OT  - Trichloroethylene
OT  - Vapor intrusion
EDAT- 2017/11/18 06:00
MHDA- 2017/11/18 06:01
CRDT- 2017/11/18 06:00
PHST- 2017/08/02 00:00 [received]
PHST- 2017/09/26 00:00 [revised]
PHST- 2017/10/20 00:00 [accepted]
PHST- 2017/11/18 06:00 [pubmed]
PHST- 2017/11/18 06:01 [medline]
PHST- 2017/11/18 06:00 [entrez]
AID - S0048-9697(17)32923-6 [pii]
AID - 10.1016/j.scitotenv.2017.10.205 [doi]
PST - ppublish
SO  - Sci Total Environ. 2018 Mar;616-617:1149-1162. doi:
      10.1016/j.scitotenv.2017.10.205. Epub 2017 Nov 14.

PMID- 29324453
OWN - NLM
STAT- MEDLINE
DCOM- 20181126
LR  - 20201215
IS  - 1423-0003 (Electronic)
IS  - 0304-324X (Linking)
VI  - 64
IP  - 3
DP  - 2018
TI  - Developmental Origins of Health Span and Life Span: A Mini-Review.
PG  - 237-245
LID - 10.1159/000485506 [doi]
AB  - BACKGROUND: A vast body of research has demonstrated that disease
      susceptibility and offspring health can be influenced by perinatal
      factors, which include both paternal and maternal behavior and
      environment. Offspring disease risk has the potential to affect the
      health span and life span of offspring. KEY FINDINGS: Various maternal
      factors, such as environmental toxicant exposure, diet, stress, exercise,
      age at conception, and longevity have the potential to influence age-
      associated diseases such as cardiovascular disease, obesity, diabetes,
      and cancer risk in offspring. Paternal factors such as diet, age at
      conception, and longevity can potentially impact offspring health span
      and life span-reducing traits as well. PRACTICAL IMPLICATIONS: Continued
      research could go a long way toward defining mechanisms of the
      developmental origins of life span and health span, and eventually
      establishing regimens to avoid negative developmental influences and to
      encourage positive interventions to potentially increase life span and
      improve health span in offspring.
CI  - (c) 2018 S. Karger AG, Basel.
FAU - Preston, Joshua D
AU  - Preston JD
AD  - Pharmacology and Nutritional Sciences, University of Kentucky College of
      Medicine, Lexington, KY, USA.
FAU - Reynolds, Leryn J
AU  - Reynolds LJ
FAU - Pearson, Kevin J
AU  - Pearson KJ
LA  - eng
GR  - P30 ES026529/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DK090460/DK/NIDDK NIH HHS/United States
GR  - R03 CA165086/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20180112
PL  - Switzerland
TA  - Gerontology
JT  - Gerontology
JID - 7601655
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/etiology
MH  - Developmental Biology
MH  - Diabetes Mellitus, Type 2/etiology
MH  - Diet/adverse effects
MH  - Disease Susceptibility
MH  - Epigenesis, Genetic
MH  - Exercise
MH  - Female
MH  - Humans
MH  - Infant, Newborn
MH  - Longevity/genetics/*physiology
MH  - Male
MH  - Obesity/etiology
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects
MH  - Seasons
MH  - Telomere Shortening
PMC - PMC5876086
MID - NIHMS922686
OTO - NOTNLM
OT  - *Aging
OT  - *Developmental origins of health and disease
OT  - *Developmental programming
OT  - *Disease
OT  - *Epigenetics
OT  - *Exercise
OT  - *Longevity
OT  - *Pregnancy
EDAT- 2018/01/13 06:00
MHDA- 2018/11/27 06:00
CRDT- 2018/01/12 06:00
PHST- 2017/06/30 00:00 [received]
PHST- 2017/11/21 00:00 [accepted]
PHST- 2018/01/13 06:00 [pubmed]
PHST- 2018/11/27 06:00 [medline]
PHST- 2018/01/12 06:00 [entrez]
AID - 000485506 [pii]
AID - 10.1159/000485506 [doi]
PST - ppublish
SO  - Gerontology. 2018;64(3):237-245. doi: 10.1159/000485506. Epub 2018 Jan
      12.

PMID- 29302630
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2470-1343 (Print)
IS  - 2470-1343 (Linking)
VI  - 2
IP  - 12
DP  - 2017 Dec 31
TI  - Synthesis and Characterization of Thermoresponsive Hydrogels Based on
      N-Isopropylacrylamide Crosslinked with 4,4'-Dihydroxybiphenyl Diacrylate.
PG  - 8723-8729
LID - 10.1021/acsomega.7b01247 [doi]
AB  - A novel crosslinker [4,4'-dihydroxybiphenyl diacrylate (44BDA)] was
      developed, and a series of temperature-responsive hydrogels were
      synthesized through free radical polymerization of N-isopropylacrylamide
      (NIPAAm) with 44BDA. The temperature-responsive behavior of the resulting
      gels was characterized by swelling studies, and the lower critical
      solution temperature (LCST) of the hydrogels was characterized through
      differential scanning calorimetry. Increased content of 44BDA led to a
      decreased swelling ratio and shifted the LCST to lower temperatures.
      These novel hydrogels also displayed resiliency through multiple
      swelling-deswelling cycles, and their temperature responsiveness was
      reversible. The successful synthesis of NIPAAm-based hydrogels
      crosslinked with 44BDA has led to a new class of temperature-responsive
      hydrogel systems with a variety of potential applications.
FAU - Tang, Shuo
AU  - Tang S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, Kentucky 40536, United States.
FAU - Floy, Martha
AU  - Floy M
AD  - Department of Chemical Engineering, Kansas State University, 1005 Durland
      Hall 1701A Platt Street, Manhattan, Kansas 66506, United States.
FAU - Bhandari, Rohit
AU  - Bhandari R
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, Kentucky 40536, United States.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Division of Cardiovascular Medicine, The Gill Heart Institute, University
      of Kentucky, 741 S. Limestone Street, Lexington, Kentucky 40506, United
      States.
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, Kentucky 40536, United States.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Division of Cardiovascular Medicine, The Gill Heart Institute, University
      of Kentucky, 741 S. Limestone Street, Lexington, Kentucky 40506, United
      States.
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, Kentucky 40536, United States.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, Kentucky 40536, United States.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, Kentucky 40536, United States.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20171207
PL  - United States
TA  - ACS Omega
JT  - ACS omega
JID - 101691658
PMC - PMC5748278
COIS- The authors declare no competing financial interest.
EDAT- 2018/01/06 06:00
MHDA- 2018/01/06 06:01
CRDT- 2018/01/06 06:00
PHST- 2017/08/24 00:00 [received]
PHST- 2017/11/21 00:00 [accepted]
PHST- 2018/01/06 06:00 [entrez]
PHST- 2018/01/06 06:00 [pubmed]
PHST- 2018/01/06 06:01 [medline]
AID - 10.1021/acsomega.7b01247 [doi]
PST - ppublish
SO  - ACS Omega. 2017 Dec 31;2(12):8723-8729. doi: 10.1021/acsomega.7b01247.
      Epub 2017 Dec 7.

PMID- 29210407
OWN - NLM
STAT- MEDLINE
DCOM- 20180426
LR  - 20181213
IS  - 2050-7895 (Electronic)
IS  - 2050-7887 (Linking)
VI  - 19
IP  - 12
DP  - 2017 Dec 13
TI  - Three-dimensional vapor intrusion modeling approach that combines wind
      and stack effects on indoor, atmospheric, and subsurface domains.
PG  - 1594-1607
LID - 10.1039/c7em00423k [doi]
AB  - Vapor intrusion (IV) exposure risks are difficult to characterize due to
      the role of atmospheric, building and subsurface processes. This study
      presents a three-dimensional VI model that extends the common subsurface
      fate and transport equations to incorporate wind and stack effects on
      indoor air pressure, building air exchange rate (AER) and indoor
      contaminant concentration to improve VI exposure risk estimates. The
      model incorporates three modeling programs: (1) COMSOL Multiphysics to
      model subsurface fate and transport processes, (2) CFD0 to model
      atmospheric air flow around the building, and (3) CONTAM to model indoor
      air quality. The combined VI model predicts AER values, zonal indoor air
      pressures and zonal indoor air contaminant concentrations as a function
      of wind speed, wind direction and outdoor and indoor temperature. Steady
      state modeling results for a single-story building with a basement
      demonstrate that wind speed, wind direction and opening locations in a
      building play important roles in changing the AER, indoor air pressure,
      and indoor air contaminant concentration. Calculated indoor air pressures
      ranged from approximately -10 Pa to +4 Pa depending on weather conditions
      and building characteristics. AER values, mass entry rates and indoor air
      concentrations vary depending on weather conditions and building
      characteristics. The presented modeling approach can be used to
      investigate the relationship between building features, AER, building
      pressures, soil gas concentrations, indoor air concentrations and VI
      exposure risks.
FAU - Shirazi, Elham
AU  - Shirazi E
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, USA. kellypennell@uky.edu.
FAU - Pennell, Kelly G
AU  - Pennell KG
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - England
TA  - Environ Sci Process Impacts
JT  - Environmental science. Processes & impacts
JID - 101601576
RN  - 0 (Air Pollutants)
RN  - 0 (Gases)
RN  - 0 (Soil)
RN  - 0 (Volatile Organic Compounds)
SB  - IM
MH  - Air Pollutants/*analysis
MH  - Air Pollution, Indoor/*analysis
MH  - Air Pressure
MH  - Gases/analysis
MH  - Housing
MH  - *Models, Theoretical
MH  - Soil/chemistry
MH  - Volatile Organic Compounds/*analysis
MH  - *Wind
PMC - PMC5755378
MID - NIHMS925178
EDAT- 2017/12/07 06:00
MHDA- 2018/04/27 06:00
CRDT- 2017/12/07 06:00
PHST- 2017/12/07 06:00 [pubmed]
PHST- 2018/04/27 06:00 [medline]
PHST- 2017/12/07 06:00 [entrez]
AID - 10.1039/c7em00423k [doi]
PST - ppublish
SO  - Environ Sci Process Impacts. 2017 Dec 13;19(12):1594-1607. doi:
      10.1039/c7em00423k.

PMID- 29391943
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2046-2069 (Print)
IS  - 2046-2069 (Linking)
VI  - 7
IP  - 88
DP  - 2017
TI  - Layer-by-layer Assembled Membranes with Immobilized Porins.
PG  - 56123-56136
LID - 10.1039/c7ra08737c [doi]
AB  - With the synthesis and functionalization of membranes for selective
      separations, reactivity, and stimuli responsive behavior arises new and
      advanced opportunities. The integration of bio-based channels is one of
      these advancements in membrane technologies. By a layer-by-layer (LbL)
      assembly of polyelectrolytes, outer membrane protein F trimers (OmpF) or
      "porins" from Escherichia coli with a central pore of ~2 nm diameter at
      its opening and ~0.7 x 1.1 nm at its constricted region are immobilized
      within the pores of poly(vinylidene fluoride) microfiltration membranes,
      as opposed to traditional ruptured lipid bilayer or vesicles processes.
      These OmpF-membranes demonstrate selective rejections of non-charged
      organics over ionic solutes, allowing the passage of salts up to 2 times
      higher than traditional nanofiltration membranes starting with rejections
      of 84% for 0.4-1.0 kDa organics. The presence of charged groups in OmpF
      membranes also leads to pH-dependent salt rejection through Donnan
      exclusion. These OmpF-membranes also show exceptional durability and
      stability, delivering consistent and constant permeability and recovery
      for over 160 h of operation. Characterization of solutions containing
      OmpF, and membranes were conducted during each stage of the process,
      including detection by fluorescence labelling (FITC), zeta potential, pH
      responsiveness, flux changes, and rejections of organic-inorganic
      solutions.
FAU - Hernandez, Sebastian
AU  - Hernandez S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY.
FAU - Porter, Cassandra
AU  - Porter C
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY.
FAU - Zhang, Xinyi
AU  - Zhang X
AD  - Department of Chemistry, University of Kentucky, Lexington, KY.
FAU - Wei, Yinan
AU  - Wei Y
AD  - Department of Chemistry, University of Kentucky, Lexington, KY.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20171213
PL  - England
TA  - RSC Adv
JT  - RSC advances
JID - 101581657
PMC - PMC5788187
MID - NIHMS936568
OTO - NOTNLM
OT  - Layer-by-layer membranes
OT  - OmpF immobilization
OT  - functional polymer
OT  - selective separation
EDAT- 2018/02/03 06:00
MHDA- 2018/02/03 06:01
CRDT- 2018/02/03 06:00
PHST- 2018/02/03 06:00 [entrez]
PHST- 2018/02/03 06:00 [pubmed]
PHST- 2018/02/03 06:01 [medline]
AID - 10.1039/c7ra08737c [doi]
PST - ppublish
SO  - RSC Adv. 2017;7(88):56123-56136. doi: 10.1039/c7ra08737c. Epub 2017 Dec
      13.

PMID- 29398952
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1385-8947 (Print)
IS  - 1385-8947 (Linking)
VI  - 327
DP  - 2017 Nov 1
TI  - Naphthenic acids removal from high TDS produced water by persulfate
      mediated iron oxide functionalized catalytic membrane, and by
      nanofiltration.
PG  - 573-583
LID - 10.1016/j.cej.2017.06.128 [doi]
AB  - Oil industries generate large amounts of produced water containing
      organic contaminants, such as naphthenic acids (NA) and very high
      concentrations of inorganic salts. Recovery of potable water from
      produced water can be highly energy intensive is some cases due to its
      high salt concentration, and safe discharge is more suitable. Here, we
      explored catalytic properties of iron oxide (FexOy nanoparticles)
      functionalized membranes in oxidizing NA from water containing high
      concentrations of total dissolved solids (TDS) using persulfate as an
      oxidizing agent. Catalytic decomposition of persulfate by FexOy
      functionalized membranes followed pseudo-first order kinetics with an
      apparent activation energy of 18 Kcal/mol. FexOy functionalized membranes
      were capable of lowering the NA concentrations to less than discharge
      limits of 10 ppm at 40 degrees C. Oxidation state of iron during reaction
      was quantified. Membrane performance was investigated for extended period
      of time. A coupled process of advanced oxidation catalyzed by membrane
      and nanofiltration was also evaluated. Commercially available
      nanofiltration membranes were found capable of retaining NA from water
      containing high concentrations of dissolved salts. Commercial NF
      membranes, Dow NF270 (Dow), and NF8 (Nanostone) had NA rejection of 79%
      and 82%, respectively. Retentate for the nanofiltration was further
      treated with advanced oxidation catalyzed by FexOy functionalized
      membrane for removal of NA.
FAU - Aher, Ashish
AU  - Aher A
AD  - Dept. of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Papp, Joseph
AU  - Papp J
AD  - Dept. of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Colburn, Andrew
AU  - Colburn A
AD  - Dept. of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Wan, Hongyi
AU  - Wan H
AD  - Dept. of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Hatakeyama, Evan
AU  - Hatakeyama E
AD  - Chevron Corporation, Richmond, CA.
FAU - Prakash, Prakhar
AU  - Prakash P
AD  - Chevron Corporation, Richmond, CA.
FAU - Weaver, Ben
AU  - Weaver B
AD  - Nanostone Corporation, Oceanside, CA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Dept. of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20170624
PL  - Switzerland
TA  - Chem Eng J
JT  - Chemical engineering journal (Lausanne, Switzerland : 1996)
JID - 9892118
PMC - PMC5791545
MID - NIHMS936579
OTO - NOTNLM
OT  - advanced oxidation
OT  - degradation
OT  - nanoparticles
OT  - oil industry
OT  - persulfate
OT  - separation
EDAT- 2018/02/06 06:00
MHDA- 2018/02/06 06:01
CRDT- 2018/02/06 06:00
PHST- 2018/02/06 06:00 [entrez]
PHST- 2018/02/06 06:00 [pubmed]
PHST- 2018/02/06 06:01 [medline]
AID - 10.1016/j.cej.2017.06.128 [doi]
PST - ppublish
SO  - Chem Eng J. 2017 Nov 1;327:573-583. doi: 10.1016/j.cej.2017.06.128. Epub
      2017 Jun 24.

PMID- 29805968
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2310-2861 (Print)
IS  - 2310-2861 (Linking)
VI  - 3
IP  - 4
DP  - 2017
TI  - Development of Novel N-isopropylacrylamide (NIPAAm) Based Hydrogels with
      Varying Content of Chrysin Multiacrylate.
LID - 40 [pii]
LID - 10.3390/gels3040040 [doi]
AB  - A series of novel temperature responsive hydrogels were synthesized by
      free radical polymerization with varying content of chrysin multiacrylate
      (ChryMA). The goal was to study the impact of this novel polyphenolic-
      based multiacrylate on the properties of N-isopropylacrylamide (NIPAAm)
      hydrogels. The temperature responsive behavior of the copolymerized gels
      was characterized by swelling studies, and their lower critical solution
      temperature (LCST) was characterized through differential scanning
      calorimetry (DSC). It was shown that the incorporation of ChryMA
      decreased the swelling ratios of the hydrogels and shifted their LCSTs to
      a lower temperature. Gels with different ChryMA content showed different
      levels of response to temperature change. Higher content gels had a
      broader phase transition and smaller temperature response, which could be
      attributed to the increased hydrophobicity being introduced by the
      ChryMA.
FAU - Tang, Shuo
AU  - Tang S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40506,
      USA.
FAU - Floy, Martha
AU  - Floy M
AD  - Department of Chemical Engineering, Kansas State University, Manhattan,
      KS 66506, USA.
FAU - Bhandari, Rohit
AU  - Bhandari R
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40506,
      USA.
FAU - Dziubla, Thomas
AU  - Dziubla T
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40506,
      USA.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40506,
      USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20171022
PL  - Switzerland
TA  - Gels
JT  - Gels (Basel, Switzerland)
JID - 101696925
PMC - PMC5967267
MID - NIHMS935870
OTO - NOTNLM
OT  - LCST
OT  - N-isopropylacrylamide
OT  - hydrogel
COIS- Conflicts of Interest: The authors declare no conflict of interest.
EDAT- 2017/01/01 00:00
MHDA- 2017/01/01 00:01
CRDT- 2018/05/29 06:00
PHST- 2018/05/29 06:00 [entrez]
PHST- 2017/01/01 00:00 [pubmed]
PHST- 2017/01/01 00:01 [medline]
AID - 10.3390/gels3040040 [doi]
PST - ppublish
SO  - Gels. 2017;3(4). doi: 10.3390/gels3040040. Epub 2017 Oct 22.

PMID- 28915320
OWN - NLM
STAT- MEDLINE
DCOM- 20180511
LR  - 20200306
IS  - 2040-4603 (Electronic)
IS  - 2040-4603 (Linking)
VI  - 7
IP  - 4
DP  - 2017 Sep 12
TI  - Adipose Tissue as a Site of Toxin Accumulation.
PG  - 1085-1135
LID - 10.1002/cphy.c160038 [doi]
AB  - We examine the role of adipose tissue, typically considered an energy
      storage site, as a potential site of toxicant accumulation. Although the
      production of most persistent organic pollutants (POPs) was banned years
      ago, these toxicants persist in the environment due to their resistance
      to biodegradation and widespread distribution in various environmental
      forms (e.g., vapor, sediment, and water). As a result, human exposure to
      these toxicants is inevitable. Largely due to their lipophilicity, POPs
      bioaccumulate in adipose tissue, resulting in greater body burdens of
      these environmental toxicants with obesity. POPs of major concern include
      polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and
      furans (PCDDs/PCDFs), and polybrominated biphenyls and diphenyl ethers
      (PBBs/PBDEs), among other organic compounds. In this review, we (i)
      highlight the physical characteristics of toxicants that enable them to
      partition into and remain stored in adipose tissue, (ii) discuss the
      specific mechanisms of action by which these toxicants act to influence
      adipocyte function, and (iii) review associations between POP exposures
      and the development of obesity and diabetes. An area of controversy
      relates to the relative potential beneficial versus hazardous health
      effects of toxicant sequestration in adipose tissue. (c) 2017 American
      Physiological Society. Compr Physiol 7:1085-1135, 2017.
CI  - Copyright (c) 2017 John Wiley & Sons, Inc.
FAU - Jackson, Erin
AU  - Jackson E
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, Kentucky, USA.
FAU - Shoemaker, Robin
AU  - Shoemaker R
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, Kentucky, USA.
FAU - Larian, Nika
AU  - Larian N
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, Kentucky, USA.
FAU - Cassis, Lisa
AU  - Cassis L
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, Kentucky, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
PT  - Research Support, N.I.H., Extramural
DEP - 20170912
PL  - United States
TA  - Compr Physiol
JT  - Comprehensive Physiology
JID - 101574442
RN  - 0 (Dioxins and Dioxin-like Compounds)
RN  - 0 (Environmental Pollutants)
SB  - IM
EIN - Compr Physiol. 2018 Jun 18;8(3):1251. PMID: 29978893
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Diabetes Mellitus/*etiology
MH  - Dioxins and Dioxin-like Compounds/chemistry/pharmacokinetics/*toxicity
MH  - Environmental Pollutants/chemistry/pharmacokinetics/*toxicity
MH  - Humans
MH  - Obesity/*etiology
PMC - PMC6101675
MID - NIHMS966074
EDAT- 2017/09/16 06:00
MHDA- 2018/05/12 06:00
CRDT- 2017/09/16 06:00
PHST- 2017/09/16 06:00 [entrez]
PHST- 2017/09/16 06:00 [pubmed]
PHST- 2018/05/12 06:00 [medline]
AID - 10.1002/cphy.c160038 [doi]
PST - epublish
SO  - Compr Physiol. 2017 Sep 12;7(4):1085-1135. doi: 10.1002/cphy.c160038.

PMID- 29176912
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 0022-0140 (Print)
IS  - 0022-0140 (Linking)
VI  - 55
IP  - 4
DP  - 2017 Aug
TI  - Older Adults' Perceptions of Nutrition as Protective Against Detrimental
      Effects of Environmental Pollution.
LID - 4RIB7 [pii]
AB  - The aging process makes older adults vulnerable to the detrimental health
      effects of environmental contaminants. Our study assessed older adults'
      perceptions regarding diet being protective against environmental
      contaminants, their levels of concern about exposure, and their interest
      in learning about protective food-related strategies. A needs assessment
      to collect such information has not been conducted among older adults.
      Health fair survey results showed that they perceived diet as beneficial
      against contaminants, were concerned about health implications of
      exposure, and were interested in learning how to protect health through
      diet-related strategies. Results suggest that a nutrition-focused
      curriculum addressing how dietary strategies can help protect against
      environmental contaminants is needed for Extension professionals.
FAU - Dunn, Kristina
AU  - Dunn K
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
FAU - Gaetke, Lisa
AU  - Gaetke L
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
FAU - Stephenson, Tammy
AU  - Stephenson T
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
FAU - Brewer, Dawn
AU  - Brewer D
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, KY 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - J Ext
JT  - Journal of extension
JID - 101649636
PMC - PMC5697776
MID - NIHMS895001
OTO - NOTNLM
OT  - environmental contaminants
OT  - fruits and vegetables
OT  - nutrition
OT  - older adults
EDAT- 2017/11/28 06:00
MHDA- 2017/11/28 06:01
CRDT- 2017/11/28 06:00
PHST- 2017/11/28 06:00 [entrez]
PHST- 2017/11/28 06:00 [pubmed]
PHST- 2017/11/28 06:01 [medline]
PST - ppublish
SO  - J Ext. 2017 Aug;55(4).

PMID- 28661687
OWN - NLM
STAT- MEDLINE
DCOM- 20170915
LR  - 20190102
IS  - 1520-6025 (Electronic)
IS  - 0163-3864 (Linking)
VI  - 80
IP  - 7
DP  - 2017 Jul 28
TI  - Curcumin Acrylation for Biological and Environmental Applications.
PG  - 1964-1971
LID - 10.1021/acs.jnatprod.6b00951 [doi]
AB  - Curcumin has recently gained interest for use in drug delivery, chemical
      sensing, and environmental applications. As a result, the development of
      synthesis strategies for the incorporation of curcumin into novel
      materials has become a priority. One such strategy, curcumin acrylation,
      involves the introduction of acrylate functional groups to the curcumin
      scaffold, with the potential generation of mono-, di-, and triacrylate
      curcumin species. The relative populations of these species in the
      resulting multiacrylate mixture can be controlled by the ratio of
      curcumin to acryloyl chloride in the initial reaction formulation.
      Characterization of the acrylation reaction and the resulting curcumin
      multiacrylate product is essential for the effective preparation of new
      curcumin-containing materials. In this work, a synthesis method for
      curcumin acrylation is presented and the resulting curcumin multiacrylate
      product is characterized via various techniques, i.e., HPLC, LCMS, and
      NMR, as a basis to establish the relationship between synthesis
      conditions and the extent of acrylation that is achieved.
FAU - Patil, Vinod S
AU  - Patil VS
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , Lexington, Kentucky 40506, United States.
FAU - Gutierrez, Angela M
AU  - Gutierrez AM
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , Lexington, Kentucky 40506, United States.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Division of Cardiovascular Medicine, Gill Heart Institute, University of
      Kentucky , Lexington, Kentucky 40536, United States.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Division of Cardiovascular Medicine, Gill Heart Institute, University of
      Kentucky , Lexington, Kentucky 40536, United States.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , Lexington, Kentucky 40506, United States.
FAU - Kalika, Douglass S
AU  - Kalika DS
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , Lexington, Kentucky 40506, United States.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AUID- ORCID: 0000-0003-2518-3926
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , Lexington, Kentucky 40506, United States.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 OD021753/OD/NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, N.I.H., Extramural
DEP - 20170629
PL  - United States
TA  - J Nat Prod
JT  - Journal of natural products
JID - 7906882
RN  - 0 (Acrylates)
RN  - 8K23O56TG5 (acryloyl chloride)
RN  - IT942ZTH98 (Curcumin)
RN  - J94PBK7X8S (acrylic acid)
SB  - IM
MH  - Acrylates/metabolism
MH  - Chromatography, High Pressure Liquid
MH  - Curcumin/*chemistry/metabolism
MH  - Drug Delivery Systems/methods
MH  - Molecular Structure
MH  - Nuclear Magnetic Resonance, Biomolecular
PMC - PMC5796414
MID - NIHMS935869
EDAT- 2017/07/01 06:00
MHDA- 2017/09/16 06:00
CRDT- 2017/06/30 06:00
PHST- 2017/07/01 06:00 [pubmed]
PHST- 2017/09/16 06:00 [medline]
PHST- 2017/06/30 06:00 [entrez]
AID - 10.1021/acs.jnatprod.6b00951 [doi]
PST - ppublish
SO  - J Nat Prod. 2017 Jul 28;80(7):1964-1971. doi:
      10.1021/acs.jnatprod.6b00951. Epub 2017 Jun 29.

PMID- 29398778
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 0887-624X (Print)
IS  - 0887-624X (Linking)
VI  - 55
IP  - 12
DP  - 2017 Jun 15
TI  - Degradation of poly(beta-amino ester) gels in alcohols through
      transesterification: A method to conjugate drugs to polymer matrices.
PG  - 2019-2026
LID - 10.1002/pola.28579 [doi]
AB  - Poly(beta amino ester) polymers have received growing attention in the
      literature, owing to their ease of synthesis, versatile co-monomer
      selection, and highly tunable degradation kinetics. As such, they have
      shown extensive potential in many biomedical applications as well. In
      this work, it is demonstrated for the first time that PbetaAE polymers
      containing primary and secondary amine groups can undergo degradation by
      primary alcohols via transesterification mechanism. While this work
      emphasizes an important aspect of solvent compatibility of these
      networks, it also represents an interesting, simple mechanism for post
      synthesis drug incorporation, with riboflavin conjugation being
      demonstrated as a model compound.
FAU - Gupta, Prachi
AU  - Gupta P
AD  - Chemical and Materials Engineering, University of Kentucky, Lexington,
      KY, 40506.
FAU - Lacerda, Caroline
AU  - Lacerda C
AD  - Chemical and Materials Engineering, University of Kentucky, Lexington,
      KY, 40506.
FAU - Patil, Vinod
AU  - Patil V
AD  - Chemical and Materials Engineering, University of Kentucky, Lexington,
      KY, 40506.
FAU - Biswal, Dipti
AU  - Biswal D
AD  - Virginia State University, Petersburg, VA, 23806.
FAU - Wattamwar, Paritosh
AU  - Wattamwar P
AD  - Chemical and Materials Engineering, University of Kentucky, Lexington,
      KY, 40506.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Chemical and Materials Engineering, University of Kentucky, Lexington,
      KY, 40506.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AD  - Chemical and Materials Engineering, University of Kentucky, Lexington,
      KY, 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20170325
PL  - United States
TA  - J Polym Sci A Polym Chem
JT  - Journal of polymer science. Part A, Polymer chemistry
JID - 9004358
PMC - PMC5796417
MID - NIHMS936226
OTO - NOTNLM
OT  - Biomaterials
OT  - Drug Delivery
OT  - Gels
OT  - Polymer Drug Conjugate
EDAT- 2018/02/06 06:00
MHDA- 2018/02/06 06:01
CRDT- 2018/02/06 06:00
PHST- 2018/02/06 06:00 [entrez]
PHST- 2018/02/06 06:00 [pubmed]
PHST- 2018/02/06 06:01 [medline]
AID - 10.1002/pola.28579 [doi]
PST - ppublish
SO  - J Polym Sci A Polym Chem. 2017 Jun 15;55(12):2019-2026. doi:
      10.1002/pola.28579. Epub 2017 Mar 25.

PMID- 28574588
OWN - NLM
STAT- MEDLINE
DCOM- 20170802
LR  - 20181113
IS  - 1749-6632 (Electronic)
IS  - 0077-8923 (Linking)
VI  - 1398
IP  - 1
DP  - 2017 Jun
TI  - Protective influence of healthful nutrition on mechanisms of
      environmental pollutant toxicity and disease risks.
PG  - 99-107
LID - 10.1111/nyas.13365 [doi]
AB  - Human exposures to environmental contaminants around the world contribute
      to the global burden of disease and thus require urgent attention.
      Exploring preventive measures against environmental exposure and disease
      risk is essential. While a sedentary lifestyle and/or poor dietary habits
      can exacerbate the deleterious effects resulting from exposure to toxic
      chemicals, much emerging evidence suggests that positive lifestyle
      changes (e.g., healthful nutrition) can modulate and/or reduce the
      toxicity of environmental pollutants. Our work has shown that diets high
      in anti-inflammatory bioactive food components (e.g., phytochemicals or
      polyphenols) are possible strategies for modulating and reducing the
      disease risks associated with exposure to toxic pollutants in the
      environment. Thus, consuming healthy diets rich in plant-derived
      bioactive nutrients may reduce the vulnerability to diseases linked to
      environmental toxic insults. This nutritional paradigm in environmental
      toxicology requires further study in order to improve our understanding
      of the relationships between nutrition and other lifestyle modifications
      and toxicant-induced diseases.
CI  - (c) 2017 New York Academy of Sciences.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
AD  - Superfund Research Center, University of Kentucky, Lexington, Kentucky.
AD  - Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, Kentucky.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, Kentucky.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, Kentucky.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20170602
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - *Diet
MH  - *Diet Therapy
MH  - Disease Susceptibility
MH  - Environmental Exposure/adverse effects
MH  - Environmental Pollutants/adverse effects
MH  - *Food
MH  - Humans
MH  - Life Style
MH  - *Nutritional Status
MH  - Risk Factors
PMC - PMC5503778
MID - NIHMS868785
OTO - NOTNLM
OT  - *anti-inflammatory nutrients
OT  - *antioxidants
OT  - *environmental pollutants
OT  - *nutrition
EDAT- 2017/06/03 06:00
MHDA- 2017/08/03 06:00
CRDT- 2017/06/03 06:00
PHST- 2017/02/28 00:00 [received]
PHST- 2017/03/29 00:00 [revised]
PHST- 2017/04/06 00:00 [accepted]
PHST- 2017/06/03 06:00 [pubmed]
PHST- 2017/08/03 06:00 [medline]
PHST- 2017/06/03 06:00 [entrez]
AID - 10.1111/nyas.13365 [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2017 Jun;1398(1):99-107. doi: 10.1111/nyas.13365. Epub
      2017 Jun 2.

PMID- 29398774
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 530
DP  - 2017 May 15
TI  - Pore Functionalized PVDF Membranes with In-Situ Synthesized Metal
      Nanoparticles: Material Characterization, and Toxic Organic Degradation.
PG  - 147-157
LID - 10.1016/j.memsci.2017.02.021 [doi]
AB  - Functionalized PVDF membrane platforms were developed for environmentally
      benign in-situ nanostructured Fe/Pd synthesis and remediation of
      chlorinated organic compounds. To prevent leaching and aggregation,
      nanoparticle catalysts were integrated into membrane domains
      functionalized with poly (acrylic acid). Nanoparticles of 16-19 nm were
      observed inside the membrane pores by using focused ion beam (FIB). This
      technique prevents mechanical deformation of the membrane, compared to
      the normal SEM preparation methods, thus providing a clean, smooth
      surface for nanoparticles characterization. This allowed quantification
      of nanoparticle properties (size and distribution) versus depth
      underneath the membrane surface (0-20 microm). The results showed that
      nanoparticles were uniformly sized and evenly distributed inside the
      membrane pores. However, the size of nanoparticles inside the membrane
      pores was 13.9% smaller than those nanoparticles located on the membrane
      surface. Investigating nanoparticles inside membrane pores increases the
      accuracy of kinetic analysis and modeling aspects. Furthermore, the Fe/Pd
      immobilized membranes showed excellent performance in the degradation of
      chlorinated organics: Over 96% degradation of
      3,3',4,4',5-pentachlorobiphenyl (PCB 126) was achieved in less than 15 s
      residence time in convective flow mode. The regeneration and reuse of
      this catalytic membrane system were also studied. Particles were examined
      in XRD upon formation, after deliberate oxidation, and after
      regeneration. The regenerated sample showed the same crystalline pattern
      as the original sample. Repeated degradation experiments demonstrated
      successful PCB 126 dechlorination with nanoparticles regenerated for four
      cycles with only a small loss in reactivity. It demonstrated that Fe/Pd
      immobilized membranes have the potential for large-scale remediation
      applications.
FAU - Wan, Hongyi
AU  - Wan H
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Briot, Nicolas J
AU  - Briot NJ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Saad, Anthony
AU  - Saad A
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - Department of Civil Engineering, University of Kentucky, Lexington,
      Kentucky 40506-0046.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC5793928
MID - NIHMS936588
OTO - NOTNLM
OT  - *Catalysis
OT  - *FIB
OT  - *Fe and Pd
OT  - *PCB Dechlorination
OT  - *Water Remediation
EDAT- 2018/02/06 06:00
MHDA- 2018/02/06 06:01
CRDT- 2018/02/06 06:00
PHST- 2018/02/06 06:00 [entrez]
PHST- 2018/02/06 06:00 [pubmed]
PHST- 2018/02/06 06:01 [medline]
AID - 10.1016/j.memsci.2017.02.021 [doi]
PST - ppublish
SO  - J Memb Sci. 2017 May 15;530:147-157. doi: 10.1016/j.memsci.2017.02.021.

PMID- 28397501
OWN - NLM
STAT- MEDLINE
DCOM- 20190109
LR  - 20190118
IS  - 1944-8252 (Electronic)
IS  - 1944-8244 (Linking)
VI  - 9
IP  - 17
DP  - 2017 May 3
TI  - Layer-by-Layer-Assembled Laccase Enzyme on Stimuli-Responsive Membranes
      for Chloro-Organics Degradation.
PG  - 14858-14867
LID - 10.1021/acsami.7b01999 [doi]
AB  - Functionalized membranes provide versatile platforms for the
      incorporation of biocatalysts and nanostructured materials for efficient
      and benign environmental remediation. The existing techniques for
      remediating chloro-organics in water consist of both physical and
      chemical means mostly using metal oxide-based catalysts, despite
      associated environmental concerns. To offer bioinspired remediation as an
      alternative, we herein demonstrate a layer-by-layer approach to
      immobilize laccase enzyme onto pH-responsive functionalized membranes for
      the degradation of chloro-organics in water. The efficacy of these
      bioinspired membranes toward dechlorination of 2,4,6-trichlorophenol
      (TCP) is demonstrated under a pressure-driven continuous flow mode
      (convective flow) for the first time to the best of our knowledge. Over
      80% of the initial TCP was degraded at an optimum flow rate under an
      applied air pressure of about 0.7 bar or lower. This corresponds to
      degradation of a substantial amount of the initial substrate in only 36 s
      residence time, whereas it takes hours for degradation in a batch
      reaction. This, in fact, demonstrates an energy efficient flow-through
      system with potentially large-scale applications. Comparison of the
      stability of the enzyme in the solution phase versus immobilized on the
      membrane phase showed a loss of some 65% of enzyme activity in the
      solution phase after 22 d, whereas the membrane-bound enzyme lost only a
      negligible percentage of the activity in a comparable time span. Finally,
      the membrane was exposed to rigorous cycles of TCP degradation trials to
      study its reusability. The primary results reveal a loss of only 14% of
      the initial activity after 4 cycles of use in a period of 25 d,
      demonstrating its potential to be reused. Regeneration of the
      functionalized membrane was also validated by dislodging the immobilized
      enzyme, followed by immobilization of fresh enzyme onto the membrane.
FAU - Sarma, Rupam
AU  - Sarma R
AUID- ORCID: http://orcid.org/0000-0003-3539-5949
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , 177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
FAU - Islam, Md Saiful
AU  - Islam MS
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , 177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
FAU - Miller, Anne-Frances
AU  - Miller AF
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , 177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AUID- ORCID: http://orcid.org/0000-0001-9948-9085
AD  - Department of Chemical and Materials Engineering, University of Kentucky
      , 177 F. Paul Anderson Tower, Lexington, Kentucky 40506, United States.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20170421
PL  - United States
TA  - ACS Appl Mater Interfaces
JT  - ACS applied materials & interfaces
JID - 101504991
RN  - 0 (Chlorophenols)
RN  - 0 (Enzymes, Immobilized)
RN  - EC 1.10.3.2 (Laccase)
SB  - IM
MH  - Chlorophenols
MH  - Enzyme Stability
MH  - Enzymes, Immobilized
MH  - Laccase/*metabolism
MH  - Membranes
PMC - PMC5787852
MID - NIHMS936573
OTO - NOTNLM
OT  - catalysis
OT  - enzyme immobilization
OT  - functionalized membrane
OT  - laccase
OT  - layer-by-layer assembly
OT  - trichlorophenol
EDAT- 2017/04/12 06:00
MHDA- 2019/01/10 06:00
CRDT- 2017/04/12 06:00
PHST- 2017/04/12 06:00 [pubmed]
PHST- 2019/01/10 06:00 [medline]
PHST- 2017/04/12 06:00 [entrez]
AID - 10.1021/acsami.7b01999 [doi]
PST - ppublish
SO  - ACS Appl Mater Interfaces. 2017 May 3;9(17):14858-14867. doi:
      10.1021/acsami.7b01999. Epub 2017 Apr 21.

PMID- 31130736
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 0008-6223 (Print)
IS  - 0008-6223 (Linking)
VI  - 116
DP  - 2017 May
TI  - Synthesis of graphene oxide membranes and their behavior in water and
      isopropanol.
PG  - 145-153
LID - 10.1016/j.carbon.2017.01.086 [doi]
AB  - Graphene oxide (GO) membrane has been synthesized on commercial
      polysulfone ultrafiltration membranes (Pore size: 17 nm) using the drop
      casting method followed by baking at 90 C for 24 h. Baking resulted in
      the reduction of GO and removal of bulk water intercalated in the GO
      sheets. Deposited GO film showed high stability under shear stress
      variation. This work shows that water adsorption on the GO membrane
      determines its permeation performance. Despite the higher viscosity of
      isopropyl alcohol (IPA), its permeability was 7 times higher than water
      through the baked ("dry") GO membranes, which were never contacted with
      water. However, IPA permeability of GO membranes dropped to 44% (of
      deionized water) when contacted with water ("hydrated" or "wet" GO
      membranes). Extensive size exclusion (rejection) studies with various dye
      and dendrimer molecules showed pore size reduced from 3.3 nm in the "dry"
      state to 1.3 nm in the "wet" state of GO membranes. FT-IR
      characterization of GO membrane suggested adsorption of water on the
      nanochannels of the active layer. Also, significant decay in flux was
      observed for water (82% of its initial flux) as compared to IPA (38% of
      its initial flux) for initially dry GO membranes.
FAU - Aher, Ashish
AU  - Aher A
AD  - Dept. Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Cai, Yuguang
AU  - Cai Y
AD  - Dept. Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Majumder, Mainak
AU  - Majumder M
AD  - Nanoscale Science and Engineering Laboratory (NSEL), Dept of Mechanical
      Engineering and Aerospace Engineering, Monash University, Clayton, VIC
      3800, Australia.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Dept. Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20170130
PL  - United States
TA  - Carbon N Y
JT  - Carbon
JID - 101204394
PMC - PMC6532981
MID - NIHMS997165
EDAT- 2017/05/01 00:00
MHDA- 2017/05/01 00:01
CRDT- 2019/05/28 06:00
PHST- 2019/05/28 06:00 [entrez]
PHST- 2017/05/01 00:00 [pubmed]
PHST- 2017/05/01 00:01 [medline]
AID - 10.1016/j.carbon.2017.01.086 [doi]
PST - ppublish
SO  - Carbon N Y. 2017 May;116:145-153. doi: 10.1016/j.carbon.2017.01.086. Epub
      2017 Jan 30.

PMID- 28163111
OWN - NLM
STAT- MEDLINE
DCOM- 20170512
LR  - 20181113
IS  - 1879-3185 (Electronic)
IS  - 0300-483X (Linking)
VI  - 380
DP  - 2017 Apr 1
TI  - A compromised liver alters polychlorinated biphenyl-mediated toxicity.
PG  - 11-22
LID - S0300-483X(17)30038-0 [pii]
LID - 10.1016/j.tox.2017.02.001 [doi]
AB  - Exposure to environmental toxicants namely polychlorinated biphenyls
      (PCBs) is correlated with multiple health disorders including liver and
      cardiovascular diseases. The liver is important for both xenobiotic and
      endobiotic metabolism. However, the responses of an injured liver to
      subsequent environmental insults has not been investigated. The current
      study aims to evaluate the role of a compromised liver in PCB-induced
      toxicity and define the implications on overall body homeostasis. Male
      C57Bl/6 mice were fed either an amino acid control diet (CD) or a
      methionine-choline deficient diet (MCD) during the 12-week study. Mice
      were subsequently exposed to either PCB126 (4.9mg/kg) or the PCB mixture,
      Arcolor1260 (20mg/kg) and analyzed for inflammatory, calorimetry and
      metabolic parameters. Consistent with the literature, MCD diet-fed mice
      demonstrated steatosis, indicative of a compromised liver. Mice fed the
      MCD-diet and subsequently exposed to PCB126 showed observable wasting
      syndrome leading to mortality. PCB126 and Aroclor1260 exposure worsened
      hepatic fibrosis exhibited by the MCD groups. Interestingly, PCB126 but
      not Aroclor1260 induced steatosis and inflammation in CD-fed mice. Mice
      with liver injury and subsequently exposed to PCBs also manifested
      metabolic disturbances due to alterations in hepatic gene expression.
      Furthermore, PCB exposure in MCD-fed mice led to extra-hepatic toxicity
      such as upregulated circulating inflammatory biomarkers, implicating
      endothelial cell dysfunction. Taken together, these results indicate that
      environmental pollution can exacerbate toxicity caused by diet-induced
      liver injury which may be partially due to dysfunctional energy
      homeostasis. This is relevant to PCB-exposed human cohorts who suffer
      from alcohol or diet-induced fatty liver diseases.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Wahlang, Banrida
AU  - Wahlang B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY, 40536, USA.
FAU - Perkins, Jordan T
AU  - Perkins JT
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY, 40536, USA.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA; Graduate Center for Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, KY 40536, USA.
FAU - Stromberg, Arnold J
AU  - Stromberg AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA; Department of Statistics, College of Arts and Sciences, University
      of Kentucky, Lexington, KY, 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY, 40536, USA;
      Graduate Center for Nutritional Sciences, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA. Electronic address:
      bhennig@uky.edu.
LA  - eng
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20170202
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Adipokines)
RN  - 0 (Aroclors)
RN  - 0 (Biomarkers)
RN  - 0 (Blood Glucose)
RN  - 11096-82-5 (aroclor 1260)
RN  - AE28F7PNPL (Methionine)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - N91BDP6H0X (Choline)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Adipokines/blood
MH  - Animals
MH  - Aroclors/toxicity
MH  - Biomarkers/blood
MH  - Blood Glucose/metabolism
MH  - Cardiovascular Diseases/blood/chemically induced/pathology
MH  - Choline/administration & dosage
MH  - Diet
MH  - Disease Models, Animal
MH  - Energy Metabolism
MH  - Fatty Liver/blood/chemically induced/*physiopathology
MH  - Gene Expression
MH  - Homeostasis/drug effects
MH  - Inflammation/blood/chemically induced
MH  - Liver/*drug effects/physiopathology
MH  - Liver Cirrhosis/blood/chemically induced/*physiopathology
MH  - Male
MH  - Methionine/administration & dosage/deficiency
MH  - Mice, Inbred C57BL
MH  - Polychlorinated Biphenyls/*toxicity
PMC - PMC5374277
MID - NIHMS853433
OTO - NOTNLM
OT  - *Aroclor1260
OT  - *Liver
OT  - *MCD
OT  - *PCB126
OT  - *Steatohepatitis
OT  - *Toxicity
EDAT- 2017/02/07 06:00
MHDA- 2017/05/13 06:00
CRDT- 2017/02/07 06:00
PHST- 2016/08/24 00:00 [received]
PHST- 2017/01/10 00:00 [revised]
PHST- 2017/02/01 00:00 [accepted]
PHST- 2017/02/07 06:00 [pubmed]
PHST- 2017/05/13 06:00 [medline]
PHST- 2017/02/07 06:00 [entrez]
AID - S0300-483X(17)30038-0 [pii]
AID - 10.1016/j.tox.2017.02.001 [doi]
PST - ppublish
SO  - Toxicology. 2017 Apr 1;380:11-22. doi: 10.1016/j.tox.2017.02.001. Epub
      2017 Feb 2.

PMID- 27837600
OWN - NLM
STAT- MEDLINE
DCOM- 20170628
LR  - 20181113
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - Air exchange rates and alternative vapor entry pathways to inform vapor
      intrusion exposure risk assessments.
PG  - 27-33
LID - 10.1515/reveh-2016-0039 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2016-0039/reveh-2016-0039.xml [pii]
AB  - Vapor intrusion (VI) is a term used to describe indoor air (IA)
      contamination that occurs due to the migration of chemical vapors in the
      soil and groundwater. The overall vapor transport process depends on
      several factors such as contaminant source characteristics, subsurface
      conditions, building characteristics, and general site conditions.
      However, the classic VI conceptual model does not adequately account for
      the physics of airflow around and inside a building and does not account
      for chemical emissions from alternative "preferential" pathways (e.g.
      sewers and other utility connections) into IA spaces. This mini-review
      provides information about recent research related to building air
      exchange rates (AERs) and alternative pathways to improve the accuracy of
      VI exposure risk assessment practices. First, results from a recently
      published AER study for residential homes across the United States (US)
      are presented and compared to AERs recommended by the US Environmental
      Protection Agency (USEPA). The comparison shows considerable differences
      in AERs when season, location, building age, and other factors are
      considered. These differences could directly impact VI assessments by
      influencing IA concentration measurements. Second, a conceptual model for
      sewer gas entry into buildings is presented and a summary of published
      field studies is reported. The results of the field studies suggest that
      alternative pathways for vapors to enter indoor spaces warrant
      consideration. Ultimately, the information presented in this mini-review
      can be incorporated into a multiple-lines-of-evidence approach for
      assessing site-specific VI exposure risks.
FAU - Reichman, Rivka
AU  - Reichman R
FAU - Roghani, Mohammadyousef
AU  - Roghani M
FAU - Willett, Evan J
AU  - Willett EJ
FAU - Shirazi, Elham
AU  - Shirazi E
FAU - Pennell, Kelly G
AU  - Pennell KG
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
SB  - IM
MH  - Air Pollution, Indoor/*analysis
MH  - Environmental Monitoring/*methods
MH  - Risk Assessment/*methods
MH  - United States
PMC - PMC5789807
MID - NIHMS935748
EDAT- 2016/11/13 06:00
MHDA- 2017/06/29 06:00
CRDT- 2016/11/13 06:00
PHST- 2016/08/04 00:00 [received]
PHST- 2016/09/22 00:00 [accepted]
PHST- 2016/11/13 06:00 [pubmed]
PHST- 2017/06/29 06:00 [medline]
PHST- 2016/11/13 06:00 [entrez]
AID - 10.1515/reveh-2016-0039 [doi]
AID - /j/reveh.ahead-of-print/reveh-2016-0039/reveh-2016-0039.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):27-33. doi:
      10.1515/reveh-2016-0039.

PMID- 27837601
OWN - NLM
STAT- MEDLINE
DCOM- 20170628
LR  - 20181113
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - Emerging roles of xenobiotic detoxification enzymes in metabolic
      diseases.
PG  - 105-110
LID - 10.1515/reveh-2016-0050 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2016-0050/reveh-2016-0050.xml [pii]
AB  - Mammalian systems have developed extensive molecular mechanisms to
      protect against the toxicity of many exogenous xenobiotic compounds.
      Interestingly, many detoxification enzymes, including cytochrome P450s
      and flavin-containing monooxygenases, and their associated
      transcriptional activators [e.g. the aryl hydrocarbon receptor (AhR)],
      have now been shown to have endogenous roles in normal physiology and the
      pathology of metabolic diseases. This mini-review will focus on two such
      instances: the role of flavin-containing monooxygenase 3 (FMO3) in the
      formation of the cardiometabolic disease biomarker trimethylamine-N-oxide
      (TMAO) and the role of AhR as a sensor of endogenous ligands such as
      those generated by the gut microbiota. Understanding the roles of
      xenobiotic sensing pathways in endogenous metabolism will undoubtedly
      lead to a better understanding of how exposure to environmental
      pollutants can perturb these physiological processes.
FAU - Petriello, Michael C
AU  - Petriello MC
FAU - Hoffman, Jessie B
AU  - Hoffman JB
FAU - Morris, Andrew J
AU  - Morris AJ
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (AHR protein, human)
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (Ligands)
RN  - 0 (Methylamines)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - EC 1.13.- (Oxygenases)
RN  - EC 1.14.13.8 (dimethylaniline monooxygenase (N-oxide forming))
RN  - FLD0K1SJ1A (trimethyloxamine)
SB  - IM
MH  - Basic Helix-Loop-Helix Transcription Factors/*metabolism
MH  - Gastrointestinal Microbiome
MH  - Humans
MH  - Ligands
MH  - Metabolic Diseases/chemically induced/metabolism
MH  - Methylamines/*metabolism
MH  - Oxygenases/*metabolism
MH  - Receptors, Aryl Hydrocarbon/*metabolism
PMC - PMC5604474
MID - NIHMS868837
EDAT- 2016/11/13 06:00
MHDA- 2017/06/29 06:00
CRDT- 2016/11/13 06:00
PHST- 2016/09/15 00:00 [received]
PHST- 2016/09/30 00:00 [accepted]
PHST- 2016/11/13 06:00 [pubmed]
PHST- 2017/06/29 06:00 [medline]
PHST- 2016/11/13 06:00 [entrez]
AID - 10.1515/reveh-2016-0050 [doi]
AID - /j/reveh.ahead-of-print/reveh-2016-0050/reveh-2016-0050.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):105-110. doi:
      10.1515/reveh-2016-0050.

PMID- 28076319
OWN - NLM
STAT- MEDLINE
DCOM- 20170628
LR  - 20181113
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - Impact of nutrition on pollutant toxicity: an update with new insights
      into epigenetic regulation.
PG  - 65-72
LID - 10.1515/reveh-2016-0041 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2016-0041/reveh-2016-0041.xml [pii]
AB  - Exposure to environmental pollutants is a global health problem and is
      associated with the development of many chronic diseases, including
      cardiovascular disease, diabetes and metabolic syndrome. There is a
      growing body of evidence that nutrition can both positively and
      negatively modulate the toxic effects of pollutant exposure. Diets high
      in proinflammatory fats, such as linoleic acid, can exacerbate pollutant
      toxicity, whereas diets rich in bioactive and anti-inflammatory food
      components, including omega-3 fatty acids and polyphenols, can attenuate
      toxicant-associated inflammation. Previously, researchers have elucidated
      direct mechanisms of nutritional modulation, including alteration of
      nuclear factor kappa-light-chain-enhancer of activated B cells (NF-
      kappaB) signaling, but recently, increased focus has been given to the
      ways in which nutrition and pollutants affect epigenetics. Nutrition has
      been demonstrated to modulate epigenetic markers that have been linked
      either to increased disease risks or to protection against diseases.
      Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been
      observed to alter prenatal epigenetic tags that may increase the risk of
      offspring developing disease later in life. Conversely, bioactive food
      components, including curcumin, have been shown to alter epigenetic
      markers that suppress the activation of NF-kappaB, thus reducing
      inflammatory responses. Exposure to pollutants also alters epigenetic
      markers and may contribute to inflammation and disease. It has been
      demonstrated that pollutants, via epigenetic modulations, can increase
      the activation of NF-kappaB and upregulate microRNAs associated with
      inflammation, cardiac injury and oxidative damage. Importantly, recent
      evidence suggests that nutritional components, including epigallocatechin
      gallate (EGCG), can protect against pollutant-induced inflammation
      through epigenetic regulation of proinflammatory target genes of NF-
      kappaB. Further research is needed to better understand how nutrition can
      modulate pollutant toxicity through epigenetic regulation. Therefore, the
      objective of this review is to elucidate the current evidence linking
      epigenetic changes to pollutant-induced diseases and how this regulation
      may be modulated by nutrients allowing for the development of future
      personalized lifestyle interventions.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
FAU - Petriello, Michael C
AU  - Petriello MC
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - *Diet
MH  - Environmental Pollutants/*toxicity
MH  - *Epigenesis, Genetic
MH  - Humans
MH  - *Nutritional Status
PMC - PMC5489226
MID - NIHMS868839
EDAT- 2017/01/12 06:00
MHDA- 2017/06/29 06:00
CRDT- 2017/01/12 06:00
PHST- 2016/08/09 00:00 [received]
PHST- 2016/11/09 00:00 [accepted]
PHST- 2017/01/12 06:00 [pubmed]
PHST- 2017/06/29 06:00 [medline]
PHST- 2017/01/12 06:00 [entrez]
AID - 10.1515/reveh-2016-0041 [doi]
AID - /j/reveh.ahead-of-print/reveh-2016-0041/reveh-2016-0041.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):65-72. doi:
      10.1515/reveh-2016-0041.

PMID- 28118146
OWN - NLM
STAT- MEDLINE
DCOM- 20170628
LR  - 20181113
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - An open-sourced statistical application for identifying complex
      toxicological interactions of environmental pollutants.
PG  - 23-26
LID - 10.1515/reveh-2016-0044 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2016-0044/reveh-2016-0044.xml [pii]
AB  - The rising number of chemicals that humans are exposed to on a daily
      basis, as well as advances in biomonitoring and detection technologies
      have highlighted the diversity of individual exposure profiles (complex
      body burdens). To address this, the toxicological sciences have begun to
      shift away from examining toxic agents or stressors individually to
      focusing on more complex models with multiple agents or stressors
      present. Literature on interactions between chemicals is fairly limited
      in comparison with dose-response studies on individual toxicants, which
      is largely due to experimental and statistical challenges. Experimental
      designs capable of identifying these complex interactions are often
      avoided or not evaluated to their fullest potential because of the
      difficulty associated with appropriate analysis as well as logistical
      factors. To assist with statistical analysis of these types of
      experiments, an online, open-sourced statistical application was created
      for investigators to use to analyze and interpret potential toxicant
      interactions in laboratory experimental data using a full-factorial
      three-way analysis of variance (ANOVA). This model utilizes backward
      selection on interaction terms to model main effects and interactions.
FAU - Perkins, Jordan T
AU  - Perkins JT
FAU - Petriello, Michael C
AU  - Petriello MC
FAU - Xu, Li
AU  - Xu L
FAU - Stromberg, Arnold
AU  - Stromberg A
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Environmental Pollutants)
RN  - 0 (Hazardous Substances)
SB  - IM
MH  - Data Interpretation, Statistical
MH  - Environmental Monitoring/*methods
MH  - Environmental Pollutants/analysis/*toxicity
MH  - Hazardous Substances/analysis/*toxicity
MH  - Humans
MH  - Models, Theoretical
PMC - PMC5489228
MID - NIHMS868865
EDAT- 2017/01/25 06:00
MHDA- 2017/06/29 06:00
CRDT- 2017/01/25 06:00
PHST- 2016/08/15 00:00 [received]
PHST- 2016/09/23 00:00 [accepted]
PHST- 2017/01/25 06:00 [pubmed]
PHST- 2017/06/29 06:00 [medline]
PHST- 2017/01/25 06:00 [entrez]
AID - 10.1515/reveh-2016-0044 [doi]
AID - /j/reveh.ahead-of-print/reveh-2016-0044/reveh-2016-0044.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):23-26. doi:
      10.1515/reveh-2016-0044.

PMID- 28222040
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20181211
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - Environmental challenges in Central and Eastern Europe.
PG  - 1
LID - 10.1515/reveh-2017-0004 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2017-0004/reveh-2017-0004.xml [pii]
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
PT  - Editorial
PT  - Introductory Journal Article
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - *Environmental Exposure/adverse effects/analysis/prevention & control
MH  - *Environmental Health
MH  - Environmental Monitoring
MH  - Environmental Pollutants/*adverse effects
MH  - Europe
MH  - Europe, Eastern
PMC - PMC5555221
MID - NIHMS873866
EDAT- 2017/02/22 06:00
MHDA- 2018/12/12 06:00
CRDT- 2017/02/22 06:00
PHST- 2017/02/22 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2017/02/22 06:00 [entrez]
AID - 10.1515/reveh-2017-0004 [doi]
AID - /j/reveh.ahead-of-print/reveh-2017-0004/reveh-2017-0004.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):1. doi: 10.1515/reveh-2017-0004.

PMID- 28231068
OWN - NLM
STAT- MEDLINE
DCOM- 20170628
LR  - 20181113
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - Recent advances on iron oxide magnetic nanoparticles as sorbents of
      organic pollutants in water and wastewater treatment.
PG  - 111-117
LID - 10.1515/reveh-2016-0063 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2016-0063/reveh-2016-0063.xml [pii]
AB  - The constant growth in population worldwide over the past decades
      continues to put forward the need to provide access to safe, clean water
      to meet human needs. There is a need for cost-effective technologies for
      water and wastewater treatment that can meet the global demands and the
      rigorous water quality standards and at the same maximizing pollutant
      efficiency removal. Current remediation technologies have failed in
      keeping up with these factors without becoming cost-prohibitive. Most
      recently, nanotechnology has been sought as the best alternative to
      increase access to water supplies by remediating those already
      contaminated and offering ways to access unconventional sources. The use
      of iron oxide magnetic nanoparticles as nanoadsorbents has led way to a
      new class of magnetic separation strategies for water treatment. This
      review focuses on highlighting some of the most recent advances in core-
      shell iron oxide magnetic nanoparticles and nanocomposites containing
      iron oxide nanoparticles currently being developed for water and
      wastewater treatment of organic pollutants. We discuss the novelty of
      these novel materials and the insight gained from their advances that can
      help develop cost-effective reusable technologies for scale-up and
      commercial use.
FAU - Gutierrez, Angela M
AU  - Gutierrez AM
FAU - Dziubla, Thomas D
AU  - Dziubla TD
FAU - Hilt, J Zach
AU  - Hilt JZ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Ferric Compounds)
RN  - 0 (Water Pollutants, Chemical)
RN  - 1K09F3G675 (ferric oxide)
SB  - IM
MH  - Adsorption
MH  - Ferric Compounds/*chemistry
MH  - Metal Nanoparticles/*chemistry
MH  - Nanocomposites/*chemistry
MH  - Waste Disposal, Fluid/economics/*methods
MH  - Water Pollutants, Chemical/*chemistry
PMC - PMC5785914
MID - NIHMS935857
EDAT- 2017/02/24 06:00
MHDA- 2017/06/29 06:00
CRDT- 2017/02/24 06:00
PHST- 2016/10/19 00:00 [received]
PHST- 2017/01/18 00:00 [accepted]
PHST- 2017/02/24 06:00 [pubmed]
PHST- 2017/06/29 06:00 [medline]
PHST- 2017/02/24 06:00 [entrez]
AID - 10.1515/reveh-2016-0063 [doi]
AID - /j/reveh.ahead-of-print/reveh-2016-0063/reveh-2016-0063.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):111-117. doi:
      10.1515/reveh-2016-0063.

PMID- 28282297
OWN - NLM
STAT- MEDLINE
DCOM- 20170628
LR  - 20181113
IS  - 2191-0308 (Electronic)
IS  - 0048-7554 (Linking)
VI  - 32
IP  - 1-2
DP  - 2017 Mar 1
TI  - Sensemaking, stakeholder discord, and long-term risk communication at a
      US Superfund site.
PG  - 165-169
LID - 10.1515/reveh-2016-0048 [doi]
LID - /j/reveh.2017.32.issue-1-2/reveh-2016-0048/reveh-2016-0048.xml [pii]
AB  - INTRODUCTION: Risk communication can help reduce exposures to
      environmental contaminants, mitigate negative health outcomes, and inform
      community-based decisions about hazardous waste sites. While
      communication best practices have long guided such efforts, little
      research has examined unintended consequences arising from such
      guidelines. As rhetoric informs stakeholder sensemaking, the language
      used in and reinforced by these guidelines can challenge relationships
      and exacerbate stakeholder tensions. OBJECTIVES: This study evaluates
      risk communication at a U.S. Superfund site to identify unintended
      consequences arising from current risk communication practices. METHODS:
      This qualitative case study crystallizes data spanning 6 years from three
      sources: 1) local newspaper coverage of site-related topics; 2) focus-
      group transcripts from a multi-year project designed to support future
      visioning of site use; and 3) published blog entries authored by a local
      environmental activist. Constant comparative analysis provides the
      study's analytic foundation, with qualitative data analysis software QSR
      NVivo 8 supporting a three-step process: 1) provisional coding to
      identify broad topic categories within datasets, 2) coding occurrences of
      sensemaking constructs and emergent intra-dataset patterns, and 3)
      grouping related codes across datasets to examine the relationships among
      them. RESULTS: Existing risk communication practices at this Superfund
      site contribute to a dichotomous conceptualization of multiple and
      diverse stakeholders as members of one of only two categories: the
      government or the public. This conceptualization minimizes perceptions of
      capacity, encourages public commitment to stances aligned with a
      preferred group, and contributes to negative expectations that can become
      self-fulfilling prophecies. CONCLUSION: Findings indicate a need to re-
      examine and adapt risk communication guidelines to encourage more
      pluralistic understanding of the stakeholder landscape.
FAU - Hoover, Anna Goodman
AU  - Hoover AG
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R13 ES026036/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Environmental Pollutants)
RN  - 0 (Hazardous Substances)
SB  - IM
MH  - *Environmental Exposure
MH  - Environmental Pollutants/*toxicity
MH  - Hazardous Substances/*toxicity
MH  - Humans
MH  - *Information Dissemination
MH  - Kentucky
MH  - *Risk
PMC - PMC5785920
MID - NIHMS935868
EDAT- 2017/03/11 06:00
MHDA- 2017/06/29 06:00
CRDT- 2017/03/11 06:00
PHST- 2016/08/26 00:00 [received]
PHST- 2016/12/13 00:00 [accepted]
PHST- 2017/03/11 06:00 [entrez]
PHST- 2017/03/11 06:00 [pubmed]
PHST- 2017/06/29 06:00 [medline]
AID - 10.1515/reveh-2016-0048 [doi]
AID - /j/reveh.2017.32.issue-1-2/reveh-2016-0048/reveh-2016-0048.xml [pii]
PST - ppublish
SO  - Rev Environ Health. 2017 Mar 1;32(1-2):165-169. doi:
      10.1515/reveh-2016-0048.

PMID- 28989952
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2352-4928 (Print)
IS  - 2352-4928 (Linking)
VI  - 10
DP  - 2017 Mar
TI  - Synthesis and characterization of thermally responsive
      N-isopropylacrylamide hydrogels copolymerized with novel hydrophobic
      polyphenolic crosslinkers.
PG  - 46-53
LID - 10.1016/j.mtcomm.2016.12.003 [doi]
AB  - Two series of thermosensitive hydrogels were synthesized by
      copolymerizing N-isopropylacrylamide (NIPAAm) with various contents of
      novel hydrophobic crosslinkers, curcumin multiacrylate (CMA) and
      quercetin multiacrylate (QMA). The compositions of the resulting
      hydrogels were characterized using solid state-NMR (ss-NMR), and the
      temperature dependent swelling behavior and lower critical solution
      temperature (LCST) were characterized using swelling studies and
      differential scanning calorimetry (DSC). Increasing the crosslinker
      content resulted in a significant decrease in the LCST and swelling ratio
      of hydrogels, which could be attributed to the increased hydrophobicity
      introduced by CMA or QMA. All of the hydrogels demonstrated temperature
      responsive swelling with the extent of swelling decreasing with
      increasing crosslinker content. The lower crosslinker content gels
      displayed sharper phase transitions, while the high crosslinker content
      gels had broader phase transitions.
FAU - Tang, Shuo
AU  - Tang S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, USA.
FAU - Bhandari, Rohit
AU  - Bhandari R
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, USA.
FAU - Delaney, Sean P
AU  - Delaney SP
AD  - Department of Pharmaceutical Sciences, University of Kentucky, Lexington,
      Kentucky 40506, USA.
FAU - Munson, Eric J
AU  - Munson EJ
AD  - Department of Pharmaceutical Sciences, University of Kentucky, Lexington,
      Kentucky 40506, USA.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, USA.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20161231
PL  - England
TA  - Mater Today Commun
JT  - Materials today. Communications
JID - 101702545
PMC - PMC5628756
MID - NIHMS854859
EDAT- 2017/10/11 06:00
MHDA- 2017/10/11 06:01
CRDT- 2017/10/10 06:00
PHST- 2017/10/10 06:00 [entrez]
PHST- 2017/10/11 06:00 [pubmed]
PHST- 2017/10/11 06:01 [medline]
AID - 10.1016/j.mtcomm.2016.12.003 [doi]
PST - ppublish
SO  - Mater Today Commun. 2017 Mar;10:46-53. doi: 10.1016/j.mtcomm.2016.12.003.
      Epub 2016 Dec 31.

PMID- 28186210
OWN - NLM
STAT- MEDLINE
DCOM- 20170512
LR  - 20181202
IS  - 2050-7895 (Electronic)
IS  - 2050-7887 (Linking)
VI  - 19
IP  - 2
DP  - 2017 Feb 22
TI  - US residential building air exchange rates: new perspectives to improve
      decision making at vapor intrusion sites.
PG  - 87-100
LID - 10.1039/c6em00504g [doi]
AB  - Vapor intrusion (VI) is well-known to be difficult to characterize
      because indoor air (IA) concentrations exhibit considerable temporal and
      spatial variability in homes throughout impacted communities. To overcome
      this and other limitations, most VI science has focused on subsurface
      processes; however there is a need to understand the role of aboveground
      processes, especially building operation, in the context of VI exposure
      risks. This tutorial review focuses on building air exchange rates (AERs)
      and provides a review of literature related building AERs to inform
      decision making at VI sites. Commonly referenced AER values used by VI
      regulators and practitioners do not account for the variability in AER
      values that have been published in indoor air quality studies. The
      information presented herein highlights that seasonal differences, short-
      term weather conditions, home age and air conditioning status, which are
      well known to influence AERs, are also likely to influence IA
      concentrations at VI sites. Results of a 3D VI model in combination with
      relevant AER values reveal that IA concentrations can vary more than one
      order of magnitude due to air conditioning status and one order of
      magnitude due to house age. Collectively, the data presented strongly
      support the need to consider AERs when making decisions at VI sites.
FAU - Reichman, Rivka
AU  - Reichman R
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, USA. kellypennell@uky.edu.
FAU - Shirazi, Elham
AU  - Shirazi E
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, USA. kellypennell@uky.edu.
FAU - Colliver, Donald G
AU  - Colliver DG
AD  - University of Kentucky, Department of Biosystems and Agricultural
      Engineering, Lexington, KY 40503, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - University of Kentucky, Department of Civil Engineering, Lexington, KY
      40506, USA. kellypennell@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - England
TA  - Environ Sci Process Impacts
JT  - Environmental science. Processes & impacts
JID - 101601576
RN  - 0 (Gases)
SB  - IM
MH  - *Air Movements
MH  - *Air Pollution, Indoor
MH  - Decision Making
MH  - Gases
MH  - Housing
MH  - *Models, Theoretical
PMC - PMC5369024
MID - NIHMS851050
EDAT- 2017/02/12 06:00
MHDA- 2017/05/13 06:00
CRDT- 2017/02/11 06:00
PHST- 2017/02/12 06:00 [pubmed]
PHST- 2017/05/13 06:00 [medline]
PHST- 2017/02/11 06:00 [entrez]
AID - 10.1039/c6em00504g [doi]
PST - ppublish
SO  - Environ Sci Process Impacts. 2017 Feb 22;19(2):87-100. doi:
      10.1039/c6em00504g.

PMID- 28367475
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2325-1034 (Print)
VI  - 3
IP  - 2
DP  - 2017
TI  - Measuring Vapor Intrusion: From Source Science Politics to a
      Transdisciplinary Approach.
PG  - 145-154
LID - 10.1080/23251042.2016.1224528 [doi]
AB  - Investigation of indoor air quality has been on the upswing in recent
      years. In this article, we focus on how the transport of subsurface
      vapors into indoor air spaces, a process known as "vapor intrusion," (VI)
      is defined and addressed. For environmental engineers and physical
      scientists who specialize in this emerging indoor environmental exposure
      science, VI is notoriously difficult to characterize, leading the
      regulatory community to seek improved science-based understandings of VI
      pathways and exposures. Yet despite the recent growth in VI science and
      competition between environmental consulting companies, VI studies have
      largely overlooked the social and political field in which VI problems
      emerge and are experienced by those at risk. To balance and inform
      current VI studies, this article explores VI science and policy and
      develops a critique of what we call "source science politics." Drawing
      inspiration from the creative synthesis of social and environmental
      science/engineering perspectives, the article offers a transdisciplinary
      approach to VI that highlights collaboration with social scientists and
      impacted communities and cultivates epistemic empathy.
FAU - Little, Peter C
AU  - Little PC
AD  - Department of Anthropology, Rhode Island College, Providence, RI, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY,
      USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20161012
PL  - England
TA  - Environ Sociol
JT  - Environmental sociology
JID - 101698478
PMC - PMC5370174
MID - NIHMS851198
OTO - NOTNLM
OT  - indoor air
OT  - risk
OT  - source science
OT  - transdisciplinarity
OT  - uncertainty
OT  - vapor intrusion
EDAT- 2017/04/04 06:00
MHDA- 2017/04/04 06:01
CRDT- 2017/04/04 06:00
PHST- 2017/04/04 06:00 [entrez]
PHST- 2017/04/04 06:00 [pubmed]
PHST- 2017/04/04 06:01 [medline]
AID - 10.1080/23251042.2016.1224528 [doi]
PST - ppublish
SO  - Environ Sociol. 2017;3(2):145-154. doi: 10.1080/23251042.2016.1224528.
      Epub 2016 Oct 12.

PMID- 31131152
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2158-2440 (Print)
IS  - 2158-2440 (Linking)
VI  - 6
IP  - 4
DP  - 2016 Oct-Dec
TI  - Applying Community-Based Participatory Research Partnership Principles to
      Public Health Practice-Based Research Networks.
LID - 10.1177/2158244016679211 [doi]
AB  - With real-world relevance and translatability as important goals, applied
      methodological approaches have arisen along the participatory continuum
      that value context and empower stakeholders to partner actively with
      academics throughout the research process. Community-based participatory
      research (CBPR) provides the gold standard for equitable, partnered
      research in traditional communities. Practice-based research networks
      (PBRNs) also have developed, coalescing communities of practice and of
      academics to identify, study, and answer practice-relevant questions. To
      optimize PBRN potential for expanding scientific knowledge, while
      bridging divides across knowledge production, dissemination, and
      implementation, we elucidate how PBRN partnerships can be strengthened by
      applying CBPR principles to build and maintain research collaboratives
      that empower practice partners. Examining the applicability of CBPR
      partnership principles to public health (PH) PBRNs, we conclude that PH-
      PBRNs can serve as authentic, sustainable CBPR partnerships, ensuring the
      co-production of new knowledge, while also improving and expanding the
      implementation and impact of research findings in real-world settings.
FAU - Winterbauer, Nancy L
AU  - Winterbauer NL
AD  - East Carolina University, Greenville, NC, USA.
FAU - Bekemeier, Betty
AU  - Bekemeier B
AD  - University of Washington, Seattle, USA.
FAU - VanRaemdonck, Lisa
AU  - VanRaemdonck L
AD  - Public Health Alliance of Colorado & Colorado Association of Local Public
      Health Officials, Denver, USA.
FAU - Hoover, Anna G
AU  - Hoover AG
AD  - University of Kentucky, Lexington, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20161101
PL  - United States
TA  - Sage Open
JT  - SAGE open
JID - 101565150
PMC - PMC6533003
MID - NIHMS995413
OTO - NOTNLM
OT  - academic-practice partnerships
OT  - communities of practice
OT  - community-based participatory research (CBPR)
OT  - knowledge co-production
OT  - practice-based research networks (PBRN)
COIS- Declaration of Conflicting Interests The author(s) declared no potential
      conflicts of interest with respect to the research, authorship, and/or
      publication of this article.
EDAT- 2016/10/01 00:00
MHDA- 2016/10/01 00:01
CRDT- 2019/05/28 06:00
PHST- 2019/05/28 06:00 [entrez]
PHST- 2016/10/01 00:00 [pubmed]
PHST- 2016/10/01 00:01 [medline]
AID - 10.1177/2158244016679211 [doi]
PST - ppublish
SO  - Sage Open. 2016 Oct-Dec;6(4). doi: 10.1177/2158244016679211. Epub 2016
      Nov 1.

PMID- 27287099
OWN - NLM
STAT- MEDLINE
DCOM- 20170406
LR  - 20190109
IS  - 1873-0191 (Electronic)
IS  - 0928-4931 (Linking)
VI  - 67
DP  - 2016 Oct 1
TI  - Single step synthesis, characterization and applications of curcumin
      functionalized iron oxide magnetic nanoparticles.
PG  - 59-64
LID - S0928-4931(16)30400-3 [pii]
LID - 10.1016/j.msec.2016.04.093 [doi]
AB  - Magnetic iron oxide nanoparticles have been well known for their
      applications in magnetic resonance imaging (MRI), hyperthermia, targeted
      drug delivery, etc. The surface modification of these magnetic
      nanoparticles has been explored extensively to achieve functionalized
      materials with potential application in biomedical, environmental and
      catalysis field. Herein, we report a novel and versatile single step
      methodology for developing curcumin functionalized magnetic Fe3O4
      nanoparticles without any additional linkers, using a simple
      coprecipitation technique. The magnetic nanoparticles (MNPs) were
      characterized using transmission electron microscopy, X-ray diffraction,
      fourier transform infrared spectroscopy and thermogravimetric analysis.
      The developed MNPs were employed in a cellular application for protection
      against an inflammatory agent, a polychlorinated biphenyl (PCB) molecule.
CI  - Copyright (c) 2016. Published by Elsevier B.V.
FAU - Bhandari, Rohit
AU  - Bhandari R
AD  - Chemical and Materials Engineering Department, University of Kentucky,
      Lexington, KY 40506.
FAU - Gupta, Prachi
AU  - Gupta P
AD  - Chemical and Materials Engineering Department, University of Kentucky,
      Lexington, KY 40506.
FAU - Dziubla, Thomas
AU  - Dziubla T
AD  - Chemical and Materials Engineering Department, University of Kentucky,
      Lexington, KY 40506.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Chemical and Materials Engineering Department, University of Kentucky,
      Lexington, KY 40506. Electronic address: zach.hilt@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160428
PL  - Netherlands
TA  - Mater Sci Eng C Mater Biol Appl
JT  - Materials science & engineering. C, Materials for biological applications
JID - 101484109
RN  - 0 (Drug Carriers)
RN  - 0 (Magnetite Nanoparticles)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - IT942ZTH98 (Curcumin)
RN  - XM0M87F357 (Ferrosoferric Oxide)
SB  - IM
MH  - *Curcumin/chemistry/pharmacokinetics/pharmacology
MH  - *Drug Carriers/chemistry/pharmacokinetics/pharmacology
MH  - *Ferrosoferric Oxide/chemistry/pharmacokinetics/pharmacology
MH  - Human Umbilical Vein Endothelial Cells/*metabolism
MH  - Humans
MH  - Magnetite Nanoparticles/*chemistry/ultrastructure
MH  - Particle Size
MH  - Polychlorinated Biphenyls/toxicity
PMC - PMC5321203
MID - NIHMS846580
OTO - NOTNLM
OT  - Anti-inflammatory
OT  - Cell viability
OT  - Curcumin
OT  - Functionalization
OT  - Iron oxide
EDAT- 2016/06/12 06:00
MHDA- 2017/04/07 06:00
CRDT- 2016/06/12 06:00
PHST- 2016/02/13 00:00 [received]
PHST- 2016/04/14 00:00 [revised]
PHST- 2016/04/27 00:00 [accepted]
PHST- 2016/06/12 06:00 [entrez]
PHST- 2016/06/12 06:00 [pubmed]
PHST- 2017/04/07 06:00 [medline]
AID - S0928-4931(16)30400-3 [pii]
AID - 10.1016/j.msec.2016.04.093 [doi]
PST - ppublish
SO  - Mater Sci Eng C Mater Biol Appl. 2016 Oct 1;67:59-64. doi:
      10.1016/j.msec.2016.04.093. Epub 2016 Apr 28.

PMID- 28090221
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1874-2882 (Print)
VI  - 10
DP  - 2016
TI  - Nutrition and Other Protective Behaviors Motivated by Environmental
      Health Risk Awareness.
PG  - 1-12
LID - 10.2174/1874288201610010001 [doi]
AB  - BACKGROUND: Research findings have suggested that exposure to
      environmental pollutants contributes to increased health risks, which may
      be modulated by certain nutrition and other protective health behaviors.
      Nutrition professionals play an important role in effectively
      disseminating this information and in devising specific community-based
      nutrition education programs for audiences located in areas with
      environmental health issues. OBJECTIVE: To assess awareness of
      environmental health problems and motivation to adopt protective health
      behaviors for use in planning nutrition education programs for
      communities exposed to environmental pollutants. METHOD: Data were
      collected from a modified, validated Environmental Health Engagement
      Profile (EHEP) survey instrument administered to adults (n=774)
      participating in community events in Kentucky based on location relative
      to hazardous waste sites. RESULTS: The modified EHEP survey instrument
      showed good internal consistency reliability, and demographic
      characteristics were evaluated. Correlation analyses revealed significant
      positive correlations in all groups, separately and combined, between
      awareness of environmental pollution in an individual's surroundings and
      the extent of concern that pollutants cause adverse health effects (P <
      0.01) and between concern that pollutants cause adverse health effects
      and taking personal actions to protect against such environmental insults
      (P < 0.01). The groups having the highest level of awareness posed by
      pollution are those residing near federally designated hazardous waste
      sites. CONCLUSION: These results suggest that determining and expanding
      an audience's knowledge and perceptions of environmental health risks
      will enhance effective nutrition education program planning.
FAU - Jones, Elizabeth W
AU  - Jones EW
AD  - Department of Dietetics and Human Nutrition, University of Kentucky, 203
      Funkhouser Bldg, Lexington, KY 40506-0054, USA.
FAU - Feng, Limin
AU  - Feng L
AD  - Department of Statistics, University of Kentucky, 817 Patterson Office
      Tower, Lexington, KY 40506-0027, USA.
FAU - Dixon, Jane K
AU  - Dixon JK
AD  - Yale University, School of Nursing, New Haven CT 06536-0740, USA.
FAU - Dixon, John P
AU  - Dixon JP
AD  - Greater New Haven Green Fund, New Haven, CT 06511, USA.
FAU - Hofe, Carolyn R
AU  - Hofe CR
AD  - Graduate Center for Nutritional Sciences, University of Kentucky, 115
      Funkhouser Bldg, Lexington, KY 40506-0054, USA.
FAU - Gaetke, Lisa M
AU  - Gaetke LM
AD  - Department of Dietetics and Human Nutrition, University of Kentucky, 203
      Funkhouser Bldg, Lexington, KY 40506-0054, USA; Graduate Center for
      Nutritional Sciences, University of Kentucky, 115 Funkhouser Bldg,
      Lexington, KY 40506-0054, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160930
PL  - Netherlands
TA  - Open Nutr J
JT  - The open nutrition journal
JID - 101532751
PMC - PMC5234471
MID - NIHMS828712
OTO - NOTNLM
OT  - Environmental health
OT  - Environmental health behavior
OT  - Hazardous exposures
OT  - Nutrition
OT  - Risk communication
COIS- The authors, E. Jones, L. Feng, J.K. Dixon, J.P. Dixon, C. Hofe, and L.
      Gaetke declare they have no financial and no non-financial conflicts of
      interest. The authors' freedom to design, conduct, interpret and publish
      research is not compromised by any controlling sponsor as a condition of
      review or publication.
EDAT- 2017/01/17 06:00
MHDA- 2017/01/17 06:01
CRDT- 2017/01/17 06:00
PHST- 2017/01/17 06:00 [entrez]
PHST- 2017/01/17 06:00 [pubmed]
PHST- 2017/01/17 06:01 [medline]
AID - 10.2174/1874288201610010001 [doi]
PST - ppublish
SO  - Open Nutr J. 2016;10:1-12. doi: 10.2174/1874288201610010001. Epub 2016
      Sep 30.

PMID- 28642630
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 0360-1277 (Print)
IS  - 0360-1277 (Linking)
VI  - 42
IP  - 11
DP  - 2016
TI  - Increased Fruit and Vegetable Intake among Older Adults Participating in
      Kentucky's Congregate Meal Site Program.
PG  - 771-784
LID - 10.1080/03601277.2016.1231511 [doi]
AB  - The purpose of this study was to determine if the amount and variety of
      fruits and vegetables consumed increased among community-dwelling older
      adults participating in Kentucky's congregate meal site program following
      a series of five nutrition education lessons. A convenience sample of
      older adults attending senior centers (n=35), two intervention (n=19) and
      two control (n=16) centers, participated in this quasi-experimental pilot
      study. Following the intervention there was a significant increase in
      actual fruit and vegetable intake in the intervention group (p<0.05) as
      assessed by plate waste measurements of the congregate lunch meal. In
      addition, from pre- to post-intervention, a trend towards increased self-
      reported intake in the variety of fruit and vegetables was observed among
      the intervention group. As well, a significant increase in the number of
      days intervention participants self-reported consuming at least 4.5 cups
      of fruits and vegetables in the last seven days (2.44+/-2.09 days to
      4.28+/-1.99 days (p=0.004)) was observed; and knowledge pertaining to
      phytochemicals increased (p<0.05). The phytochemical index (PI) score of
      the lunch meal, taking into account that the older adults consumption of
      meal components, including phytochemical-rich foods, was 26.9. Overall,
      study results indicated that a short theory-based nutrition education
      program offered to community-dwelling older adults was linked to an
      increase in fruit and vegetable consumption and phytochemical knowledge.
FAU - Brewer, Dawn
AU  - Brewer D
AD  - Department of Dietetics and Human Nutrition, University of Kentucky,
      Lexington, Kentucky 40506.
FAU - Dickens, Emily
AU  - Dickens E
AD  - Department of Dietetics and Human Nutrition, University of Kentucky,
      Lexington, Kentucky 40506.
FAU - Humphrey, Alyson
AU  - Humphrey A
AD  - Department of Dietetics and Human Nutrition, University of Kentucky,
      Lexington, Kentucky 40506.
FAU - Stephenson, Tammy
AU  - Stephenson T
AD  - Department of Dietetics and Human Nutrition, University of Kentucky,
      Lexington, Kentucky 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160903
PL  - United States
TA  - Educ Gerontol
JT  - Educational gerontology
JID - 7802138
PMC - PMC5476306
MID - NIHMS830699
OTO - NOTNLM
OT  - Fruits and vegetables
OT  - older adults
OT  - phytochemicals
OT  - plate waste
EDAT- 2016/01/01 00:00
MHDA- 2016/01/01 00:01
CRDT- 2017/06/24 06:00
PHST- 2017/06/24 06:00 [entrez]
PHST- 2016/01/01 00:00 [pubmed]
PHST- 2016/01/01 00:01 [medline]
AID - 10.1080/03601277.2016.1231511 [doi]
PST - ppublish
SO  - Educ Gerontol. 2016;42(11):771-784. doi: 10.1080/03601277.2016.1231511.
      Epub 2016 Sep 3.

PMID- 27288564
OWN - NLM
STAT- MEDLINE
DCOM- 20170404
LR  - 20181113
IS  - 1879-3177 (Electronic)
IS  - 0887-2333 (Linking)
VI  - 35
DP  - 2016 Sep
TI  - Polychlorinated biphenyl exposure alters the expression profile of
      microRNAs associated with vascular diseases.
PG  - 180-7
LID - 10.1016/j.tiv.2016.06.001 [doi]
LID - S0887-2333(16)30115-1 [pii]
AB  - Exposure to persistent organic pollutants, including polychlorinated
      biphenyls (PCBs) is correlated with multiple vascular complications
      including endothelial cell dysfunction and atherosclerosis. PCB-induced
      activation of the vasculature subsequently leads to oxidative stress and
      induction of pro-inflammatory cytokines and adhesion proteins. Gene
      expression of these cytokines/proteins is known to be regulated by small,
      endogenous oligonucleotides known as microRNAs that interact with
      messenger RNA. MicroRNAs are an acknowledged component of the epigenome,
      but the role of environmentally-driven epigenetic changes such as
      toxicant-induced changes in microRNA profiles is currently understudied.
      The objective of this study was to determine the effects of PCB exposure
      on microRNA expression profile in primary human endothelial cells using
      the commercial PCB mixture Aroclor 1260. Samples were analyzed using
      Affymetrix GeneChip(R) miRNA 4.0 arrays for high throughput detection and
      selected microRNA gene expression was validated (RT-PCR). Microarray
      analysis identified 557 out of 6658 microRNAs that were changed with PCB
      exposure (p<0.05). In-silico analysis using MetaCore database identified
      21 of these microRNAs to be associated with vascular diseases. Further
      validation showed that Aroclor 1260 increased miR-21, miR-31, miR-126,
      miR-221 and miR-222 expression levels. Upregulated miR-21 has been
      reported in cardiac injury while miR-126 and miR-31 modulate
      inflammation. Our results demonstrated evidence of altered microRNA
      expression with PCB exposure, thus providing novel insights into
      mechanisms of PCB toxicity.
CI  - Copyright (c) 2016 Elsevier B.V. All rights reserved.
FAU - Wahlang, Banrida
AU  - Wahlang B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture,
      Food, and Environment, University of Kentucky, Lexington, KY 40536, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture,
      Food, and Environment, University of Kentucky, Lexington, KY 40536, USA.
FAU - Perkins, Jordan T
AU  - Perkins JT
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA.
FAU - Shen, Shu
AU  - Shen S
AD  - Department of Statistics, College of Arts and Sciences, University of
      Kentucky, Lexington, KY 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture,
      Food, and Environment, University of Kentucky, Lexington, KY 40536, USA;
      Graduate Center for Nutritional Sciences, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA. Electronic address:
      bhennig@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160608
PL  - England
TA  - Toxicol In Vitro
JT  - Toxicology in vitro : an international journal published in association
      with BIBRA
JID - 8712158
RN  - 0 (MicroRNAs)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Cells, Cultured
MH  - Gene Expression Profiling
MH  - Human Umbilical Vein Endothelial Cells/*drug effects/metabolism
MH  - MicroRNAs/*genetics
MH  - Oligonucleotide Array Sequence Analysis
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Vascular Diseases/*genetics
PMC - PMC4949395
MID - NIHMS798607
OTO - NOTNLM
OT  - Aroclor 1260
OT  - Endothelial cells
OT  - PCBs
OT  - Vascular diseases
OT  - miRNAs
EDAT- 2016/06/12 06:00
MHDA- 2017/04/05 06:00
CRDT- 2016/06/12 06:00
PHST- 2016/03/14 00:00 [received]
PHST- 2016/05/05 00:00 [revised]
PHST- 2016/06/07 00:00 [accepted]
PHST- 2016/06/12 06:00 [entrez]
PHST- 2016/06/12 06:00 [pubmed]
PHST- 2017/04/05 06:00 [medline]
AID - S0887-2333(16)30115-1 [pii]
AID - 10.1016/j.tiv.2016.06.001 [doi]
PST - ppublish
SO  - Toxicol In Vitro. 2016 Sep;35:180-7. doi: 10.1016/j.tiv.2016.06.001. Epub
      2016 Jun 8.

PMID- 27155921
OWN - NLM
STAT- MEDLINE
DCOM- 20171120
LR  - 20181113
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 33
DP  - 2016 Jul
TI  - Dioxin-like pollutants increase hepatic flavin containing monooxygenase
      (FMO3) expression to promote synthesis of the pro-atherogenic nutrient
      biomarker trimethylamine N-oxide from dietary precursors.
PG  - 145-53
LID - 10.1016/j.jnutbio.2016.03.016 [doi]
LID - S0955-2863(16)30036-5 [pii]
AB  - The etiology of cardiovascular disease (CVD) is impacted by multiple
      modifiable and non-modifiable risk factors including dietary choices,
      genetic predisposition, and environmental exposures. However, mechanisms
      linking diet, exposure to pollutants, and CVD risk are largely unclear.
      Recent studies identified a strong link between plasma levels of
      nutrient-derived Trimethylamine N-oxide (TMAO) and coronary artery
      disease. Dietary precursors of TMAO include carnitine and
      phosphatidylcholine, which are abundant in animal-derived foods. Dioxin-
      like pollutants can upregulate a critical enzyme responsible for TMAO
      formation, hepatic flavin containing monooxygenase 3 (FMO3), but a link
      between dioxin-like PCBs, upregulation of FMO3, and increased TMAO has
      not been reported. Here, we show that mice exposed acutely to dioxin-like
      PCBs exhibit increased hepatic FMO3 mRNA, protein, as well as an increase
      in circulating levels of TMAO following oral administration of its
      metabolic precursors. C57BL/6 mice were exposed to 5mumol PCB 126/kg
      mouse weight (1.63mg/kg). At 48h post-PCB exposure, mice were
      subsequently given a single gavage of phosphatidylcholine dissolved in
      corn oil. Exposure to 5 mumole/kg PCB 126 resulted in greater than
      100-fold increase in FMO3 mRNA expression, robust induction of FMO3
      protein, and a 5-fold increase in TMAO levels compared with vehicle
      treated mice. We made similar observations in mice exposed to PCB 77
      (49.6mg/kg twice); stable isotope tracer studies revealed increased
      formation of plasma TMAO from an orally administered precursor
      trimethylamine (TMA). Taken together, these observations suggest a novel
      diet-toxicant interaction that results in increased production of a
      circulating biomarker of cardiovascular disease risk.
CI  - Copyright (c) 2016 Elsevier Inc. All rights reserved.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, 40536; Lexington
      Veterans Affairs Medical Center, Lexington, KY, USA.
FAU - Hoffman, Jessie B
AU  - Hoffman JB
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536;
      Graduate Center for Nutritional Sciences, College of Medicine, University
      of Kentucky, Lexington, KY, 40536.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536;
      Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, 40536.
FAU - Wahlang, Banrida
AU  - Wahlang B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, 40536.
FAU - Perkins, Jordan T
AU  - Perkins JT
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536;
      Lexington Veterans Affairs Medical Center, Lexington, KY, USA; Division
      of Cardiovascular Medicine, College of Medicine, University of Kentucky,
      Lexington, KY, 40536.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY, 40536;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, 40536. Electronic
      address: bhennig@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, N.I.H., Extramural
DEP - 20160401
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Biomarkers)
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Methylamines)
RN  - 0 (Phosphatidylcholines)
RN  - AR09D82C7G (Deuterium)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.13.- (Oxygenases)
RN  - EC 1.14.13.8 (dimethylaniline monooxygenase (N-oxide forming))
RN  - FLD0K1SJ1A (trimethyloxamine)
RN  - LHH7G8O305 (trimethylamine)
RN  - N91BDP6H0X (Choline)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Administration, Oral
MH  - Animals
MH  - Atherosclerosis/blood/*etiology/metabolism
MH  - Biomarkers/blood
MH  - Choline/administration & dosage/*metabolism
MH  - Deuterium
MH  - Dietary Fats/metabolism
MH  - Environmental Pollutants/administration & dosage/*toxicity
MH  - Enzyme Induction/drug effects
MH  - Food-Drug Interactions
MH  - Liver/*drug effects/enzymology/metabolism
MH  - Male
MH  - Methylamines/administration & dosage/*blood/metabolism
MH  - Mice, Inbred C57BL
MH  - Oxygenases/chemistry/genetics/*metabolism
MH  - Phosphatidylcholines/administration & dosage/metabolism
MH  - Polychlorinated Biphenyls/administration & dosage/*toxicity
MH  - Random Allocation
MH  - Up-Regulation/drug effects
PMC - PMC4893916
MID - NIHMS774509
OTO - NOTNLM
OT  - *Cardiovascular disease
OT  - *FMO3
OT  - *Nutrition
OT  - *PCB toxicity
OT  - *TMAO
EDAT- 2016/05/09 06:00
MHDA- 2017/11/29 06:00
CRDT- 2016/05/09 06:00
PHST- 2016/02/03 00:00 [received]
PHST- 2016/03/22 00:00 [revised]
PHST- 2016/03/28 00:00 [accepted]
PHST- 2016/05/09 06:00 [entrez]
PHST- 2016/05/09 06:00 [pubmed]
PHST- 2017/11/29 06:00 [medline]
AID - S0955-2863(16)30036-5 [pii]
AID - 10.1016/j.jnutbio.2016.03.016 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2016 Jul;33:145-53. doi: 10.1016/j.jnutbio.2016.03.016.
      Epub 2016 Apr 1.

PMID- 26977535
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20181113
IS  - 1879-1026 (Electronic)
IS  - 0048-9697 (Linking)
VI  - 556
DP  - 2016 Jun 15
TI  - Field data and numerical modeling: A multiple lines of evidence approach
      for assessing vapor intrusion exposure risks.
PG  - 291-301
LID - 10.1016/j.scitotenv.2016.02.185 [doi]
LID - S0048-9697(16)30396-5 [pii]
AB  - USEPA recommends a multiple lines of evidence approach to make informed
      decisions at vapor intrusion sites because the vapor intrusion pathway is
      notoriously difficult to characterize. Our study uses this approach by
      incorporating groundwater, soil gas, indoor air field measurements and
      numerical models to evaluate vapor intrusion exposure risks in a Metro-
      Boston neighborhood known to exhibit lower than anticipated indoor air
      concentrations based on groundwater concentrations. We collected and
      evaluated five rounds of field sampling data over the period of one year.
      Field data results show a steep gradient in soil gas concentrations near
      the groundwater surface; however as the depth decreases, soil gas
      concentration gradients also decrease. Together, the field data and the
      numerical model results suggest that a subsurface feature is limiting
      vapor transport into indoor air spaces at the study site and that
      groundwater concentrations are not appropriate indicators of vapor
      intrusion exposure risks in this neighborhood. This research also reveals
      the importance of including relevant physical models when evaluating
      vapor intrusion exposure risks using the multiple lines of evidence
      approach. Overall, the findings provide insight about how the multiple
      lines of evidence approach can be used to inform decisions by using field
      data collected using regulatory-relevant sampling techniques, and a well-
      established 3-D vapor intrusion model.
CI  - Copyright (c) 2016 Elsevier B.V. All rights reserved.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - University of Kentucky, Civil Engineering Department, Lexington, KY
      40506, United States. Electronic address: kellypennell@uky.edu.
FAU - Scammell, Madeleine K
AU  - Scammell MK
AD  - Boston University School of Public Health, Boston, MA 02118, United
      States.
FAU - McClean, Michael D
AU  - McClean MD
AD  - Boston University School of Public Health, Boston, MA 02118, United
      States.
FAU - Suuberg, Eric M
AU  - Suuberg EM
AD  - Brown University, School of Engineering, Providence, RI 02912, United
      States.
FAU - Moradi, Ali
AU  - Moradi A
AD  - Colorado School of Mines, Department of Civil & Environmental
      Engineering, Golden, CO 80401, United States.
FAU - Roghani, Mohammadyousef
AU  - Roghani M
AD  - University of Kentucky, Civil Engineering Department, Lexington, KY
      40506, United States.
FAU - Ames, Jennifer
AU  - Ames J
AD  - Boston University School of Public Health, Boston, MA 02118, United
      States.
FAU - Friguglietti, Leigh
AU  - Friguglietti L
AD  - Boston University School of Public Health, Boston, MA 02118, United
      States.
FAU - Indeglia, Paul A
AU  - Indeglia PA
AD  - Colorado School of Mines, Department of Civil & Environmental
      Engineering, Golden, CO 80401, United States.
FAU - Shen, Rui
AU  - Shen R
AD  - Brown University, School of Engineering, Providence, RI 02912, United
      States.
FAU - Yao, Yijun
AU  - Yao Y
AD  - College of Environmental and Resource Sciences, Zhejiang University,
      Hangzhou 310058, China.
FAU - Heiger-Bernays, Wendy J
AU  - Heiger-Bernays WJ
AD  - Boston University School of Public Health, Boston, MA 02118, United
      States.
LA  - eng
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
GR  - P42 ES007381/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES07381/ES/NIEHS NIH HHS/United States
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20160312
PL  - Netherlands
TA  - Sci Total Environ
JT  - The Science of the total environment
JID - 0330500
RN  - 0 (Air Pollutants)
RN  - 0 (Gases)
SB  - IM
MH  - Air Pollutants/*analysis
MH  - Air Pollution/*statistics & numerical data
MH  - Air Pollution, Indoor/statistics & numerical data
MH  - Boston
MH  - Environmental Exposure/*statistics & numerical data
MH  - Gases/analysis
MH  - Groundwater/chemistry
MH  - Humans
MH  - Models, Chemical
MH  - Volatilization
PMC - PMC4844003
MID - NIHMS768480
OTO - NOTNLM
OT  - Hazardous waste
OT  - Indoor air
OT  - Numerical modeling
OT  - Soil gas
OT  - Vapor intrusion
EDAT- 2016/03/16 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/03/16 06:00
PHST- 2015/12/11 00:00 [received]
PHST- 2016/02/25 00:00 [revised]
PHST- 2016/02/26 00:00 [accepted]
PHST- 2016/03/16 06:00 [entrez]
PHST- 2016/03/16 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - S0048-9697(16)30396-5 [pii]
AID - 10.1016/j.scitotenv.2016.02.185 [doi]
PST - ppublish
SO  - Sci Total Environ. 2016 Jun 15;556:291-301. doi:
      10.1016/j.scitotenv.2016.02.185. Epub 2016 Mar 12.

PMID- 31130776
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 55
IP  - 14
DP  - 2016 Apr 13
TI  - High Total Dissolved Solids Water Treatment by Charged Nanofiltration
      Membranes Relating to Power Plant Applications.
PG  - 4089-4097
LID - 10.1021/acs.iecr.6b00098 [doi]
AB  - Selective desalination through nanofiltration (NF) is of great interest
      for many industrial applications including reuse of power plant scrubber
      wastewater and treatment of water containing high concentrations of TDS
      (total dissolved solids). This work seeks to understand the effect ion
      interactions at the membrane interface have on rejection and flux
      performance of charged NF membranes. NF membranes were also effective for
      low energy desalination of scrubber wastewater from Georgia Power Plant
      Bowen, composed primarily of Ca(2+), Mg(2+), Cl(-), and SO4 (2-). As NF
      membranes have the capability for selective separations, 80% water
      recovery was achieved experimentally while maintaining an overall
      rejection of over 60% for Ca(2+) and Cl(-). The occurrence of CaSO4
      precipitation at high water recovery was observed. The effect of
      precipitation on osmotic pressure and the effect of Cl(-) counterions on
      increasing gypsum solubility were explored for water recovery operation.
      This work expands on a previous work on the topics of desalination of
      multi-ionic solutions by incorporating the use of large scale membrane
      modules (0.59 m(2)) with several synthetic solutions as well as actual
      scrubber water containing precipitating elements, Ca(2+) and SO4 (2-). It
      was observed that the spiral wound membrane modules maintained a stable
      water permeability over the 144 day course of tests.
FAU - Colburn, Andrew S
AU  - Colburn AS
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, United States.
FAU - Meeks, Noah
AU  - Meeks N
AD  - Southern Company Services, Inc., Birmingham, Alabama 35203, United
      States.
FAU - Weinman, Steven T
AU  - Weinman ST
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, United States.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506, United States.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160321
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC6532996
MID - NIHMS997164
COIS- The authors declare no competing financial interest.
EDAT- 2016/04/13 00:00
MHDA- 2016/04/13 00:01
CRDT- 2019/05/28 06:00
PHST- 2019/05/28 06:00 [entrez]
PHST- 2016/04/13 00:00 [pubmed]
PHST- 2016/04/13 00:01 [medline]
AID - 10.1021/acs.iecr.6b00098 [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2016 Apr 13;55(14):4089-4097. doi:
      10.1021/acs.iecr.6b00098. Epub 2016 Mar 21.

PMID- 29170756
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 2372-0980 (Print)
IS  - 2372-0980 (Linking)
VI  - 4
IP  - 1
DP  - 2016
TI  - Healthy Hunger-Free Kids Act Increases Phytochemicals in Menus and
      Curriculum Furthers Identification of Phytochemical-Rich Foods.
LID - 10.15226/jnhfs.2016.00156 [doi]
AB  - Objective: This study evaluated whether providing the Fruits and
      Vegetables (F/V) required by the Healthy Hunger-Free Kids Act (HHFKA)
      increased phytochemical/antioxidant content of school lunches.
      Additionally, the ability of adolescents to apply their nutritional
      knowledge following participation in a nutrition-focused science-based
      curriculum was assessed. Methods: Changes in antioxidant/phytochemical
      content from F/V offered in school lunch menus were analyzed Pre-and
      Post-HHFKA. Food logs completed by 717 youth aged 10-18 were analyzed for
      correctly identifying "fighting foods". Results: Significant increases in
      antioxidant/phytochemical content resulted following implementation of
      HHFKA (P<0.05). Seventy-five percent [0, 100] of the time students
      accurately identified "fighting foods" in their one-day in-school food
      log (n=468). Conclusions and Implications: Creatively incorporating
      nutrition education into core curriculum, when paired with a supportive
      built environment that increases F/V access (HHFKA), generates a
      multilevel intervention promoting F/V consumption among school-aged
      youth.
FAU - Brewer, D
AU  - Brewer D
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, USA.
FAU - Hershberger, S
AU  - Hershberger S
AD  - Miami University of Ohio, Department of Chemistry and Biochemistry,
      Oxford, USA.
FAU - Gaetke, L
AU  - Gaetke L
AD  - University of Kentucky, Department of Dietetics and Human Nutrition,
      Lexington, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R25 OD011090/OD/NIH HHS/United States
GR  - R25 RR032208/RR/NCRR NIH HHS/United States
PT  - Journal Article
DEP - 20160309
PL  - United States
TA  - J Nutrit Health Food Sci
JT  - Journal of nutritional health & food science
JID - 101643744
PMC - PMC5697734
MID - NIHMS849928
OTO - NOTNLM
OT  - Environmental contaminants
OT  - Healthy Hunger-Free Kids Act
OT  - Phytochemicals
OT  - School lunch and/or National school lunch program
EDAT- 2016/01/01 00:00
MHDA- 2016/01/01 00:01
CRDT- 2017/11/25 06:00
PHST- 2017/11/25 06:00 [entrez]
PHST- 2016/01/01 00:00 [pubmed]
PHST- 2016/01/01 00:01 [medline]
AID - 10.15226/jnhfs.2016.00156 [doi]
PST - ppublish
SO  - J Nutrit Health Food Sci. 2016;4(1). doi: 10.15226/jnhfs.2016.00156. Epub
      2016 Mar 9.

PMID- 29392097
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 2168-0485 (Print)
IS  - 2168-0485 (Linking)
VI  - 4
IP  - 3
DP  - 2016 Mar 7
TI  - Functionalization of flat sheet and hollow fiber microfiltration
      membranes for water applications.
PG  - 907-918
LID - 10.1021/acssuschemeng.5b01005 [doi]
AB  - Functionalized membranes containing nanoparticles provide a novel
      platform for organic pollutant degradation reactions and for selective
      removal of contaminants without the drawback of potential nanoparticle
      loss to the environment. These eco-friendly and sustainable technology
      approaches allow various water treatment applications through enhanced
      water transport through the membrane pores. This paper presents "green"
      techniques to create nanocomposite materials based on sponge-like
      membranes for water remediation applications involving chlorinated
      organic compounds. First, hydrophobic hollow fiber microfiltration
      membranes (HF) of polyvinylidene fluoride were hydrophilized using a
      water-based green chemistry process with polyvinylpyrrolidone and
      persulfate. HF and flat sheet membrane pores were then functionalized
      with poly(acrylic acid) and synthesized Fe/Pd nanoparticles. Surface
      modifications were determined by contact angle, surface free energy and
      infrared spectroscopy. The synthesized nanoparticles were characterized
      by electronic microscopy, X-ray spectrometry and image analysis.
      Nanoparticle sizes of 193 and 301 nm were obtained for each of the
      membranes. Depending on the concentration of the dopant (Pd) in the
      membrane, catalytic activity (established by trichloroethylene (TCE)
      reduction), was enhanced up to tenfold compared to other reported
      results. Chloride produced in reduction was close to the stoichiometric
      3/1 (Cl(-)/TCE), indicating complete absence of reaction intermediates.
FAU - Hernandez, Sebastian
AU  - Hernandez S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Lei, Shi
AU  - Lei S
AD  - Singapore Membrane Technology Centre, Nanyang Technological University,
      639798, Singapore.
FAU - Rong, Wang
AU  - Rong W
AD  - Singapore Membrane Technology Centre, Nanyang Technological University,
      639798, Singapore.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20151214
PL  - United States
TA  - ACS Sustain Chem Eng
JT  - ACS sustainable chemistry & engineering
JID - 101608852
PMC - PMC5790112
MID - NIHMS936563
OTO - NOTNLM
OT  - Sponge-like membranes
OT  - TCE dechlorination
OT  - nanoparticles
OT  - surface modification
COIS- Notes The authors declare no competing financial interest.
EDAT- 2016/03/07 00:00
MHDA- 2016/03/07 00:01
CRDT- 2018/02/03 06:00
PHST- 2018/02/03 06:00 [entrez]
PHST- 2016/03/07 00:00 [pubmed]
PHST- 2016/03/07 00:01 [medline]
AID - 10.1021/acssuschemeng.5b01005 [doi]
PST - ppublish
SO  - ACS Sustain Chem Eng. 2016 Mar 7;4(3):907-918. doi:
      10.1021/acssuschemeng.5b01005. Epub 2015 Dec 14.

PMID- 25586614
OWN - NLM
STAT- MEDLINE
DCOM- 20161013
LR  - 20181202
IS  - 1614-7499 (Electronic)
IS  - 0944-1344 (Linking)
VI  - 23
IP  - 3
DP  - 2016 Feb
TI  - Exercise protects against PCB-induced inflammation and associated
      cardiovascular risk factors.
PG  - 2201-11
LID - 10.1007/s11356-014-4062-6 [doi]
AB  - Polychlorinated biphenyls (PCBs) are persistent environmental pollutants
      that contribute to the initiation of cardiovascular disease. Exercise has
      been shown to reduce the risk of cardiovascular disease; however, whether
      exercise can modulate PCB-induced vascular endothelial dysfunction and
      associated cardiovascular risk factors is unknown. We examined the
      effects of exercise on coplanar PCB-induced cardiovascular risk factors
      including oxidative stress, inflammation, impaired glucose tolerance,
      hypercholesteremia, and endothelium-dependent relaxation. Male ApoE(-/-)
      mice were divided into sedentary and exercise groups (voluntary wheel
      running) over a 12-week period. Half of each group was exposed to vehicle
      or PCB 77 at weeks 1, 2, 9, and 10. For ex vivo studies, male C57BL/6
      mice exercised via voluntary wheel training for 5 weeks and then were
      administered with vehicle or PCB 77 24 h before vascular reactivity
      studies were performed. Exposure to coplanar PCB increased risk factors
      associated with cardiovascular disease, including oxidative stress and
      systemic inflammation, glucose intolerance, and hypercholesteremia. The
      12-week exercise intervention significantly reduced these proatherogenic
      parameters. Exercise also upregulated antioxidant enzymes including phase
      II detoxification enzymes. Sedentary animals exposed to PCB 77 exhibited
      endothelial dysfunction as demonstrated by significant impairment of
      endothelium-dependent relaxation, which was prevented by exercise.
      Lifestyle modifications such as aerobic exercise could be utilized as a
      therapeutic approach for the prevention of adverse cardiovascular health
      effects induced by environmental pollutants such as PCBs.
FAU - Murphy, Margaret O
AU  - Murphy MO
AD  - Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, KY, 40536, USA.
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      900 S. Limestone Street, Lexington, KY, 40536, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      900 S. Limestone Street, Lexington, KY, 40536, USA.
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA.
FAU - Han, Sung Gu
AU  - Han SG
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      900 S. Limestone Street, Lexington, KY, 40536, USA.
AD  - Department of Food Science and Biotechnology of Animal Resources, College
      of Animal Bioscience and Technology, Konkuk University, Seoul, 143-701,
      Republic of Korea.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      900 S. Limestone Street, Lexington, KY, 40536, USA.
AD  - Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      900 S. Limestone Street, Lexington, KY, 40536, USA.
AD  - Division of Cardiovascular Medicine, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA.
FAU - Esser, Karyn
AU  - Esser K
AD  - Department of Physiology, College of Medicine, University of Kentucky,
      Lexington, KY, 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Department of Pharmacology and Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, KY, 40536, USA. bhennig@uky.edu.
AD  - University of Kentucky Superfund Research Center, University of Kentucky,
      900 S. Limestone Street, Lexington, KY, 40536, USA. bhennig@uky.edu.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY, 40536, USA.
      bhennig@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 RR026884/RR/NCRR NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
GR  - R01 HL120507/HL/NHLBI NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20150115
PL  - Germany
TA  - Environ Sci Pollut Res Int
JT  - Environmental science and pollution research international
JID - 9441769
RN  - 0 (Environmental Pollutants)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/*etiology/immunology/physiopathology/*prevention
      & control
MH  - Environmental Pollutants/toxicity
MH  - *Exercise
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Motor Activity
MH  - Oxidative Stress/drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Risk Factors
PMC - PMC4503535
MID - NIHMS655864
OTO - NOTNLM
OT  - Antioxidant response
OT  - Cardiovascular disease
OT  - Endothelial function
OT  - Exercise
OT  - Inflammation
OT  - Oxidative stress
OT  - Polychlorinated biphenyl
EDAT- 2015/01/15 06:00
MHDA- 2016/10/14 06:00
CRDT- 2015/01/15 06:00
PHST- 2014/10/31 00:00 [received]
PHST- 2014/12/30 00:00 [accepted]
PHST- 2015/01/15 06:00 [entrez]
PHST- 2015/01/15 06:00 [pubmed]
PHST- 2016/10/14 06:00 [medline]
AID - 10.1007/s11356-014-4062-6 [doi]
AID - 10.1007/s11356-014-4062-6 [pii]
PST - ppublish
SO  - Environ Sci Pollut Res Int. 2016 Feb;23(3):2201-11. doi:
      10.1007/s11356-014-4062-6. Epub 2015 Jan 15.

PMID- 25877901
OWN - NLM
STAT- MEDLINE
DCOM- 20161013
LR  - 20181202
IS  - 1614-7499 (Electronic)
IS  - 0944-1344 (Linking)
VI  - 23
IP  - 3
DP  - 2016 Feb
TI  - Polychlorinated biphenyls and links to cardiovascular disease.
PG  - 2160-72
LID - 10.1007/s11356-015-4479-6 [doi]
AB  - The pathology of cardiovascular disease is multi-faceted, with links to
      many modifiable and non-modifiable risk factors. Epidemiological evidence
      now implicates exposure to persistent organic pollutants, such as
      polychlorinated biphenyls (PCBs), with an increased risk of developing
      diabetes, hypertension, and obesity; all of which are clinically relevant
      to the onset and progression of cardiovascular disease. PCBs exert their
      cardiovascular toxicity either directly or indirectly via multiple
      mechanisms, which are highly dependent on the type and concentration of
      PCBs present. However, many PCBs may modulate cellular signaling pathways
      leading to common detrimental outcomes including induction of chronic
      oxidative stress, inflammation, and endocrine disruption. With the
      abundance of potential toxic pollutants increasing globally, it is
      critical to identify sensible means of decreasing associated disease
      risks. Emerging evidence now implicates a protective role of lifestyle
      modifications such as increased exercise and/or nutritional modulation
      via anti-inflammatory foods, which may help to decrease the vascular
      toxicity of PCBs. This review will outline the current state of knowledge
      linking coplanar and non-coplanar PCBs to cardiovascular disease and
      describe the possible molecular mechanism of this association.
FAU - Perkins, Jordan T
AU  - Perkins JT
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, KY, 40536, USA.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food, and
      Environment, University of Kentucky, Lexington, KY, 40536, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, KY, 40536, USA.
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA.
FAU - Newsome, Bradley J
AU  - Newsome BJ
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, KY, 40536, USA.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food, and
      Environment, University of Kentucky, Lexington, KY, 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, 900 S. Limestone
      Street, Lexington, KY, 40536, USA. bhennig@uky.edu.
AD  - Department of Animal and Food Sciences, College of Agriculture, Food, and
      Environment, University of Kentucky, Lexington, KY, 40536, USA.
      bhennig@uky.edu.
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY, 40536, USA. bhennig@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20150417
PL  - Germany
TA  - Environ Sci Pollut Res Int
JT  - Environmental science and pollution research international
JID - 9441769
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/*etiology/metabolism
MH  - Humans
MH  - Oxidative Stress
MH  - Polychlorinated Biphenyls/*toxicity
PMC - PMC4609220
MID - NIHMS681912
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Cardiovascular risk factors
OT  - Inflammation
OT  - Nutritional modulation
OT  - Oxidative stress
OT  - Persistent organic pollutants
OT  - Polychlorinated biphenyls
EDAT- 2015/04/17 06:00
MHDA- 2016/10/14 06:00
CRDT- 2015/04/17 06:00
PHST- 2015/01/19 00:00 [received]
PHST- 2015/03/31 00:00 [accepted]
PHST- 2015/04/17 06:00 [entrez]
PHST- 2015/04/17 06:00 [pubmed]
PHST- 2016/10/14 06:00 [medline]
AID - 10.1007/s11356-015-4479-6 [doi]
AID - 10.1007/s11356-015-4479-6 [pii]
PST - ppublish
SO  - Environ Sci Pollut Res Int. 2016 Feb;23(3):2160-72. doi:
      10.1007/s11356-015-4479-6. Epub 2015 Apr 17.

PMID- 26878794
OWN - NLM
STAT- MEDLINE
DCOM- 20161107
LR  - 20181113
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 28
DP  - 2016 Feb
TI  - EGCG prevents PCB-126-induced endothelial cell inflammation via
      epigenetic modifications of NF-kappaB target genes in human endothelial
      cells.
PG  - 164-70
LID - 10.1016/j.jnutbio.2015.10.003 [doi]
LID - S0955-2863(15)00296-X [pii]
AB  - Anti-inflammatory polyphenols, such as epigallocatechin-3-gallate (EGCG),
      have been shown to protect against the toxicity of environmental
      pollutants. It is well known that bioactive food compounds such as
      polyphenols may exert their protection by modulating inflammatory
      pathways regulated through nuclear factor-kappa B (NF-kappaB) signaling.
      EGCG has been reported to inhibit NF-kappaB activation. We hypothesize
      that EGCG can protect against polychlorinated biphenyl (PCB)-induced
      endothelial inflammation in part through epigenetic regulation of NF-
      kappaB-regulated inflammatory genes. In order to test this hypothesis,
      human endothelial cells (EA.hy926) were exposed to physiologically
      relevant levels of coplanar PCB 126 and/or 15 or 30 muM of EGCG, followed
      by quantification of NF-kappaB subunit p65, histone acetyltransferase
      p300 and histone deacetylases (HDACs) accumulation through chromatin
      immunoprecipitation assay in the promoter region of inflammatory genes.
      In addition, the enrichment of the acetylated H3 was also quantified. PCB
      126 exposure increased the expression of vascular inflammatory mediators,
      including interleukin (IL)-6, C-reactive protein, intercellular adhesion
      molecule-1, vascular cell adhesion molecule-1 and IL-1alpha/beta, which
      were prevented by pretreatment with EGCG. This inhibitory effect by EGCG
      correlated with abolished nuclear import of p65, decreased chromatin
      binding of p65 and p300, as well as increased chromatin binding of HDAC
      1/2. Furthermore, EGCG induced hypoacetylation of H3, which accounts for
      deactivation of downstream genes. These data suggest that EGCG-induced
      epigenetic modifications can decrease PCB-induced vascular toxicity.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Liu, Dandan
AU  - Liu D
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY 40536.
FAU - Perkins, Jordan T
AU  - Perkins JT
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY 40536.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536;
      Department of Animal and Food Sciences, College of Agriculture, Food and
      Environment, University of Kentucky, Lexington, KY 40536. Electronic
      address: bhennig@uky.edu.
LA  - eng
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 8 P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20151026
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Chromatin)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Transcription Factor RelA)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Acetylation
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cell Line
MH  - Cell Nucleus/metabolism
MH  - Chromatin/metabolism
MH  - Endothelium, Vascular/cytology/*drug effects
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Inflammation/chemically induced/*prevention & control
MH  - Inflammation Mediators/metabolism
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Protein Transport
MH  - Transcription Factor RelA/metabolism
PMC - PMC4757812
MID - NIHMS733643
OTO - NOTNLM
OT  - EGCG
OT  - HDACs
OT  - PCB 126
OT  - Vascular inflammation
OT  - p300
OT  - p65
EDAT- 2016/02/18 06:00
MHDA- 2016/11/08 06:00
CRDT- 2016/02/17 06:00
PHST- 2015/08/27 00:00 [received]
PHST- 2015/10/19 00:00 [revised]
PHST- 2015/10/22 00:00 [accepted]
PHST- 2016/02/17 06:00 [entrez]
PHST- 2016/02/18 06:00 [pubmed]
PHST- 2016/11/08 06:00 [medline]
AID - S0955-2863(15)00296-X [pii]
AID - 10.1016/j.jnutbio.2015.10.003 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2016 Feb;28:164-70. doi: 10.1016/j.jnutbio.2015.10.003.
      Epub 2015 Oct 26.

PMID- 30979126
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2073-4360 (Electronic)
IS  - 2073-4360 (Linking)
VI  - 8
IP  - 2
DP  - 2016 Jan 27
TI  - Development of PVDF Membrane Nanocomposites via Various Functionalization
      Approaches for Environmental Applications.
LID - E32 [pii]
LID - 10.3390/polym8020032 [doi]
AB  - Membranes are finding wide applications in various fields spanning
      biological, water, and energy areas. Synthesis of membranes to provide
      tunable flux, metal sorption, and catalysis has been done through pore
      functionalization of microfiltration (MF) type membranes with responsive
      behavior. This methodology provides an opportunity to improve synthetic
      membrane performance via polymer fabrication and surface modification. By
      optimizing the polymer coagulation conditions in phase inversion
      fabrication, spongy polyvinylidene fluoride (PVDF) membranes with high
      porosity and large internal pore volume were created in lab and full
      scale. This robust membrane shows a promising mechanical strength as well
      as high capacity for loading of adsorptive and catalytic materials. By
      applying surface modification techniques, synthetic membranes with
      different functionality (carboxyl, amine, and nanoparticle-based) were
      obtained. These functionalities provide an opportunity to fine-tune the
      membrane surface properties such as charge and reactivity. The
      incorporation of stimuli-responsive acrylic polymers (polyacrylic acid or
      sodium polyacrylate) in membrane pores also results in tunable pore size
      and ion-exchange capacity. This provides the added benefits of adjustable
      membrane permeability and metal capture efficiency. The equilibrium and
      dynamic binding capacity of these functionalized spongy membranes were
      studied via calcium ion-exchange. Iron/palladium catalytic nanoparticles
      were immobilized in the polymer matrix in order to perform the
      challenging degradation of the environmental pollutant trichloroethylene
      (TCE).
FAU - Davenport, Douglas M
AU  - Davenport DM
AD  - Department of Chemical and Materials Engineering, and Center of Membrane
      Sciences, University of Kentucky, Lexington, KY 40506, USA.
      dougdvnprt@gmail.com.
FAU - Gui, Minghui
AU  - Gui M
AD  - Department of Chemical and Materials Engineering, and Center of Membrane
      Sciences, University of Kentucky, Lexington, KY 40506, USA.
      guiminghui@gmail.com.
FAU - Ormsbee, Lindell R
AU  - Ormsbee LR
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506, USA. lindell.ormsbee@uky.edu.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, and Center of Membrane
      Sciences, University of Kentucky, Lexington, KY 40506, USA. db@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20160127
PL  - Switzerland
TA  - Polymers (Basel)
JT  - Polymers
JID - 101545357
PMC - PMC6432535
OTO - NOTNLM
OT  - free radical polymerization
OT  - phase inversion
OT  - polyelectrolyte
OT  - water remediation
EDAT- 2016/01/27 00:00
MHDA- 2016/01/27 00:01
CRDT- 2019/04/14 06:00
PHST- 2015/11/01 00:00 [received]
PHST- 2016/01/21 00:00 [revised]
PHST- 2016/01/22 00:00 [accepted]
PHST- 2019/04/14 06:00 [entrez]
PHST- 2016/01/27 00:00 [pubmed]
PHST- 2016/01/27 00:01 [medline]
AID - polym8020032 [pii]
AID - 10.3390/polym8020032 [doi]
PST - epublish
SO  - Polymers (Basel). 2016 Jan 27;8(2). pii: polym8020032. doi:
      10.3390/polym8020032.

PMID- 26716948
OWN - NLM
STAT- MEDLINE
DCOM- 20161220
LR  - 20181113
IS  - 1939-022X (Electronic)
IS  - 1939-0211 (Linking)
VI  - 13
IP  - 5
DP  - 2016
TI  - Branched-Chain Amino Acid Supplementation in Combination with Voluntary
      Running Improves Body Composition in Female C57BL/6 Mice.
PG  - 473-86
LID - 10.3109/19390211.2015.1112866 [doi]
AB  - Exercise is an inexpensive intervention that may be used to reduce
      obesity and its consequences. In addition, many individuals who regularly
      exercise utilize dietary supplements to enhance their exercise routine
      and to accelerate fat loss or increase lean mass. Branched-chain amino
      acids (BCAAs) are a popular supplement and have been shown to produce a
      number of beneficial effects in rodent models and humans. Therefore, we
      hypothesized that BCAA supplementation would protect against high fat
      diet (HFD)-induced glucose intolerance and obesity in mice with and
      without access to exercise. We subjected 80 female C57BL/6 mice to a
      paradigm of HFD feeding, exercise in the form of voluntary wheel running,
      and BCAA supplementation in the drinking water for 16 weeks (n = 10 per
      group). Body weight was monitored weekly, while food and water
      consumption were recorded twice weekly. During the 5th, 10th, and 15th
      weeks of treatment, glucose tolerance and body composition were analyzed.
      Exercise significantly improved glucose tolerance in both control-fed and
      HFD-fed mice. BCAA supplementation, however, did not significantly alter
      glucose tolerance in any treatment group. While BCAA supplements did not
      improve lean to fat mass ratio in sedentary mice, it significantly
      augmented the effects of exercise on this parameter.
FAU - Platt, Kristen M
AU  - Platt KM
AD  - a Department of Pharmacology and Nutritional Sciences, College of
      Medicine , University of Kentucky , Lexington , KY , USA.
FAU - Charnigo, Richard J
AU  - Charnigo RJ
AD  - b Department of Biostatistics, College of Public Health , University of
      Kentucky , Lexington , KY , USA.
FAU - Shertzer, Howard G
AU  - Shertzer HG
AD  - c Department of Environmental Health and Center for Environmental
      Genetics , University of Cincinnati Medical Center , Cincinnati , OH ,
      USA.
FAU - Pearson, Kevin J
AU  - Pearson KJ
AD  - a Department of Pharmacology and Nutritional Sciences, College of
      Medicine , University of Kentucky , Lexington , KY , USA.
LA  - eng
GR  - 5P20 RR021954-05/RR/NCRR NIH HHS/United States
GR  - DK07778/DK/NIDDK NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 8P20 GM103527-05/GM/NIGMS NIH HHS/United States
GR  - R01 DK090460/DK/NIDDK NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P20 RR021954/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20151230
PL  - England
TA  - J Diet Suppl
JT  - Journal of dietary supplements
JID - 101249830
RN  - 0 (Amino Acids, Branched-Chain)
RN  - 0 (Drinking Water)
SB  - IM
MH  - Amino Acids, Branched-Chain/*administration & dosage
MH  - Animals
MH  - Body Composition/*drug effects
MH  - Body Weight
MH  - Diet, High-Fat/adverse effects
MH  - *Dietary Supplements
MH  - Drinking Water
MH  - Female
MH  - Glucose Intolerance/drug therapy
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Obesity/drug therapy
MH  - *Physical Conditioning, Animal
PMC - PMC4788571
MID - NIHMS752357
OTO - NOTNLM
OT  - BCAA
OT  - exercise
OT  - high fat diet
OT  - obesity
OT  - rodent
OT  - supplement
EDAT- 2015/12/31 06:00
MHDA- 2016/12/21 06:00
CRDT- 2015/12/31 06:00
PHST- 2015/12/31 06:00 [entrez]
PHST- 2015/12/31 06:00 [pubmed]
PHST- 2016/12/21 06:00 [medline]
AID - 10.3109/19390211.2015.1112866 [doi]
PST - ppublish
SO  - J Diet Suppl. 2016;13(5):473-86. doi: 10.3109/19390211.2015.1112866. Epub
      2015 Dec 30.

PMID- 26519613
OWN - NLM
STAT- MEDLINE
DCOM- 20160307
LR  - 20181113
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 289
IP  - 3
DP  - 2015 Dec 15
TI  - Exposure to coplanar PCBs induces endothelial cell inflammation through
      epigenetic regulation of NF-kappaB subunit p65.
PG  - 457-65
LID - 10.1016/j.taap.2015.10.015 [doi]
LID - S0041-008X(15)30118-6 [pii]
AB  - Epigenetic modifications of DNA and histones alter cellular phenotypes
      without changing genetic codes. Alterations of epigenetic marks can be
      induced by exposure to environmental pollutants and may contribute to
      associated disease risks. Here we test the hypothesis that endothelial
      cell dysfunction induced by exposure to polychlorinated biphenyls (PCBs)
      is mediated in part though histone modifications. In this study, human
      vascular endothelial cells were exposed to physiologically relevant
      concentrations of several PCBs congeners (e.g., PCBs 77, 118, 126 and
      153) followed by quantification of inflammatory gene expression and
      changes of histone methylation. Only exposure to coplanar PCBs 77 and 126
      induced the expression of histone H3K9 trimethyl demethylase jumonji
      domain-containing protein 2B (JMJD2B) and nuclear factor-kappa B (NF-
      kappaB) subunit p65, activated NF-kappaB signaling as evidenced by
      nuclear translocation of p65, and up-regulated p65 target inflammatory
      genes, such as interleukin (IL)-6, C-reactive protein (CRP),
      intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion
      molecule-1 (VCAM-1), and IL-1alpha/beta. The increased accumulation of
      JMJD2B in the p65 promoter led to a depletion of H3K9me3 repression mark,
      which accounts for the observed up-regulation of p65 and associated
      inflammatory genes. JMJD2B gene knockdown confirmed a critical role for
      this histone demethylase in mediating PCB-induced inflammation of the
      vascular endothelium. Finally, it was determined, via chemical
      inhibition, that PCB-induced up-regulation of JMJD2B was estrogen
      receptor-alpha (ER-alpha) dependent. These data suggest that coplanar
      PCBs may exert endothelial cell toxicity through changes in histone
      modifications.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Liu, Dandan
AU  - Liu D
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      United States; Department of Animal and Food Sciences, College of
      Agriculture, Food and Environment, University of Kentucky, Lexington, KY
      40536, United States.
FAU - Perkins, Jordan T
AU  - Perkins JT
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      United States; Department of Animal and Food Sciences, College of
      Agriculture, Food and Environment, University of Kentucky, Lexington, KY
      40536, United States.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      United States; Graduate Center for Toxicology and Cancer Biology, College
      of Medicine, University of Kentucky, Lexington, KY 40536, United States.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      United States; Department of Animal and Food Sciences, College of
      Agriculture, Food and Environment, University of Kentucky, Lexington, KY
      40536, United States. Electronic address: bhennig@uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 8 P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20151028
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Environmental Pollutants)
RN  - 0 (Histones)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.11.1 (eIF-2 Kinase)
SB  - IM
MH  - C-Reactive Protein/genetics
MH  - Cell Adhesion/drug effects/genetics
MH  - Cells, Cultured
MH  - Endothelial Cells/*drug effects
MH  - Endothelium, Vascular/drug effects
MH  - Environmental Pollutants/*adverse effects
MH  - Epigenesis, Genetic/*drug effects/genetics
MH  - Histones/genetics
MH  - Humans
MH  - Inflammation/*chemically induced/genetics
MH  - Intercellular Adhesion Molecule-1/genetics
MH  - Interleukin-6/genetics
MH  - Methylation/drug effects
MH  - NF-kappa B/*genetics
MH  - Polychlorinated Biphenyls/*adverse effects
MH  - Signal Transduction/drug effects/genetics
MH  - Tumor Necrosis Factor-alpha/genetics
MH  - Up-Regulation/drug effects/genetics
MH  - Vascular Cell Adhesion Molecule-1/genetics
MH  - eIF-2 Kinase/*genetics
PMC - PMC4662647
MID - NIHMS734966
OTO - NOTNLM
OT  - ER-alpha
OT  - Epigenetics and vascular inflammation
OT  - H3K9me3
OT  - JMJD2B
OT  - PCBs
OT  - p65
EDAT- 2015/11/01 06:00
MHDA- 2016/03/08 06:00
CRDT- 2015/11/01 06:00
PHST- 2015/08/05 00:00 [received]
PHST- 2015/10/23 00:00 [revised]
PHST- 2015/10/26 00:00 [accepted]
PHST- 2015/11/01 06:00 [entrez]
PHST- 2015/11/01 06:00 [pubmed]
PHST- 2016/03/08 06:00 [medline]
AID - S0041-008X(15)30118-6 [pii]
AID - 10.1016/j.taap.2015.10.015 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2015 Dec 15;289(3):457-65. doi:
      10.1016/j.taap.2015.10.015. Epub 2015 Oct 28.

PMID- 26354995
OWN - NLM
STAT- MEDLINE
DCOM- 20160104
LR  - 20181113
IS  - 1521-0103 (Electronic)
IS  - 0022-3565 (Linking)
VI  - 355
IP  - 2
DP  - 2015 Nov
TI  - Loss of multidrug resistance-associated protein 1 potentiates chronic
      doxorubicin-induced cardiac dysfunction in mice.
PG  - 280-7
LID - 10.1124/jpet.115.225581 [doi]
AB  - Doxorubicin (DOX), an effective cancer chemotherapeutic agent, induces
      dose-dependent cardiotoxicity, in part due to its ability to cause
      oxidative stress. We investigated the role of multidrug resistance-
      associated protein 1 (Mrp1/Abcc1) in DOX-induced cardiotoxicity in C57BL
      wild-type (WT) mice and their Mrp1 null (Mrp1(-/-)) littermates. Male
      mice were administered intraperitoneal DOX (3 or 2 mg/kg body weight) or
      saline twice a week for 3 weeks and examined 2 weeks after the last dose
      (protocol A total dose: 18 mg/kg) or for 5 weeks, and mice were examined
      48 hours and 2 weeks after the last dose (protocol B total dose: 20
      mg/kg). Chronic DOX induced body weight loss and hemotoxicity, adverse
      effects significantly exacerbated in Mrp1(-/-) versus WT mice. In the
      heart, significantly higher basal levels of glutathione (1.41-fold +/-
      0.27-fold) and glutathione disulfide (1.35-fold +/- 0.16-fold) were
      detected in Mrp1(-/-) versus WT mice, and there were comparable decreases
      in the glutathione/glutathione disulfide ratio in WT and Mrp1(-/-) mice
      after DOX administration. Surprisingly, DOX induced comparable increases
      in 4-hydroxynonenal glutathione conjugate concentration in hearts from WT
      and Mrp1(-/-) mice. However, more DOX-induced apoptosis was detected in
      Mrp1(-/-) versus WT hearts (P < 0.05) (protocol A), and cardiac function,
      assessed by measurement of fractional shortening and ejection fraction
      with echocardiography, was significantly decreased by DOX in Mrp1(-/-)
      versus WT mice (P < 0.05; 95% confidence intervals of 20.0%-24.3% versus
      23.7%-29.5% for fractional shortening, and 41.5%-48.4% versus 47.7%-56.7%
      for ejection fraction; protocol B). Together, these data indicate that
      Mrp1 protects the mouse heart against chronic DOX-induced cardiotoxicity.
CI  - Copyright (c) 2015 by The American Society for Pharmacology and
      Experimental Therapeutics.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky.
FAU - Deng, Jun
AU  - Deng J
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky.
FAU - Wang, Chi
AU  - Wang C
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky.
FAU - St Clair, Daret
AU  - St Clair D
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky.
FAU - Vore, Mary
AU  - Vore M
AD  - Department of Toxicology and Cancer Biology (W.Z., J.D., D.S.C., M.V.),
      Division of Cardiovascular Medicine, (M.S., A.J.M), and Markey Cancer
      Center (C.W.), College of Medicine, University of Kentucky, Lexington,
      Kentucky maryv@email.uky.edu.
LA  - eng
GR  - R01CA139844/CA/NCI NIH HHS/United States
GR  - P30CA177558/CA/NCI NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P30 CA177558/CA/NCI NIH HHS/United States
GR  - R01 CA139844/CA/NCI NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20150909
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Antibiotics, Antineoplastic)
RN  - 0 (Multidrug Resistance-Associated Proteins)
RN  - 0 (glutathionyl 4-hydroxy-2-nonenal conjugate)
RN  - 80168379AG (Doxorubicin)
RN  - GAN16C9B8O (Glutathione)
RN  - ULW86O013H (Glutathione Disulfide)
RN  - Y49M64GZ4Q (multidrug resistance-associated protein 1)
SB  - IM
MH  - Animals
MH  - Antibiotics, Antineoplastic/*toxicity
MH  - Apoptosis
MH  - Cardiotoxicity/metabolism/pathology/*physiopathology
MH  - Doxorubicin/*toxicity
MH  - Glutathione/analogs & derivatives/metabolism
MH  - Glutathione Disulfide/metabolism
MH  - Leukocyte Count
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Multidrug Resistance-Associated Proteins/*genetics
MH  - Myocardial Contraction
MH  - Myocardium/metabolism/pathology
MH  - Systole
MH  - Ventricular Dysfunction, Left/chemically induced/physiopathology
PMC - PMC4613956
EDAT- 2015/09/12 06:00
MHDA- 2016/01/05 06:00
CRDT- 2015/09/11 06:00
PHST- 2015/04/29 00:00 [received]
PHST- 2015/08/26 00:00 [accepted]
PHST- 2015/09/11 06:00 [entrez]
PHST- 2015/09/12 06:00 [pubmed]
PHST- 2016/01/05 06:00 [medline]
AID - jpet.115.225581 [pii]
AID - 10.1124/jpet.115.225581 [doi]
PST - ppublish
SO  - J Pharmacol Exp Ther. 2015 Nov;355(2):280-7. doi:
      10.1124/jpet.115.225581. Epub 2015 Sep 9.

PMID- 26354996
OWN - NLM
STAT- MEDLINE
DCOM- 20160104
LR  - 20181113
IS  - 1521-0103 (Electronic)
IS  - 0022-3565 (Linking)
VI  - 355
IP  - 2
DP  - 2015 Nov
TI  - Elevated glutathione is not sufficient to protect against doxorubicin-
      induced nuclear damage in heart in multidrug resistance-associated
      protein 1 (Mrp1/Abcc1) null mice.
PG  - 272-9
LID - 10.1124/jpet.115.225490 [doi]
AB  - Cardiotoxicity is a major dose-limiting adverse effect of doxorubicin
      (DOX), mediated in part by overproduction of reactive oxygen species and
      oxidative stress. Abcc1 (Mrp1) mediates the efflux of reduced and
      oxidized glutathione (GSH, GSSG) and is also a major transporter that
      effluxes the GSH conjugate of 4-hydroxy-2-nonenal (HNE; GS-HNE), a toxic
      product of lipid peroxidation formed during oxidative stress. To assess
      the role of Mrp1 in protecting the heart from DOX-induced cardiac injury,
      wild-type (WT) and Mrp1 null (Mrp1(-/-)) C57BL/6 littermate mice were
      administered DOX (15 mg/kg) or saline (7.5 ml/kg) i.v., and heart
      ventricles were examined at 72 hours. Morphometric analysis by electron
      microscopy revealed extensive injuries in cytosol, mitochondria, and
      nuclei of DOX-treated mice in both genotypes. Significantly more severely
      injured nuclei were observed in Mrp1(-/-) versus WT mice (P = 0.031). GSH
      and the GSH/GSSG ratio were significantly increased in treatment-naive
      Mrp1(-/-) versus WT mice; GSH remained significantly higher in Mrp1(-/-)
      versus WT mice after saline and DOX treatment, with no changes in GSSG or
      GSH/GSSG. GS-HNE, measured by mass spectrometry, was lower in the hearts
      of treatment-naive Mrp1(-/-) versus WT mice (P < 0.05). DOX treatment
      decreased GS-HNE in WT but not Mrp1(-/-) mice, so that GS-HNE was
      modestly but significantly higher in Mrp1(-/-) versus WT hearts after
      DOX. Expression of enzymes mediating GSH synthesis and antioxidant
      proteins did not differ between genotypes. Thus, despite elevated GSH
      levels in Mrp1(-/-) hearts, DOX induced significantly more injury in the
      nuclei of Mrp1(-/-) versus WT hearts.
CI  - Copyright (c) 2015 by The American Society for Pharmacology and
      Experimental Therapeutics.
FAU - Deng, Jun
AU  - Deng J
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Coy, Donna
AU  - Coy D
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Wang, Chi
AU  - Wang C
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Chaiswing, Luksana
AU  - Chaiswing L
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - St Clair, Daret
AU  - St Clair D
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.).
FAU - Vore, Mary
AU  - Vore M
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.)
      maryv@email.uky.edu paiboon@fdu.edu.
FAU - Jungsuwadee, Paiboon
AU  - Jungsuwadee P
AD  - Department of Toxicology and Cancer Biology (J.D., D.C., L.C., W.Z.,
      D.St.C., M.V.), Division of Cardiovascular Medicine (M.S., A.J.M.),
      Markey Cancer Center (C.W.) University of Kentucky, Lexington, Kentucky;
      Department of Pathology and Laboratory Medicine, William S. Middleton
      Memorial Veterans Administration Hospital and University of Wisconsin
      Medical School, Madison Wisconsin (L.C.); and School of Pharmacy,
      Fairleigh Dickinson University, Florham Park, New Jersey (P.J.)
      maryv@email.uky.edu paiboon@fdu.edu.
LA  - eng
GR  - R01CA139844/CA/NCI NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P30 CA177558/CA/NCI NIH HHS/United States
GR  - R01 CA139844/CA/NCI NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P20 RR021954/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20150909
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Antibiotics, Antineoplastic)
RN  - 0 (Multidrug Resistance-Associated Proteins)
RN  - 0 (glutathionyl 4-hydroxy-2-nonenal conjugate)
RN  - 80168379AG (Doxorubicin)
RN  - GAN16C9B8O (Glutathione)
RN  - ULW86O013H (Glutathione Disulfide)
RN  - Y49M64GZ4Q (multidrug resistance-associated protein 1)
SB  - IM
MH  - Animals
MH  - Antibiotics, Antineoplastic/*toxicity
MH  - Cardiotoxicity/metabolism
MH  - Cell Nucleus/*drug effects
MH  - Doxorubicin/*toxicity
MH  - Glutathione/analogs & derivatives/*metabolism
MH  - Glutathione Disulfide/metabolism
MH  - Lipid Peroxidation
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Multidrug Resistance-Associated Proteins/*genetics
MH  - Myocardium/*metabolism/*ultrastructure
MH  - Oxidative Stress
PMC - PMC4613962
EDAT- 2015/09/12 06:00
MHDA- 2016/01/05 06:00
CRDT- 2015/09/11 06:00
PHST- 2015/04/29 00:00 [received]
PHST- 2015/08/26 00:00 [accepted]
PHST- 2015/09/11 06:00 [entrez]
PHST- 2015/09/12 06:00 [pubmed]
PHST- 2016/01/05 06:00 [medline]
AID - jpet.115.225490 [pii]
AID - 10.1124/jpet.115.225490 [doi]
PST - ppublish
SO  - J Pharmacol Exp Ther. 2015 Nov;355(2):272-9. doi:
      10.1124/jpet.115.225490. Epub 2015 Sep 9.

PMID- 25734695
OWN - NLM
STAT- MEDLINE
DCOM- 20160713
LR  - 20181113
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Linking)
VI  - 123
IP  - 10
DP  - 2015 Oct
TI  - Effects of Adipocyte Aryl Hydrocarbon Receptor Deficiency on PCB-Induced
      Disruption of Glucose Homeostasis in Lean and Obese Mice.
PG  - 944-50
LID - 10.1289/ehp.1408594 [doi]
AB  - BACKGROUND: Coplanar polychlorinated biphenyls (PCBs) promote adipocyte
      inflammation and impair glucose homeostasis in lean mice. The diabetes-
      promoting effects of lipophilic PCBs have been observed only during
      weight loss in obese mice. The molecular mechanisms linking PCB exposures
      to impaired glucose metabolism are unclear. OBJECTIVES: In this study we
      tested the hypothesis that coplanar PCBs act at adipocyte aryl
      hydrocarbon receptors (AhRs) to promote adipose inflammation and impair
      glucose homeostasis in lean mice and in obese mice during weight loss.
      METHODS AND RESULTS: PCB-77 administration impaired glucose and insulin
      tolerance in LF (low fat diet)-fed control (AhR(fl/fl)) mice but not in
      adipocyte AhR-deficient mice (AhR(AdQ)). Unexpectedly, AhR(AdQ) mice
      exhibited increased fat mass when fed a standard LF or high fat (HF)
      diet. In mice fed a HF diet, both genotypes became obese, but AhR(AdQ)
      mice administered vehicle (VEH) exhibited increased body weight, adipose
      mass, adipose inflammation, and impaired glucose tolerance compared with
      AhR(fl/fl) controls. Impairment of glucose homeostasis in response to
      PCB-77 was not observed in obese mice of either genotype. However, upon
      weight loss, AhR(fl/fl) mice administered PCB-77 exhibited increased
      abundance of adipose tumor necrosis factor-alpha (TNF-alpha) mRNA and
      impaired glucose homeostasis compared with those administered VEH. In
      contrast, PCB-77 had no effect on TNF-alpha or glucose homeostasis in
      AhR(AdQ) mice exhibiting weight loss. CONCLUSIONS: Our results
      demonstrate that adipocyte AhR mediates PCB-induced adipose inflammation
      and impairment of glucose homeostasis in mice. Moreover, deficiency of
      AhR in adipocytes augmented the development of obesity, indicating that
      endogenous ligand(s) for AhR regulate adipose homeostasis.
FAU - Baker, Nicki A
AU  - Baker NA
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, Kentucky, USA.
FAU - Shoemaker, Robin
AU  - Shoemaker R
FAU - English, Victoria
AU  - English V
FAU - Larian, Nika
AU  - Larian N
FAU - Sunkara, Manjula
AU  - Sunkara M
FAU - Morris, Andrew J
AU  - Morris AJ
FAU - Walker, Mary
AU  - Walker M
FAU - Yiannikouris, Frederique
AU  - Yiannikouris F
FAU - Cassis, Lisa A
AU  - Cassis LA
LA  - eng
GR  - NIH T32 3048107792/PHS HHS/United States
GR  - P42 ES 007380/ES/NIEHS NIH HHS/United States
GR  - P20 GM103527-06/GM/NIGMS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20150303
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - IY9XDZ35W2 (Glucose)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Adipocytes/metabolism
MH  - Animals
MH  - Diet, Fat-Restricted
MH  - Diet, High-Fat/adverse effects
MH  - Female
MH  - Glucose/*metabolism
MH  - Homeostasis/*drug effects
MH  - *Insulin Resistance
MH  - Male
MH  - Mice
MH  - Obesity/etiology
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Receptors, Aryl Hydrocarbon/deficiency/*metabolism
MH  - Weight Loss
PMC - PMC4590748
EDAT- 2015/03/04 06:00
MHDA- 2016/07/14 06:00
CRDT- 2015/03/04 06:00
PHST- 2014/04/23 00:00 [received]
PHST- 2015/03/02 00:00 [accepted]
PHST- 2015/03/04 06:00 [entrez]
PHST- 2015/03/04 06:00 [pubmed]
PHST- 2016/07/14 06:00 [medline]
AID - 10.1289/ehp.1408594 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2015 Oct;123(10):944-50. doi:
      10.1289/ehp.1408594. Epub 2015 Mar 3.

PMID- 26261284
OWN - NLM
STAT- MEDLINE
DCOM- 20160531
LR  - 20181113
IS  - 1521-009X (Electronic)
IS  - 0090-9556 (Linking)
VI  - 43
IP  - 10
DP  - 2015 Oct
TI  - Drug Metabolism by the Host and Gut Microbiota: A Partnership or Rivalry?
PG  - 1499-504
LID - 10.1124/dmd.115.065714 [doi]
AB  - The importance of the gut microbiome in determining not only overall
      health, but also in the metabolism of drugs and xenobiotics, is rapidly
      emerging. It is becoming increasingly clear that the gut microbiota can
      act in concert with the host cells to maintain intestinal homeostasis,
      cometabolize drugs and xenobiotics, and alter the expression levels of
      drug-metabolizing enzymes and transporters and the expression and
      activity levels of nuclear receptors. In this myriad of activities, the
      impact of the microbiota may be beneficial or detrimental to the host.
      Given that the interplay between the gut microbiota and host cells is
      likely subject to high interindividual variability, this work has
      tremendous implications for our ability to predict accurately a
      particular drug's pharmacokinetics and a given patient population's
      response to drugs. In this issue of Drug Metabolism and Disposition, a
      series of articles is presented that illustrate the progress and
      challenges that lie ahead as we unravel the intricacies associated with
      drug and xenobiotic metabolism by the gut microbiota. These articles
      highlight the underlying mechanisms that are involved and the use of in
      vivo and in vitro approaches that are currently available for elucidating
      the role of the gut microbiota in drug and xenobiotic metabolism. These
      articles also shed light on exciting new avenues of research that may be
      pursued as we consider the role of the gut microbiota as an endocrine
      organ, a component of the brain-gut axis, and whether the gut microbiota
      is an appropriate and amenable target for new drugs.
CI  - Copyright (c) 2015 by The American Society for Pharmacology and
      Experimental Therapeutics.
FAU - Swanson, Hollie I
AU  - Swanson HI
AD  - Department of Pharmacology and Nutritional Sciences, University of
      Kentucky, Lexington, Kentucky hswan@email.uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20150810
PL  - United States
TA  - Drug Metab Dispos
JT  - Drug metabolism and disposition: the biological fate of chemicals
JID - 9421550
RN  - 0 (Pharmaceutical Preparations)
RN  - 0 (Xenobiotics)
SB  - IM
MH  - Animals
MH  - Gastrointestinal Microbiome/*drug effects/*physiology
MH  - Gastrointestinal Tract/drug effects/metabolism
MH  - Homeostasis/drug effects/physiology
MH  - Humans
MH  - Microbiota/drug effects/physiology
MH  - Pharmaceutical Preparations/administration & dosage/*metabolism
MH  - Xenobiotics/metabolism/pharmacology
PMC - PMC4576677
EDAT- 2015/08/12 06:00
MHDA- 2016/06/01 06:00
CRDT- 2015/08/12 06:00
PHST- 2015/05/26 00:00 [received]
PHST- 2015/07/10 00:00 [accepted]
PHST- 2015/08/12 06:00 [entrez]
PHST- 2015/08/12 06:00 [pubmed]
PHST- 2016/06/01 06:00 [medline]
AID - dmd.115.065714 [pii]
AID - 10.1124/dmd.115.065714 [doi]
PST - ppublish
SO  - Drug Metab Dispos. 2015 Oct;43(10):1499-504. doi: 10.1124/dmd.115.065714.
      Epub 2015 Aug 10.

PMID- 26327740
OWN - NLM
STAT- Publisher
LR  - 20191120
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 488
DP  - 2015 Aug 15
TI  - Engineered Iron/Iron Oxide Functionalized Membranes for Selenium and
      Other Toxic Metal Removal from Power Plant Scrubber Water.
PG  - 79-91
AB  - The remediation of toxic metals from water with high concentrations of
      salt has been an emerging area for membrane separation. Cost-effective
      nanomaterials such as iron and iron oxide nanoparticles have been widely
      used in reductive and oxidative degradation of toxic organics. Similar
      procedures can be used for redox transformations of metal species (e.g.
      metal oxyanions to elemental metal), and/or adsorption of species on iron
      oxide surface. In this study, iron-functionalized membranes were
      developed for reduction and adsorption of selenium from coal-fired power
      plant scrubber water. Iron-functionalized membranes have advantages over
      iron suspension as the membrane prevents particle aggregation and
      dissolution. Both lab-scale and full-scale membranes were prepared first
      by coating polyvinylidene fluoride (PVDF) membranes with polyacrylic acid
      (PAA), followed by ion exchange of ferrous ions and subsequent reduction
      to zero-valent iron nanoparticles. Water permeability of membrane
      decreased as the percent PAA functionalization increased, and the highest
      ion exchange capacity (IEC) was obtained at 20% PAA with highly pH
      responsive pores. Although high concentrations of sulfate and chloride in
      scrubber water decreased the reaction rate of selenium reduction, this
      was shown to be overcome by integration of nanofiltration (NF) and iron-
      functionalized membranes, and selenium concentration below 10 mug/L was
      achieved.
FAU - Gui, Minghui
AU  - Gui M
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Papp, Joseph K
AU  - Papp JK
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Colburn, Andrew S
AU  - Colburn AS
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Meeks, Noah D
AU  - Meeks ND
AD  - Southern Company Services, Inc., Birmingham, AL 35203, USA.
FAU - Weaver, Benjamin
AU  - Weaver B
AD  - Nanostone/Sepro Membranes, Inc., Oceanside, CA 92056, USA.
FAU - Wilf, Ilan
AU  - Wilf I
AD  - Nanostone/Sepro Membranes, Inc., Oceanside, CA 92056, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC4552196
MID - NIHMS683379
OTO - NOTNLM
OT  - Nanocomposite membrane
OT  - Nanoparticles
OT  - Polyelectrolyte
OT  - Surface modification
EDAT- 2015/09/04 06:00
MHDA- 2015/09/04 06:00
CRDT- 2015/09/02 06:00
PHST- 2015/09/02 06:00 [entrez]
PHST- 2015/09/04 06:00 [pubmed]
PHST- 2015/09/04 06:00 [medline]
AID - 10.1016/j.memsci.2015.03.089 [doi]
PST - ppublish
SO  - J Memb Sci. 2015 Aug 15;488:79-91. doi: 10.1016/j.memsci.2015.03.089.

PMID- 26074669
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 54
IP  - 16
DP  - 2015 Apr 29
TI  - Polymerization and Functionalization of Membrane Pores for Water Related
      Applications.
PG  - 4174-4182
AB  - Poly(vinylidene fluoride) (PVDF) was modified by chemical treatments in
      order to create active double bonds to obtain covalent grafting of
      poly(acrylic acid) (PAA) on membrane. The attenuated total reflectance
      Fourier transform infrared (ATR-FTIR) spectrum confirms the formation of
      conjugated C=C double bonds with surface dehydrofluorination. The
      membrane morphology was studied by scanning electron microscopy (SEM).
      The surface composition was characterized by X-ray photoelectron
      spectroscopy (XPS). The thermal stability of the dehydrofluorinated
      membrane (Def-PVDF) and functionalized membranes were investigated by
      differential scanning calorimetry (DSC) analysis. The influence of
      covalently attached PAA on Def-PVDF membrane has been investigated to
      determine its effect on the transport of water and charged solute.
      Variations in the solution pH show an effect on both permeability and
      solute retention in a reversible fashion. Metal nanoparticles were also
      immobilized in the membrane for the degradation of toxic chlorinated
      organics from water. In addition, PVDF membranes with an asymmetric and
      sponge-like morphology were developed by immersion-precipitation phase-
      inversion methods in both lab-scale and large-scale. The new type of
      spongy PVDF membrane shows high surface area with higher yield of PAA
      functionalization. The ion-capacity with Ca(2+) ions was also
      investigated.
FAU - Xiao, Li
AU  - Xiao L
AD  - Department of Chemical and Materials Engineering and Department of Civil
      Engineering, University of Kentucky , Lexington, Kentucky 40506, United
      States.
FAU - Davenport, Douglas M
AU  - Davenport DM
AD  - Department of Chemical and Materials Engineering and Department of Civil
      Engineering, University of Kentucky , Lexington, Kentucky 40506, United
      States.
FAU - Ormsbee, Lindell
AU  - Ormsbee L
AD  - Department of Chemical and Materials Engineering and Department of Civil
      Engineering, University of Kentucky , Lexington, Kentucky 40506, United
      States.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering and Department of Civil
      Engineering, University of Kentucky , Lexington, Kentucky 40506, United
      States.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20141215
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC4461045
EDAT- 2015/06/16 06:00
MHDA- 2015/06/16 06:01
CRDT- 2015/06/16 06:00
PHST- 2014/10/20 00:00 [received]
PHST- 2014/12/15 00:00 [revised]
PHST- 2014/12/15 00:00 [accepted]
PHST- 2015/06/16 06:00 [entrez]
PHST- 2015/06/16 06:00 [pubmed]
PHST- 2015/06/16 06:01 [medline]
AID - 10.1021/ie504149t [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2015 Apr 29;54(16):4174-4182. doi: 10.1021/ie504149t.
      Epub 2014 Dec 15.

PMID- 25947051
OWN - NLM
STAT- MEDLINE
DCOM- 20150929
LR  - 20181113
IS  - 1096-2247 (Print)
IS  - 1096-2247 (Linking)
VI  - 65
IP  - 2
DP  - 2015 Feb
TI  - A variance decomposition approach to uncertainty quantification and
      sensitivity analysis of the Johnson and Ettinger model.
PG  - 154-64
LID - 10.1080/10962247.2014.980469 [doi]
AB  - The Johnson and Ettinger (J&E) model is the most widely used vapor
      intrusion model in the United States. It is routinely used as part of
      hazardous waste site assessments to evaluate the potential for vapor
      intrusion exposure risks. This study incorporates mathematical approaches
      that allow sensitivity and uncertainty of the J&E model to be evaluated.
      In addition to performing Monte Carlo simulations to examine the
      uncertainty in the J&E model output, a powerful global sensitivity
      analysis technique based on Sobol indices is used to evaluate J&E model
      sensitivity to variations in the input parameters. The results suggest
      that the J&E model is most sensitive to the building air exchange rate,
      regardless of soil type and source depth. Building air exchange rate is
      not routinely measured during vapor intrusion investigations, but clearly
      improved estimates and/or measurements of the air exchange rate would
      lead to improved model predictions. It is also found that the J&E model
      is more sensitive to effective diffusivity than to effective
      permeability. Field measurements of effective diffusivity are not
      commonly collected during vapor intrusion investigations; however,
      consideration of this parameter warrants additional attention. Finally,
      the effects of input uncertainties on model predictions for different
      scenarios (e.g., sandy soil as compared to clayey soil, and "shallow"
      sources as compared to "deep" sources) are evaluated. Our results not
      only identify the range of variability to be expected depending on the
      scenario at hand, but also mark the important cases where special care is
      needed when estimating the input parameters to which the J&E model is
      most sensitive.
FAU - Moradi, Ali
AU  - Moradi A
AD  - a Department of Civil & Environmental Engineering , University of
      Massachusetts-Dartmouth , North Dartmouth , MA , USA.
FAU - Tootkaboni, Mazdak
AU  - Tootkaboni M
FAU - Pennell, Kelly G
AU  - Pennell KG
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Air Waste Manag Assoc
JT  - Journal of the Air & Waste Management Association (1995)
JID - 9503111
RN  - 0 (Air Pollutants)
RN  - 0 (Soil)
SB  - IM
MH  - Air Pollutants/*analysis
MH  - Air Pollution, Indoor/*analysis
MH  - Analysis of Variance
MH  - Environmental Monitoring/*methods
MH  - *Models, Theoretical
MH  - Monte Carlo Method
MH  - Sensitivity and Specificity
MH  - Soil/*chemistry
MH  - Uncertainty
PMC - PMC4425250
MID - NIHMS651396
EDAT- 2015/05/08 06:00
MHDA- 2015/09/30 06:00
CRDT- 2015/05/08 06:00
PHST- 2015/05/08 06:00 [entrez]
PHST- 2015/05/08 06:00 [pubmed]
PHST- 2015/09/30 06:00 [medline]
AID - 10.1080/10962247.2014.980469 [doi]
PST - ppublish
SO  - J Air Waste Manag Assoc. 2015 Feb;65(2):154-64. doi:
      10.1080/10962247.2014.980469.

PMID- 25199685
OWN - NLM
STAT- MEDLINE
DCOM- 20150619
LR  - 20211021
IS  - 1432-0738 (Electronic)
IS  - 0340-5761 (Linking)
VI  - 88
IP  - 11
DP  - 2014 Nov
TI  - Copper: toxicological relevance and mechanisms.
PG  - 1929-38
LID - 10.1007/s00204-014-1355-y [doi]
AB  - Copper (Cu) is a vital mineral essential for many biological processes.
      The vast majority of all Cu in healthy humans is associated with enzyme
      prosthetic groups or bound to proteins. Cu homeostasis is tightly
      regulated through a complex system of Cu transporters and chaperone
      proteins. Excess or toxicity of Cu, which is associated with the
      pathogenesis of hepatic disorder, neurodegenerative changes and other
      disease conditions, can occur when Cu homeostasis is disrupted. The
      capacity to initiate oxidative damage is most commonly attributed to Cu-
      induced cellular toxicity. Recently, altered cellular events, including
      lipid metabolism, gene expression, alpha-synuclein aggregation,
      activation of acidic sphingomyelinase and release of ceramide, and
      temporal and spatial distribution of Cu in hepatocytes, as well as Cu-
      protein interaction in the nerve system, have been suggested to play a
      role in Cu toxicity. However, whether these changes are independent of,
      or secondary to, an altered cellular redox state of Cu remain to be
      elucidated.
FAU - Gaetke, Lisa M
AU  - Gaetke LM
AD  - Department of Dietetics and Human Nutrition, University of Kentucky,
      Lexington, KY, 40506, USA.
FAU - Chow-Johnson, Hannah S
AU  - Chow-Johnson HS
FAU - Chow, Ching K
AU  - Chow CK
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20140909
PL  - Germany
TA  - Arch Toxicol
JT  - Archives of toxicology
JID - 0417615
RN  - 0 (Molecular Chaperones)
RN  - 0 (Proteins)
RN  - 789U1901C5 (Copper)
SB  - IM
MH  - Animals
MH  - Biological Transport
MH  - Copper/metabolism/*toxicity
MH  - Homeostasis/physiology
MH  - Humans
MH  - Molecular Chaperones/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/*drug effects
MH  - Proteins/*metabolism
PMC - PMC4339675
MID - NIHMS659791
EDAT- 2014/09/10 06:00
MHDA- 2015/06/20 06:00
CRDT- 2014/09/10 06:00
PHST- 2014/08/08 00:00 [received]
PHST- 2014/08/28 00:00 [accepted]
PHST- 2014/09/10 06:00 [entrez]
PHST- 2014/09/10 06:00 [pubmed]
PHST- 2015/06/20 06:00 [medline]
AID - 10.1007/s00204-014-1355-y [doi]
PST - ppublish
SO  - Arch Toxicol. 2014 Nov;88(11):1929-38. doi: 10.1007/s00204-014-1355-y.
      Epub 2014 Sep 9.

PMID- 24530186
OWN - NLM
STAT- MEDLINE
DCOM- 20141219
LR  - 20211021
IS  - 1879-1026 (Electronic)
IS  - 0048-9697 (Linking)
VI  - 491-492
DP  - 2014 Sep 1
TI  - Modulation of persistent organic pollutant toxicity through nutritional
      intervention: emerging opportunities in biomedicine and environmental
      remediation.
PG  - 11-6
LID - 10.1016/j.scitotenv.2014.01.109 [doi]
LID - S0048-9697(14)00138-7 [pii]
AB  - Environmental pollution is increasing worldwide, and there is evidence
      that exposure to halogenated persistent organic pollutants (POPs) such as
      polychlorinated biphenyls can contribute to the pathology of inflammatory
      diseases such as atherosclerosis, diabetes, and cancer. Pollutant removal
      from contaminated sites and subsequent pollutant degradation are critical
      for reducing the long-term health risks associated with exposure.
      However, complete remediation of a toxicant from the environment is very
      difficult and cost-prohibitive. Furthermore, remediation technologies
      often result in the generation of secondary toxicants. Considering these
      circumstances, environmentally-friendly and sustainable remediation
      technologies and biomedical solutions to reduce vulnerability to
      environmental chemical insults need to be explored to reduce the overall
      health risks associated with exposure to environmental pollutants. We
      propose that positive lifestyle changes such as healthful nutrition and
      consumption of diets rich in fruits and vegetables or bioactive nutrients
      with antioxidant and/or anti-inflammatory properties will reduce the
      body's vulnerability to environmental stressors and thus reduce toxicant-
      mediated disease pathologies. Interestingly, emerging evidence now
      implicates the incorporation of bioactive nutrients, such as plant-
      derived polyphenols, in technologies focused on the capture, sensing and
      remediation of halogenated POPs. We propose that human nutritional
      intervention in concert with the use of natural polyphenol sensing and
      remediation platforms may provide a sensible means to develop primary and
      long-term prevention strategies of diseases associated with many
      environmental toxic insults including halogenated POPs.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA.
FAU - Newsome, Bradley J
AU  - Newsome BJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Chemistry, College of Arts and Sciences, University of
      Kentucky, Lexington, KY 40506, USA.
FAU - Dziubla, Thomas D
AU  - Dziubla TD
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Chemical and Materials Engineering, College of
      Engineering, University of Kentucky, Lexington, KY 40506, USA.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Chemical and Materials Engineering, College of
      Engineering, University of Kentucky, Lexington, KY 40506, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Chemical and Materials Engineering, College of
      Engineering, University of Kentucky, Lexington, KY 40506, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA; Department of Animal and Food
      Sciences, College of Agriculture Food and Environment, University of
      Kentucky, Lexington, KY 40546, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140213
PL  - Netherlands
TA  - Sci Total Environ
JT  - The Science of the total environment
JID - 0330500
RN  - 0 (Antioxidants)
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - *Antioxidants
MH  - Environmental Pollutants/*toxicity
MH  - Environmental Pollution/*statistics & numerical data
MH  - Environmental Restoration and Remediation/*methods
MH  - Food
MH  - Humans
MH  - Nutritive Value
PMC - PMC4077968
MID - NIHMS567838
OTO - NOTNLM
OT  - Antioxidant response
OT  - Nutrition
OT  - Oxidative stress
OT  - POP toxicity
OT  - Polyphenol
OT  - Sustainable remediation
EDAT- 2014/02/18 06:00
MHDA- 2014/12/20 06:00
CRDT- 2014/02/18 06:00
PHST- 2013/11/04 00:00 [received]
PHST- 2014/01/27 00:00 [revised]
PHST- 2014/01/28 00:00 [accepted]
PHST- 2014/02/18 06:00 [entrez]
PHST- 2014/02/18 06:00 [pubmed]
PHST- 2014/12/20 06:00 [medline]
AID - S0048-9697(14)00138-7 [pii]
AID - 10.1016/j.scitotenv.2014.01.109 [doi]
PST - ppublish
SO  - Sci Total Environ. 2014 Sep 1;491-492:11-6. doi:
      10.1016/j.scitotenv.2014.01.109. Epub 2014 Feb 13.

PMID- 24709675
OWN - NLM
STAT- MEDLINE
DCOM- 20140706
LR  - 20211021
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 277
IP  - 2
DP  - 2014 Jun 1
TI  - PCB 126 toxicity is modulated by cross-talk between caveolae and Nrf2
      signaling.
PG  - 192-9
LID - 10.1016/j.taap.2014.03.018 [doi]
LID - S0041-008X(14)00114-8 [pii]
AB  - Environmental toxicants such as polychlorinated biphenyls (PCBs) have
      been implicated in the promotion of multiple inflammatory disorders
      including cardiovascular disease, but information regarding mechanisms of
      toxicity and cross-talk between relevant cell signaling pathways is
      lacking. To examine the hypothesis that cross-talk between membrane
      domains called caveolae and nuclear factor (erythroid-derived 2)-like 2
      (Nrf2) pathways alters PCB-induced inflammation, caveolin-1 was silenced
      in vascular endothelial cells, resulting in a decreased PCB-induced
      inflammatory response. Cav-1 silencing (siRNA treatment) also increased
      levels of Nrf2-ARE transcriptional binding, resulting in higher mRNA
      levels of the antioxidant genes glutathione s-transferase and NADPH
      dehydrogenase quinone-1 in both vehicle and PCB-treated systems. Along
      with this upregulated antioxidant response, Cav-1 siRNA treated cells
      exhibited decreased mRNA levels of the Nrf2 inhibitory protein Keap1 in
      both vehicle and PCB-treated samples. Silencing Cav-1 also decreased
      protein levels of Nrf2 inhibitory proteins Keap1 and Fyn kinase,
      especially in PCB-treated cells. Further, endothelial cells from wildtype
      and Cav-1-/- mice were isolated and treated with PCB to better elucidate
      the role of functional caveolae in PCB-induced endothelial inflammation.
      Cav-1-/- endothelial cells were protected from PCB-induced cellular
      dysfunction as evidenced by decreased vascular cell adhesion molecule
      (VCAM-1) protein induction. Compared to wildtype cells, Cav-1-/-
      endothelial cells also allowed for a more effective antioxidant response,
      as observed by higher levels of the antioxidant genes. These data
      demonstrate novel cross-talk mechanisms between Cav-1 and Nrf2 and
      implicate the reduction of Cav-1 as a protective mechanism for PCB-
      induced cellular dysfunction and inflammation.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA; University of Kentucky Superfund
      Research Center, Lexington, KY 40536, USA.
FAU - Han, Sung Gu
AU  - Han SG
AD  - University of Kentucky Superfund Research Center, Lexington, KY 40536,
      USA; Department of Food Science and Biotechnology of Animal Resources,
      College of Animal Bioscience and Technology, Konkuk University, Seoul
      143-701, Republic of Korea.
FAU - Newsome, Bradley J
AU  - Newsome BJ
AD  - University of Kentucky Superfund Research Center, Lexington, KY 40536,
      USA; Department of Chemistry, College of Arts and Sciences, University of
      Kentucky, Lexington, KY 40506, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA; University of Kentucky Superfund
      Research Center, Lexington, KY 40536, USA; Department of Animal and Food
      Sciences, College of Agriculture, Food and Environment, University of
      Kentucky, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20140404
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (CAV1 protein, human)
RN  - 0 (Cav1 protein, mouse)
RN  - 0 (Caveolin 1)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (KEAP1 protein, human)
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NFE2L2 protein, human)
RN  - 0 (Nfe2l2 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.6.99.3 (NADH Dehydrogenase)
RN  - EC 2.5.1.18 (Glutathione Transferase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Caveolae/*drug effects/metabolism/pathology
MH  - Caveolin 1/genetics/metabolism
MH  - Cell Line
MH  - Endothelial Cells/*drug effects/metabolism/pathology
MH  - Environmental Pollutants/*toxicity
MH  - Gene Expression Regulation, Enzymologic/drug effects
MH  - Glutathione Transferase/genetics/metabolism
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Intracellular Signaling Peptides and Proteins/genetics/metabolism
MH  - Kelch-Like ECH-Associated Protein 1
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NADH Dehydrogenase/genetics/metabolism
MH  - NF-E2-Related Factor 2/*metabolism
MH  - Phosphorylation
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA Interference
MH  - RNA, Messenger/metabolism
MH  - Signal Transduction/*drug effects
MH  - Swine
MH  - Transfection
MH  - Vascular Cell Adhesion Molecule-1/metabolism
PMC - PMC4041015
MID - NIHMS584439
OTO - NOTNLM
OT  - Antioxidant response
OT  - Caveolin-1
OT  - Endothelial cell dysfunction
OT  - Nrf2
OT  - Oxidative stress
OT  - Polychlorinated biphenyl
EDAT- 2014/04/09 06:00
MHDA- 2014/07/07 06:00
CRDT- 2014/04/09 06:00
PHST- 2013/12/03 00:00 [received]
PHST- 2014/03/18 00:00 [revised]
PHST- 2014/03/22 00:00 [accepted]
PHST- 2014/04/09 06:00 [entrez]
PHST- 2014/04/09 06:00 [pubmed]
PHST- 2014/07/07 06:00 [medline]
AID - S0041-008X(14)00114-8 [pii]
AID - 10.1016/j.taap.2014.03.018 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2014 Jun 1;277(2):192-9. doi:
      10.1016/j.taap.2014.03.018. Epub 2014 Apr 4.

PMID- 23417440
OWN - NLM
STAT- MEDLINE
DCOM- 20150123
LR  - 20211021
IS  - 1614-7499 (Electronic)
IS  - 0944-1344 (Linking)
VI  - 21
IP  - 10
DP  - 2014 May
TI  - Influence of nutrition in PCB-induced vascular inflammation.
PG  - 6410-8
LID - 10.1007/s11356-013-1549-5 [doi]
AB  - The nutritional profile of an individual can influence the toxicity of
      persistent environmental toxicants. Polychlorinated biphenyls (PCBs),
      prevalent environmental pollutants, are highly lipid-soluble toxic
      compounds that biomagnify through trophic levels and pose cancer,
      neurocognitive, and atherosclerotic risk to human populations. There is a
      growing body of knowledge that PCBs can initiate inflammatory responses
      in vivo, and this inflammation can be either exacerbated or ameliorated
      by nutrition. Data indicate that diets high in certain dietary lipids
      such as omega-6 fatty acids can worsen PCB-induced vascular toxicity
      while diets enriched with bioactive food components such as polyphenols
      and omega-3 polyunsaturated fatty acids can improve the toxicant-induced
      inflammation. There is evidence that bioactive nutrients protect through
      multiple cell signaling pathways, but we have shown that lipid raft
      caveolae and the antioxidant defense controller nuclear factor
      (erythroid-derived 2)-like 2 (Nrf2) both play a predominant role in
      nutritional modulation of PCB-induced vascular toxicity. Interestingly,
      there appears to be an intimate cross-talk between caveolae-related
      proteins and cellular Nrf2, and focusing on the use of specific bioactive
      food components that simultaneously alter both pathways may produce a
      more effective and efficient cytoprotective response to toxicant
      exposure. The use of nutrition as a protective tool is an economically
      beneficial means to address the toxicity of persistent environmental
      toxicants and may become a sensible means to protect human populations
      from PCB-induced vascular inflammation and associated chronic diseases.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington, KY,
      40536-0200, USA.
FAU - Newsome, Bradley
AU  - Newsome B
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 ES07266/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130217
PL  - Germany
TA  - Environ Sci Pollut Res Int
JT  - Environmental science and pollution research international
JID - 9441769
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Diet/statistics & numerical data
MH  - Dietary Fats
MH  - Environmental Exposure/statistics & numerical data
MH  - Environmental Pollutants/*toxicity
MH  - Humans
MH  - Nutritional Status/*drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Signal Transduction/drug effects
MH  - Vasculitis/*chemically induced
PMC - PMC3686851
MID - NIHMS447055
EDAT- 2013/02/19 06:00
MHDA- 2015/01/24 06:00
CRDT- 2013/02/19 06:00
PHST- 2012/11/09 00:00 [received]
PHST- 2013/02/04 00:00 [accepted]
PHST- 2013/02/19 06:00 [entrez]
PHST- 2013/02/19 06:00 [pubmed]
PHST- 2015/01/24 06:00 [medline]
AID - 10.1007/s11356-013-1549-5 [doi]
PST - ppublish
SO  - Environ Sci Pollut Res Int. 2014 May;21(10):6410-8. doi:
      10.1007/s11356-013-1549-5. Epub 2013 Feb 17.

PMID- 23504249
OWN - NLM
STAT- MEDLINE
DCOM- 20150123
LR  - 20211021
IS  - 1614-7499 (Electronic)
IS  - 0944-1344 (Linking)
VI  - 21
IP  - 10
DP  - 2014 May
TI  - PCB 77 dechlorination products modulate pro-inflammatory events in
      vascular endothelial cells.
PG  - 6354-64
LID - 10.1007/s11356-013-1591-3 [doi]
AB  - Persistent organic pollutants such as polychlorinated biphenyls (PCBs)
      are associated with detrimental health outcomes including cardiovascular
      diseases. Remediation of these compounds is a critical component of
      environmental policy. Although remediation efforts aim to completely
      remove toxicants, little is known about the effects of potential
      remediation byproducts. We previously published that Fe/Pd nanoparticles
      effectively dechlorinate PCB 77 to biphenyl, thus eliminating PCB-induced
      endothelial dysfunction using primary vascular endothelial cells. Herein,
      we analyzed the toxic effects of PCB congener mixtures (representative
      mixtures of commercial PCBs based on previous dechlorination data)
      produced at multiple time points during the dechlorination of PCB 77 to
      biphenyl. Compared with pure PCB 77, exposing endothelial cells to lower
      chlorinated PCB byproducts led to improved cellular viability, decreased
      superoxide production, and decreased nuclear factor kappa B activation
      based on duration of remediation. Presence of the parent compound, PCB
      77, led to significant increases in mRNA and protein inflammatory marker
      expression. These data implicate that PCB dechlorination reduces
      biological toxicity to vascular endothelial cells.
FAU - Eske, Katryn
AU  - Eske K
AD  - University of Kentucky SRP Center, University of Kentucky, Lexington, KY,
      40536-0200, USA.
FAU - Newsome, Bradley
AU  - Newsome B
FAU - Han, Sung Gu
AU  - Han SG
FAU - Murphy, Margaret
AU  - Murphy M
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - 3P42ES007380-13S1/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, American Recovery and Reinvestment Act
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130316
PL  - Germany
TA  - Environ Sci Pollut Res Int
JT  - Environmental science and pollution research international
JID - 9441769
RN  - 0 (Hazardous Substances)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Endothelial Cells
MH  - Gene Expression/drug effects
MH  - Hazardous Substances/*toxicity
MH  - Polychlorinated Biphenyls/*toxicity
PMC - PMC3728165
MID - NIHMS456831
EDAT- 2013/03/19 06:00
MHDA- 2015/01/24 06:00
CRDT- 2013/03/19 06:00
PHST- 2012/11/16 00:00 [received]
PHST- 2013/02/20 00:00 [accepted]
PHST- 2013/03/19 06:00 [entrez]
PHST- 2013/03/19 06:00 [pubmed]
PHST- 2015/01/24 06:00 [medline]
AID - 10.1007/s11356-013-1591-3 [doi]
PST - ppublish
SO  - Environ Sci Pollut Res Int. 2014 May;21(10):6354-64. doi:
      10.1007/s11356-013-1591-3. Epub 2013 Mar 16.

PMID- 24944434
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 457
DP  - 2014 May 1
TI  - Development of Bench and Full-Scale Temperature and pH Responsive
      Functionalized PVDF Membranes with Tunable Properties.
PG  - 39-49
AB  - Temperature and pH responsive polymers (poly(N-isopropylacrylamide)
      (PNIPAAm), and polyacrylic acid, PAA) were synthesized in one common
      macrofiltration PVDF membrane platform by pore-filling method. The
      microstructure and morphology of the PNIPAAm-PVDF, and PNIPAAm-FPAA-PVDF
      membranes were studied by attenuated total reflectance Fourier transform
      infrared (ATR-FTIR), thermogravimetric analysis (TGA), scanning electron
      microscopy (SEM) and atomic force microscopy (AFM). The membrane pore
      size was controlled by the swelling and shrinking of the PNIPAAm at the
      temperature around lower critical solution temperature (LCST). The
      composite membrane demonstrated a rapid and reversible swelling and
      deswelling change within a small temperature range. The controllable flux
      makes it possible to utilize this temperature responsive membrane as a
      valve to regulate filtration properties by temperature change. Dextran
      solution (Mw=2,000,000g/mol, 26 nm diameter) was used to evaluate the
      separation performance of the temperature responsive membranes. The
      ranges of dextran rejection are from 4% to 95% depending on the
      temperature, monomer amount and pressure. The full-scale membrane was
      also developed to confirm the feasibility of our bench-scale experimental
      results. The full-scale membrane also exhibited both temperature and pH
      responsivity. This system was also used for controlled nanoparticles
      synthesis and for dechlorination reaction.
FAU - Xiao, Li
AU  - Xiao L
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Isner, Austin
AU  - Isner A
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Waldrop, Krysta
AU  - Waldrop K
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Saad, Anthony
AU  - Saad A
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Takigawa, Doreen
AU  - Takigawa D
AD  - Sepro Membranes, Inc. Oceanside, CA 92056, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC4058347
MID - NIHMS560566
OTO - NOTNLM
OT  - Poly(N-isopropylacrylamide)
OT  - nanoparticle synthesis
OT  - polyacrylic acid
OT  - polymerization
OT  - tunable separation
EDAT- 2014/06/20 06:00
MHDA- 2014/06/20 06:01
CRDT- 2014/06/20 06:00
PHST- 2014/06/20 06:00 [entrez]
PHST- 2014/06/20 06:00 [pubmed]
PHST- 2014/06/20 06:01 [medline]
AID - 10.1016/j.memsci.2014.01.033 [doi]
PST - ppublish
SO  - J Memb Sci. 2014 May 1;457:39-49. doi: 10.1016/j.memsci.2014.01.033.

PMID- 24755147
OWN - NLM
STAT- MEDLINE
DCOM- 20141118
LR  - 20211021
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 3
IP  - 2
DP  - 2014 Apr 22
TI  - Bisphenol A increases atherosclerosis in pregnane X receptor-humanized
      ApoE deficient mice.
PG  - e000492
LID - 10.1161/JAHA.113.000492 [doi]
AB  - BACKGROUND: Bisphenol A (BPA) is a base chemical used extensively in many
      consumer products. BPA has recently been associated with increased risk
      of cardiovascular disease (CVD) in multiple large-scale human population
      studies, but the underlying mechanisms remain elusive. We previously
      reported that BPA activates the pregnane X receptor (PXR), which acts as
      a xenobiotic sensor to regulate xenobiotic metabolism and has pro-
      atherogenic effects in animal models upon activation. Interestingly, BPA
      is a potent agonist of human PXR but does not activate mouse or rat PXR
      signaling, which confounds the use of rodent models to evaluate
      mechanisms of BPA-mediated CVD risk. This study aimed to investigate the
      atherogenic mechanism of BPA using a PXR-humanized mouse model. METHODS
      AND RESULTS: A PXR-humanized ApoE deficient (huPXR*ApoE(-/-)) mouse line
      was generated that respond to human PXR ligands and feeding studies were
      performed to determine the effects of BPA exposure on atherosclerosis
      development. Exposure to BPA significantly increased atherosclerotic
      lesion area in the aortic root and brachiocephalic artery of
      huPXR*ApoE(-/-) mice by 104% (P<0.001) and 120% (P<0.05), respectively.
      By contrast, BPA did not affect atherosclerosis development in the
      control littermates without human PXR. BPA exposure did not affect plasma
      lipid levels but increased CD36 expression and lipid accumulation in
      macrophages of huPXR*ApoE(-/-) mice. CONCLUSION: These findings identify
      a molecular mechanism that could link BPA exposure to increased risk of
      CVD in exposed individuals. PXR is therefore a relevant target for future
      risk assessment of BPA and related environmental chemicals in humans.
FAU - Sui, Yipeng
AU  - Sui Y
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, KY.
FAU - Park, Se-Hyung
AU  - Park SH
FAU - Helsley, Robert N
AU  - Helsley RN
FAU - Sunkara, Manjula
AU  - Sunkara M
FAU - Gonzalez, Frank J
AU  - Gonzalez FJ
FAU - Morris, Andrew J
AU  - Morris AJ
FAU - Zhou, Changcheng
AU  - Zhou C
LA  - eng
GR  - P30HL101300/HL/NHLBI NIH HHS/United States
GR  - R01ES023470/ES/NIEHS NIH HHS/United States
GR  - T32 HL072743/HL/NHLBI NIH HHS/United States
GR  - S10 RR026884/RR/NCRR NIH HHS/United States
GR  - R01 ES023470/ES/NIEHS NIH HHS/United States
GR  - P20GM103527/GM/NIGMS NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - P30 HL101300/HL/NHLBI NIH HHS/United States
GR  - R21 ES022745/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P20 RR021954/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20140422
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Apolipoproteins E)
RN  - 0 (Benzhydryl Compounds)
RN  - 0 (CD36 Antigens)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Lipids)
RN  - 0 (Phenols)
RN  - 0 (Pregnane X Receptor)
RN  - 0 (Receptors, Steroid)
RN  - MLT3645I99 (bisphenol A)
SB  - IM
MH  - Animals
MH  - Aorta/drug effects/metabolism/pathology
MH  - Apolipoproteins E/*deficiency/genetics
MH  - Atherosclerosis/*chemically induced/genetics/metabolism/pathology
MH  - Benzhydryl Compounds/*toxicity
MH  - Brachiocephalic Trunk/drug effects/metabolism/pathology
MH  - CD36 Antigens/metabolism
MH  - Environmental Pollutants/*toxicity
MH  - Humans
MH  - Lipids/blood
MH  - Macrophages/drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Phenols/*toxicity
MH  - Pregnane X Receptor
MH  - Receptors, Steroid/*agonists/genetics/metabolism
MH  - Risk Assessment
MH  - Risk Factors
PMC - PMC4187496
OTO - NOTNLM
OT  - atherosclerosis
OT  - cells
OT  - receptors
OT  - risk factors
EDAT- 2014/04/24 06:00
MHDA- 2014/11/19 06:00
CRDT- 2014/04/24 06:00
PHST- 2014/04/24 06:00 [entrez]
PHST- 2014/04/24 06:00 [pubmed]
PHST- 2014/11/19 06:00 [medline]
AID - jah3508 [pii]
AID - 10.1161/JAHA.113.000492 [doi]
PST - epublish
SO  - J Am Heart Assoc. 2014 Apr 22;3(2):e000492. doi: 10.1161/JAHA.113.000492.

PMID- 24774064
OWN - NLM
STAT- MEDLINE
DCOM- 20141209
LR  - 20211021
IS  - 1879-0739 (Electronic)
IS  - 0271-5317 (Linking)
VI  - 34
IP  - 4
DP  - 2014 Apr
TI  - Fruit and vegetable intake, as reflected by serum carotenoid
      concentrations, predicts reduced probability of polychlorinated biphenyl-
      associated risk for type 2 diabetes: National Health and Nutrition
      Examination Survey 2003-2004.
PG  - 285-93
LID - 10.1016/j.nutres.2014.02.001 [doi]
LID - S0271-5317(14)00022-0 [pii]
AB  - Type 2 diabetes has been shown to occur in response to environmental and
      genetic influences, among them nutrition; food intake patterns; sedentary
      lifestyle; body mass index; and exposure to persistent organic
      pollutants, such as polychlorinated biphenyls (PCBs). Nutrition is
      essential in the prevention and management of type 2 diabetes and has
      been shown to modulate the toxicity of PCBs. Serum carotenoid
      concentrations, considered a reliable biomarker of fruit and vegetable
      intake, are associated with the reduced probability of chronic diseases,
      such as type 2 diabetes and cardiovascular disease. Our hypothesis is
      that fruit and vegetable intake, reflected by serum carotenoid
      concentrations, is associated with the reduced probability of developing
      type 2 diabetes in US adults with elevated serum concentrations of PCBs
      118, 126, and 153. This cross-sectional study used the Center for Disease
      Control and Prevention database, National Health and Nutrition
      Examination Survey 2003-2004, in logistic regression analyses. Overall
      prevalence of type 2 diabetes was approximately 11.6% depending on the
      specific PCB. All 3 PCBs were positively associated with the probability
      of type 2 diabetes. For participants at higher PCB percentiles (eg, 75th
      and 90th) for PCB 118 and 126, increasing serum carotenoid concentrations
      were associated with a smaller probability of type 2 diabetes. Fruit and
      vegetable intake, as reflected by serum carotenoid concentrations,
      predicted notably reduced probability of dioxin-like PCB-associated risk
      for type 2 diabetes.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Hofe, Carolyn R
AU  - Hofe CR
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, KY 40506.
FAU - Feng, Limin
AU  - Feng L
AD  - Department of Statistics, University of Kentucky, Lexington, KY 40506.
FAU - Zephyr, Dominique
AU  - Zephyr D
AD  - Department of Statistics, University of Kentucky, Lexington, KY 40506.
FAU - Stromberg, Arnold J
AU  - Stromberg AJ
AD  - Department of Statistics, University of Kentucky, Lexington, KY 40506.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, KY 40506; Molecular and Cell Nutrition Laboratory, University
      of Kentucky, Lexington, KY 40506.
FAU - Gaetke, Lisa M
AU  - Gaetke LM
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, KY 40506; Department of Dietetics and Human Nutrition,
      University of Kentucky, Lexington, KY 40506. Electronic address:
      lgaetke@email.uky.edu.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20140210
PL  - United States
TA  - Nutr Res
JT  - Nutrition research (New York, N.Y.)
JID - 8303331
RN  - 0 (Dioxins)
RN  - 36-88-4 (Carotenoids)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Adult
MH  - Carotenoids/blood/*pharmacology
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 2/chemically induced/epidemiology/*prevention &
      control
MH  - *Diet
MH  - Dioxins/adverse effects
MH  - Female
MH  - Fruit/*chemistry
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Nutrition Surveys
MH  - Nutritional Status
MH  - Polychlorinated Biphenyls/*adverse effects
MH  - Prevalence
MH  - Vegetables/*chemistry
PMC - PMC4008967
MID - NIHMS569053
OTO - NOTNLM
OT  - Environmental health
OT  - NHANES, type 2 diabetes
OT  - Nutrition
OT  - Polychlorinated biphenyls, PCBs
OT  - Serum carotenoids
EDAT- 2014/04/30 06:00
MHDA- 2014/12/15 06:00
CRDT- 2014/04/30 06:00
PHST- 2013/10/29 00:00 [received]
PHST- 2014/01/28 00:00 [revised]
PHST- 2014/02/03 00:00 [accepted]
PHST- 2014/04/30 06:00 [entrez]
PHST- 2014/04/30 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - S0271-5317(14)00022-0 [pii]
AID - 10.1016/j.nutres.2014.02.001 [doi]
PST - ppublish
SO  - Nutr Res. 2014 Apr;34(4):285-93. doi: 10.1016/j.nutres.2014.02.001. Epub
      2014 Feb 10.

PMID- 24378064
OWN - NLM
STAT- MEDLINE
DCOM- 20140915
LR  - 20211021
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 25
IP  - 2
DP  - 2014 Feb
TI  - Green tea diet decreases PCB 126-induced oxidative stress in mice by up-
      regulating antioxidant enzymes.
PG  - 126-35
LID - 10.1016/j.jnutbio.2013.10.003 [doi]
LID - S0955-2863(13)00221-0 [pii]
AB  - Superfund chemicals such as polychlorinated biphenyls pose a serious
      human health risk due to their environmental persistence and link to
      multiple diseases. Selective bioactive food components such as flavonoids
      have been shown to ameliorate PCB toxicity, but primarily in an in vitro
      setting. Here, we show that mice fed a green tea-enriched diet and
      subsequently exposed to environmentally relevant doses of coplanar PCB
      exhibit decreased overall oxidative stress primarily due to the up-
      regulation of a battery of antioxidant enzymes. C57BL/6 mice were fed a
      low-fat diet supplemented with green tea extract (GTE) for 12 weeks and
      exposed to 5 mumol PCB 126/kg mouse weight (1.63 mg/kg-day) on weeks 10,
      11 and 12 (total body burden: 4.9 mg/kg). F2-isoprostane and its
      metabolites, established markers of in vivo oxidative stress, measured in
      plasma via HPLC-MS/MS exhibited fivefold decreased levels in mice
      supplemented with GTE and subsequently exposed to PCB compared to animals
      on a control diet exposed to PCB. Livers were collected and harvested for
      both messenger RNA and protein analyses, and it was determined that many
      genes transcriptionally controlled by aryl hydrocarbon receptor and
      nuclear factor (erythroid-derived 2)-like 2 proteins were up-regulated in
      PCB-exposed mice fed the green tea-supplemented diet. An increased
      induction of genes such as SOD1, GSR, NQO1 and GST, key antioxidant
      enzymes, in these mice (green tea plus PCB) may explain the observed
      decrease in overall oxidative stress. A diet supplemented with green tea
      allows for an efficient antioxidant response in the presence of PCB 126,
      which supports the emerging paradigm that healthful nutrition may be able
      to bolster and buffer a physiological system against the toxicities of
      environmental pollutants.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Newsome, Bradley J
AU  - Newsome BJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Chemistry, College of Arts and Sciences, University of
      Kentucky, Lexington, KY 40506, USA.
FAU - Petriello, Michael C
AU  - Petriello MC
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY 40536, USA.
FAU - Han, Sung Gu
AU  - Han SG
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Food Science and Biotechnology of Animal Resources,
      College of Animal Bioscience and Technology, Konkuk University, Seoul
      143-701, Republic of Korea.
FAU - Murphy, Margaret O
AU  - Murphy MO
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Graduate Center for Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, KY 40536, USA.
FAU - Eske, Katryn E
AU  - Eske KE
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Graduate Center for Nutritional Sciences, College of Medicine,
      University of Kentucky, Lexington, KY 40536, USA.
FAU - Sunkara, Manjula
AU  - Sunkara M
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Division of Cardiovascular Medicine, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA.
FAU - Morris, Andrew J
AU  - Morris AJ
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Division of Cardiovascular Medicine, College of Medicine, University
      of Kentucky, Lexington, KY 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Superfund Research Center, University of Kentucky, Lexington, KY 40536,
      USA; Department of Animal and Food Sciences, College of Agriculture, Food
      and Environment, University of Kentucky, Lexington, KY 40536, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 RR026884/RR/NCRR NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20131106
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Antioxidants)
RN  - 0 (DNA Primers)
RN  - 0 (Enzymes)
RN  - 0 (Tea)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Antioxidants/*metabolism
MH  - Base Sequence
MH  - Chromatography, High Pressure Liquid
MH  - DNA Primers
MH  - *Diet
MH  - Enzymes/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Oxidative Stress/*drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Polymerase Chain Reaction
MH  - Tandem Mass Spectrometry
MH  - *Tea
MH  - Up-Regulation/*drug effects
PMC - PMC3946959
MID - NIHMS538756
OTO - NOTNLM
OT  - AhR
OT  - Antioxidant response
OT  - Green tea
OT  - Nrf2
OT  - Oxidative stress
OT  - PCB toxicity
EDAT- 2014/01/01 06:00
MHDA- 2014/09/16 06:00
CRDT- 2014/01/01 06:00
PHST- 2013/08/21 00:00 [received]
PHST- 2013/10/22 00:00 [revised]
PHST- 2013/10/28 00:00 [accepted]
PHST- 2014/01/01 06:00 [entrez]
PHST- 2014/01/01 06:00 [pubmed]
PHST- 2014/09/16 06:00 [medline]
AID - S0955-2863(13)00221-0 [pii]
AID - 10.1016/j.jnutbio.2013.10.003 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2014 Feb;25(2):126-35. doi:
      10.1016/j.jnutbio.2013.10.003. Epub 2013 Nov 6.

PMID- 24954975
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 53
IP  - 3
DP  - 2014 Jan 22
TI  - Iron-Based Redox Polymerization of Acrylic Acid for Direct Synthesis of
      Hydrogel/Membranes, and Metal Nanoparticles for Water Treatment.
PG  - 1130-1142
AB  - Functionalized polymer materials with ion exchange groups and integration
      of nano-structured materials is an emerging area for catalytic and water
      pollution control applications. The polymerization of materials such as
      acrylic acid often requires persulfate initiator and a high temperature
      start. However, is generally known that metal ions accelerate such
      polymerizations starting from room temperature. If the metal is properly
      selected, it can be used in environmental applications adding two
      advantages simultaneously. This paper deals with this by polymerizing
      acrylic acid using iron as accelerant and its subsequent use for
      nanoparticle synthesis in hydrogel and PVDF membranes. Characterizations
      of hydrogel, membranes and nanoparticles were carried out with different
      techniques. Nanoparticles sizes of 30-60 nm were synthesized.
      Permeability and swelling measurements demonstrate an inverse
      relationship between hydrogel mesh size (6.30 to 8.34 nm) and membrane
      pores (222 to 110 nm). Quantitative reduction of
      trichloroethylene/chloride generation by Fe/Pd nanoparticles in
      hydrogel/membrane platforms was also performed.
FAU - Hernandez, Sebastian
AU  - Hernandez S
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506-0046.
FAU - Papp, Joseph K
AU  - Papp JK
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506-0046.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506-0046.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC4061718
MID - NIHMS546276
OTO - NOTNLM
OT  - TCE
OT  - catalysis
OT  - iron nanoparticles
OT  - membrane functionalization
OT  - responsive behavior
OT  - xerogel
EDAT- 2014/06/24 06:00
MHDA- 2014/06/24 06:01
CRDT- 2014/06/24 06:00
PHST- 2014/06/24 06:00 [entrez]
PHST- 2014/06/24 06:00 [pubmed]
PHST- 2014/06/24 06:01 [medline]
AID - 10.1021/ie403353g [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2014 Jan 22;53(3):1130-1142. doi: 10.1021/ie403353g.

PMID- 24034829
OWN - NLM
STAT- MEDLINE
DCOM- 20140828
LR  - 20211021
IS  - 1879-1298 (Electronic)
IS  - 0045-6535 (Linking)
VI  - 95
DP  - 2014 Jan
TI  - Analytical modeling of the subsurface volatile organic vapor
      concentration in vapor intrusion.
PG  - 140-9
LID - 10.1016/j.chemosphere.2013.08.051 [doi]
LID - S0045-6535(13)01167-3 [pii]
AB  - The inhalation of volatile and semi-volatile organic compounds that
      intrude from a subsurface contaminant source into indoor air has become
      the subject of health and safety concerns over the last twenty years.
      Building subslab and soil gas contaminant vapor concentration sampling
      have become integral parts of vapor intrusion field investigations. While
      numerical models can be of use in analyzing field data and in helping
      understand the subslab and soil gas vapor concentrations, they are not
      widely used due to the perceived effort in setting them up. In this
      manuscript, we present a new closed-form analytical expression describing
      subsurface contaminant vapor concentrations, including subslab vapor
      concentrations. The expression was derived using Schwarz-Christoffel
      mapping. Results from this analytical model match well the numerical
      modeling results. This manuscript also explores the relationship between
      subslab and exterior soil gas vapor concentrations, and offers insights
      on what parameters need to receive greater focus in field studies.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Shen, Rui
AU  - Shen R
AD  - School of Engineering, Brown University, Providence, RI 02912, USA.
      Electronic address: rui_shen@brown.edu.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130910
PL  - England
TA  - Chemosphere
JT  - Chemosphere
JID - 0320657
RN  - 0 (Air Pollutants)
RN  - 0 (Soil)
RN  - 0 (Soil Pollutants)
RN  - 0 (Volatile Organic Compounds)
SB  - IM
MH  - Air Pollutants/analysis/*chemistry
MH  - Environmental Monitoring
MH  - Humans
MH  - *Models, Chemical
MH  - Soil/*chemistry
MH  - Soil Pollutants/analysis/*chemistry
MH  - Volatile Organic Compounds/analysis/*chemistry
PMC - PMC3941444
MID - NIHMS519153
OTO - NOTNLM
OT  - Chemical fate and transport
OT  - Modeling
OT  - Vapor intrusion
OT  - Volatile organic compounds
EDAT- 2013/09/17 06:00
MHDA- 2014/08/29 06:00
CRDT- 2013/09/17 06:00
PHST- 2013/05/21 00:00 [received]
PHST- 2013/08/07 00:00 [revised]
PHST- 2013/08/15 00:00 [accepted]
PHST- 2013/09/17 06:00 [entrez]
PHST- 2013/09/17 06:00 [pubmed]
PHST- 2014/08/29 06:00 [medline]
AID - S0045-6535(13)01167-3 [pii]
AID - 10.1016/j.chemosphere.2013.08.051 [doi]
PST - ppublish
SO  - Chemosphere. 2014 Jan;95:140-9. doi: 10.1016/j.chemosphere.2013.08.051.
      Epub 2013 Sep 10.

PMID- 24197079
OWN - NLM
STAT- MEDLINE
DCOM- 20140711
LR  - 20211021
IS  - 2050-7895 (Electronic)
IS  - 2050-7887 (Linking)
VI  - 15
IP  - 12
DP  - 2013 Dec
TI  - A numerical investigation of oxygen concentration dependence on
      biodegradation rate laws in vapor intrusion.
PG  - 2345-54
LID - 10.1039/c3em00421j [doi]
AB  - In subsurface vapor intrusion, aerobic biodegradation has been considered
      as a major environmental factor that determines the soil gas
      concentration attenuation factors for contaminants such as petroleum
      hydrocarbons. The site investigation has shown that oxygen can play an
      important role in this biodegradation rate, and this paper explores the
      influence of oxygen concentration on biodegradation reactions included in
      vapor intrusion (VI) models. Two different three dimensional (3-D)
      numerical models of vapor intrusion were explored for their sensitivity
      to the form of the biodegradation rate law. A second order biodegradation
      rate law, explicitly including oxygen concentration dependence, was
      introduced into one model. The results indicate that the aerobic/anoxic
      interface depth is determined by the ratio of contaminant source vapor to
      atmospheric oxygen concentration, and that the contaminant concentration
      profile in the aerobic zone was significantly influenced by the choice of
      rate law.
FAU - Yao, Yijun
AU  - Yao Y
AD  - IJRC-PTS, MOE Key Laboratory of Environmental Remediation and Ecosystem
      Health, College of Environmental and Resource Sciences, Zhejiang
      University, Hangzhou 310058, China.
FAU - Shen, Rui
AU  - Shen R
FAU - Pennel, Kelly G
AU  - Pennel KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Environ Sci Process Impacts
JT  - Environmental science. Processes & impacts
JID - 101601576
RN  - 0 (Environmental Pollutants)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - *Biodegradation, Environmental
MH  - Environmental Pollutants/*metabolism
MH  - *Models, Theoretical
MH  - Oxygen/*metabolism
PMC - PMC3897126
MID - NIHMS537566
EDAT- 2013/11/08 06:00
MHDA- 2014/07/12 06:00
CRDT- 2013/11/08 06:00
PHST- 2013/11/08 06:00 [entrez]
PHST- 2013/11/08 06:00 [pubmed]
PHST- 2014/07/12 06:00 [medline]
AID - 10.1039/c3em00421j [doi]
PST - ppublish
SO  - Environ Sci Process Impacts. 2013 Dec;15(12):2345-54. doi:
      10.1039/c3em00421j.

PMID- 24237919
OWN - NLM
STAT- MEDLINE
DCOM- 20140717
LR  - 20211021
IS  - 1873-2607 (Electronic)
IS  - 0749-3797 (Linking)
VI  - 45
IP  - 6
DP  - 2013 Dec
TI  - Public health research implementation and translation: evidence from
      practice-based research networks.
PG  - 752-62
LID - 10.1016/j.amepre.2013.08.011 [doi]
LID - S0749-3797(13)00489-3 [pii]
AB  - BACKGROUND: Research on how best to deliver efficacious public health
      strategies in heterogeneous community and organizational contexts remains
      limited. Such studies require the active engagement of public health
      practice settings in the design, implementation, and translation of
      research. Practice-based research networks (PBRNs) provide mechanisms for
      research engagement, but until now they have not been tested in public
      health settings. PURPOSE: This study uses data from participants in 14
      public health PBRNs and a national comparison group of public health
      agencies to study processes influencing the engagement of public health
      settings in research implementation and translation activities. METHODS:
      A cross-sectional network analysis survey was fielded with participants
      in public health PBRNs approximately 1 year after network formation
      (n=357) and with a nationally representative comparison group of U.S.
      local health departments not participating in PBRNs (n=625). Hierarchic
      regression models were used to estimate how organizational attributes and
      PBRN network structures influence engagement in research implementation
      and translation activities. Data were collected in 2010-2012 and analyzed
      in 2012. RESULTS: Among PBRN participants, both researchers and practice
      agencies reported high levels of engagement in research activities. Local
      public health agencies participating in PBRNs were two to three times
      more likely than nonparticipating agencies to engage in research
      implementation and translation activities (p<0.05). Participants in less
      densely connected PBRN networks and in more peripheral locations within
      these networks reported higher levels of research engagement, greater
      perceived benefits from engagement, and greater likelihood of continued
      participation. CONCLUSIONS: PBRN networks can serve as effective
      mechanisms for facilitating research implementation and translation among
      public health practice settings.
CI  - (c) 2013 Published by American Journal of Preventive Medicine on behalf
      of American Journal of Preventive Medicine.
FAU - Mays, Glen P
AU  - Mays GP
AD  - Department of Health Services Management, College of Public Health,
      University of Kentucky, Lexington, Kentucky.
FAU - Hogg, Rachel A
AU  - Hogg RA
FAU - Castellanos-Cruz, Doris M
AU  - Castellanos-Cruz DM
FAU - Hoover, Anna G
AU  - Hoover AG
FAU - Fowler, Lizeth C
AU  - Fowler LC
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - UL1 TR000117/TR/NCATS NIH HHS/United States
GR  - UL1TR000117/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Am J Prev Med
JT  - American journal of preventive medicine
JID - 8704773
SB  - IM
MH  - Community Networks/*organization & administration
MH  - Cross-Sectional Studies
MH  - Health Services Research/*organization & administration
MH  - Humans
MH  - *Public Health
MH  - Public Health Practice
MH  - Regression Analysis
MH  - Translational Medical Research/*organization & administration
MH  - United States
PMC - PMC4366056
MID - NIHMS669660
EDAT- 2013/11/19 06:00
MHDA- 2014/07/18 06:00
CRDT- 2013/11/19 06:00
PHST- 2013/03/08 00:00 [received]
PHST- 2013/07/23 00:00 [revised]
PHST- 2013/08/13 00:00 [accepted]
PHST- 2013/11/19 06:00 [entrez]
PHST- 2013/11/19 06:00 [pubmed]
PHST- 2014/07/18 06:00 [medline]
AID - S0749-3797(13)00489-3 [pii]
AID - 10.1016/j.amepre.2013.08.011 [doi]
PST - ppublish
SO  - Am J Prev Med. 2013 Dec;45(6):752-62. doi: 10.1016/j.amepre.2013.08.011.

PMID- 24083557
OWN - NLM
STAT- MEDLINE
DCOM- 20150930
LR  - 20211021
IS  - 1520-5851 (Electronic)
IS  - 0013-936X (Linking)
VI  - 47
IP  - 21
DP  - 2013
TI  - Bridging research and environmental regulatory processes: the role of
      knowledge brokers.
PG  - 11985-92
LID - 10.1021/es4025244 [doi]
AB  - Federal funding agencies increasingly require research investigators to
      ensure that federally sponsored research demonstrates broader societal
      impact. Specifically, the National Institutes of Environmental Health
      Sciences (NIEHS) Superfund Research Program (SRP) requires research
      centers to include research translation and community engagement cores to
      achieve broader impacts, with special emphasis on improving environmental
      health policies through better scientific understanding. This paper draws
      on theoretical insights from the social sciences to show how
      incorporating knowledge brokers in research centers can facilitate
      translation of scientific expertise to influence regulatory processes and
      thus promote public health. Knowledge brokers connect academic
      researchers with decision-makers, to facilitate the translation of
      research findings into policies and programs. In this article, we
      describe the stages of the regulatory process and highlight the role of
      the knowledge broker and scientific expert at each stage. We illustrate
      the cooperation of knowledge brokers, scientific experts and policymakers
      using a case from the Brown University (Brown) SRP. We show how the Brown
      SRP incorporated knowledge brokers to engage scientific experts with
      regulatory officials around the emerging public health problem of vapor
      intrusion (VI). In the Brown SRP, the knowledge broker brought regulatory
      officials into the research process, to help scientific experts
      understand the critical nature of this emerging public health threat, and
      helped scientific experts develop a research agenda that would inform the
      development of timely measures to protect public health. Our experience
      shows that knowledge brokers can enhance the impact of environmental
      research on public health by connecting policy decision-makers with
      scientific experts at critical points throughout the regulatory process.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - Department of Civil Engineering, University of Kentucky , Lexington,
      Kentucky 40506, United States.
FAU - Thompson, Marcella
AU  - Thompson M
FAU - Rice, James W
AU  - Rice JW
FAU - Senier, Laura
AU  - Senier L
FAU - Brown, Phil
AU  - Brown P
FAU - Suuberg, Eric
AU  - Suuberg E
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20131022
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
SB  - IM
MH  - Decision Making
MH  - Environmental Health/economics/*legislation & jurisprudence
MH  - Environmental Policy/economics/*legislation & jurisprudence
MH  - *Financing, Government
MH  - *Government Regulation
MH  - Health Knowledge, Attitudes, Practice
MH  - Health Policy/economics/*legislation & jurisprudence
MH  - Humans
MH  - National Institute of Environmental Health Sciences (U.S.)
MH  - Research/economics/*legislation & jurisprudence
MH  - United States
PMC - PMC3875357
MID - NIHMS533926
EDAT- 2013/10/03 06:00
MHDA- 2015/10/01 06:00
CRDT- 2013/10/03 06:00
PHST- 2013/10/03 06:00 [entrez]
PHST- 2013/10/03 06:00 [pubmed]
PHST- 2015/10/01 06:00 [medline]
AID - 10.1021/es4025244 [doi]
PST - ppublish
SO  - Environ Sci Technol. 2013;47(21):11985-92. doi: 10.1021/es4025244. Epub
      2013 Oct 22.

PMID- 23595851
OWN - NLM
STAT- MEDLINE
DCOM- 20131212
LR  - 20211021
IS  - 1552-8618 (Electronic)
IS  - 0730-7268 (Linking)
VI  - 32
IP  - 10
DP  - 2013 Oct
TI  - Performance of passive samplers for monitoring estuarine water column
      concentrations: 2. Emerging contaminants.
PG  - 2190-6
LID - 10.1002/etc.2248 [doi]
AB  - Measuring dissolved concentrations of emerging contaminants, such as
      polybrominated diphenyl ethers (PBDEs) and triclosan, can be challenging
      due to their physicochemical properties resulting in low aqueous
      solubilities and association with particles. Passive sampling methods
      have been applied to assess dissolved concentrations in water and
      sediments primarily for legacy contaminants. Although the technology is
      applicable to some emerging contaminants, the use of passive samplers
      with emerging contaminants is limited. In the present study, the
      performance of 3 common passive samplers was evaluated for sampling PBDEs
      and triclosan. Passive sampling polymers included low-density
      polyethylene (PE) and polyoxymethylene (POM) sheets, and
      polydimethylsiloxane (PDMS)-coated solid-phase microextraction (SPME)
      fibers. Dissolved concentrations were calculated using measured sampler
      concentrations and laboratory-derived partition coefficients. Dissolved
      tri-, tetra-, and pentabrominated PBDE congeners were detected at several
      of the study sites at very low pg/L concentrations using PE and POM.
      Calculated dissolved water concentrations of triclosan ranged from 1.7
      ng/L to 18 ng/L for POM and 8.8 ng/L to 13 ng/L for PE using performance
      reference compound equilibrium adjustments. Concentrations in SPME were
      not reported due to lack of detectable chemical in the PDMS polymer
      deployed. Although both PE and POM were found to effectively accumulate
      emerging contaminants from the water column, further research is needed
      to determine their utility as passive sampling devices for emerging
      contaminants.
CI  - (c) 2013 SETAC.
FAU - Perron, Monique M
AU  - Perron MM
AD  - National Research Council, US Environmental Protection Agency,
      ORD/NHEERL, Narragansett, Rhode Island, USA. perron.monique@epa.gov
FAU - Burgess, Robert M
AU  - Burgess RM
FAU - Suuberg, Eric M
AU  - Suuberg EM
FAU - Cantwell, Mark G
AU  - Cantwell MG
FAU - Pennell, Kelly G
AU  - Pennell KG
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130719
PL  - United States
TA  - Environ Toxicol Chem
JT  - Environmental toxicology and chemistry
JID - 8308958
RN  - 0 (Dimethylpolysiloxanes)
RN  - 0 (Halogenated Diphenyl Ethers)
RN  - 0 (Resins, Synthetic)
RN  - 0 (Water Pollutants, Chemical)
RN  - 4NM5039Y5X (Triclosan)
RN  - 63148-62-9 (baysilon)
RN  - 9002-88-4 (Polyethylene)
RN  - 9085-38-5 (delrin)
SB  - IM
MH  - Dimethylpolysiloxanes
MH  - Environmental Monitoring
MH  - *Estuaries
MH  - Halogenated Diphenyl Ethers/*analysis
MH  - Polyethylene
MH  - Resins, Synthetic
MH  - Seawater/*chemistry
MH  - Solid Phase Microextraction
MH  - Triclosan/*analysis
MH  - Water Pollutants, Chemical/*analysis
PMC - PMC4006789
MID - NIHMS569291
OTO - NOTNLM
OT  - Emerging contaminants
OT  - Passive sampling
OT  - Polyethylene
OT  - Polyoxymethylene
OT  - Solid-phase microextraction fibers
EDAT- 2013/04/19 06:00
MHDA- 2013/12/18 06:00
CRDT- 2013/04/19 06:00
PHST- 2013/01/17 00:00 [received]
PHST- 2013/02/08 00:00 [revised]
PHST- 2013/04/08 00:00 [accepted]
PHST- 2013/04/19 06:00 [entrez]
PHST- 2013/04/19 06:00 [pubmed]
PHST- 2013/12/18 06:00 [medline]
AID - 10.1002/etc.2248 [doi]
PST - ppublish
SO  - Environ Toxicol Chem. 2013 Oct;32(10):2190-6. doi: 10.1002/etc.2248. Epub
      2013 Jul 19.

PMID- 23832638
OWN - NLM
STAT- MEDLINE
DCOM- 20131212
LR  - 20211021
IS  - 1552-8618 (Electronic)
IS  - 0730-7268 (Linking)
VI  - 32
IP  - 10
DP  - 2013 Oct
TI  - Performance of passive samplers for monitoring estuarine water column
      concentrations: 1. Contaminants of concern.
PG  - 2182-9
AB  - Contaminants enter marine and estuarine environments and pose a risk to
      human and ecological health. Recently, passive sampling devices have been
      utilized to estimate dissolved concentrations of contaminants of concern
      (COCs), such as polycyclic aromatic hydrocarbons (PAHs) and
      polychlorinated biphenyls (PCBs). In the present study, the performance
      of 3 common passive samplers was evaluated for sampling PAHs and PCBs at
      several stations in the temperate estuary Narragansett Bay, Rhode Island,
      USA. Sampler polymers included polyethylene (PE), polydimethylsiloxane
      (PDMS)-coated solid-phase microextraction (SPME) fibers, and
      polyoxymethylene (POM). Dissolved concentrations of each contaminant were
      calculated using measured sampler concentrations adjusted for equilibrium
      conditions with performance reference compounds (PRCs) and chemical-
      specific partition coefficients derived in the laboratory. Despite
      differences in PE and POM sampler concentrations, calculated total
      dissolved concentrations ranged from 14 ng/L to 93 ng/L and from 13 pg/L
      to 465 pg/L for PAHs and PCBs, respectively. Dissolved concentrations of
      PAHs were approximately 3 times greater based on POM compared to PE,
      while dissolved concentrations of PCBs based on PE were approximately 3
      times greater than those based on POM. Concentrations in SPME were not
      reported due to the lack of detectable chemical in the amount of PDMS
      polymer deployed. Continued research is needed to improve and support PE
      and POM use for the routine monitoring of COCs. For example, a better
      understanding of the use of PRCs with POM is critically needed.
CI  - (c) 2013 SETAC.
FAU - Perron, Monique M
AU  - Perron MM
AD  - National Research Council, US Environmental Protection Agency,
      ORD/NHEERL, Narragansett, Rhode Island, USA. perron.monique@epa.gov
FAU - Burgess, Robert M
AU  - Burgess RM
FAU - Suuberg, Eric M
AU  - Suuberg EM
FAU - Cantwell, Mark G
AU  - Cantwell MG
FAU - Pennell, Kelly G
AU  - Pennell KG
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Environ Toxicol Chem
JT  - Environmental toxicology and chemistry
JID - 8308958
RN  - 0 (Dimethylpolysiloxanes)
RN  - 0 (Polycyclic Aromatic Hydrocarbons)
RN  - 0 (Resins, Synthetic)
RN  - 0 (Water Pollutants, Chemical)
RN  - 63148-62-9 (baysilon)
RN  - 9002-88-4 (Polyethylene)
RN  - 9085-38-5 (delrin)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Dimethylpolysiloxanes
MH  - Environmental Monitoring
MH  - *Estuaries
MH  - Humans
MH  - Polychlorinated Biphenyls/*analysis
MH  - Polycyclic Aromatic Hydrocarbons/*analysis
MH  - Polyethylene
MH  - Resins, Synthetic
MH  - Rhode Island
MH  - Seawater/*chemistry
MH  - Solid Phase Microextraction
MH  - Water Pollutants, Chemical/*analysis
PMC - PMC3979968
MID - NIHMS569192
EDAT- 2013/07/09 06:00
MHDA- 2013/12/18 06:00
CRDT- 2013/07/09 06:00
PHST- 2013/01/16 00:00 [received]
PHST- 2013/02/21 00:00 [revised]
PHST- 2013/07/02 00:00 [accepted]
PHST- 2013/07/09 06:00 [entrez]
PHST- 2013/07/09 06:00 [pubmed]
PHST- 2013/12/18 06:00 [medline]
AID - 10.1002/etc.2321 [doi]
PST - ppublish
SO  - Environ Toxicol Chem. 2013 Oct;32(10):2182-9. doi: 10.1002/etc.2321.

PMID- 24170970
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1092-8758 (Print)
IS  - 1092-8758 (Linking)
VI  - 30
IP  - 10
DP  - 2013 Oct
TI  - Influence of Soil Moisture on Soil Gas Vapor Concentration for Vapor
      Intrusion.
PG  - 628-637
AB  - Mathematical models have been widely used in analyzing the effects of
      various environmental factors in the vapor intrusion process. Soil
      moisture content is one of the key factors determining the subsurface
      vapor concentration profile. This manuscript considers the effects of
      soil moisture profiles on the soil gas vapor concentration away from any
      surface capping by buildings or pavement. The "open field" soil gas vapor
      concentration profile is observed to be sensitive to the soil moisture
      distribution. The van Genuchten relations can be used for describing the
      soil moisture retention curve, and give results consistent with the
      results from a previous experimental study. Other modeling methods that
      account for soil moisture are evaluated. These modeling results are also
      compared with the measured subsurface concentration profiles in the U.S.
      EPA vapor intrusion database.
FAU - Shen, Rui
AU  - Shen R
AD  - School of Engineering, Brown University , Providence, Rhode Island.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Environ Eng Sci
JT  - Environmental engineering science
JID - 9891639
PMC - PMC3804323
OTO - NOTNLM
OT  - modeling
OT  - soil gas vapor concentration
OT  - soil moisture
OT  - vapor intrusion
EDAT- 2013/10/31 06:00
MHDA- 2013/10/31 06:01
CRDT- 2013/10/31 06:00
PHST- 2013/04/19 00:00 [received]
PHST- 2013/07/17 00:00 [accepted]
PHST- 2013/10/31 06:00 [entrez]
PHST- 2013/10/31 06:00 [pubmed]
PHST- 2013/10/31 06:01 [medline]
AID - 10.1089/ees.2013.0133 [doi]
AID - 10.1089/ees.2013.0133 [pii]
PST - ppublish
SO  - Environ Eng Sci. 2013 Oct;30(10):628-637. doi: 10.1089/ees.2013.0133.

PMID- 24954974
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 52
IP  - 31
DP  - 2013 Aug 7
TI  - Reactive Functionalized Membranes for Polychlorinated Biphenyl
      Degradation.
PG  - 10430-10440
AB  - Membranes have been widely used in water remediation (e.g. desalination
      and heavy metal removal) because of the ability to control membrane pore
      size and surface charge. The incorporation of nanomaterials into the
      membranes provides added benefits through increased reactivity with
      different functionality. In this study, we report the dechlorination of
      2-chlorobiphenyl in the aqueous phase by a reactive membrane system.
      Fe/Pd bimetallic nanoparticles (NPs) were synthesized (in-situ) within
      polyacrylic acid (PAA) functionalized polyvinylidene fluoride (PVDF)
      membranes for degradation of polychlorinated biphenyls (PCBs). Biphenyl
      formed in the reduction was further oxidized into hydroxylated biphenyls
      and benzoic acid by an iron-catalyzed hydroxyl radical (OH*) reaction.
      The formation of magnetite on Fe surface was observed. This combined
      pathway (reductive/oxidative) could reduce the toxicity of PCBs
      effectively while eliminating the formation of chlorinated degradation
      byproducts. The successful manufacturing of full-scale functionalized
      membranes demonstrates the possibility of applying reactive membranes in
      practical water treatment.
FAU - Gui, Minghui
AU  - Gui M
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
FAU - Ormsbee, Lindell E
AU  - Ormsbee LE
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC4061716
MID - NIHMS481940
OTO - NOTNLM
OT  - Fenton reaction
OT  - PVDF membrane
OT  - catalysis
OT  - hydroxyl radical
OT  - iron oxide
OT  - nanoparticles
EDAT- 2014/06/24 06:00
MHDA- 2014/06/24 06:01
CRDT- 2014/06/24 06:00
PHST- 2014/06/24 06:00 [entrez]
PHST- 2014/06/24 06:00 [pubmed]
PHST- 2014/06/24 06:01 [medline]
AID - 10.1021/ie400507c [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2013 Aug 7;52(31):10430-10440. doi: 10.1021/ie400507c.

PMID- 23278296
OWN - NLM
STAT- MEDLINE
DCOM- 20140422
LR  - 20211021
IS  - 1600-0668 (Electronic)
IS  - 0905-6947 (Linking)
VI  - 23
IP  - 4
DP  - 2013 Aug
TI  - Formaldehyde concentrations in household air of asthma patients
      determined using colorimetric detector tubes.
PG  - 285-94
LID - 10.1111/ina.12024 [doi]
AB  - Formaldehyde is a colorless, pungent gas commonly found in homes and is a
      respiratory irritant, sensitizer, carcinogen, and asthma trigger. Typical
      household sources include plywood and particleboard, cleaners, cosmetics,
      pesticides, and others. Development of a fast and simple measurement
      technique could facilitate continued research on this important chemical.
      The goal of this research is to apply an inexpensive short-term
      measurement method to find correlations between formaldehyde sources and
      concentration, and formaldehyde concentration and asthma control.
      Formaldehyde was measured using 30-min grab samples in length-of-stain
      detector tubes in homes (n = 70) of asthmatics in the Boston, MA area.
      Clinical status and potential formaldehyde sources were determined. The
      geometric mean formaldehyde level was 35.1 ppb and ranged from 5 to 132
      ppb. Based on one-way ANOVA, t-tests, and linear regression, predictors
      of log-transformed formaldehyde concentration included absolute humidity,
      season, and the presence of decorative laminates, fiberglass, or
      permanent press fabrics (P < 0.05), as well as temperature and household
      cleaner use (P < 0.10). The geometric mean formaldehyde concentration was
      57% higher in homes of children with very poorly controlled asthma
      compared to homes of other asthmatic children (P = 0.078). This study
      provides a simple method for measuring household formaldehyde and
      suggests that exposure is related to poorly controlled asthma.
CI  - (c) 2012 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Dannemiller, K C
AU  - Dannemiller KC
AD  - Department of Chemical and Environmental Engineering, Yale University,
      New Haven, CT, USA.
FAU - Murphy, J S
AU  - Murphy JS
FAU - Dixon, S L
AU  - Dixon SL
FAU - Pennell, K G
AU  - Pennell KG
FAU - Suuberg, E M
AU  - Suuberg EM
FAU - Jacobs, D E
AU  - Jacobs DE
FAU - Sandel, M
AU  - Sandel M
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20130131
PL  - England
TA  - Indoor Air
JT  - Indoor air
JID - 9423515
RN  - 1HG84L3525 (Formaldehyde)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Air/analysis
MH  - Asthma/*epidemiology
MH  - Boston/epidemiology
MH  - Child
MH  - Child, Preschool
MH  - Colorimetry
MH  - Environmental Monitoring/*methods
MH  - Female
MH  - Formaldehyde/*analysis
MH  - Housing
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Regression Analysis
MH  - Young Adult
PMC - PMC3710296
MID - NIHMS459380
OTO - NOTNLM
OT  - Absolute humidity
OT  - Asthma
OT  - Colorimetric detector tubes
OT  - Formaldehyde
OT  - Household chemical exposure
OT  - Housing
EDAT- 2013/01/03 06:00
MHDA- 2014/04/23 06:00
CRDT- 2013/01/03 06:00
PHST- 2012/07/09 00:00 [received]
PHST- 2012/12/15 00:00 [accepted]
PHST- 2013/01/03 06:00 [entrez]
PHST- 2013/01/03 06:00 [pubmed]
PHST- 2014/04/23 06:00 [medline]
AID - 10.1111/ina.12024 [doi]
PST - ppublish
SO  - Indoor Air. 2013 Aug;23(4):285-94. doi: 10.1111/ina.12024. Epub 2013 Jan
      31.

PMID- 24795543
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1539-1663 (Print)
IS  - 1539-1663 (Linking)
VI  - 12
IP  - 3
DP  - 2013 Aug
TI  - Estimation of Contaminant Subslab Concentration in Vapor Intrusion
      Including Lateral Source-Building Separation.
LID - 10.2136/vzj2012.0157 [doi]
AB  - Most current vapor-intrusion screening models employ the assumption of a
      subsurface homogenous source distribution, and groundwater data obtained
      from nearby monitoring wells are usually taken to reflect the source
      concentration for several nearby buildings. This practice makes it
      necessary to consider the possible influence of lateral source-building
      separation. In this study, a new way to estimate subslab
      (nonbiodegradable) contaminant concentration is introduced that includes
      the influence of source offset with the help of a conformal transform
      technique. Results from this method are compared with those from a three-
      dimensional numerical model. Based on this newly developed method, a
      possible explanation is provided here for the great variation in the
      attenuation factors of the soil vapor concentrations of groundwater-to-
      subslab contaminants found in the EPA vapor-intrusion database.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown Univ., Providence RI 02912.
FAU - Shen, Rui
AU  - Shen R
AD  - School of Engineering, Brown Univ., Providence RI 02912.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - School of Engineering, Brown Univ., Providence RI 02912.
FAU - Suuberg, Eric M
AU  - Suuberg EM
AD  - School of Engineering, Brown Univ., Providence RI 02912.
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Vadose Zone J
JT  - Vadose zone journal : VZJ
JID - 101235416
PMC - PMC4006780
MID - NIHMS568536
EDAT- 2014/05/06 06:00
MHDA- 2014/05/06 06:01
CRDT- 2014/05/06 06:00
PHST- 2014/05/06 06:00 [entrez]
PHST- 2014/05/06 06:00 [pubmed]
PHST- 2014/05/06 06:01 [medline]
AID - 10.2136/vzj2012.0157 [doi]
PST - ppublish
SO  - Vadose Zone J. 2013 Aug;12(3). doi: 10.2136/vzj2012.0157.

PMID- 23752876
OWN - NLM
STAT- MEDLINE
DCOM- 20140123
LR  - 20211021
IS  - 2050-7895 (Electronic)
IS  - 2050-7887 (Linking)
VI  - 15
IP  - 7
DP  - 2013 Jul
TI  - Modeling quantification of the influence of soil moisture on subslab
      vapor concentration.
PG  - 1444-51
LID - 10.1039/c3em00225j [doi]
AB  - The U.S. EPA has developed a database of field data obtained from vapor
      intrusion sites throughout the United States. Large variations in
      reported subsurface contaminant vapor concentration ratios (e.g. building
      subslab to groundwater source) present challenges for the analysis of
      subsurface vapor transport processes. Meanwhile, numerical models have
      been used by the U.S. EPA and others to describe the transport processes
      governing vapor intrusion. The influence of the capillary fringe has
      often been ignored in these models. In this manuscript, the influence of
      soil moisture content on the subslab vapor concentration is analyzed in
      the context of mathematical models. Results are compared to those from
      other modeling methods that do not account for the soil moisture content.
      The slab capping effect is observed to interact with the effect of soil
      moisture in determining the subslab contaminant vapor concentration. The
      slab capping effect is observed to be significant when the building-
      source separation distance is less than half of the slab size.
FAU - Shen, Rui
AU  - Shen R
AD  - School of Engineering, Brown University, Providence, RI 02912, USA.
      rui_shen@brown.edu
FAU - Yao, Yijun
AU  - Yao Y
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Environ Sci Process Impacts
JT  - Environmental science. Processes & impacts
JID - 101601576
RN  - 0 (Soil)
RN  - 0 (Soil Pollutants)
RN  - 059QF0KO0R (Water)
SB  - IM
MH  - Air Pollution, Indoor
MH  - *Models, Theoretical
MH  - Soil/*chemistry
MH  - Soil Pollutants/*analysis/chemistry
MH  - Volatilization
MH  - Water/*analysis
PMC - PMC3756691
MID - NIHMS504032
EDAT- 2013/06/12 06:00
MHDA- 2014/01/24 06:00
CRDT- 2013/06/12 06:00
PHST- 2013/06/12 06:00 [entrez]
PHST- 2013/06/12 06:00 [pubmed]
PHST- 2014/01/24 06:00 [medline]
AID - 10.1039/c3em00225j [doi]
PST - ppublish
SO  - Environ Sci Process Impacts. 2013 Jul;15(7):1444-51. doi:
      10.1039/c3em00225j.

PMID- 23950637
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1069-3629 (Print)
IS  - 1069-3629 (Linking)
VI  - 33
IP  - 3
DP  - 2013 Summer
TI  - Sewer Gas: An Indoor Air Source of PCE to Consider During Vapor Intrusion
      Investigations.
PG  - 119-126
AB  - The United States Environmental Protection Agency (USEPA) is finalizing
      its vapor intrusion guidelines. One of the important issues related to
      vapor intrusion is background concentrations of volatile organic
      chemicals (VOCs) in indoor air, typically attributed to consumer products
      and building materials. Background concentrations can exist even in the
      absence of vapor intrusion and are an important consideration when
      conducting site assessments. In addition, the development of accurate
      conceptual models that depict pathways for vapor entry into buildings is
      important during vapor intrusion site assessments. Sewer gas, either as a
      contributor to background concentrations or as part of the site
      conceptual model, is not routinely evaluated during vapor intrusion site
      assessments. The research described herein identifies an instance where
      vapors emanating directly from a sanitary sewer pipe within a residence
      were determined to be a source of tetrachloroethylene (PCE) detected in
      indoor air. Concentrations of PCE in the bathroom range from 2.1 to 190
      ug/m(3) and exceed typical indoor air concentrations by orders of
      magnitude resulting in human health risk classified as an "Imminent
      Hazard" condition. The results suggest that infiltration of sewer gas
      resulted in PCE concentrations in indoor air that were nearly two-orders
      of magnitude higher as compared to when infiltration of sewer gas was not
      known to be occurring. This previously understudied pathway whereby
      sewers serve as sources of PCE (and potentially other VOC) vapors is
      highlighted. Implications for vapor intrusion investigations are also
      discussed.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - University of Massachusetts-Dartmouth, Civil and Environmental
      Engineering Department, North Dartmouth MA 02747.
FAU - Scammell, Madeleine Kangsen
AU  - Scammell MK
FAU - McClean, Michael D
AU  - McClean MD
FAU - Ames, Jennifer
AU  - Ames J
FAU - Weldon, Brittany
AU  - Weldon B
FAU - Friguglietti, Leigh
AU  - Friguglietti L
FAU - Suuberg, Eric M
AU  - Suuberg EM
FAU - Shen, Rui
AU  - Shen R
FAU - Indeglia, Paul A
AU  - Indeglia PA
FAU - Heiger-Bernays, Wendy J
AU  - Heiger-Bernays WJ
LA  - eng
GR  - P42 ES007381/ES/NIEHS NIH HHS/United States
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Ground Water Monit Remediat
JT  - Ground water monitoring & remediation
JID - 100911134
PMC - PMC3740581
MID - NIHMS482227
OTO - NOTNLM
OT  - Vapor Intrusion
OT  - groundwater
OT  - indoor air
OT  - sewer gas
EDAT- 2013/08/21 06:00
MHDA- 2013/08/21 06:01
CRDT- 2013/08/17 06:00
PHST- 2013/08/17 06:00 [entrez]
PHST- 2013/08/21 06:00 [pubmed]
PHST- 2013/08/21 06:01 [medline]
AID - 10.1111/gwmr.12021 [doi]
PST - ppublish
SO  - Ground Water Monit Remediat. 2013 Summer;33(3):119-126. doi:
      10.1111/gwmr.12021.

PMID- 30518988
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 0021-8995 (Print)
IS  - 0021-8995 (Linking)
VI  - 128
IP  - 3
DP  - 2013 May 5
TI  - Temperature Responsive Hydrogel with Reactive Nanoparticles.
PG  - 1804-1814
LID - 10.1002/APP.38335 [doi]
AB  - The application of temperature responsive hydrogels with ion-exchange
      domain for nanoscale catalytic reactions is an emerging and attractive
      area because of the combination of individual unique features:
      temperature responsive tunability by the polymer domain and the high
      catalytic reactivity of the nanomaterial. Here, we report the entrapment
      and/or direct synthesis of reactive Fe and Fe/Pd nanoparticles (about
      40-70 nm) in a temperature responsive hydrogel network
      (N-isopropylacrylamide (NIPAAm), and NIPAAm-PAA). These nanoparticles are
      stabilized in the hydrogel network and the dechlorination (using
      trichloroethylene, TCE, as a model compound) reactivity in water is
      enhanced and controllable in the temperature range of 30-34 degrees C
      involving polymer domain transitions at lower critical solution
      temperature (LCST) from hydrophilic to collapsed hydrophobic state. Water
      fraction modulation of the network and the enhancement of pollutant
      partitioning by the thermally responsive polymers play an important role
      in the catalytic activity.
FAU - Xiao, Li
AU  - Xiao L
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Isner, Austin B
AU  - Isner AB
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Hilt, J Zach
AU  - Hilt JZ
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20120801
PL  - United States
TA  - J Appl Polym Sci
JT  - Journal of applied polymer science
JID - 9891577
PMC - PMC6276787
MID - NIHMS997162
OTO - NOTNLM
OT  - catalysts
OT  - copolymers
OT  - gels
OT  - nanoparticles
OT  - stimuli-sensitive polymers
EDAT- 2013/05/05 00:00
MHDA- 2013/05/05 00:01
CRDT- 2018/12/07 06:00
PHST- 2018/12/07 06:00 [entrez]
PHST- 2013/05/05 00:00 [pubmed]
PHST- 2013/05/05 00:01 [medline]
AID - 10.1002/APP.38335 [doi]
PST - ppublish
SO  - J Appl Polym Sci. 2013 May 5;128(3):1804-1814. doi: 10.1002/APP.38335.
      Epub 2012 Aug 1.

PMID- 23380242
OWN - NLM
STAT- MEDLINE
DCOM- 20130913
LR  - 20211021
IS  - 1879-3185 (Electronic)
IS  - 0300-483X (Linking)
VI  - 306
DP  - 2013 Apr 5
TI  - Titanium dioxide nanoparticles increase inflammatory responses in
      vascular endothelial cells.
PG  - 1-8
LID - 10.1016/j.tox.2013.01.014 [doi]
LID - S0300-483X(13)00019-X [pii]
AB  - Atherosclerosis is a chronic inflammatory disease that remains the
      leading cause of death in the United States. Numerous risk factors for
      endothelial cell inflammation and the development of atherosclerosis have
      been identified, including inhalation of ultrafine particles. Recently,
      engineered nanoparticles (NPs) such as titanium (TiO2) NPs have attracted
      much attention due to their wide range of applications. However, there
      are also great concerns surrounding potential adverse health effects in
      vascular systems. Although TiO2 NPs are known to induce oxidative stress
      and inflammation, the associated signaling pathways have not been well
      studied. The focus of this work, therefore, deals with examination of the
      cellular signaling pathways responsible for TiO2 NP-induced endothelial
      oxidative stress and inflammation. In this study, primary vascular
      endothelial cells were treated with TiO2 NPs for 2-16h at concentrations
      of 0-50 mug/mL. TiO2 NP exposure increased cellular oxidative stress and
      DNA binding of NF-kappaB. Further, phosphorylation of Akt, ERK, JNK and
      p38 was increased in cells exposed to TiO2 NPs. TiO2 NPs also
      significantly increased induction of mRNA and protein levels of vascular
      cell adhesion molecule-1 (VCAM-1) and mRNA levels of monocyte
      chemoattractant protein-1 (MCP-1). Pretreatment with inhibitors for NF-
      kappaB (pyrrolidine dithiocarbamate), oxidative stress (epigallocatechin
      gallate and apocynin), Akt (LY294002), ERK (PD98059), JNK (SP600125) and
      p38 (SB203580) significantly attenuated TiO2 NP-induced MCP-1 and VCAM-1
      gene expression. These data indicate that TiO2 NPs can induce endothelial
      inflammatory responses via redox-sensitive cellular signaling pathways.
CI  - Copyright (c) 2013 Elsevier Ireland Ltd. All rights reserved.
FAU - Han, Sung Gu
AU  - Han SG
AD  - Superfund Research Program, University of Kentucky, Lexington, KY 40536,
      USA.
FAU - Newsome, Bradley
AU  - Newsome B
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130201
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Chemokine CCL2)
RN  - 0 (Peptide Fragments)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 0 (monocyte chemoattractant protein 1 (66-77))
RN  - 15FIX9V2JP (titanium dioxide)
RN  - D1JT611TNE (Titanium)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/genetics/metabolism
MH  - Electrophoretic Mobility Shift Assay
MH  - Endothelial Cells/cytology/*drug effects/metabolism
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Inflammation/*chemically induced
MH  - MAP Kinase Signaling System/drug effects
MH  - Microscopy, Electron, Scanning
MH  - Nanoparticles/*toxicity
MH  - Oxidative Stress/*drug effects
MH  - Peptide Fragments/genetics/metabolism
MH  - Protein Kinase Inhibitors/pharmacology
MH  - RNA, Messenger/chemistry/genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Titanium/*toxicity
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
PMC - PMC3631470
MID - NIHMS441884
EDAT- 2013/02/06 06:00
MHDA- 2013/09/14 06:00
CRDT- 2013/02/06 06:00
PHST- 2012/10/29 00:00 [received]
PHST- 2013/01/10 00:00 [revised]
PHST- 2013/01/22 00:00 [accepted]
PHST- 2013/02/06 06:00 [entrez]
PHST- 2013/02/06 06:00 [pubmed]
PHST- 2013/09/14 06:00 [medline]
AID - S0300-483X(13)00019-X [pii]
AID - 10.1016/j.tox.2013.01.014 [doi]
PST - ppublish
SO  - Toxicology. 2013 Apr 5;306:1-8. doi: 10.1016/j.tox.2013.01.014. Epub 2013
      Feb 1.

PMID- 23360069
OWN - NLM
STAT- MEDLINE
DCOM- 20140319
LR  - 20211021
IS  - 1520-5851 (Electronic)
IS  - 0013-936X (Linking)
VI  - 47
IP  - 6
DP  - 2013 Mar 19
TI  - A review of vapor intrusion models.
PG  - 2457-70
LID - 10.1021/es302714g [doi]
AB  - A complete vapor intrusion (VI) model, describing vapor entry of volatile
      organic chemicals (VOCs) into buildings located on contaminated sites,
      generally consists of two main parts: one part describing vapor transport
      in the soil and the other describing its entry into the building.
      Modeling the soil vapor transport part involves either analytically or
      numerically solving the equations of vapor advection and diffusion in the
      subsurface. Contaminant biodegradation must often also be included in
      this simulation, and can increase the difficulty of obtaining a solution,
      especially when explicitly considering coupled oxygen transport and
      consumption. The models of contaminant building entry pathway are often
      coupled to calculations of indoor air contaminant concentration, and both
      are influenced by building construction and operational features. The
      description of entry pathway involves consideration of building
      foundation characteristics, while calculation of indoor air contaminant
      levels requires characterization of building enclosed space and air
      exchange within this. This review summarizes existing VI models, and
      discusses the limits of current screening tools commonly used in this
      field.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown University , Providence, Rhode Island 02912,
      USA.
FAU - Shen, Rui
AU  - Shen R
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20130227
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
RN  - 0 (Environmental Pollutants)
RN  - 0 (Soil)
RN  - 0 (Volatile Organic Compounds)
SB  - IM
MH  - Air Pollution, Indoor/*analysis
MH  - Biodegradation, Environmental
MH  - Computer Simulation
MH  - Diffusion
MH  - Environmental Pollutants/*analysis/metabolism
MH  - Models, Chemical
MH  - Soil/chemistry
MH  - Volatile Organic Compounds/*analysis/metabolism
MH  - Volatilization
PMC - PMC3604123
MID - NIHMS443228
EDAT- 2013/01/31 06:00
MHDA- 2014/03/22 06:00
CRDT- 2013/01/31 06:00
PHST- 2013/01/31 06:00 [entrez]
PHST- 2013/01/31 06:00 [pubmed]
PHST- 2014/03/22 06:00 [medline]
AID - 10.1021/es302714g [doi]
PST - ppublish
SO  - Environ Sci Technol. 2013 Mar 19;47(6):2457-70. doi: 10.1021/es302714g.
      Epub 2013 Feb 27.

PMID- 23293835
OWN - NLM
STAT- MEDLINE
DCOM- 20130723
LR  - 20211021
IS  - 1520-5851 (Electronic)
IS  - 0013-936X (Linking)
VI  - 47
IP  - 3
DP  - 2013 Feb 5
TI  - Examination of the U.S. EPA's vapor intrusion database based on models.
PG  - 1425-33
LID - 10.1021/es304546f [doi]
AB  - In the United States Environmental Protection Agency (U.S. EPA)'s vapor
      intrusion (VI) database, there appears to be a trend showing an inverse
      relationship between the indoor air concentration attenuation factor and
      the subsurface source vapor concentration. This is inconsistent with the
      physical understanding in current vapor intrusion models. This article
      explores possible reasons for this apparent discrepancy. Soil vapor
      transport processes occur independently of the actual building entry
      process and are consistent with the trends in the database results. A
      recent EPA technical report provided a list of factors affecting vapor
      intrusion, and the influence of some of these are explored in the context
      of the database results.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown University, Providence, RI 02912, USA.
FAU - Shen, Rui
AU  - Shen R
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130114
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
RN  - 0 (Air Pollutants)
SB  - IM
MH  - Air Pollutants/analysis
MH  - Air Pollution, Indoor/*analysis
MH  - Computer Simulation
MH  - Groundwater/chemistry
MH  - *Models, Theoretical
MH  - United States
MH  - *United States Environmental Protection Agency
MH  - Volatilization
PMC - PMC3565061
MID - NIHMS436116
EDAT- 2013/01/09 06:00
MHDA- 2013/07/24 06:00
CRDT- 2013/01/09 06:00
PHST- 2013/01/09 06:00 [entrez]
PHST- 2013/01/09 06:00 [pubmed]
PHST- 2013/07/24 06:00 [medline]
AID - 10.1021/es304546f [doi]
PST - ppublish
SO  - Environ Sci Technol. 2013 Feb 5;47(3):1425-33. doi: 10.1021/es304546f.
      Epub 2013 Jan 14.

PMID- 23252837
OWN - NLM
STAT- MEDLINE
DCOM- 20130624
LR  - 20211021
IS  - 1520-5851 (Electronic)
IS  - 0013-936X (Linking)
VI  - 47
IP  - 2
DP  - 2013 Jan 15
TI  - Examination of the influence of environmental factors on contaminant
      vapor concentration attenuation factors using the U.S. EPA's vapor
      intrusion database.
PG  - 906-13
LID - 10.1021/es303441x [doi]
AB  - Those charged with the responsibility of estimating the risk posed by
      vapor intrusion (VI) processes have often looked to information contained
      in the U.S. Environmental Protection Agency (EPA)'s VI database for
      insight. Indoor air concentration attenuation factors have always been a
      key focus of this database, but the roles of different environmental
      factors in these attenuation processes are still unclear. This study aims
      to examine the influences of these factors in the context of the
      information in the VI database. The database shows that the attenuation
      factors vary over many orders of magnitude and that no simple statistical
      fluctuation around any typical mean value exists. Thus far, no simple
      explanation of this phenomenon has been presented. This paper examines
      various possible contributing factors to the enormous range of observed
      values, looking at which ones can plausibly contribute to explaining
      them.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown University, Providence, Rhode Island 02912,
      USA.
FAU - Shen, Rui
AU  - Shen R
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130104
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
RN  - 0 (Environmental Pollutants)
RN  - 0 (Soil)
SB  - IM
MH  - Air Pollution, Indoor/*analysis
MH  - *Databases, Factual
MH  - Diffusion
MH  - Environmental Monitoring
MH  - Environmental Pollutants/*analysis
MH  - Groundwater/*analysis
MH  - Models, Chemical
MH  - Soil/analysis
MH  - United States
MH  - *United States Environmental Protection Agency
MH  - Volatilization
MH  - Water Pollution/*analysis
PMC - PMC3557812
MID - NIHMS431328
EDAT- 2012/12/21 06:00
MHDA- 2013/06/26 06:00
CRDT- 2012/12/21 06:00
PHST- 2012/12/21 06:00 [entrez]
PHST- 2012/12/21 06:00 [pubmed]
PHST- 2013/06/26 06:00 [medline]
AID - 10.1021/es303441x [doi]
PST - ppublish
SO  - Environ Sci Technol. 2013 Jan 15;47(2):906-13. doi: 10.1021/es303441x.
      Epub 2013 Jan 4.

PMID- 23359620
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 0360-1323 (Print)
IS  - 0360-1323 (Linking)
VI  - 59
DP  - 2013 Jan 1
TI  - Simulating the effect of slab features on vapor intrusion of crack entry.
PG  - 417-425
AB  - In vapor intrusion screening models, a most widely employed assumption in
      simulating the entry of contaminant into a building is that of a crack in
      the building foundation slab. Some modelers employed a perimeter crack
      hypothesis while others chose not to identify the crack type. However,
      few studies have systematically investigated the influence on vapor
      intrusion predictions of slab crack features, such as the shape and
      distribution of slab cracks and related to this overall building
      foundation footprint size. In this paper, predictions from a three-
      dimensional model of vapor intrusion are used to compare the contaminant
      mass flow rates into buildings with different foundation slab crack
      features. The simulations show that the contaminant mass flow rate into
      the building does not change much for different assumed slab crack shapes
      and locations, and the foundation footprint size does not play a
      significant role in determining contaminant mass flow rate through a unit
      area of crack. Moreover, the simulation helped reveal the distribution of
      subslab contaminant soil vapor concentration beneath the foundation, and
      the results suggest that in most cases involving no biodegradation, the
      variation in subslab concentration should not exceed an order of
      magnitude, and is often significantly less than this.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown University, Providence RI02912.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - England
TA  - Build Environ
JT  - Building and environment
JID - 101562928
PMC - PMC3555425
MID - NIHMS409775
EDAT- 2013/01/30 06:00
MHDA- 2013/01/30 06:01
CRDT- 2013/01/30 06:00
PHST- 2013/01/30 06:00 [entrez]
PHST- 2013/01/30 06:00 [pubmed]
PHST- 2013/01/30 06:01 [medline]
AID - 10.1016/j.buildenv.2012.09.007 [doi]
PST - ppublish
SO  - Build Environ. 2013 Jan 1;59:417-425. doi:
      10.1016/j.buildenv.2012.09.007.

PMID- 23099484
OWN - NLM
STAT- MEDLINE
DCOM- 20130708
LR  - 20211021
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Linking)
VI  - 121
IP  - 1
DP  - 2013 Jan
TI  - Coplanar polychlorinated biphenyls impair glucose homeostasis in lean
      C57BL/6 mice and mitigate beneficial effects of weight loss on glucose
      homeostasis in obese mice.
PG  - 105-10
LID - 10.1289/ehp.1205421 [doi]
AB  - BACKGROUND: Previous studies demonstrated that coplanar polychlorinated
      biphenyls (PCBs) promote proinflammatory gene expression in adipocytes.
      PCBs are highly lipophilic and accumulate in adipose tissue, a site of
      insulin resistance in persons with type 2 diabetes. OBJECTIVES: We
      investigated the in vitro and in vivo effects of coplanar PCBs on adipose
      expression of tumor necrosis factor alpha (TNF-alpha) and on glucose and
      insulin homeostasis in lean and obese mice. METHODS: We quantified
      glucose and insulin tolerance, as well as TNF-alpha levels, in liver,
      muscle, and adipose tissue of male C57BL/6 mice administered vehicle,
      PCB-77, or PCB-126 and fed a low fat (LF) diet. Another group of mice
      administered vehicle or PCB-77 were fed a high fat (HF) diet for 12
      weeks; the diet was then switched from HF to LF for 4 weeks to induce
      weight loss. We quantified glucose and insulin tolerance and adipose TNF-
      alpha expression in these mice. In addition, we used in vitro and in vivo
      studies to quantify aryl hydrocarbon receptor (AhR)-dependent effects of
      PCB-77 on parameters of glucose homeostasis. RESULTS: Treatment with
      coplanar PCBs resulted in sustained impairment of glucose and insulin
      tolerance in mice fed the LF diet. In PCB-77-treated mice, TNF-alpha
      expression was increased in adipose tissue but not in liver or muscle.
      PCB-77 levels were strikingly higher in adipose tissue than in liver or
      serum. Antagonism of AhR abolished both in vitro and in vivo effects of
      PCB-77. In obese mice, PCB-77 had no effect on glucose homeostasis, but
      glucose homeostasis was impaired after weight loss. CONCLUSIONS: Coplanar
      PCBs impaired glucose homeostasis in lean mice and in obese mice
      following weight loss. Adipose-specific elevations in TNF-alpha
      expression by PCBs may contribute to impaired glucose homeostasis.
FAU - Baker, Nicki A
AU  - Baker NA
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, Kentucky 40536-0200, USA.
FAU - Karounos, Michael
AU  - Karounos M
FAU - English, Victoria
AU  - English V
FAU - Fang, Jun
AU  - Fang J
FAU - Wei, Yinan
AU  - Wei Y
FAU - Stromberg, Arnold
AU  - Stromberg A
FAU - Sunkara, Manjula
AU  - Sunkara M
FAU - Morris, Andrew J
AU  - Morris AJ
FAU - Swanson, Hollie I
AU  - Swanson HI
FAU - Cassis, Lisa A
AU  - Cassis LA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - 8 P20 GM103527-05/GM/NIGMS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20121024
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
CIN - Environ Health Perspect. 2013 Jan;121(1):A32. PMID: 23286978
MH  - Adipose Tissue/drug effects/metabolism
MH  - Animals
MH  - Glucose/*metabolism
MH  - Homeostasis/*drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Obese
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Weight Loss/*physiology
PMC - PMC3553436
EDAT- 2012/10/27 06:00
MHDA- 2013/07/09 06:00
CRDT- 2012/10/27 06:00
PHST- 2012/05/03 00:00 [received]
PHST- 2012/10/24 00:00 [accepted]
PHST- 2012/10/27 06:00 [entrez]
PHST- 2012/10/27 06:00 [pubmed]
PHST- 2013/07/09 06:00 [medline]
AID - 10.1289/ehp.1205421 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2013 Jan;121(1):105-10. doi:
      10.1289/ehp.1205421. Epub 2012 Oct 24.

PMID- 23741283
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1879-5390 (Print)
IS  - 1879-5390 (Linking)
VI  - 3
IP  - 1
DP  - 2013 Jan 1
TI  - Perinatal Polychlorinated Biphenyl 126 Exposure Alters Offspring Body
      Composition.
PG  - 47-53
AB  - Polychlorinated biphenyls (PCBs) are ubiquitous environmental
      contaminants whose exposure levels are associated with various health
      hazards. We hypothesized that in utero and lactational exposure to PCBs
      can cause changes in body composition and obesity in a mouse model.
      Pregnant mice were exposed biweekly to two concentrations of PCB 126 via
      oral gavage. Maternal PCB exposure did not result in heavier offspring,
      however, dose-dependent and sex specific changes in body composition were
      observed. Female offspring displayed the most susceptibility to PCB-
      induced alterations in body composition, having less percent lean body
      mass and increased adiposity compared to females born to control dams,
      and these effects were largely dose-dependent. In contrast to females,
      and independent of the exposure level of PCB 126, male offspring had
      reduced lean body mass but no change in fat mass compared to males born
      to control dams. In conclusion, perinatal PCB 126 exposure did not affect
      body weight, but rather modulated body composition in a dose-dependent
      and gender-specific manner.
FAU - Rashid, Cetewayo S
AU  - Rashid CS
AD  - Graduate Center for Nutritional Sciences, College of Medicine, University
      of Kentucky, 900 South Limestone, Lexington, KY 40536-0200, USA.
FAU - Carter, Lindsay G
AU  - Carter LG
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Pearson, Kevin J
AU  - Pearson KJ
LA  - eng
GR  - P20 GM103527/GM/NIGMS NIH HHS/United States
GR  - P20 RR021954/RR/NCRR NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PL  - Germany
TA  - J Pediatr Biochem
JT  - Journal of pediatric biochemistry
JID - 101531615
PMC - PMC3670830
MID - NIHMS433425
OTO - NOTNLM
OT  - Programming
OT  - aryl hydrocarbon receptor
OT  - coplanar
OT  - mice
OT  - obesity
OT  - persistent organic pollutants
EDAT- 2013/06/07 06:00
MHDA- 2013/06/07 06:01
CRDT- 2013/06/07 06:00
PHST- 2013/06/07 06:00 [entrez]
PHST- 2013/06/07 06:00 [pubmed]
PHST- 2013/06/07 06:01 [medline]
AID - 10.3233/JPB-120072 [doi]
PST - ppublish
SO  - J Pediatr Biochem. 2013 Jan 1;3(1):47-53. doi: 10.3233/JPB-120072.

PMID- 23081707
OWN - NLM
STAT- MEDLINE
DCOM- 20130524
LR  - 20211021
IS  - 1557-1904 (Electronic)
IS  - 1557-1890 (Linking)
VI  - 7
IP  - 4
DP  - 2012 Dec
TI  - Cerebrovascular toxicity of PCB153 is enhanced by binding to silica
      nanoparticles.
PG  - 991-1001
LID - 10.1007/s11481-012-9403-y [doi]
AB  - Environmental polychlorinated biphenyls (PCBs) are frequently bound onto
      nanoparticles (NPs). However, the toxicity and health effects of PCBs
      assembled onto nanoparticles are unknown. The aim of this study was to
      study the hypothesis that binding PCBs to silica NPs potentiates PCB-
      induced cerebrovascular toxicity and brain damage in an experimental
      stroke model. Mice (C57BL/6, males, 12-week-old) were exposed to PCB153
      bound to NPs (PCB153-NPs), PCB153, or vehicle. PCB153 was administered in
      the amount of 5 ng/g body weight. A group of treated animals was
      subjected to a 40 min ischemia, followed by a 24 h reperfusion. The
      blood-brain barrier (BBB) permeability, brain infarct volume, expression
      of tight junction (TJ) proteins, and inflammatory mediators were
      assessed. As compared to controls, a 24 h exposure to PCB153-NPs injected
      into cerebral vasculature resulted in significant elevation of the BBB
      permeability, disruption of TJ protein expression, increased
      proinflammatory responses, and enhanced monocyte transmigration in mouse
      brain capillaries. Importantly, exposure to PCB153-NPs increased stroke
      volume and potentiated brain damage in mice subjected to
      ischemia/reperfusion. A long-term (30 days) oral exposure to PCB153-NPs
      resulted in a higher PCB153 content in the abdominal adipose tissue and
      amplified adhesion of leukocytes to the brain endothelium as compared to
      treatment with PCB153 alone. This study provides the first evidence that
      binding to NPs increases cerebrovascular toxicity of environmental
      toxicants, such as PCB153.
FAU - Zhang, Bei
AU  - Zhang B
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, KY, USA.
FAU - Chen, Lei
AU  - Chen L
FAU - Choi, Jeong June
AU  - Choi JJ
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 CA133257/CA/NCI NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - DA027569/DA/NIDA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - CA133257/CA/NCI NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20121019
PL  - United States
TA  - J Neuroimmune Pharmacol
JT  - Journal of neuroimmune pharmacology : the official journal of the Society
      on NeuroImmune Pharmacology
JID - 101256586
RN  - 7631-86-9 (Silicon Dioxide)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - ZRU0C9E32O (2,4,5,2',4',5'-hexachlorobiphenyl)
SB  - IM
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Blood-Brain Barrier/metabolism
MH  - Capillaries/pathology
MH  - Carotid Artery, Internal
MH  - Cell Movement
MH  - Cerebrovascular Disorders/*chemically induced/pathology
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/metabolism
MH  - Gas Chromatography-Mass Spectrometry
MH  - Immunohistochemistry
MH  - Injections, Intra-Arterial
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nanoparticles
MH  - Polychlorinated Biphenyls/administration &
      dosage/pharmacokinetics/*toxicity
MH  - Real-Time Polymerase Chain Reaction
MH  - Silicon Dioxide
MH  - Stroke/chemically induced/pathology
MH  - Tight Junctions/metabolism
PMC - PMC3518694
MID - NIHMS416367
EDAT- 2012/10/20 06:00
MHDA- 2013/05/28 06:00
CRDT- 2012/10/20 06:00
PHST- 2012/07/16 00:00 [received]
PHST- 2012/09/09 00:00 [accepted]
PHST- 2012/10/20 06:00 [entrez]
PHST- 2012/10/20 06:00 [pubmed]
PHST- 2013/05/28 06:00 [medline]
AID - 10.1007/s11481-012-9403-y [doi]
PST - ppublish
SO  - J Neuroimmune Pharmacol. 2012 Dec;7(4):991-1001. doi:
      10.1007/s11481-012-9403-y. Epub 2012 Oct 19.

PMID- 22922135
OWN - NLM
STAT- MEDLINE
DCOM- 20130411
LR  - 20211021
IS  - 1879-1026 (Electronic)
IS  - 0048-9697 (Linking)
VI  - 437
DP  - 2012 Oct 15
TI  - A numerical investigation of vapor intrusion--the dynamic response of
      contaminant vapors to rainfall events.
PG  - 110-20
LID - 10.1016/j.scitotenv.2012.07.054 [doi]
LID - S0048-9697(12)00999-0 [pii]
AB  - The U.S. government and various agencies have published guidelines for
      field investigation of vapor intrusion, most of which suggest soil gas
      sampling as an integral part of the investigation. Contaminant soil gas
      data are often relatively more stable than indoor air vapor concentration
      measurements, but meteorological conditions might influence soil gas
      values. Although a few field and numerical studies have considered some
      temporal effects on soil gas vapor transport, a full explanation of the
      contaminant vapor concentration response to rainfall events is not
      available. This manuscript seeks to demonstrate the effects on soil vapor
      transport during and after different rainfall events, by applying a
      coupled numerical model of fluid flow and vapor transport. Both a single
      rainfall event and seasonal rainfall events were modeled. For the single
      rainfall event models, the vapor response process could be divided into
      three steps: namely, infiltration, water redistribution, and
      establishment of a water lens atop the groundwater source. In the
      infiltration step, rainfall intensity was found to determine the speed of
      the wetting front and wash-out effect on the vapor. The passage of the
      wetting front led to an increase of the vapor concentration in both the
      infiltration and water redistribution steps and this effect is noted at
      soil probes located 1m below the ground surface. When the mixing of
      groundwater with infiltrated water was not allowed, a clean water lens
      accumulated above the groundwater source and led to a capping effect
      which can reduce diffusion rates of contaminant from the source. Seasonal
      rainfall with short time intervals involved superposition of the
      individual rainfall events. This modeling results indicated that for
      relatively deeper soil that the infiltration wetting front could not
      flood, the effects were damped out in less than a month after rain; while
      in the long term (years), possible formation of a water lens played a
      larger role in determining the vapor intrusion risk. In addition, soil
      organic carbon retarded the transport process, and damped the contaminant
      concentration fluctuations.
CI  - Copyright (c) 2012 Elsevier B.V. All rights reserved.
FAU - Shen, Rui
AU  - Shen R
AD  - School of Engineering, Brown University, Providence, RI 02912, USA.
      rui_shen@brown.edu
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20120822
PL  - Netherlands
TA  - Sci Total Environ
JT  - The Science of the total environment
JID - 0330500
RN  - 0 (Soil)
RN  - 0 (Soil Pollutants)
SB  - IM
MH  - *Air Pollution
MH  - Diffusion
MH  - Groundwater/chemistry
MH  - Models, Chemical
MH  - Numerical Analysis, Computer-Assisted
MH  - Rain/*chemistry
MH  - Seasons
MH  - Soil/chemistry
MH  - Soil Pollutants/*chemistry
MH  - Volatilization
PMC - PMC3756695
MID - NIHMS503171
EDAT- 2012/08/28 06:00
MHDA- 2013/04/12 06:00
CRDT- 2012/08/28 06:00
PHST- 2012/06/09 00:00 [received]
PHST- 2012/07/13 00:00 [revised]
PHST- 2012/07/13 00:00 [accepted]
PHST- 2012/08/28 06:00 [entrez]
PHST- 2012/08/28 06:00 [pubmed]
PHST- 2013/04/12 06:00 [medline]
AID - S0048-9697(12)00999-0 [pii]
AID - 10.1016/j.scitotenv.2012.07.054 [doi]
PST - ppublish
SO  - Sci Total Environ. 2012 Oct 15;437:110-20. doi:
      10.1016/j.scitotenv.2012.07.054. Epub 2012 Aug 22.

PMID- 22776832
OWN - NLM
STAT- MEDLINE
DCOM- 20121205
LR  - 20211021
IS  - 1873-3336 (Electronic)
IS  - 0304-3894 (Linking)
VI  - 231-232
DP  - 2012 Sep 15
TI  - Estimation of contaminant subslab concentration in vapor intrusion.
PG  - 10-7
LID - 10.1016/j.jhazmat.2012.06.016 [doi]
AB  - This study is concerned with developing a method to estimate subslab
      perimeter crack contaminant concentration for structures built atop a
      vapor source. A simple alternative to the widely-used but restrictive
      one-dimensional (1-D) screening models is presented and justified by
      comparing to predictions from a three-dimensional (3-D) CFD model. A
      series of simulations were prepared for steady-state transport of a non-
      biodegradable contaminant in homogenous soil for different structure
      construction features and site characteristics. The results showed that
      subslab concentration does not strongly depend on the soil diffusivity,
      indoor air pressure, or foundation footprint size. It is determined by
      the geometry of the domain, represented by a characteristic length which
      is the ratio of foundation depth to source depth. An extension of this
      analytical approximation was developed for multi-layer soil cases.
CI  - Copyright (c) 2012 Elsevier B.V. All rights reserved.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown University, Providence, RI 02912, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20120616
PL  - Netherlands
TA  - J Hazard Mater
JT  - Journal of hazardous materials
JID - 9422688
RN  - 0 (Air Pollutants)
RN  - 0 (Soil Pollutants)
SB  - IM
MH  - Air Pollutants/*analysis
MH  - Air Pollution, Indoor/*analysis
MH  - Computer Simulation
MH  - *Models, Theoretical
MH  - Soil Pollutants/*analysis
PMC - PMC3439146
MID - NIHMS392202
EDAT- 2012/07/11 06:00
MHDA- 2012/12/10 06:00
CRDT- 2012/07/11 06:00
PHST- 2012/04/16 00:00 [received]
PHST- 2012/06/05 00:00 [revised]
PHST- 2012/06/09 00:00 [accepted]
PHST- 2012/07/11 06:00 [entrez]
PHST- 2012/07/11 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
AID - S0304-3894(12)00636-X [pii]
AID - 10.1016/j.jhazmat.2012.06.016 [doi]
PST - ppublish
SO  - J Hazard Mater. 2012 Sep 15;231-232:10-7. doi:
      10.1016/j.jhazmat.2012.06.016. Epub 2012 Jun 16.

PMID- 21764480
OWN - NLM
STAT- MEDLINE
DCOM- 20121024
LR  - 20211020
IS  - 1558-1497 (Electronic)
IS  - 0197-4580 (Linking)
VI  - 33
IP  - 8
DP  - 2012 Aug
TI  - HIV-1 Tat-induced cerebrovascular toxicity is enhanced in mice with
      amyloid deposits.
PG  - 1579-90
LID - 10.1016/j.neurobiolaging.2011.06.004 [doi]
AB  - HIV-1-infected brains are characterized by elevated depositions of
      amyloid beta (Abeta); however, the interactions between Abeta and HIV-1
      are poorly understood. In the present study, we administered specific
      HIV-1 protein Tat into the cerebral vasculature of 50-52-week-old double
      transgenic (B6C3-Tg) mice that express a chimeric mouse/human amyloid
      precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1
      (PS1-dE9) and are characterized by increased Abeta depositions in the
      brain. Exposure to Tat increased permeability across cerebral
      capillaries, enhanced disruption of zonula occludens (ZO)-1 tight
      junction protein, and elevated brain expression of matrix
      metalloproteinase-9 (MMP-9) in B6C3-Tg mice as compared with age-matched
      littermate controls. These changes were associated with increased
      leukocyte attachment and their transcapillary migration. The majority of
      Tat-induced effects were attenuated by treatment with a specific Rho
      inhibitor, hydroxyfasudil. The results of animal experiments were
      reproduced in cultured brain endothelial cells exposed to Abeta and/or
      Tat. The present data indicate that increased brain levels of Abeta can
      enhance vascular toxicity and proinflammatory responses induced by HIV-1
      protein Tat.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Chen, Lei
AU  - Chen L
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, KY 40536, USA.
FAU - Choi, Jeong June
AU  - Choi JJ
FAU - Choi, Yean Jung
AU  - Choi YJ
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - DA027569/DA/NIDA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-06/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 RR15592/RR/NCRR NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - CA133257/CA/NCI NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P42 ES007380-10/ES/NIEHS NIH HHS/United States
GR  - R01 MH063022-10/MH/NIMH NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 DA027569-03/DA/NIDA NIH HHS/United States
GR  - R01 CA133257/CA/NCI NIH HHS/United States
GR  - ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 CA133257-03/CA/NCI NIH HHS/United States
GR  - R01 MH063022-05/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110718
PL  - United States
TA  - Neurobiol Aging
JT  - Neurobiology of aging
JID - 8100437
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Gene Products, tat)
SB  - IM
MH  - Amyloid beta-Peptides/*metabolism
MH  - Animals
MH  - Cerebral Arteries/drug effects/physiopathology
MH  - Cerebrovascular Disorders/*chemically induced/*physiopathology
MH  - Gene Products, tat/*toxicity
MH  - Mice
MH  - Mice, Transgenic
MH  - Plaque, Amyloid/*metabolism
MH  - Vasculitis/*chemically induced/*physiopathology
PMC - PMC3206197
MID - NIHMS312094
EDAT- 2011/07/19 06:00
MHDA- 2012/10/25 06:00
CRDT- 2011/07/19 06:00
PHST- 2010/11/19 00:00 [received]
PHST- 2011/04/04 00:00 [revised]
PHST- 2011/06/04 00:00 [accepted]
PHST- 2011/07/19 06:00 [entrez]
PHST- 2011/07/19 06:00 [pubmed]
PHST- 2012/10/25 06:00 [medline]
AID - S0197-4580(11)00213-2 [pii]
AID - 10.1016/j.neurobiolaging.2011.06.004 [doi]
PST - ppublish
SO  - Neurobiol Aging. 2012 Aug;33(8):1579-90. doi:
      10.1016/j.neurobiolaging.2011.06.004. Epub 2011 Jul 18.

PMID- 22357258
OWN - NLM
STAT- MEDLINE
DCOM- 20121001
LR  - 20211021
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Linking)
VI  - 120
IP  - 6
DP  - 2012 Jun
TI  - Nutrition can modulate the toxicity of environmental pollutants:
      implications in risk assessment and human health.
PG  - 771-4
LID - 10.1289/ehp.1104712 [doi]
AB  - BACKGROUND: The paradigm of human risk assessment includes many variables
      that must be viewed collectively in order to improve human health and
      prevent chronic disease. The pathology of chronic diseases is complex,
      however, and may be influenced by exposure to environmental pollutants, a
      sedentary lifestyle, and poor dietary habits. Much of the emerging
      evidence suggests that nutrition can modulate the toxicity of
      environmental pollutants, which may alter human risks associated with
      toxicant exposures. OBJECTIVES: In this commentary, we discuss the basis
      for recommending that nutrition be considered a critical variable in
      disease outcomes associated with exposure to environmental pollutants,
      thus establishing the importance of incorporating nutrition within the
      context of cumulative risk assessment. DISCUSSION: A convincing body of
      research indicates that nutrition is a modulator of vulnerability to
      environmental insults; thus, it is timely to consider nutrition as a
      vital component of human risk assessment. Nutrition may serve as either
      an agonist or an antagonist (e.g., high-fat foods or foods rich in
      antioxidants, respectively) of the health impacts associated with
      exposure to environmental pollutants. Dietary practices and food choices
      may help explain the large variability observed in human risk assessment.
      CONCLUSION: We recommend that nutrition and dietary practices be
      incorporated into future environmental research and the development of
      risk assessment paradigms. Healthful nutrition interventions might be a
      powerful approach to reduce disease risks associated with many
      environmental toxic insults and should be considered a variable within
      the context of cumulative risk assessment and, where appropriate, a
      potential tool for subsequent risk reduction.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - University of Kentucky Superfund Research Program, Lexington, Kentucky
      40536, USA. bhennig@uky.edu
FAU - Ormsbee, Lindell
AU  - Ormsbee L
FAU - McClain, Craig J
AU  - McClain CJ
FAU - Watkins, Bruce A
AU  - Watkins BA
FAU - Blumberg, Bruce
AU  - Blumberg B
FAU - Bachas, Leonidas G
AU  - Bachas LG
FAU - Sanderson, Wayne
AU  - Sanderson W
FAU - Thompson, Claudia
AU  - Thompson C
FAU - Suk, William A
AU  - Suk WA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20120222
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - Environmental Exposure/*adverse effects
MH  - Environmental Pollutants/*toxicity
MH  - *Health Status
MH  - Humans
MH  - Nutritional Status/*physiology
MH  - Risk Assessment
PMC - PMC3385446
EDAT- 2012/02/24 06:00
MHDA- 2012/10/02 06:00
CRDT- 2012/02/24 06:00
PHST- 2011/11/07 00:00 [received]
PHST- 2012/02/22 00:00 [accepted]
PHST- 2012/02/24 06:00 [entrez]
PHST- 2012/02/24 06:00 [pubmed]
PHST- 2012/10/02 06:00 [medline]
AID - 10.1289/ehp.1104712 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2012 Jun;120(6):771-4. doi: 10.1289/ehp.1104712.
      Epub 2012 Feb 22.

PMID- 22521609
OWN - NLM
STAT- MEDLINE
DCOM- 20120723
LR  - 20211021
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 261
IP  - 2
DP  - 2012 Jun 1
TI  - EGCG protects endothelial cells against PCB 126-induced inflammation
      through inhibition of AhR and induction of Nrf2-regulated genes.
PG  - 181-8
LID - 10.1016/j.taap.2012.03.024 [doi]
AB  - Tea flavonoids such as epigallocatechin gallate (EGCG) protect against
      vascular diseases such as atherosclerosis via their antioxidant and anti-
      inflammatory functions. Persistent and widespread environmental
      pollutants, including polychlorinated biphenyls (PCB), can induce
      oxidative stress and inflammation in vascular endothelial cells. Even
      though PCBs are no longer produced, they are still detected in human
      blood and tissues and thus considered a risk for vascular dysfunction. We
      hypothesized that EGCG can protect endothelial cells against PCB-induced
      cell damage via its antioxidant and anti-inflammatory properties. To test
      this hypothesis, primary vascular endothelial cells were pretreated with
      EGCG, followed by exposure to the coplanar PCB 126. Exposure to PCB 126
      significantly increased cytochrome P450 1A1 (Cyp1A1) mRNA and protein
      expression and superoxide production, events which were significantly
      attenuated following pretreatment with EGCG. Similarly, EGCG also reduced
      DNA binding of NF-kappaB and downstream expression of inflammatory
      markers such as monocyte chemotactic protein-1 (MCP-1) and vascular cell
      adhesion protein-1 (VCAM-1) after PCB exposure. Furthermore, EGCG
      decreased endogenous or base-line levels of Cyp1A1, MCP-1 and VCAM-1 in
      endothelial cells. Most of all, treatment of EGCG upregulated expression
      of NF-E2-related factor 2 (Nrf2)-controlled antioxidant genes, including
      glutathione S transferase (GST) and NAD(P)H:quinone oxidoreductase 1
      (NQO1), in a dose-dependent manner. In contrast, silencing of Nrf2
      increased Cyp1A1, MCP-1 and VCAM-1 and decreased GST and NQO1 expression,
      respectively. These data suggest that EGCG can inhibit AhR regulated
      genes and induce Nrf2-regulated antioxidant enzymes, thus providing
      protection against PCB-induced inflammatory responses in endothelial
      cells.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Han, Sung Gu
AU  - Han SG
AD  - Superfund Research Program, University of Kentucky, Lexington, KY
      40536-0200, USA.
FAU - Han, Seong-Su
AU  - Han SS
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120406
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone))
RN  - EC 2.5.1.18 (Glutathione Transferase)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics
MH  - Cytochrome P-450 CYP1A1/biosynthesis
MH  - Cytoprotection
MH  - Endothelial Cells/*drug effects
MH  - Gene Expression Regulation/*drug effects
MH  - Glutathione Transferase/genetics
MH  - NAD(P)H Dehydrogenase (Quinone)/genetics
MH  - NF-E2-Related Factor 2/*physiology
MH  - NF-kappa B/metabolism
MH  - Oxidative Stress/drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Receptors, Aryl Hydrocarbon/*antagonists & inhibitors/metabolism
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/genetics
PMC - PMC3358429
MID - NIHMS369113
EDAT- 2012/04/24 06:00
MHDA- 2012/07/24 06:00
CRDT- 2012/04/24 06:00
PHST- 2012/03/05 00:00 [received]
PHST- 2012/03/30 00:00 [accepted]
PHST- 2012/04/24 06:00 [entrez]
PHST- 2012/04/24 06:00 [pubmed]
PHST- 2012/07/24 06:00 [medline]
AID - S0041-008X(12)00127-5 [pii]
AID - 10.1016/j.taap.2012.03.024 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2012 Jun 1;261(2):181-8. doi:
      10.1016/j.taap.2012.03.024. Epub 2012 Apr 6.

PMID- 31130817
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1388-0764 (Print)
IS  - 1388-0764 (Linking)
VI  - 14
IP  - 5
DP  - 2012 May
TI  - Iron oxide nanoparticle synthesis in aqueous and membrane systems for
      oxidative degradation of trichloroethylene from water.
LID - 861 [pii]
LID - 10.1007/s11051-012-0861-1 [doi]
AB  - The potential for using hydroxyl radical (OH(*)) reactions catalyzed by
      iron oxide nanoparticles (NPs) to remediate toxic organic compounds was
      investigated. Iron oxide NPs were synthesized by controlled oxidation of
      iron NPs prior to their use for contaminant oxidation (by H2O2 addition)
      at near-neutral pH values. Cross-linked polyacrylic acid (PAA)
      functionalized polyvinylidene fluoride (PVDF) microfiltration membranes
      were prepared by in situ polymerization of acrylic acid inside the
      membrane pores. Iron and iron oxide NPs (80-100 nm) were directly
      synthesized in the polymer matrix of PAA/PVDF membranes, which prevented
      the agglomeration of particles and controlled the particle size. The
      conversion of iron to iron oxide in aqueous solution with air oxidation
      was studied based on X-ray diffraction, Mossbauer spectroscopy and BET
      surface area test methods. Trichloroethylene (TCE) was selected as the
      model contaminant because of its environmental importance. Degradations
      of TCE and H2O2 by NP surface generated OH(*) were investigated.
      Depending on the ratio of iron and H2O2, TCE conversions as high as 100 %
      (with about 91 % dechlorination) were obtained. TCE dechlorination was
      also achieved in real groundwater samples with the reactive membranes.
FAU - Gui, Minghui
AU  - Gui M
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Smuleac, Vasile
AU  - Smuleac V
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
FAU - Ormsbee, Lindell E
AU  - Ormsbee LE
AD  - Department of Civil Engineering, University of Kentucky, Lexington, KY
      40506, USA.
FAU - Sedlak, David L
AU  - Sedlak DL
AD  - Department of Civil and Environmental Engineering, University of
      California at Berkeley, Berkeley, CA 94720, USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506, USA.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20120429
PL  - Netherlands
TA  - J Nanopart Res
JT  - Journal of nanoparticle research : an interdisciplinary forum for
      nanoscale science and technology
JID - 101088075
PMC - PMC6532989
MID - NIHMS997111
OTO - NOTNLM
OT  - Functionalized membrane
OT  - Heterogeneous Fenton
OT  - Hydrogen peroxide
OT  - Hydroxyl radical
OT  - Iron oxide nanoparticles
OT  - TCE dechlorination
EDAT- 2012/05/01 00:00
MHDA- 2012/05/01 00:01
CRDT- 2019/05/28 06:00
PHST- 2019/05/28 06:00 [entrez]
PHST- 2012/05/01 00:00 [pubmed]
PHST- 2012/05/01 00:01 [medline]
AID - 10.1007/s11051-012-0861-1 [doi]
PST - ppublish
SO  - J Nanopart Res. 2012 May;14(5). doi: 10.1007/s11051-012-0861-1. Epub 2012
      Apr 29.

PMID- 21435178
OWN - NLM
STAT- MEDLINE
DCOM- 20120625
LR  - 20211020
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Linking)
VI  - 16
IP  - 2
DP  - 2012 Feb
TI  - Methamphetamine alters occludin expression via NADPH oxidase-induced
      oxidative insult and intact caveolae.
PG  - 362-75
LID - 10.1111/j.1582-4934.2011.01320.x [doi]
AB  - Methamphetamine (METH) is a drug of abuse with neurotoxic and vascular
      effects that may be mediated by reactive oxygen species (ROS). However,
      potential sources of METH-induced generation of ROS are not fully
      understood. This study is focused on the role of NAD(P)H oxidase (NOX) in
      METH-induced dysfunction of brain endothelial cells. Treatment with METH
      induced a time-dependent increase in phosphorylation of NOX subunit p47,
      followed by its binding with gp91 and p22, and the formation of an active
      NOX complex. An increase in NOX activity was associated with elevated
      production of ROS, alterations of occludin levels and increased
      transendothelial migration of monocytes. Inhibition of NOX by NSC 23766
      attenuated METH-induced ROS generation, changes in occludin protein
      levels and monocyte migration. Because an active NOX complex is localized
      to caveolae, we next evaluated the role of caveolae in METH-mediated
      toxicity to brain endothelial cells. Treatment with METH induced
      phosphorylation of ERK1/2 and caveolin-1 protein. Inhibition of ERK1/2
      activity or caveolin-1 silencing protected against METH-induced
      alterations of occludin levels. These findings indicate an important role
      of NOX and functional caveolae in METH-induced oxidative stress in brain
      endothelial cells that contribute to the subsequent alterations of
      occludin levels and transendothelial migration of inflammatory cells.
CI  - (c) 2011 The Authors Journal of Cellular and Molecular Medicine (c) 2011
      Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
FAU - Park, Minseon
AU  - Park M
AD  - Department of Neurosurgery, University of Kentucky, KY 40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 CA133257/CA/NCI NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - DA027569/DA/NIDA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 CA133257-02/CA/NCI NIH HHS/United States
GR  - R01 MH072567-01A2/MH/NIMH NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH063022-06A2/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 DA027569-01/DA/NIDA NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (Caveolin 1)
RN  - 0 (Cytochrome b Group)
RN  - 0 (Membrane Proteins)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, mouse)
RN  - 0 (Pirb protein, mouse)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, Immunologic)
RN  - 44RAL3456C (Methamphetamine)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.1 (Cyba protein, mouse)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Brain/metabolism/*pathology
MH  - Caveolae/*metabolism
MH  - Caveolin 1/genetics/metabolism
MH  - Cell Line
MH  - Cell Movement
MH  - Cytochrome b Group/antagonists & inhibitors/metabolism
MH  - Endothelial Cells/metabolism/*pathology
MH  - MAP Kinase Signaling System/drug effects
MH  - Membrane Proteins/*metabolism
MH  - Methamphetamine/*metabolism/pharmacology/toxicity
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - NADPH Oxidases/antagonists & inhibitors/metabolism
MH  - Occludin
MH  - Oxidation-Reduction
MH  - Oxidative Stress
MH  - Reactive Oxygen Species
MH  - Receptors, Immunologic/metabolism
PMC - PMC3133868
MID - NIHMS283236
EDAT- 2011/03/26 06:00
MHDA- 2012/06/26 06:00
CRDT- 2011/03/26 06:00
PHST- 2011/03/26 06:00 [entrez]
PHST- 2011/03/26 06:00 [pubmed]
PHST- 2012/06/26 06:00 [medline]
AID - 10.1111/j.1582-4934.2011.01320.x [doi]
PST - ppublish
SO  - J Cell Mol Med. 2012 Feb;16(2):362-75. doi:
      10.1111/j.1582-4934.2011.01320.x.

PMID- 21447442
OWN - NLM
STAT- MEDLINE
DCOM- 20120516
LR  - 20211020
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 23
IP  - 2
DP  - 2012 Feb
TI  - Epigallocatechin-gallate stimulates NF-E2-related factor and heme
      oxygenase-1 via caveolin-1 displacement.
PG  - 163-8
LID - 10.1016/j.jnutbio.2010.12.002 [doi]
AB  - Flavonoids, such as the tea catechin epigallocatechin-gallate (EGCG), can
      protect against atherosclerosis by decreasing vascular endothelial cell
      inflammation. Heme oxygenase-1 (HO-1) is an enzyme that plays an
      important role in vascular physiology, and its induction may provide
      protection against atherosclerosis. Heme oxygenase-1 can be
      compartmentalized in caveolae in endothelial cells. Caveolae are plasma
      microdomains important in vesicular transport and the regulation of
      signaling pathways associated with the pathology of vascular diseases. We
      hypothesize that caveolae play a role in the uptake and transport of EGCG
      and mechanisms associated with the anti-inflammatory properties of this
      flavonoid. To test this hypothesis, we explored the effect of EGCG on the
      induction of NF-E2-related factor (Nrf2) and HO-1 in endothelial cells
      with or without functional caveolae. Treatment with EGCG activated Nrf2
      and increased HO-1 expression and cellular production of bilirubin. In
      addition, EGCG rapidly accumulated in caveolae, which was associated with
      caveolin-1 displacement from the plasma membrane towards the cytosol.
      Similar to EGCG treatment, silencing of caveolin-1 by siRNA technique
      also resulted in up-regulation of Nrf2, HO-1 and bilirubin production.
      These data suggest that EGCG-induced caveolin-1 displacement may reduce
      endothelial inflammation.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Zheng, Yuanyuan
AU  - Zheng Y
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture, KY
      40536, USA.
FAU - Morris, Andrew
AU  - Morris A
FAU - Sunkara, Manjula
AU  - Sunkara M
FAU - Layne, Joseph
AU  - Layne J
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - GM50388/GM/NIGMS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P20RR021954/RR/NCRR NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110329
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Caveolin 1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (RNA, Small Interfering)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - RFM9X3LJ49 (Bilirubin)
SB  - IM
MH  - Animals
MH  - Bilirubin/metabolism
MH  - Catechin/*analogs & derivatives/pharmacokinetics/pharmacology
MH  - Caveolae/drug effects/metabolism
MH  - Caveolin 1/genetics/*metabolism
MH  - Cells, Cultured
MH  - Endothelial Cells/drug effects/metabolism
MH  - Endothelium, Vascular/cytology/drug effects
MH  - Heme Oxygenase-1/*metabolism
MH  - NF-E2-Related Factor 2/genetics/*metabolism
MH  - RNA, Small Interfering
MH  - Swine
PMC - PMC4309924
MID - NIHMS656587
EDAT- 2011/03/31 06:00
MHDA- 2012/05/17 06:00
CRDT- 2011/03/31 06:00
PHST- 2010/11/19 00:00 [received]
PHST- 2010/12/06 00:00 [revised]
PHST- 2010/12/10 00:00 [accepted]
PHST- 2011/03/31 06:00 [entrez]
PHST- 2011/03/31 06:00 [pubmed]
PHST- 2012/05/17 06:00 [medline]
AID - S0955-2863(11)00015-5 [pii]
AID - 10.1016/j.jnutbio.2010.12.002 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2012 Feb;23(2):163-8. doi: 10.1016/j.jnutbio.2010.12.002.
      Epub 2011 Mar 29.

PMID- 21925196
OWN - NLM
STAT- MEDLINE
DCOM- 20120113
LR  - 20211020
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 257
IP  - 1
DP  - 2011 Nov 15
TI  - Polychlorinated biphenyl 77 augments angiotensin II-induced
      atherosclerosis and abdominal aortic aneurysms in male apolipoprotein E
      deficient mice.
PG  - 148-54
LID - 10.1016/j.taap.2011.08.028 [doi]
AB  - Infusion of angiotensin II (AngII) to hyperlipidemic mice augments
      atherosclerosis and causes formation of abdominal aortic aneurysms
      (AAAs). Each of these AngII-induced vascular pathologies exhibit
      pronounced inflammation. Previous studies demonstrated that coplanar
      polychlorinated biphenyls (PCBs) promote inflammation in endothelial
      cells and adipocytes, two cell types implicated in AngII-induced vascular
      pathologies. The purpose of this study was to test the hypothesis that
      administration of PCB77 to male apolipoprotein E (ApoE) -/- mice promotes
      AngII-induced atherosclerosis and AAA formation. Male ApoE-/- mice were
      administered vehicle or PCB77 (49 mg/kg, i.p.) during week 1 and 4 (2
      divided doses/week) of AngII infusion. Body weights and total serum
      cholesterol concentrations were not influenced by administration of
      PCB77. Systolic blood pressure was increased in AngII-infused mice
      administered PCB77 compared to vehicle (156+/-6 vs 137+/-5 mmHg,
      respectively). The percentage of aortic arch covered by atherosclerotic
      lesions was increased in AngII-infused mice administered PCB77 compared
      to vehicle (2.0+/-0.4 vs 0.9+/-0.1%, respectively). Lumen diameters of
      abdominal aortas determined by in vivo ultrasound and external diameters
      of excised suprarenal aortas were increased in AngII-infused mice
      administered PCB77 compared to vehicle. In addition, AAA incidence
      increased from 47 to 85% in AngII-infused mice administered PCB77.
      Adipose tissue in close proximity to AAAs from mice administered PCB77
      exhibited increased mRNA abundance of proinflammatory cytokines and
      elevated expression of components of the renin-angiotensin system
      (angiotensinogen, angiotensin type 1a receptor (AT1aR)). These results
      demonstrate that PCB77 augments AngII-induced atherosclerosis and AAA
      formation.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Arsenescu, Violeta
AU  - Arsenescu V
AD  - Graduate Center for Nutritional Sciences, University of Kentucky, 800
      Rose Street, Lexington, KY 40536-0200, USA.
FAU - Arsenescu, Razvan
AU  - Arsenescu R
FAU - Parulkar, Madhura
AU  - Parulkar M
FAU - Karounos, Michael
AU  - Karounos M
FAU - Zhang, Xuan
AU  - Zhang X
FAU - Baker, Nicki
AU  - Baker N
FAU - Cassis, Lisa A
AU  - Cassis LA
LA  - eng
GR  - T32 DK007778-11/DK/NIDDK NIH HHS/United States
GR  - P42 ES007380-11/ES/NIEHS NIH HHS/United States
GR  - P42ES0078380/ES/NIEHS NIH HHS/United States
GR  - T32 DK007778/DK/NIDDK NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110907
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Apolipoproteins E)
RN  - 11128-99-7 (Angiotensin II)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Animals
MH  - Aortic Aneurysm, Abdominal/*chemically induced
MH  - Apolipoproteins E/*deficiency
MH  - Atherosclerosis/*chemically induced
MH  - Blood Pressure/drug effects
MH  - Drug Synergism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Mutant Strains
MH  - Polychlorinated Biphenyls/*adverse effects
MH  - Real-Time Polymerase Chain Reaction
PMC - PMC3220787
MID - NIHMS329809
EDAT- 2011/09/20 06:00
MHDA- 2012/01/14 06:00
CRDT- 2011/09/20 06:00
PHST- 2011/06/15 00:00 [received]
PHST- 2011/08/22 00:00 [revised]
PHST- 2011/08/29 00:00 [accepted]
PHST- 2011/09/20 06:00 [entrez]
PHST- 2011/09/20 06:00 [pubmed]
PHST- 2012/01/14 06:00 [medline]
AID - S0041-008X(11)00342-5 [pii]
AID - 10.1016/j.taap.2011.08.028 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2011 Nov 15;257(1):148-54. doi:
      10.1016/j.taap.2011.08.028. Epub 2011 Sep 7.

PMID- 21840940
OWN - NLM
STAT- MEDLINE
DCOM- 20111227
LR  - 20211020
IS  - 1530-6860 (Electronic)
IS  - 0892-6638 (Linking)
VI  - 25
IP  - 11
DP  - 2011 Nov
TI  - PPARalpha and PPARgamma protect against HIV-1-induced MMP-9
      overexpression via caveolae-associated ERK and Akt signaling.
PG  - 3979-88
LID - 10.1096/fj.11-188607 [doi]
AB  - Activation of matrix metalloproteinase-9 (MMP-9) is involved in
      HIV-1-induced disruption of the blood-brain barrier (BBB). In the present
      study, we hypothesize that peroxisome proliferator-activated receptor
      (PPAR)-alpha or PPARgamma can protect against HIV-1-induced MMP-9
      overexpression in brain endothelial cells (hCMEC cell line) by
      attenuating cellular oxidative stress and down-regulation of caveolae-
      associated redox signaling. Exposure to HIV-1-infected monocytes induced
      phosphorylation of ERK1/2 and Akt in hCMEC by 2.5- and 3.6-fold,
      respectively; however, these effects were attenuated by overexpression of
      PPARalpha or PPARgamma and by silencing of caveolin-1 (cav-1). Coculture
      of hCMEC with HIV-1-infected monocytes significantly induced MMP-9
      promoter and enzyme activity by 3- to 3.5-fold. Promoter mutation studies
      indicated that SP-1 (g1940t_g1941t) is an essential transcription factor
      involved in induction of MMP-9 promoter by HIV-1. In addition,
      HIV-1-stimulated activity of MMP-9 promoter was inhibited by mutation of
      AP-1 site 2 (c1918t_a1919g) and both (but not individual) NF-kappaB
      binding sites (g1389c and g1664c). PPAR overexpression, ERK1/2 or Akt
      inhibition, and silencing of cav-1 all effectively protected against
      HIV-1-induced MMP-9 promoter activity, indicating a close relationship
      among HIV-1-induced cerebrovascular toxicity, redox-regulated mechanisms,
      and functional caveolae. Such a link was further confirmed in
      MMP-9-deficient mice exposed to PPARalpha or PPARgamma agonist and
      injected with the HIV-1-specific protein Tat into cerebral vasculature.
      Overall, our results indicate that ERK1/2, Akt, and cav-1 are involved in
      the regulatory mechanisms of PPAR-mediated protection against
      HIV-1-induced MMP-9 expression in brain endothelial cells.
FAU - Huang, Wen
AU  - Huang W
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, Kentucky, USA.
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Rha, Geun Bae
AU  - Rha GB
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - DA027569/DA/NIDA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 RR15592/RR/NCRR NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - P20 RR015592/RR/NCRR NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110812
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American
      Societies for Experimental Biology
JID - 8804484
RN  - 0 (Caveolin 1)
RN  - 0 (PPAR alpha)
RN  - 0 (PPAR gamma)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/metabolism
MH  - Caveolae/metabolism
MH  - Caveolin 1/*physiology
MH  - Extracellular Signal-Regulated MAP Kinases/*physiology
MH  - HEK293 Cells
MH  - HIV-1/*metabolism
MH  - Humans
MH  - Matrix Metalloproteinase 9/*biosynthesis
MH  - Mice
MH  - Mitogen-Activated Protein Kinase 1/*physiology
MH  - Mitogen-Activated Protein Kinase 3/*physiology
MH  - PPAR alpha/*physiology
MH  - PPAR gamma/*physiology
MH  - Phosphorylation/drug effects
MH  - Proto-Oncogene Proteins c-akt/*physiology
MH  - Signal Transduction/drug effects
MH  - U937 Cells
PMC - PMC3205841
EDAT- 2011/08/16 06:00
MHDA- 2011/12/28 06:00
CRDT- 2011/08/16 06:00
PHST- 2011/08/16 06:00 [entrez]
PHST- 2011/08/16 06:00 [pubmed]
PHST- 2011/12/28 06:00 [medline]
AID - fj.11-188607 [pii]
AID - 10.1096/fj.11-188607 [doi]
PST - ppublish
SO  - FASEB J. 2011 Nov;25(11):3979-88. doi: 10.1096/fj.11-188607. Epub 2011
      Aug 12.

PMID- 21770469
OWN - NLM
STAT- MEDLINE
DCOM- 20120202
LR  - 20211020
IS  - 1520-5851 (Electronic)
IS  - 0013-936X (Linking)
VI  - 45
IP  - 17
DP  - 2011 Sep 1
TI  - Kinetics and mechanisms of nanosilver oxysulfidation.
PG  - 7345-53
LID - 10.1021/es201539s [doi]
AB  - Among the many new engineered nanomaterials, nanosilver is one of the
      highest priority cases for environmental risk assessment. Recent analysis
      of field samples from water treatment facilities suggests that silver is
      converted to silver sulfide, whose very low solubility may limit the
      bioavailability and adverse impact of silver in the environment. The
      present study demonstrates that silver nanoparticles react with dissolved
      sulfide species (H(2)S, HS(-)) under relevant but controlled laboratory
      conditions to produce silver sulfide nanostructures similar to those
      observed in the field. The reaction is tracked by time-resolved sulfide
      depletion measurements to yield quantitative reaction rates and
      stoichiometries. The reaction requires dissolved oxygen, and it is
      sensitive to pH and natural organic matter. Focused-ion-beam analysis of
      surface films reveals an irregular coarse-grained sulfide phase that
      allows deep (>1 mum) conversion of silver surfaces without passivation.
      At high sulfide concentrations, nanosilver oxysulfidation occurs by a
      direct particle-fluid reaction. At low sulfide concentration,
      quantitative kinetic analysis suggests a mechanistic switch to an
      oxidative dissolution/precipitation mechanism, in which the biologically
      active Ag(+) ion is generated as an intermediate. The environmental
      transformation pathways for nanosilver will vary depending on the media-
      specific competing rates of oxidative dissolution and direct
      oxysulfidation.
FAU - Liu, Jingyu
AU  - Liu J
AD  - Department of Chemistry, Brown University, Providence, Rhode Island
      02912, United States.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Hurt, Robert H
AU  - Hurt RH
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42 ES013660-07/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20110804
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
RN  - 0 (Environmental Pollutants)
RN  - 0 (Silver Compounds)
RN  - 0 (Sulfides)
RN  - 3M4G523W1G (Silver)
RN  - 9ZB10YHC1C (silver sulfide)
SB  - IM
MH  - Environmental Pollutants/chemistry
MH  - Hydrogen-Ion Concentration
MH  - Metal Nanoparticles/*chemistry/ultrastructure
MH  - Oxidation-Reduction
MH  - Particle Size
MH  - Risk Assessment
MH  - Silver/*chemistry
MH  - Silver Compounds/*chemical synthesis/*chemistry
MH  - Sulfides/*chemistry
PMC - PMC3164758
MID - NIHMS314322
EDAT- 2011/07/21 06:00
MHDA- 2012/02/03 06:00
CRDT- 2011/07/21 06:00
PHST- 2011/07/21 06:00 [entrez]
PHST- 2011/07/21 06:00 [pubmed]
PHST- 2012/02/03 06:00 [medline]
AID - 10.1021/es201539s [doi]
PST - ppublish
SO  - Environ Sci Technol. 2011 Sep 1;45(17):7345-53. doi: 10.1021/es201539s.
      Epub 2011 Aug 4.

PMID- 21292468
OWN - NLM
STAT- MEDLINE
DCOM- 20120222
LR  - 20211020
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 22
IP  - 9
DP  - 2011 Sep
TI  - Caveolae: a regulatory platform for nutritional modulation of
      inflammatory diseases.
PG  - 807-11
LID - 10.1016/j.jnutbio.2010.09.013 [doi]
AB  - Dietary intervention strategies have proven to be an effective means of
      decreasing several risk factors associated with the development of
      atherosclerosis. Endothelial cell dysfunction influences vascular
      inflammation and is involved in promoting the earliest stages of lesion
      formation. Caveolae are lipid raft microdomains abundant within the
      plasma membrane of endothelial cells and are responsible for modulating
      receptor-mediated signal transduction, thus influencing endothelial
      activation. Caveolae have been implicated in the regulation of enzymes
      associated with several key signaling pathways capable of determining
      intracellular redox status. Diet and plasma-derived nutrients may
      modulate an inflammatory outcome by interacting with and altering
      caveolae-associated cellular signaling. For example, omega-3 fatty acids
      and several polyphenolics have been shown to improve endothelial cell
      function by decreasing the formation of ROS and increasing NO
      bioavailability, events associated with altered caveolae composition.
      Thus, nutritional modulation of caveolae-mediated signaling events may
      provide an opportunity to ameliorate inflammatory signaling pathways
      capable of promoting the formation of vascular diseases, including
      atherosclerosis.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Layne, Joseph
AU  - Layne J
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 60536, USA.
FAU - Majkova, Zuzana
AU  - Majkova Z
FAU - Smart, Eric J
AU  - Smart EJ
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-14/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110202
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Caveolin 1)
RN  - 0 (Fatty Acids, Omega-3)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Polyphenols)
RN  - 0 (Reactive Oxygen Species)
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Atherosclerosis/*metabolism/prevention & control
MH  - Caveolae/*metabolism
MH  - Caveolin 1/metabolism
MH  - Dietary Supplements
MH  - Endothelial Cells/metabolism
MH  - Fatty Acids, Omega-3/*pharmacology
MH  - Humans
MH  - Inflammation/*metabolism/prevention & control
MH  - NF-E2-Related Factor 2/metabolism
MH  - Nitric Oxide/metabolism
MH  - Oxidative Stress
MH  - Polyphenols/*pharmacology
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
PMC - PMC3139026
MID - NIHMS252260
EDAT- 2011/02/05 06:00
MHDA- 2012/02/23 06:00
CRDT- 2011/02/05 06:00
PHST- 2010/07/23 00:00 [received]
PHST- 2010/09/13 00:00 [revised]
PHST- 2010/09/30 00:00 [accepted]
PHST- 2011/02/05 06:00 [entrez]
PHST- 2011/02/05 06:00 [pubmed]
PHST- 2012/02/23 06:00 [medline]
AID - S0955-2863(10)00241-X [pii]
AID - 10.1016/j.jnutbio.2010.09.013 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2011 Sep;22(9):807-11. doi:
      10.1016/j.jnutbio.2010.09.013. Epub 2011 Feb 2.

PMID- 21294658
OWN - NLM
STAT- MEDLINE
DCOM- 20111122
LR  - 20211020
IS  - 1557-7716 (Electronic)
IS  - 1523-0864 (Linking)
VI  - 15
IP  - 5
DP  - 2011 Sep 1
TI  - Oxidative stress and blood-brain barrier dysfunction under particular
      consideration of matrix metalloproteinases.
PG  - 1305-23
LID - 10.1089/ars.2011.3923 [doi]
AB  - A cell's "redox" (oxidation and reduction) state is determined by the sum
      of all redox processes yielding reactive oxygen species (ROS), reactive
      nitrogen species (RNS), and other reactive intermediates. Low amounts of
      ROS/RNS are generated by different mechanisms in every cell and are
      important regulatory mediators in many signaling processes (redox
      signaling). When the physiological balance between the generation and
      elimination of ROS/RNS is disrupted, oxidative/nitrosative stress with
      persistent oxidative damage of the organism occurs. Oxidative stress has
      been suggested to act as initiator and/or mediator of many human
      diseases. The cerebral vasculature is particularly susceptible to
      oxidative stress, which is critical since cerebral endothelial cells play
      a major role in the creation and maintenance of the blood-brain barrier
      (BBB). This article will only contain a focused introduction on the
      biochemical background of redox signaling, since this has been reported
      already in a series of excellent recent reviews. The goal of this work is
      to increase the understanding of basic mechanisms underlying ROS/RNS-
      induced BBB disruption, with a focus on the role of matrix
      metalloproteinases, which, after all, appear to be a key mediator in the
      initiation and progression of BBB damage elicited by oxidative stress.
FAU - Lehner, Christine
AU  - Lehner C
AD  - Department of Organismic Biology, Development Biology Group, University
      Hospital of Salzburg, Salzburg, Austria.
FAU - Gehwolf, Renate
AU  - Gehwolf R
FAU - Tempfer, Herbert
AU  - Tempfer H
FAU - Krizbai, Istvan
AU  - Krizbai I
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Bauer, Hans-Christian
AU  - Bauer HC
FAU - Bauer, Hannelore
AU  - Bauer H
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20110519
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (Cytokines)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/*metabolism/*physiopathology
MH  - Brain/metabolism/physiopathology
MH  - Cytokines/metabolism
MH  - Endothelial Cells/metabolism
MH  - Endothelium/metabolism
MH  - Gene Expression Regulation
MH  - Humans
MH  - Leukocytes/metabolism
MH  - Matrix Metalloproteinases/*metabolism
MH  - Oxidation-Reduction
MH  - *Oxidative Stress
MH  - Reactive Oxygen Species/metabolism
MH  - Transcription, Genetic
PMC - PMC6464004
EDAT- 2011/02/08 06:00
MHDA- 2011/12/13 00:00
CRDT- 2011/02/08 06:00
PHST- 2011/02/08 06:00 [entrez]
PHST- 2011/02/08 06:00 [pubmed]
PHST- 2011/12/13 00:00 [medline]
AID - 10.1089/ars.2011.3923 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2011 Sep 1;15(5):1305-23. doi:
      10.1089/ars.2011.3923. Epub 2011 May 19.

PMID- 22228920
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 0376-7388 (Print)
IS  - 0376-7388 (Linking)
VI  - 379
IP  - 1-2
DP  - 2011 Sep 1
TI  - Green Synthesis of Fe and Fe/Pd Bimetallic Nanoparticles in Membranes for
      Reductive Degradation of Chlorinated Organics.
PG  - 131-137
AB  - Membranes containing reactive nanoparticles (Fe and Fe/Pd) immobilized in
      a polymer film (polyacrylic acid, PAA-coated polyvinylidene fluoride,
      PVDF membrane) are prepared by a new method. In the present work a
      biodegradable, non-toxic -"green" reducing agent, green tea extract was
      used for nanoparticle (NP) synthesis, instead of the well-known sodium
      borohydride. Green tea extract contains a number of polyphenols that can
      act as both chelating/reducing and capping agents for the nanoparticles.
      Therefore, the particles are protected from oxidation and aggregation,
      which increases their stability and longevity. The membrane supported NPs
      were successfully used for the degradation of a common and highly
      important pollutant, trichloroethylene (TCE). The rate of TCE degradation
      was found to increase linearly with the amount of Fe immobilized on the
      membrane, the surface normalized rate constant (k(SA)) being 0.005
      L/m(2)h. The addition of a second catalytic metal, Pd, to form bimetallic
      Fe/Pd increased the k(SA) value to 0.008 L/m(2)h. For comparison
      purposes, Fe and Fe/Pd nanoparticles were synthesized in membranes using
      sodium borohydride as a reducing agent. Although the initial k(SA) values
      for this case (for Fe) are one order of magnitude higher than the tea
      extract synthesized NPs, the rapid oxidation reduced their reactivity to
      less than 20 % within 4 cycles. For the green tea extract NPs, the
      initial reactivity in the membrane domain was preserved even after 3
      months of repeated use. The reactivity of TCE was verified with "real"
      water system.
FAU - Smuleac, V
AU  - Smuleac V
AD  - Dept. of Chemical and Materials Engineering, University of Kentucky
      Lexington, KY 40506 USA.
FAU - Varma, R
AU  - Varma R
FAU - Sikdar, S
AU  - Sikdar S
FAU - Bhattacharyya, D
AU  - Bhattacharyya D
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-13S2/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-15/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - J Memb Sci
JT  - Journal of membrane science
JID - 7606202
PMC - PMC3252031
MID - NIHMS306630
EDAT- 2012/01/10 06:00
MHDA- 2012/01/10 06:01
CRDT- 2012/01/10 06:00
PHST- 2012/01/10 06:00 [entrez]
PHST- 2012/01/10 06:00 [pubmed]
PHST- 2012/01/10 06:01 [medline]
AID - 10.1016/j.memsci.2011.05.054 [doi]
PST - ppublish
SO  - J Memb Sci. 2011 Sep 1;379(1-2):131-137. doi:
      10.1016/j.memsci.2011.05.054.

PMID- 30505074
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 0959-9428 (Print)
IS  - 0959-9428 (Linking)
VI  - 21
IP  - 28
DP  - 2011 Jul 28
TI  - Development of reactive Pd/Fe bimetallic nanotubes for dechlorination
      reactions.
PG  - 10454-10462
LID - 10.1039/c1jm11435b [doi]
AB  - We described the synthesis and characterization of a new class of
      bimetallic nanotubes based on Pd/Fe and demonstrated their efficacy in
      the dechlorination of PCB 77, a polychlorinated biphenyl. Onedimensional
      iron metal nanotubes of different diameters were prepared by electroless
      deposition within the pores of PVP-coated polycarbonate membranes using a
      simple technique under ambient conditions. The longitudinal nucleation of
      the nanotubes along the pore walls was achieved by mounting the PC
      membrane between two halves of a U-shape reaction tube. The composition,
      morphology, and structure of the Pd/Fe nanotubes were characterized by
      transmission electron microscopy, scanning electron microscopy,
      inductively coupled plasma-atomic emission spectroscopy, and X-ray powder
      diffraction spectroscopy. The as-prepared Pd/Fe bimetallic nanotubes were
      used in dechlorination of 3,3',4,4'-tetrachlorobiphenyl (PCB 77). In
      comparison with Pd/Fe nanoparticles, the Pd/Fe nanotubes demonstrated
      higher efficiency and faster dechlorination of the PCB.
FAU - Zahran, Elsayed M
AU  - Zahran EM
AD  - Department of Chemistry, University of Kentucky, Lexington, KY, 40506,
      USA.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Material Engineering, University of Kentucky,
      Lexington, KY, 40506, USA.
FAU - Bachas, Leonidas G
AU  - Bachas LG
AD  - Department of Chemistry, University of Kentucky, Lexington, KY, 40506,
      USA.
AD  - Department of Chemistry, University of Miami, Coral Gables, FL, 33146,
      USA. bachas@miami.edu; ; Tel: +1 859 257-6350.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20110611
PL  - England
TA  - J Mater Chem
JT  - Journal of materials chemistry
JID - 9889099
PMC - PMC6262226
MID - NIHMS997116
EDAT- 2011/07/28 00:00
MHDA- 2011/07/28 00:01
CRDT- 2018/12/04 06:00
PHST- 2018/12/04 06:00 [entrez]
PHST- 2011/07/28 00:00 [pubmed]
PHST- 2011/07/28 00:01 [medline]
AID - 10.1039/c1jm11435b [doi]
PST - ppublish
SO  - J Mater Chem. 2011 Jul 28;21(28):10454-10462. doi: 10.1039/c1jm11435b.
      Epub 2011 Jun 11.

PMID- 21606340
OWN - NLM
STAT- MEDLINE
DCOM- 20111007
LR  - 20211020
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 108
IP  - 21
DP  - 2011 May 24
TI  - Reactive nanostructured membranes for water purification.
PG  - 8577-82
LID - 10.1073/pnas.1101144108 [doi]
AB  - Many current treatments for the reclamation of contaminated water sources
      are chemical-intensive, energy-intensive, and/or require posttreatment
      due to unwanted by-product formation. We demonstrate that through the
      integration of nanostructured materials, enzymatic catalysis, and iron-
      catalyzed free radical reactions within pore-functionalized synthetic
      membrane platforms, we are able to conduct environmentally important
      oxidative reactions for toxic organic degradation and detoxification from
      water without the addition of expensive or harmful chemicals. In contrast
      to conventional, passive membrane technologies, our approach utilizes two
      independently controlled, nanostructured membranes in a stacked
      configuration for the generation of the necessary oxidants. These include
      biocatalytic and organic/inorganic (polymer/iron) nanocomposite
      membranes. The bioactive (top) membrane contains an electrostatically
      immobilized enzyme for the catalytic production of one of the main
      reactants, hydrogen peroxide (H(2)O(2)), from glucose. The bottom
      membrane contains either immobilized iron ions or ferrihydrite/iron oxide
      nanoparticles for the decomposition of hydrogen peroxide to form powerful
      free radical oxidants. By permeating (at low pressure) a solution
      containing a model organic contaminant, such as trichlorophenol, with
      glucose in oxygen-saturated water through the membrane stack, significant
      contaminant degradation was realized. To illustrate the effectiveness of
      this membrane platform in real-world applications, membrane-immobilized
      ferrihydrite/iron oxide nanoparticles were reacted with hydrogen peroxide
      to form free radicals for the degradation of a chlorinated organic
      contaminant in actual groundwater. Although we establish the development
      of these nanostructured materials for environmental applications, the
      practical and methodological advances demonstrated here permit the
      extension of their use to applications including disinfection and/or
      virus inactivation.
FAU - Lewis, Scott R
AU  - Lewis SR
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, KY 40506-0046, USA.
FAU - Datta, Saurav
AU  - Datta S
FAU - Gui, Minghui
AU  - Gui M
FAU - Coker, Eric L
AU  - Coker EL
FAU - Huggins, Frank E
AU  - Huggins FE
FAU - Daunert, Sylvia
AU  - Daunert S
FAU - Bachas, Leonidas
AU  - Bachas L
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20110523
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of
      America
JID - 7505876
RN  - 0 (Enzymes, Immobilized)
RN  - 0 (Membranes, Artificial)
RN  - 0 (Organic Chemicals)
RN  - 0 (Water Pollutants, Chemical)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - E1UOL152H7 (Iron)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Enzymes, Immobilized
MH  - Glucose/chemistry
MH  - Hydrogen Peroxide
MH  - Iron/chemistry
MH  - *Membranes, Artificial
MH  - Nanostructures/*chemistry
MH  - Organic Chemicals
MH  - Water Pollutants, Chemical/chemistry
MH  - Water Purification/*methods
PMC - PMC3102394
EDAT- 2011/05/25 06:00
MHDA- 2011/10/08 06:00
CRDT- 2011/05/25 06:00
PHST- 2011/05/25 06:00 [entrez]
PHST- 2011/05/25 06:00 [pubmed]
PHST- 2011/10/08 06:00 [medline]
AID - 1101144108 [pii]
AID - 10.1073/pnas.1101144108 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2011 May 24;108(21):8577-82. doi:
      10.1073/pnas.1101144108. Epub 2011 May 23.

PMID- 21344848
OWN - NLM
STAT- MEDLINE
DCOM- 20110519
LR  - 20211020
IS  - 1520-5851 (Electronic)
IS  - 0013-936X (Linking)
VI  - 45
IP  - 6
DP  - 2011 Mar 15
TI  - Comparison of the Johnson-Ettinger vapor intrusion screening model
      predictions with full three-dimensional model results.
PG  - 2227-35
LID - 10.1021/es102602s [doi]
AB  - The Johnson-Ettinger vapor intrusion model (J-E model) is the most widely
      used screening tool for evaluating vapor intrusion potential because of
      its simplicity and convenience of use. Since its introduction about
      twenty years ago, the J-E model has become a cornerstone in guidance
      related to the potential for significant vapor intrusion-related
      exposures. A few papers have been published that claim it is a
      conservative predictor of exposure, but there has not been a systematic
      comparison in the open literature of the J-E model predictions with the
      results of more complete full three-dimensional descriptions of the
      phenomenon. In this paper, predictions from a three-dimensional model of
      vapor intrusion, based upon finite element calculations of homogeneous
      soil scenarios, are directly compared with the results of the J-E model.
      These results suggest that there are conditions under which the J-E model
      predictions might be quite reasonable but that there are also others in
      which the predictions are low as well as high. Some small modifications
      to the J-E model are also suggested that can bring its predictions into
      excellent agreement with those of the much more elaborate 3-D models, in
      some specific cases of homogeneous soils. Finally, both models were
      compared with actual field data.
FAU - Yao, Yijun
AU  - Yao Y
AD  - School of Engineering, Brown University, Providence, Rhode Island 02912,
      United States.
FAU - Shen, Rui
AU  - Shen R
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110223
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
RN  - 0 (Air Pollutants)
RN  - 0 (Gases)
RN  - 0 (Soil)
RN  - 0 (Soil Pollutants)
SB  - IM
MH  - Air Pollutants/*analysis/chemistry
MH  - Environmental Exposure/*analysis/statistics & numerical data
MH  - Gases/*analysis/chemistry
MH  - *Models, Chemical
MH  - Soil/chemistry
MH  - Soil Pollutants/*analysis/chemistry
PMC - PMC3664551
MID - NIHMS459373
EDAT- 2011/02/25 06:00
MHDA- 2011/05/20 06:00
CRDT- 2011/02/25 06:00
PHST- 2011/02/25 06:00 [entrez]
PHST- 2011/02/25 06:00 [pubmed]
PHST- 2011/05/20 06:00 [medline]
AID - 10.1021/es102602s [doi]
PST - ppublish
SO  - Environ Sci Technol. 2011 Mar 15;45(6):2227-35. doi: 10.1021/es102602s.
      Epub 2011 Feb 23.

PMID- 21130106
OWN - NLM
STAT- MEDLINE
DCOM- 20110224
LR  - 20211020
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 251
IP  - 1
DP  - 2011 Feb 15
TI  - Omega-3 fatty acid oxidation products prevent vascular endothelial cell
      activation by coplanar polychlorinated biphenyls.
PG  - 41-9
LID - 10.1016/j.taap.2010.11.013 [doi]
AB  - Coplanar polychlorinated biphenyls (PCBs) may facilitate development of
      atherosclerosis by stimulating pro-inflammatory pathways in the vascular
      endothelium. Nutrition, including fish oil-derived long-chain omega-3
      fatty acids, such as docosahexaenoic acid (DHA, 22:6omega-3), can reduce
      inflammation and thus the risk of atherosclerosis. We tested the
      hypothesis that cyclopentenone metabolites produced by oxidation of DHA
      can protect against PCB-induced endothelial cell dysfunction. Oxidized
      DHA (oxDHA) was prepared by incubation of the fatty acid with the free
      radical generator 2,2-azo-bis(2-amidinopropane) dihydrochloride (AAPH).
      Cellular pretreatment with oxDHA prevented production of superoxide
      induced by PCB77, and subsequent activation of nuclear factor-kappaB (NF-
      kappaB). A(4)/J(4)-neuroprostanes (NPs) were identified and quantitated
      using HPLC ESI tandem mass spectrometry. Levels of these NPs were
      markedly increased after DHA oxidation with AAPH. The protective actions
      of oxDHA were reversed by treatment with sodium borohydride (NaBH(4)),
      which concurrently abrogated A(4)/J(4)-NP formation. Up-regulation of
      monocyte chemoattractant protein-1 (MCP-1) by PCB77 was markedly reduced
      by oxDHA, but not by un-oxidized DHA. These protective effects were
      proportional to the abundance of A(4)/J(4) NPs in the oxidized DHA
      sample. Treatment of cells with oxidized eicosapentaenoic acid (EPA,
      20:5omega-3) also reduced MCP-1 expression, but less than oxDHA.
      Treatment with DHA-derived cyclopentenones also increased DNA binding of
      NF-E2-related factor-2 (Nrf2) and downstream expression of
      NAD(P)H:quinone oxidoreductase (NQO1), similarly to the Nrf-2 activator
      sulforaphane. Furthermore, sulforaphane prevented PCB77-induced MCP-1
      expression, suggesting that activation of Nrf-2 mediates the observed
      protection against PCB77 toxicity. Our data implicate A(4)/J(4)-NPs as
      mediators of omega-3 fatty acid-mediated protection against the
      endothelial toxicity of coplanar PCBs.
CI  - (c) 2010 Elsevier Inc. All rights reserved.
FAU - Majkova, Zuzana
AU  - Majkova Z
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington, KY
      40536-0200, USA.
FAU - Layne, Joseph
AU  - Layne J
FAU - Sunkara, Manjula
AU  - Sunkara M
FAU - Morris, Andrew J
AU  - Morris AJ
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - GM50388/GM/NIGMS NIH HHS/United States
GR  - P20 RR021954-03/RR/NCRR NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - S10 RR024598/RR/NCRR NIH HHS/United States
GR  - R01 GM050388/GM/NIGMS NIH HHS/United States
GR  - P42 ES007380-14/ES/NIEHS NIH HHS/United States
GR  - P20RR021954/RR/NCRR NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 RR021954/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20101201
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Antioxidants)
RN  - 0 (Borohydrides)
RN  - 0 (Cyclopentanes)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - 0 (Neuroprostanes)
RN  - 11062-77-4 (Superoxides)
RN  - 25167-62-8 (Docosahexaenoic Acids)
RN  - 87L0B9CPPA (sodium borohydride)
RN  - AAN7QOV9EA (Eicosapentaenoic Acid)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone))
RN  - Q0U2IGF9CK (cyclopentenone)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Antioxidants/metabolism
MH  - Borohydrides/pharmacology
MH  - Cells, Cultured
MH  - Cyclopentanes/metabolism
MH  - Cytoprotection
MH  - Docosahexaenoic Acids/*metabolism
MH  - Eicosapentaenoic Acid/*metabolism
MH  - Endothelial Cells/*drug effects/metabolism
MH  - NAD(P)H Dehydrogenase (Quinone)/metabolism
MH  - NF-E2-Related Factor 2/metabolism
MH  - NF-kappa B/metabolism
MH  - Neuroprostanes/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/*drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Superoxides/metabolism
MH  - Swine
MH  - Time Factors
PMC - PMC3026064
MID - NIHMS262963
EDAT- 2010/12/07 06:00
MHDA- 2011/02/25 06:00
CRDT- 2010/12/07 06:00
PHST- 2010/07/01 00:00 [received]
PHST- 2010/11/22 00:00 [revised]
PHST- 2010/11/22 00:00 [accepted]
PHST- 2010/12/07 06:00 [entrez]
PHST- 2010/12/07 06:00 [pubmed]
PHST- 2011/02/25 06:00 [medline]
AID - S0041-008X(10)00445-X [pii]
AID - 10.1016/j.taap.2010.11.013 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2011 Feb 15;251(1):41-9. doi:
      10.1016/j.taap.2010.11.013. Epub 2010 Dec 1.

PMID- 24619471
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1878-0296 (Print)
IS  - 1878-0296 (Linking)
VI  - 4
DP  - 2011
TI  - Vapor intrusion in urban settings: effect of foundation features and
      source location.
PG  - 245-250
AB  - In many urban settings, groundwater contains volatile organic compounds,
      such as tricholoroethene, tetrachloroethene, benzene, etc., at
      concentrations that are at or slightly below non-potable groundwater
      standards. Some non-potable groundwater standards do not protect against
      human health risks that might result from vapor intrusion. Vapor
      intrusion is a process by which vapor phase contaminants present in the
      subsurface migrate through the soil and ultimately enter a building
      through foundation cracks. The end result is a decrease in air quality
      within the building. Predicting whether or not vapor intrusion will occur
      at rates sufficient to cause health risks is extremely difficult and
      depends on many factors. In many cities, a wide-range of property uses
      take place over a relatively small area. For instance, schools,
      commercial buildings and residential buildings may all reside within a
      few city blocks. Most conceptual site models assume the ground surface is
      open to the atmosphere (i.e. green space); however the effect that an
      impervious surface (e.g. paving) may have on vapor transport rates is not
      routinely considered. Using a 3-D computational fluid dynamics model, we
      are investigating how the presence of impervious surfaces affects vapor
      intrusion rates. To complement our modeling efforts, we are in the
      initial stages of conducting a field study in a neighborhood where vapor
      intrusion is occurring.
FAU - Yao, Yijun
AU  - Yao Y
AD  - Brown University School of Engineering, Providence, RI 02912, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - Brown University School of Engineering, Providence, RI 02912, USA.
FAU - Suuberg, Eric
AU  - Suuberg E
AD  - Brown University School of Engineering, Providence, RI 02912, USA.
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - Procedia Environ Sci
JT  - Procedia environmental sciences
JID - 101556816
PMC - PMC3947568
MID - NIHMS459407
OTO - NOTNLM
OT  - Vapor intrusion
OT  - capping
OT  - perimeter crack
OT  - urban
OT  - wall crack
EDAT- 2011/01/01 00:00
MHDA- 2011/01/01 00:01
CRDT- 2014/03/13 06:00
PHST- 2014/03/13 06:00 [entrez]
PHST- 2011/01/01 00:00 [pubmed]
PHST- 2011/01/01 00:01 [medline]
AID - 10.1016/j.proenv.2011.03.029 [doi]
PST - ppublish
SO  - Procedia Environ Sci. 2011;4:245-250. doi: 10.1016/j.proenv.2011.03.029.

PMID- 19608276
OWN - NLM
STAT- MEDLINE
DCOM- 20110111
LR  - 20211020
IS  - 1873-6750 (Electronic)
IS  - 0160-4120 (Linking)
VI  - 36
IP  - 8
DP  - 2010 Nov
TI  - Quercetin blocks caveolae-dependent pro-inflammatory responses induced by
      co-planar PCBs.
PG  - 931-4
LID - 10.1016/j.envint.2009.06.009 [doi]
AB  - Polychlorinated biphenyls (PCBs) are widespread environmental
      contaminants, and co-planar PCBs can induce oxidative stress and
      activation of pro-inflammatory signaling cascades which are associated
      with atherosclerosis. The majority of the toxicological effects elicited
      by the co-planar PCB exposure are associated to the activation of the
      aryl hydrocarbon receptor (AHR) and subsequent induction of responsive
      genes. Previous studies from our group have shown that quercetin, a
      nutritionally relevant flavonoid can significantly reduce PCB77 induction
      of oxidative stress and expression of the AHR responsive gene cytochrome
      P450 1A1 (CYP1A1). We also have evidence that membrane domains called
      caveolae may regulate PCB-induced inflammatory parameters. Thus, we
      hypothesized that quercetin can modulate PCB-induced endothelial
      inflammation associated with caveolae. To test this hypothesis,
      endothelial cells were exposed to co-planar PCBs in combination with
      quercetin, and the expression of pro-inflammatory genes was analyzed by
      real-time PCR. Quercetin co-treatment significantly blocked both PCB77
      and PCB126 induction of CYP1A1, vascular cell adhesion molecule 1
      (VCAM-1), E-selectin and P-selectin. Exposure to PCB77 also induced
      caveolin-1 protein expression, which was reduced by co-treatment with
      quercetin. Our results suggest that inflammatory pathways induced by co-
      planar PCBs can be down-regulated by the dietary flavonoid quercetin
      through mechanisms associated with functional caveolae.
CI  - Copyright (c) 2009 Elsevier Ltd. All rights reserved.
FAU - Choi, Yean Jung
AU  - Choi YJ
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington KY 40536-0200, USA.
FAU - Arzuaga, Xabier
AU  - Arzuaga X
FAU - Kluemper, Chase T
AU  - Kluemper CT
FAU - Caraballo, Adelka
AU  - Caraballo A
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R25 ES016248/ES/NIEHS NIH HHS/United States
GR  - R25ES016248/ES/NIEHS NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20090715
PL  - Netherlands
TA  - Environ Int
JT  - Environment international
JID - 7807270
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Caveolin 1)
RN  - 0 (E-Selectin)
RN  - 0 (P-Selectin)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 9IKM0I5T1E (Quercetin)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Caveolae/*metabolism
MH  - Caveolin 1/biosynthesis
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/biosynthesis
MH  - E-Selectin/biosynthesis
MH  - Endothelial Cells/drug effects
MH  - Gene Expression Profiling
MH  - Humans
MH  - Inflammation/*chemically induced
MH  - P-Selectin/biosynthesis
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Quercetin/*pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Vascular Cell Adhesion Molecule-1/biosynthesis
PMC - PMC2889233
MID - NIHMS128446
EDAT- 2009/07/18 09:00
MHDA- 2011/01/12 06:00
CRDT- 2009/07/18 09:00
PHST- 2008/10/10 00:00 [received]
PHST- 2009/01/13 00:00 [revised]
PHST- 2009/06/07 00:00 [accepted]
PHST- 2009/07/18 09:00 [entrez]
PHST- 2009/07/18 09:00 [pubmed]
PHST- 2011/01/12 06:00 [medline]
AID - S0160-4120(09)00146-9 [pii]
AID - 10.1016/j.envint.2009.06.009 [doi]
PST - ppublish
SO  - Environ Int. 2010 Nov;36(8):931-4. doi: 10.1016/j.envint.2009.06.009.
      Epub 2009 Jul 15.

PMID- 20406324
OWN - NLM
STAT- MEDLINE
DCOM- 20110210
LR  - 20211020
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Linking)
VI  - 14
IP  - 10
DP  - 2010 Oct
TI  - The role of caveolae in endothelial cell dysfunction with a focus on
      nutrition and environmental toxicants.
PG  - 2359-70
LID - 10.1111/j.1582-4934.2010.01064.x [doi]
AB  - Complications of vascular diseases, including atherosclerosis, are the
      number one cause of death in Western societies. Dysfunction of
      endothelial cells is a critical underlying cause of the pathology of
      atherosclerosis. Lipid rafts, and especially caveolae, are enriched in
      endothelial cells, and down-regulation of the caveolin-1 gene may provide
      protection against the development of atherosclerosis. There is
      substantial evidence that exposure to environmental pollution is linked
      to cardiovascular mortality, and that persistent organic pollutants can
      markedly contribute to endothelial cell dysfunction and an increase in
      vascular inflammation. Nutrition can modulate the toxicity of
      environmental pollutants, and evidence suggests that these affect health
      and disease outcome associated with chemical insults. Because caveolae
      can provide a regulatory platform for pro-inflammatory signalling
      associated with vascular diseases such as atherosclerosis, we suggest a
      link between atherogenic risk and functional changes of caveolae by
      environmental factors such as dietary lipids and organic pollutants. For
      example, we have evidence that endothelial caveolae play a role in uptake
      of persistent organic pollutants, an event associated with subsequent
      production of inflammatory mediators. Functional properties of caveolae
      can be modulated by nutrition, such as dietary lipids (e.g. fatty acids)
      and plant-derived polyphenols (e.g. flavonoids), which change activation
      of caveolae-associated signalling proteins. The following review will
      focus on caveolae providing a platform for pro-inflammatory signalling,
      and the role of caveolae in endothelial cell functional changes
      associated with environmental mediators such as nutrients and toxicants,
      which are known to modulate the pathology of vascular diseases.
CI  - (c) 2010 The Authors Journal compilation (c) 2010 Foundation for Cellular
      and Molecular Medicine/Blackwell Publishing Ltd.
FAU - Majkova, Zuzana
AU  - Majkova Z
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington, KY,
      USA.
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (Caveolin 1)
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Flavonoids)
RN  - 0 (Polycyclic Aromatic Hydrocarbons)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/genetics/metabolism
MH  - Caveolae/*metabolism
MH  - Caveolin 1/genetics/metabolism
MH  - *Diet
MH  - Dietary Fats/*pharmacology
MH  - Down-Regulation
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Environmental Pollutants/*antagonists & inhibitors/toxicity
MH  - Flavonoids/pharmacology
MH  - Humans
MH  - Mice
MH  - Nutritional Sciences
MH  - Polychlorinated Biphenyls/toxicity
MH  - Polycyclic Aromatic Hydrocarbons/toxicity
MH  - Signal Transduction
PMC - PMC2965309
MID - NIHMS225915
EDAT- 2010/04/22 06:00
MHDA- 2011/02/11 06:00
CRDT- 2010/04/22 06:00
PHST- 2010/04/22 06:00 [entrez]
PHST- 2010/04/22 06:00 [pubmed]
PHST- 2011/02/11 06:00 [medline]
AID - JCMM1064 [pii]
AID - 10.1111/j.1582-4934.2010.01064.x [doi]
PST - ppublish
SO  - J Cell Mol Med. 2010 Oct;14(10):2359-70. doi:
      10.1111/j.1582-4934.2010.01064.x.

PMID- 20564349
OWN - NLM
STAT- MEDLINE
DCOM- 20101206
LR  - 20211020
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 88
IP  - 13
DP  - 2010 Oct
TI  - Deficiency of telomerase activity aggravates the blood-brain barrier
      disruption and neuroinflammatory responses in a model of experimental
      stroke.
PG  - 2859-68
LID - 10.1002/jnr.22450 [doi]
AB  - Epidemiology and genetic studies indicate that patients with telomere
      length shorter than average are at higher risk of dying from heart
      disease or stroke. Telomeres are located at the ends of eukaryotic
      chromosomes, which demonstrate progressive length reduction in most
      somatic cells during aging. The enzyme telomerase can compensate for
      telomere loss during cell replication. The present study sought to
      investigate the contribution of telomerase to stroke and blood-brain
      barrier (BBB) dysfunction. Telomerase reverse transcriptase knockout
      (TERT(-/-)) mice and littermate controls with normal TERT expression were
      subjected to a 24-hr permanent middle cerebral artery occlusion (pMCAO).
      The stroke outcomes were assessed in terms of neurological scores and
      infarct volumes. In addition, we evaluated oxidative stress, permeability
      across the BBB, and integrity of tight junctions in brain microvessels.
      Neurological testing revealed that TERT(-/-) mice showed enhanced
      deficits compared with controls. These changes were associated with a
      greater infarct volume. The expression of tight junction protein ZO-1
      decreased markedly in ischemic hemispheres of TERT(-/-) mice. The brain
      microvessels of TERT(-/-) mice also were more susceptible to oxidative
      stress, revealing higher superoxide and lower glutathione levels compared
      with mice with normal TERT expression. Importantly, TERT deficiency
      potentiated the production of inflammatory mediators, such as tumor
      necrosis factor-alpha, interleukin-1 beta, and intercellular adhesion
      molecule-1, in the ischemic hemispheres of mice with pMCAO. Our study
      suggests that TERT deficiency can predispose to the development of stroke
      in an experimental model of this disease.
CI  - (c) 2010 Wiley-Liss, Inc.
FAU - Zhang, Bei
AU  - Zhang B
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, Kentucky 40536, USA.
FAU - Chen, Lei
AU  - Chen L
FAU - Swartz, Karin R
AU  - Swartz KR
FAU - Bruemmer, Dennis
AU  - Bruemmer D
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Huang, Wen
AU  - Huang W
FAU - Seelbach, Melissa
AU  - Seelbach M
FAU - Choi, Yean Jung
AU  - Choi YJ
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 CA133257/CA/NCI NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Cytokines)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 11062-77-4 (Superoxides)
RN  - EC 2.7.7.49 (Telomerase)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/*physiopathology
MH  - Brain/pathology
MH  - Brain Infarction/etiology/pathology
MH  - Cytokines/genetics/metabolism
MH  - Disease Models, Animal
MH  - Encephalitis/*etiology/*genetics
MH  - Gene Expression Regulation/genetics
MH  - Glutathione/metabolism
MH  - Infarction, Middle Cerebral Artery/*complications
MH  - Mice
MH  - Mice, Knockout
MH  - Microvessels/physiopathology
MH  - Nervous System Diseases/etiology/genetics
MH  - Oxidative Stress/genetics/physiology
MH  - Proto-Oncogene Proteins/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - Statistics, Nonparametric
MH  - Superoxides/metabolism
MH  - Telomerase/*deficiency
PMC - PMC2919635
MID - NIHMS209270
EDAT- 2010/06/22 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/06/22 06:00
PHST- 2010/06/22 06:00 [entrez]
PHST- 2010/06/22 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
AID - 10.1002/jnr.22450 [doi]
PST - ppublish
SO  - J Neurosci Res. 2010 Oct;88(13):2859-68. doi: 10.1002/jnr.22450.

PMID- 20299304
OWN - NLM
STAT- MEDLINE
DCOM- 20101019
LR  - 20181113
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Linking)
VI  - 118
IP  - 7
DP  - 2010 Jul
TI  - Polychlorinated biphenyls disrupt intestinal integrity via NADPH oxidase-
      induced alterations of tight junction protein expression.
PG  - 976-81
LID - 10.1289/ehp.0901751 [doi]
AB  - BACKGROUND: Polychlorinated biphenyls (PCBs) are widely distributed
      environmental toxicants that contribute to numerous disease states. The
      main route of exposure to PCBs is through the gastrointestinal tract;
      however, little is known about the effects of PCBs on intestinal
      epithelial barrier functions. OBJECTIVE: The aim of the present study was
      to address the hypothesis that highly chlorinated PCBs can disrupt gut
      integrity at the level of tight junction (TJ) proteins. METHODS: Caco-2
      human colon adenocarcinoma cells were exposed to one of the following PCB
      congeners: PCB153, PCB118, PCB104, and PCB126. We then assessed NAD(P)H
      oxidase (NOX) activity and expression and the barrier function of Caco-2
      cells. In addition, the integrity of intestinal barrier function and
      expression of TJ proteins were evaluated in C57BL/6 mice exposed to
      individual PCBs by oral gavage. RESULTS: Exposure of Caco-2 cells to
      individual PCB congeners resulted in activation of NOX and increased
      permeability of fluorescein isothiocyanate (FITC)-labeled dextran (4
      kDa). Treatment with PCB congeners also disrupted expression of TJ
      proteins zonula occludens-1 (ZO-1) and occludin in Caco-2 cells.
      Importantly, inhibition of NOX by apocynin significantly protected
      against PCB-mediated increase in epithelial permeability and alterations
      of ZO-1 protein expression. Exposure to PCBs also resulted in alterations
      of gut permeability via decreased expression of TJ proteins in an intact
      physiological animal model. CONCLUSIONS: These results suggest that oral
      exposure to highly chlorinated PCBs disrupts intestinal epithelial
      integrity and may directly contribute to the systemic effects of these
      toxicants.
FAU - Choi, Yean Jung
AU  - Choi YJ
AD  - Department of Neurosurgery, University of Kentucky, Lexington, 40536,
      USA.
FAU - Seelbach, Melissa J
AU  - Seelbach MJ
FAU - Pu, Hong
AU  - Pu H
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Chen, Lei
AU  - Chen L
FAU - Zhang, Bei
AU  - Zhang B
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20100318
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Environmental Pollutants)
RN  - 0 (Membrane Proteins)
RN  - 0 (OCLN protein, human)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, mouse)
RN  - 0 (Phosphoproteins)
RN  - 0 (TJP1 protein, human)
RN  - 0 (Tjp1 protein, mouse)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.6.3.- (NADPH Oxidases)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Blotting, Western
MH  - Caco-2 Cells
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Environmental Pollutants/*toxicity
MH  - Enzyme Activation/drug effects
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Immunohistochemistry
MH  - Immunoprecipitation
MH  - Intestinal Mucosa/*drug effects
MH  - Male
MH  - Membrane Proteins/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NADPH Oxidases/*metabolism
MH  - Occludin
MH  - Phosphoproteins/metabolism
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Tight Junctions/*drug effects
MH  - Zonula Occludens-1 Protein
PMC - PMC2920918
EDAT- 2010/03/20 06:00
MHDA- 2010/10/20 06:00
CRDT- 2010/03/20 06:00
PHST- 2009/11/30 00:00 [received]
PHST- 2010/03/18 00:00 [accepted]
PHST- 2010/03/20 06:00 [entrez]
PHST- 2010/03/20 06:00 [pubmed]
PHST- 2010/10/20 06:00 [medline]
AID - 10.1289/ehp.0901751 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2010 Jul;118(7):976-81. doi:
      10.1289/ehp.0901751. Epub 2010 Mar 18.

PMID- 20406653
OWN - NLM
STAT- MEDLINE
DCOM- 20100628
LR  - 20211020
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 246
IP  - 1-2
DP  - 2010 Jul
TI  - Polychlorinated biphenyl-induced VCAM-1 expression is attenuated in
      aortic endothelial cells isolated from caveolin-1 deficient mice.
PG  - 74-82
LID - 10.1016/j.taap.2010.04.009 [doi]
AB  - Exposure to environmental contaminants, such as polychlorinated biphenyls
      (PCBs), is a risk factor for the development of cardiovascular diseases
      such as atherosclerosis. Vascular cell adhesion molecule-1 (VCAM-1) is a
      critical mediator for adhesion and uptake of monocytes across the
      endothelium in the early stages of atherosclerosis development. The
      upregulation of VCAM-1 by PCBs may be dependent on functional membrane
      domains called caveolae. Caveolae are particularly abundant in
      endothelial cell membranes and involved in trafficking and signal
      transduction. The objective of this study was to investigate the role of
      caveolae in PCB-induced endothelial cell dysfunction. Primary mouse
      aortic endothelial cells (MAECs) isolated from caveolin-1-deficient mice
      and background C57BL/6 mice were treated with coplanar PCBs, such as
      PCB77 and PCB126. In addition, siRNA gene silencing technique was used to
      knockdown caveolin-1 in porcine vascular endothelial cells. In MAECs with
      functional caveolae, VCAM-1 protein levels were increased after exposure
      to both coplanar PCBs, whereas expression levels of VCAM-1 were not
      significantly altered in cells deficient of caveolin-1. Furthermore, PCB-
      induced monocyte adhesion was attenuated in caveolin-1-deficient MAECs.
      Similarly, siRNA silencing of caveolin-1 in porcine endothelial cells
      confirmed the caveolin-1-dependent VCAM-1 expression. Treatment of cells
      with PCB77 and PCB126 resulted in phosphorylation of extracellular
      signal-regulated kinase-1/2 (ERK1/2), and pharmacological inhibition of
      ERK1/2 diminished the observed PCB-induced increase in monocyte adhesion.
      These findings suggest that coplanar PCBs induce adhesion molecule
      expression, such as VCAM-1, in endothelial cells, and that this response
      is regulated by caveolin-1 and functional caveolae. Our data demonstrate
      a critical role of functional caveolae in the activation and dysfunction
      of endothelial cells by coplanar PCBs.
CI  - 2010 Elsevier Inc. All rights reserved.
FAU - Han, Sung Gu
AU  - Han SG
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40536, USA.
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Toborek, Michal
AU  - Toborek M
FAU - Smart, Eric
AU  - Smart E
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-130002/ES/NIEHS NIH HHS/United States
GR  - P42ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20100418
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Caveolin 1)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Aorta
MH  - Blotting, Western
MH  - Caveolin 1/*deficiency/genetics
MH  - Cell Adhesion/drug effects
MH  - Endothelial Cells/chemistry/*drug effects/metabolism
MH  - Fluorescent Antibody Technique
MH  - Gene Expression/drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout/genetics
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - Monocytes/drug effects
MH  - Polychlorinated Biphenyls/*pharmacology
MH  - RNA Interference/drug effects
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/analysis/*biosynthesis
PMC - PMC2895770
MID - NIHMS208486
EDAT- 2010/04/22 06:00
MHDA- 2010/06/29 06:00
CRDT- 2010/04/22 06:00
PHST- 2010/01/25 00:00 [received]
PHST- 2010/04/09 00:00 [revised]
PHST- 2010/04/12 00:00 [accepted]
PHST- 2010/04/22 06:00 [entrez]
PHST- 2010/04/22 06:00 [pubmed]
PHST- 2010/06/29 06:00 [medline]
AID - S0041-008X(10)00136-5 [pii]
AID - 10.1016/j.taap.2010.04.009 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2010 Jul;246(1-2):74-82. doi:
      10.1016/j.taap.2010.04.009. Epub 2010 Apr 18.

PMID- 31354185
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 49
DP  - 2010 May 19
TI  - Sulfur-Functionalization of Porous Silica Particles and Application to
      Mercury Vapor Sorption.
PG  - 4687-4693
LID - 10.1021/ie901580k [doi]
AB  - Silanol (SiOH) groups on silica particle surfaces undergo silylation
      reactions with organosilane molecules to give functionalized particles,
      which are used in many applications. The determination of the extent of
      this reaction is important for proper design of functionalized materials,
      depending upon the application. Two types of porous silica particles (206
      and 484 m(2) g(-1); 9.6 and 2.9 nm average pore diameter, respectively),
      and colloidal silica (Ludox) with a nonporous base particle of 22 nm
      diameter, were functionalized with sulfur-containing silanes,
      3-mercaptopropyl trimethoxy silane (MPTMS), and bis[3-(triethoxysilyl)
      propyl]-tetrasulfide (S4). Maximum extent of functionalization was
      determined with S4 using Fourier transform infrared spectrometry (FTIR),
      thermogravimetric analysis (TGA), and total S analysis. For the two types
      of porous silica particles, FTIR indicated that 54 and 17% of the silanol
      groups were functionalized with S4, and TGA indicated that the
      functionalized particles were 12 and 11 mass % MPTMS, respectively. These
      results were independently confirmed with total sulfur analysis. Extents
      of functionalization were determined for varying the silane structure on
      the same silica particle. MPTMS reacted with 38% of functional groups,
      while S4 reacted with 17%; the mass % of silane is the same regardless of
      silane structure on the same silica particle. Characterization by DSC
      indicated a glass transition occurs in the silane layer of the
      S4-functionalized silica at about 85 degrees C, but not in the MPTMS
      functionalized particles. Finally, mercury sorption breakthrough curves
      indicate the pore characteristics of the S4 functionalized samples.
FAU - Meeks, Noah D
AU  - Meeks ND
AD  - University of Kentucky, Department of Chemical and Materials Engineering,
      Lexington, Kentucky 40506.
FAU - Rankin, Stephen
AU  - Rankin S
AD  - University of Kentucky, Department of Chemical and Materials Engineering,
      Lexington, Kentucky 40506.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - University of Kentucky, Department of Chemical and Materials Engineering,
      Lexington, Kentucky 40506.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20100426
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC6660182
MID - NIHMS997160
EDAT- 2010/05/19 00:00
MHDA- 2010/05/19 00:01
CRDT- 2019/07/30 06:00
PHST- 2019/07/30 06:00 [entrez]
PHST- 2010/05/19 00:00 [pubmed]
PHST- 2010/05/19 00:01 [medline]
AID - 10.1021/ie901580k [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2010 May 19;49:4687-4693. doi: 10.1021/ie901580k. Epub
      2010 Apr 26.

PMID- 20064788
OWN - NLM
STAT- MEDLINE
DCOM- 20100715
LR  - 20211020
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Linking)
VI  - 118
IP  - 4
DP  - 2010 Apr
TI  - Polychlorinated biphenyls disrupt blood-brain barrier integrity and
      promote brain metastasis formation.
PG  - 479-84
LID - 10.1289/ehp.0901334 [doi]
AB  - BACKGROUND: Polychlorinated biphenyls (PCBs) comprise a ubiquitous class
      of toxic substances associated with carcinogenic and tumor-promoting
      effects as well as neurotoxic properties in the brain. However, the
      effects of PCBs on the development of tumor metastases are not fully
      understood. OBJECTIVE: We evaluated the hypothesis that exposure to
      individual PCB congeners can facilitate the development of brain
      metastases in immunocompetent mice via the disruption of the integrity of
      the blood-brain barrier (BBB). METHODS: C57/Bl6 mice were exposed to
      individual PCBs by oral gavage, and 48 hr later they were injected with
      luciferase-labeled K1735 M2 melanoma cells into the internal carotid
      artery. The development of metastatic nodules was monitored by
      bioluminescent imaging. In addition, we evaluated the functional
      permeability of the BBB by measuring permeability of sodium fluorescein
      across the brain microvessels. Expression and colocalization of tight
      junction (TJ) proteins were studied by Western blotting and
      immunofluorescence microscopy. RESULTS: Oral administration of coplanar
      PCB126, mono-ortho-substituted PCB118, and non-coplanar PCB153 (each at
      150 micromol/kg body weight) differentially altered expression of the TJ
      proteins claudin-5, occludin, and zonula occludens-1 in brain
      capillaries. These alterations were associated with increased
      permeability of the BBB. Most importantly, exposure to individual PCB
      congeners enhanced the rate of formation and progression of brain
      metastases of luciferase-tagged melanoma cells. CONCLUSIONS: Our results
      show for the first time that exposure to individual PCBs can facilitate
      the formation of bloodborne metastases via alterations of the integrity
      of the brain capillary endothelium.
FAU - Seelbach, Melissa
AU  - Seelbach M
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky Medical Center, Lexington, Kentucky
      40536, USA.
FAU - Chen, Lei
AU  - Chen L
FAU - Powell, Anita
AU  - Powell A
FAU - Choi, Yean Jung
AU  - Choi YJ
FAU - Zhang, Bei
AU  - Zhang B
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - P42 ES07380/ES/NIEHS NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20091028
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Environmental Pollutants)
RN  - 0 (Membrane Proteins)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, mouse)
RN  - 0 (Phosphoproteins)
RN  - 0 (Tjp1 protein, mouse)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/*drug effects/metabolism
MH  - Blotting, Western
MH  - Brain Neoplasms/*chemically induced/pathology
MH  - Cell Line, Tumor
MH  - Environmental Pollutants/*toxicity
MH  - Male
MH  - Melanoma/*chemically induced/pathology
MH  - Membrane Proteins/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microscopy, Fluorescence
MH  - Occludin
MH  - Phosphoproteins/metabolism
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Zonula Occludens-1 Protein
PMC - PMC2854723
EDAT- 2010/01/13 06:00
MHDA- 2010/07/16 06:00
CRDT- 2010/01/13 06:00
PHST- 2009/08/15 00:00 [received]
PHST- 2009/10/28 00:00 [accepted]
PHST- 2010/01/13 06:00 [entrez]
PHST- 2010/01/13 06:00 [pubmed]
PHST- 2010/07/16 06:00 [medline]
AID - 10.1289/ehp.0901334 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2010 Apr;118(4):479-84. doi:
      10.1289/ehp.0901334. Epub 2009 Oct 28.

PMID- 20139322
OWN - NLM
STAT- MEDLINE
DCOM- 20100412
LR  - 20211020
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Linking)
VI  - 298
IP  - 4
DP  - 2010 Apr
TI  - Inhibition of telomerase activity alters tight junction protein
      expression and induces transendothelial migration of HIV-1-infected
      cells.
PG  - H1136-45
LID - 10.1152/ajpheart.01126.2009 [doi]
AB  - Telomerase, via its catalytic component telomerase reverse transcriptase
      (TERT), extends telomeres of eukaryotic chromosomes. The importance of
      this reaction is related to the fact that telomere shortening is a rate-
      limiting mechanism for human life span that induces cell senescence and
      contributes to the development of age-related pathologies. The aim of the
      present study was to evaluate whether the modulation of telomerase
      activity can influence human immunodeficiency virus type 1
      (HIV-1)-mediated dysfunction of human brain endothelial cells (hCMEC/D3
      cells) and transendothelial migration of HIV-1-infected cells. Telomerase
      activity was modulated in hCMEC/D3 cells via small interfering RNA-
      targeting human TERT (hTERT) or by using a specific pharmacological
      inhibitor of telomerase, TAG-6. The inhibition of hTERT resulted in the
      upregulation of HIV-1-induced overexpression of intercellular adhesion
      molecule-1 via the nuclear factor-kappaB-regulated mechanism and induced
      the transendothelial migration of HIV-1-infected monocytic U937 cells. In
      addition, the blocking of hTERT activity potentiated a HIV-induced
      downregulation of the expression of tight junction proteins. These
      results were confirmed in TERT-deficient mice injected with
      HIV-1-specific protein Tat into the cerebral vasculature. Further studies
      revealed that the upregulation of matrix metalloproteinase-9 is the
      underlying mechanisms of disruption of tight junction proteins in
      hCMEC/D3 cells with inhibited TERT and exposed to HIV-1. These results
      indicate that the senescence of brain endothelial cells may predispose to
      the HIV-induced upregulation of inflammatory mediators and the disruption
      of the barrier function at the level of the brain endothelium.
FAU - Huang, Wen
AU  - Huang W
AD  - Dept. of Neurosurgery, Univ. of Kentucky, Lexington, 40536, USA.
FAU - Rha, Geun Bae
AU  - Rha GB
FAU - Chen, Lei
AU  - Chen L
FAU - Seelbach, Melissa J
AU  - Seelbach MJ
FAU - Zhang, Bei
AU  - Zhang B
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Bruemmer, Dennis
AU  - Bruemmer D
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - NS-39254/NS/NINDS NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - MH-072567/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 RR015592/RR/NCRR NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH-63022/MH/NIMH NIH HHS/United States
GR  - P20-RR-15592/RR/NCRR NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20100205
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (CLDN5 protein, human)
RN  - 0 (Claudin-5)
RN  - 0 (Membrane Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 2.7.7.49 (Telomerase)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Cell Movement/*physiology
MH  - Cells, Cultured
MH  - Claudin-5
MH  - Disease Models, Animal
MH  - Endothelium, Vascular/drug effects/pathology/*virology
MH  - Female
MH  - Gene Silencing
MH  - HIV Infections/metabolism/pathology
MH  - HIV-1/*isolation & purification
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Matrix Metalloproteinase 9/metabolism
MH  - Membrane Proteins/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NF-kappa B/metabolism
MH  - Telomerase/*antagonists & inhibitors/genetics/metabolism
MH  - Tight Junctions/*metabolism
MH  - U937 Cells
MH  - tat Gene Products, Human Immunodeficiency Virus/pharmacology
PMC - PMC2853419
EDAT- 2010/02/09 06:00
MHDA- 2010/04/13 06:00
CRDT- 2010/02/09 06:00
PHST- 2010/02/09 06:00 [entrez]
PHST- 2010/02/09 06:00 [pubmed]
PHST- 2010/04/13 06:00 [medline]
AID - 01126.2009 [pii]
AID - 10.1152/ajpheart.01126.2009 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2010 Apr;298(4):H1136-45. doi:
      10.1152/ajpheart.01126.2009. Epub 2010 Feb 5.

PMID- 19794400
OWN - NLM
STAT- MEDLINE
DCOM- 20100402
LR  - 20211020
IS  - 1559-7016 (Electronic)
IS  - 0271-678X (Linking)
VI  - 30
IP  - 3
DP  - 2010 Mar
TI  - Intact lipid rafts regulate HIV-1 Tat protein-induced activation of the
      Rho signaling and upregulation of P-glycoprotein in brain endothelial
      cells.
PG  - 522-33
LID - 10.1038/jcbfm.2009.214 [doi]
AB  - The Rho signaling has an essential function in human immunodeficiency
      virus (HIV)-1-mediated disruption of the integrity of the blood-brain
      barrier (BBB). However, it is unknown how membrane domains, such as lipid
      rafts, can influence HIV-1-mediated activation of the Rho pathway and how
      these processes can affect the expression of the efflux transporters at
      the BBB level. This study is focused on the function of HIV-1 protein Tat
      in activation of the Rho signaling and upregulation of P-glycoprotein
      (P-gp) in human brain endothelial cells. Treatment with Tat markedly
      elevated GTP-RhoA levels and the potential downstream effectors, such as
      myosin phosphatase target subunit 1 and myosin light chain. In addition,
      Tat upregulated expression and promoter activity of P-gp as well as its
      efflux function. Inhibition of the Rho signaling cascade effectively
      blocked P-gp overexpression at the level of promoter activity. Disruption
      of lipid rafts by depletion of membrane cholesterol by methyl-beta-
      cyclodextrin, but not caveolin-1 silencing, also abolished Tat-mediated
      RhoA activation and P-gp upregulation. The present data indicate the
      critical function of intact lipid rafts and the Rho signaling in
      HIV-1-mediated upregulation of P-gp and potential development of drug
      resistance in brain endothelial cells.
FAU - Zhong, Yu
AU  - Zhong Y
AD  - Department of Neurosurgery, Molecular Neuroscience and Vascular Biology
      Laboratory, University of Kentucky Medical Center, Lexington, Kentucky
      40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - MH063022/MH/NIMH NIH HHS/United States
GR  - P01 DA019398/DA/NIDA NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P01 DA19398/DA/NIDA NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20090930
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (Caveolin 1)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Myosin Light Chains)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 1N3CZ14C5O (Rhodamine 123)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - EC 3.6.5.2 (rho GTP-Binding Proteins)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/*biosynthesis
MH  - Adenoviridae/immunology
MH  - Blotting, Western
MH  - Brain/cytology
MH  - Caveolin 1/genetics/physiology
MH  - Cells, Cultured
MH  - Cerebrovascular Circulation/physiology
MH  - Cholesterol/physiology
MH  - Endothelial Cells/*metabolism/physiology
MH  - Fluorescent Dyes
MH  - Genetic Vectors
MH  - HIV-1/*metabolism
MH  - Humans
MH  - Membrane Microdomains/*physiology
MH  - Myosin Light Chains/metabolism
MH  - Promoter Regions, Genetic
MH  - Rhodamine 123
MH  - Signal Transduction/*physiology
MH  - Up-Regulation
MH  - rho GTP-Binding Proteins/*physiology
MH  - tat Gene Products, Human Immunodeficiency Virus/*physiology
PMC - PMC2949153
EDAT- 2009/10/02 06:00
MHDA- 2010/04/03 06:00
CRDT- 2009/10/02 06:00
PHST- 2009/10/02 06:00 [entrez]
PHST- 2009/10/02 06:00 [pubmed]
PHST- 2010/04/03 06:00 [medline]
AID - jcbfm2009214 [pii]
AID - 10.1038/jcbfm.2009.214 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2010 Mar;30(3):522-33. doi:
      10.1038/jcbfm.2009.214. Epub 2009 Sep 30.

PMID- 19944163
OWN - NLM
STAT- MEDLINE
DCOM- 20100423
LR  - 20211020
IS  - 1095-9327 (Electronic)
IS  - 1044-7431 (Linking)
VI  - 43
IP  - 2
DP  - 2010 Feb
TI  - HIV-1-induced amyloid beta accumulation in brain endothelial cells is
      attenuated by simvastatin.
PG  - 232-43
LID - 10.1016/j.mcn.2009.11.004 [doi]
AB  - HIV-1-infected brains are characterized by increased amyloid deposition.
      To study the influence of HIV-1 on amyloid beta (Abeta) homeostasis at
      the blood-brain barrier (BBB) level, we employed a model of brain
      microvascular endothelial cells exposed to HIV-1 in the presence or
      absence of Abeta. HIV-1 markedly increased endogenous Abeta levels and
      elevated accumulation of exogenous Abeta. Simvastatin, the HMG-CoA
      reductase inhibitor, blocked these effects. We next evaluated the effects
      of HIV-1 and/or simvastatin on expression of the receptor for lipoprotein
      related protein (LRP1) and the receptor for advanced glycation end
      products (RAGE), known to regulate Abeta transport across the BBB. LRP1
      expression was not affected by HIV-1; however, it was increased by
      simvastatin. Importantly, simvastatin attenuated HIV-1-induced RAGE
      expression. These results suggest that HIV-1 may directly contribute to
      Abeta accumulation at the BBB level. In addition, statins may protect
      against increased Abeta levels associated with HIV-1 infection in the
      brain.
CI  - Copyright 2009 Elsevier Inc. All rights reserved.
FAU - Andras, Ibolya E
AU  - Andras IE
AD  - Department of Neurosurgery, University of Kentucky Medical Center,
      Lexington, KY 40536, USA.
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Huang, Wen
AU  - Huang W
FAU - Zhong, Yu
AU  - Zhong Y
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 NS039254-10/NS/NINDS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P42 ES007380-13S19005/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-130009/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-139005/ES/NIEHS NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 MH063022-07/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-13S10009/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20091126
PL  - United States
TA  - Mol Cell Neurosci
JT  - Molecular and cellular neurosciences
JID - 9100095
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Low Density Lipoprotein Receptor-Related Protein-1)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (amyloid beta-protein (1-40))
RN  - AGG2FN16EV (Simvastatin)
SB  - IM
MH  - Amyloid beta-Peptides/*metabolism/pharmacology
MH  - Brain/cytology
MH  - Cell Line, Transformed
MH  - Coculture Techniques/methods
MH  - *Endothelial Cells/drug effects/metabolism/virology
MH  - Gene Expression Regulation/drug effects
MH  - HIV-1/*metabolism
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology
MH  - Intercellular Signaling Peptides and Proteins/pharmacology
MH  - Low Density Lipoprotein Receptor-Related Protein-1/metabolism
MH  - Peptide Fragments/pharmacology
MH  - Receptor for Advanced Glycation End Products
MH  - Receptors, Immunologic/metabolism
MH  - Simvastatin/*pharmacology
MH  - Time Factors
PMC - PMC2818553
MID - NIHMS161840
EDAT- 2009/12/01 06:00
MHDA- 2010/04/24 06:00
CRDT- 2009/12/01 06:00
PHST- 2009/08/05 00:00 [received]
PHST- 2009/11/16 00:00 [revised]
PHST- 2009/11/17 00:00 [accepted]
PHST- 2009/12/01 06:00 [entrez]
PHST- 2009/12/01 06:00 [pubmed]
PHST- 2010/04/24 06:00 [medline]
AID - S1044-7431(09)00243-7 [pii]
AID - 10.1016/j.mcn.2009.11.004 [doi]
PST - ppublish
SO  - Mol Cell Neurosci. 2010 Feb;43(2):232-43. doi: 10.1016/j.mcn.2009.11.004.
      Epub 2009 Nov 26.

PMID- 19632255
OWN - NLM
STAT- MEDLINE
DCOM- 20091008
LR  - 20211020
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 240
IP  - 2
DP  - 2009 Oct 15
TI  - NADPH oxidase and lipid raft-associated redox signaling are required for
      PCB153-induced upregulation of cell adhesion molecules in human brain
      endothelial cells.
PG  - 299-305
LID - 10.1016/j.taap.2009.07.022 [doi]
AB  - Exposure to persistent organic pollutants, such as polychlorinated
      biphenyls (PCBs), can lead to chronic inflammation and the development of
      vascular diseases. Because cell adhesion molecules (CAMs) of the
      cerebrovascular endothelium regulate infiltration of inflammatory cells
      into the brain, we have explored the molecular mechanisms by which ortho-
      substituted polychlorinated biphenyls (PCBs), such as PCB153, can
      upregulate CAMs in brain endothelial cells. Exposure to PCB153 increased
      expression of intercellular adhesion molecule-1 (ICAM-1) and vascular
      cell adhesion molecule-1 (VCAM-1), as well as elevated adhesion of
      leukocytes to brain endothelial cells. These effects were impeded by
      inhibitors of EGFR, JAKs, or Src activity. In addition, pharmacological
      inhibition of NADPH oxidase or disruption of lipid rafts by cholesterol
      depleting agents blocked PCB153-induced phosphorylation of JAK and Src
      kinases and upregulation of CAMs. In contrast, silencing of caveolin-1 by
      siRNA interference did not affect upregulation of ICAM-1 and VCAM-1 in
      brain endothelial cells stimulated by PCB153. Results of the present
      study indicate that lipid raft-dependent NADPH oxidase/JAK/EGFR signaling
      mechanisms regulate the expression of CAMs in brain endothelial cells and
      adhesion of leukocytes to endothelial monolayers. Due to its role in
      leukocyte infiltration, induction of CAMs may contribute to PCB-induced
      cerebrovascular disorders and neurotoxic effects in the CNS.
FAU - Eum, Sung Yong
AU  - Eum SY
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, KY 40536, USA.
      sungyongeum@uky.edu
FAU - Andras, Ibolya
AU  - Andras I
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-139005/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P41 ES 07380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-130009/ES/NIEHS NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 MH063022-07/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - MH93022/MH/NIMH NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 NS039254-09/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20090724
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (CAV1 protein, human)
RN  - 0 (Caveolin 1)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.1 (neutrophil cytosolic factor 1)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.2 (Janus Kinases)
RN  - EC 2.7.10.2 (src-Family Kinases)
RN  - ZRU0C9E32O (2,4,5,2',4',5'-hexachlorobiphenyl)
SB  - IM
MH  - Brain/*blood supply
MH  - Caveolin 1/genetics/metabolism
MH  - Cell Adhesion/drug effects
MH  - Cell Adhesion Molecules/*metabolism
MH  - Cell Line, Transformed
MH  - Cholesterol/metabolism
MH  - Coculture Techniques
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/*drug effects/enzymology
MH  - Environmental Pollutants/*toxicity
MH  - ErbB Receptors/drug effects/metabolism
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Janus Kinases/metabolism
MH  - Leukocytes/drug effects/metabolism
MH  - Membrane Microdomains/*drug effects/enzymology
MH  - NADPH Oxidases/*metabolism
MH  - Oxidation-Reduction
MH  - Phosphorylation
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Protein Kinase Inhibitors/pharmacology
MH  - RNA Interference
MH  - Signal Transduction/*drug effects
MH  - Time Factors
MH  - U937 Cells
MH  - Up-Regulation
MH  - Vascular Cell Adhesion Molecule-1/metabolism
MH  - src-Family Kinases/metabolism
PMC - PMC2760772
MID - NIHMS135139
EDAT- 2009/07/28 09:00
MHDA- 2009/10/09 06:00
CRDT- 2009/07/28 09:00
PHST- 2009/05/30 00:00 [received]
PHST- 2009/07/17 00:00 [revised]
PHST- 2009/07/20 00:00 [accepted]
PHST- 2009/07/28 09:00 [entrez]
PHST- 2009/07/28 09:00 [pubmed]
PHST- 2009/10/09 06:00 [medline]
AID - S0041-008X(09)00303-2 [pii]
AID - 10.1016/j.taap.2009.07.022 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2009 Oct 15;240(2):299-305. doi:
      10.1016/j.taap.2009.07.022. Epub 2009 Jul 24.

PMID- 19467301
OWN - NLM
STAT- MEDLINE
DCOM- 20090730
LR  - 20211020
IS  - 1879-3169 (Electronic)
IS  - 0378-4274 (Linking)
VI  - 189
IP  - 2
DP  - 2009 Sep 10
TI  - Induction of gene pattern changes associated with dysfunctional lipid
      metabolism induced by dietary fat and exposure to a persistent organic
      pollutant.
PG  - 96-101
LID - 10.1016/j.toxlet.2009.05.008 [doi]
AB  - Environmental modulators of chronic diseases can include nutrition,
      lifestyle, as well as exposure to environmental toxicants such as
      persistent organic pollutants. A study was designed to explore gene
      expression changes as affected by both dietary fat and exposure to the
      polychlorinated biphenyl PCB77. Mice were fed for 4 months diets enriched
      with high-linoleic acid oils (20% and 40% as calories), and during the
      last 2 months half of each group was exposed to PCB77. Ribonucleic acids
      (RNA) were extracted from liver tissue to determine gene expression
      changes using DNA microarray analysis. Our microarray data demonstrated a
      significant interaction between dietary fat and PCB exposure. Deregulated
      genes were organized into patterns describing the interaction of diet and
      PCB exposure. Annotation of the deregulated genes matching these probe
      sets revealed a significant high-fat mediated induction of genes
      associated with fatty acid metabolism, triacylglycerol synthesis and
      cholesterol catabolism, which was down-regulated in animals exposed to
      PCB77. Many of these genes are regulated by the peroxisome proliferator
      activated receptor-alpha (PPARalpha), and changes in PPARalpha gene
      expression followed the same gene pattern as described above. These
      results provide insight into molecular mechanisms of how dietary fat can
      interact with environmental pollutants to compromise lipid metabolism.
FAU - Arzuaga, Xabier
AU  - Arzuaga X
AD  - Molecular and Cell Nutrition Laboratory, Department of Animal and Food
      Sciences, University of Kentucky, Lexington, KY 40536, USA.
FAU - Ren, Na
AU  - Ren N
FAU - Stromberg, Arnold
AU  - Stromberg A
FAU - Black, Esther P
AU  - Black EP
FAU - Arsenescu, Violeta
AU  - Arsenescu V
FAU - Cassis, Lisa A
AU  - Cassis LA
FAU - Majkova, Zuzana
AU  - Majkova Z
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P20 RR016481/RR/NCRR NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
GR  - P20 RR16481/RR/NCRR NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-12/ES/NIEHS NIH HHS/United States
GR  - P20 RR021954/RR/NCRR NIH HHS/United States
GR  - P20 RR021954-02/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20090523
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Dietary Fats)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Body Weight
MH  - Dietary Fats/*pharmacology
MH  - *Gene Expression Profiling
MH  - Gene Expression Regulation/*drug effects
MH  - Lipid Metabolism/*drug effects
MH  - Liver/anatomy & histology/drug effects
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Organ Size
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Protein Array Analysis
PMC - PMC2729430
MID - NIHMS119922
EDAT- 2009/05/27 09:00
MHDA- 2009/07/31 09:00
CRDT- 2009/05/27 09:00
PHST- 2009/04/07 00:00 [received]
PHST- 2009/05/08 00:00 [revised]
PHST- 2009/05/12 00:00 [accepted]
PHST- 2009/05/27 09:00 [entrez]
PHST- 2009/05/27 09:00 [pubmed]
PHST- 2009/07/31 09:00 [medline]
AID - S0378-4274(09)00255-0 [pii]
AID - 10.1016/j.toxlet.2009.05.008 [doi]
PST - ppublish
SO  - Toxicol Lett. 2009 Sep 10;189(2):96-101. doi:
      10.1016/j.toxlet.2009.05.008. Epub 2009 May 23.

PMID- 19265715
OWN - NLM
STAT- MEDLINE
DCOM- 20090609
LR  - 20211020
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 237
IP  - 1
DP  - 2009 May 15
TI  - Up-regulation of endothelial monocyte chemoattractant protein-1 by
      coplanar PCB77 is caveolin-1-dependent.
PG  - 1-7
LID - 10.1016/j.taap.2009.02.016 [doi]
AB  - Atherosclerosis, the primary cause of heart disease and stroke is
      initiated in the vascular endothelium, and risk factors for its
      development include environmental exposure to persistent organic
      pollutants. Caveolae are membrane microdomains involved in regulation of
      many signaling pathways, and in particular in endothelial cells. We
      tested the hypothesis that intact caveolae are required for coplanar
      PCB77-induced up-regulation of monocyte chemoattractant protein-1
      (MCP-1), an endothelium-derived chemokine that attracts monocytes into
      sub-endothelial space in early stages of the atherosclerosis development.
      Atherosclerosis-prone LDL-R(-/-) mice (control) or
      caveolin-1(-/-)/LDL-R(-/-) mice were treated with PCB77. PCB77 induced
      aortic mRNA expression and plasma protein levels of MCP-1 in control, but
      not caveolin-1(-/-)/LDL-R(-/-) mice. To study the mechanism of this
      effect, primary endothelial cells were used. PCB77 increased MCP-1 levels
      in endothelial cells in a time- and concentration-dependent manner. This
      effect was abolished by caveolin-1 silencing using siRNA. Also, MCP-1 up-
      regulation by PCB77 was prevented by inhibiting p38 and c-Jun N-terminal
      kinase (JNK), but not ERK1/2, suggesting regulatory functions via p38 and
      JNK MAPK pathways. Finally, pre-treatment of endothelial cells with the
      aryl hydrocarbon receptor (AhR) inhibitor alpha-naphthoflavone (alpha-NF)
      partially blocked MCP-1 up-regulation. Thus, our data demonstrate that
      coplanar PCB77 can induce MCP-1 expression by endothelial cells and that
      this effect is mediated by AhR, as well as p 38 and JNK MAPK pathways.
      Intact caveolae are required for these processes both in vivo and in
      vitro. This further supports a key role for caveolae in vascular
      inflammation induced by persistent organic pollutants.
FAU - Majkova, Zuzana
AU  - Majkova Z
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington, KY
      40536-0200, USA.
FAU - Smart, Eric
AU  - Smart E
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - R01 CA133257/CA/NCI NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
GR  - R01 NS039254-05/NS/NINDS NIH HHS/United States
GR  - R01 MH063022-05/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-139005/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - P42 ES007380-130009/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-12/ES/NIEHS NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20090302
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Caveolin 1)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Environmental Pollutants)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Receptors, LDL)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Atherosclerosis/chemically induced/genetics/*metabolism
MH  - Caveolae/drug effects/metabolism
MH  - Caveolin 1/*drug effects/genetics/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/drug effects/genetics/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/cytology/drug effects/*metabolism
MH  - Environmental Pollutants/*toxicity
MH  - Gene Expression Regulation/drug effects
MH  - Gene Silencing/physiology
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Polychlorinated Biphenyls/*toxicity
MH  - RNA, Messenger/analysis
MH  - RNA, Small Interfering/metabolism
MH  - Receptors, Aryl Hydrocarbon/drug effects/metabolism
MH  - Receptors, LDL/deficiency/genetics
MH  - Second Messenger Systems
MH  - Signal Transduction/drug effects/physiology
MH  - Statistics, Nonparametric
MH  - Swine
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC2680936
MID - NIHMS100416
EDAT- 2009/03/07 09:00
MHDA- 2009/06/10 09:00
CRDT- 2009/03/07 09:00
PHST- 2009/01/08 00:00 [received]
PHST- 2009/02/11 00:00 [revised]
PHST- 2009/02/13 00:00 [accepted]
PHST- 2009/03/07 09:00 [entrez]
PHST- 2009/03/07 09:00 [pubmed]
PHST- 2009/06/10 09:00 [medline]
AID - S0041-008X(09)00084-2 [pii]
AID - 10.1016/j.taap.2009.02.016 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2009 May 15;237(1):1-7. doi:
      10.1016/j.taap.2009.02.016. Epub 2009 Mar 2.

PMID- 19141539
OWN - NLM
STAT- MEDLINE
DCOM- 20090526
LR  - 20211020
IS  - 1530-6860 (Electronic)
IS  - 0892-6638 (Linking)
VI  - 23
IP  - 5
DP  - 2009 May
TI  - PPARalpha and PPARgamma attenuate HIV-induced dysregulation of tight
      junction proteins by modulations of matrix metalloproteinase and
      proteasome activities.
PG  - 1596-606
LID - 10.1096/fj.08-121624 [doi]
AB  - The blood-brain barrier (BBB) plays an important role in HIV trafficking
      into the brain and the development of the central nervous system
      complications in HIV infection. Tight junctions are the main structural
      and functional elements that regulate the BBB integrity. Exposure of
      human brain microvascular endothelial cells (hCMEC/D3 cell line) to HIV-
      infected monocytes resulted in decreased expression of tight junction
      proteins, such as junctional adhesion molecule-A (JAM)-A, occludin, and
      zonula occludens (ZO)-1. Control experiments involved exposure to
      uninfected monocytes. Alterations of tight junction protein expression
      were associated with increased endothelial permeability and elevated
      transendothelial migration of HIV-infected monocytes across an in vitro
      model of the BBB. Notably, overexpression of the peroxisome proliferator-
      activated receptor (PPAR)alpha or PPARgamma attenuated HIV-mediated
      dysregulation of tight junction proteins. With the use of exogenous
      PPARgamma agonists and silencing of PPARalpha or PPARgamma, these
      protective effects were connected to down-regulation of matrix
      metalloproteinase (MMP) and proteasome activities. Indeed, the HIV-
      induced decrease in the expression of JAM-A and occludin was restored by
      inhibition of MMP activity. Moreover, both MMP and proteasome inhibitors
      attenuated HIV-mediated altered expression of ZO-1. The present data
      indicate that down-regulation of MMP and proteasome activities
      constitutes a novel mechanism of PPAR-induced protections against HIV-
      induced disruption of brain endothelial cells.
FAU - Huang, Wen
AU  - Huang W
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky Medical Center, 593 Wethington
      Bldg., 900 S Limestone, Lexington, KY 40536, USA.
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - NS-39254/NS/NINDS NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - MH-072567/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH-63022/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20090113
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American
      Societies for Experimental Biology
JID - 8804484
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (F11R protein, human)
RN  - 0 (Immunoglobulins)
RN  - 0 (Membrane Proteins)
RN  - 0 (OCLN protein, human)
RN  - 0 (Occludin)
RN  - 0 (PPAR alpha)
RN  - 0 (PPAR gamma)
RN  - 0 (Phosphoproteins)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (TJP1 protein, human)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - EC 3.4.- (Endopeptidases)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
RN  - EC 3.4.99.- (peptidylglutamylpeptide hydrolase)
SB  - IM
MH  - Blood-Brain Barrier/*physiopathology
MH  - Brain/metabolism
MH  - Cell Adhesion Molecules/biosynthesis
MH  - Cell Line
MH  - Coculture Techniques
MH  - Endopeptidases/metabolism
MH  - Endothelial Cells/metabolism
MH  - Gene Silencing
MH  - HIV-1/*physiology
MH  - Humans
MH  - Immunoglobulins/biosynthesis
MH  - Matrix Metalloproteinase 2/metabolism
MH  - Matrix Metalloproteinase 9/metabolism
MH  - Membrane Proteins/biosynthesis
MH  - Occludin
MH  - PPAR alpha/*physiology
MH  - PPAR gamma/*physiology
MH  - Phosphoproteins/biosynthesis
MH  - Proteasome Endopeptidase Complex/*metabolism
MH  - Receptors, Cell Surface
MH  - Tight Junctions/*metabolism
MH  - Zonula Occludens-1 Protein
PMC - PMC2669424
EDAT- 2009/01/15 09:00
MHDA- 2009/05/27 09:00
CRDT- 2009/01/15 09:00
PHST- 2009/01/15 09:00 [entrez]
PHST- 2009/01/15 09:00 [pubmed]
PHST- 2009/05/27 09:00 [medline]
AID - fj.08-121624 [pii]
AID - 10.1096/fj.08-121624 [doi]
PST - ppublish
SO  - FASEB J. 2009 May;23(5):1596-606. doi: 10.1096/fj.08-121624. Epub 2009
      Jan 13.

PMID- 19418819
OWN - NLM
STAT- MEDLINE
DCOM- 20090701
LR  - 20211020
IS  - 1096-2247 (Print)
IS  - 1096-2247 (Linking)
VI  - 59
IP  - 4
DP  - 2009 Apr
TI  - Development and application of a three-dimensional finite element vapor
      intrusion model.
PG  - 447-60
AB  - Details of a three-dimensional finite element model of soil vapor
      intrusion, including the overall modeling process and the stepwise
      approach, are provided. The model is a quantitative modeling tool that
      can help guide vapor intrusion characterization efforts. It solves the
      soil gas continuity equation coupled with the chemical transport
      equation, allowing for both advective and diffusive transport. Three-
      dimensional pressure, velocity, and chemical concentration fields are
      produced from the model. Results from simulations involving common site
      features, such as impervious surfaces, porous foundation sub-base
      material, and adjacent structures are summarized herein. The results
      suggest that site-specific features are important to consider when
      characterizing vapor intrusion risks. More importantly, the results
      suggest that soil gas or subslab gas samples taken without proper regard
      for particular site features may not be suitable for evaluating vapor
      intrusion risks; rather, careful attention needs to be given to the many
      factors that affect chemical transport into and around buildings.
FAU - Pennell, Kelly G
AU  - Pennell KG
AD  - Division of Engineering, Brown University, Providence, RI 02912, USA.
      Kelly_pennell@brown.edu
FAU - Bozkurt, Ozgur
AU  - Bozkurt O
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42 ES013660-05/ES/NIEHS NIH HHS/United States
GR  - P42ES013660/ES/NIEHS NIH HHS/United States
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Air Waste Manag Assoc
JT  - Journal of the Air & Waste Management Association (1995)
JID - 9503111
RN  - 0 (Soil Pollutants)
RN  - 0 (Volatile Organic Compounds)
SB  - IM
MH  - Computer Simulation
MH  - Environmental Exposure
MH  - *Models, Chemical
MH  - Pressure
MH  - Risk Assessment
MH  - Soil Pollutants/*analysis/chemistry
MH  - Volatile Organic Compounds/*analysis/chemistry
PMC - PMC2835946
MID - NIHMS175349
EDAT- 2009/05/08 09:00
MHDA- 2009/07/02 09:00
CRDT- 2009/05/08 09:00
PHST- 2009/05/08 09:00 [entrez]
PHST- 2009/05/08 09:00 [pubmed]
PHST- 2009/07/02 09:00 [medline]
AID - 10.3155/1047-3289.59.4.447 [doi]
PST - ppublish
SO  - J Air Waste Manag Assoc. 2009 Apr;59(4):447-60. doi:
      10.3155/1047-3289.59.4.447.

PMID- 18656337
OWN - NLM
STAT- MEDLINE
DCOM- 20090326
LR  - 20211020
IS  - 0955-2863 (Print)
IS  - 0955-2863 (Linking)
VI  - 20
IP  - 3
DP  - 2009 Mar
TI  - Role of caveolin-1 in EGCG-mediated protection against linoleic-acid-
      induced endothelial cell activation.
PG  - 202-9
LID - 10.1016/j.jnutbio.2008.02.004 [doi]
AB  - Flavonoids can protect against inflammatory diseases such as
      atherosclerosis by decreasing vascular endothelial cell activation.
      Plasma microdomains called caveolae may be critical in regulating
      endothelial activation. Caveolae are particularly abundant in endothelial
      cells and play a major role in endothelial trafficking and the regulation
      of signaling pathways associated with the pathology of vascular diseases.
      We hypothesize that flavonoids can down-regulate endothelial inflammatory
      parameters by modulating caveolae-regulated cell signaling. We focused on
      the role of caveolae and its major protein, caveolin-1, in mechanisms of
      linoleic-acid-induced endothelial cell activation and protection by the
      catechin epigallocatechin-3-gallate (EGCG). Exposure to linoleic acid for
      6 h induced expression of both caveolin-1 and cyclooxygenase (COX)-2.
      Pretreatment with EGCG blocked fatty-acid-induced caveolin-1 and COX-2
      expression in a time- and concentration-dependent manner. Similar results
      were observed with nuclear factor-kappa B DNA binding activity, which was
      also reduced by caveolin-1 silencing. Exposure to linoleic acid rapidly
      increased phosphorylation of several kinases, including p38 MAPK,
      extracellular signal regulated kinase 1/2 (ERK1/2) and amino kinase
      terminal (Akt), with maximal induction at about 10 min. Inhibitors of
      ERK1/2 and Akt down-regulated the linoleic-acid-induced increase in COX-2
      protein, which also occurred after pretreatment with EGCG. Caveolin-1
      silencing blocked linoleic-acid-induced phosphorylation of ERK1/2 and
      protein expression of COX-2, suggesting that specific MAPK signaling is
      caveolae dependent. Our data provide evidence that caveolae may play a
      critical role in regulating vascular endothelial cell activation and
      protection by flavonoids such as EGCG.
FAU - Zheng, Yuanyuan
AU  - Zheng Y
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, 40536-0200, USA.
FAU - Lim, Eum Jin
AU  - Lim EJ
FAU - Wang, Lei
AU  - Wang L
FAU - Smart, Eric J
AU  - Smart EJ
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-11/ES/NIEHS NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080724
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Caveolin 1)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Small Interfering)
RN  - 8R1V1STN48 (Catechin)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Caveolin 1/*physiology
MH  - Cell Line
MH  - Cyclooxygenase 2/biosynthesis
MH  - Down-Regulation
MH  - Endothelium, Vascular/*drug effects/*metabolism
MH  - Humans
MH  - Linoleic Acid/*pharmacology
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - NF-kappa B/drug effects/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Small Interfering/pharmacology
MH  - Up-Regulation
PMC - PMC2655117
MID - NIHMS95616
EDAT- 2008/07/29 09:00
MHDA- 2009/03/27 09:00
CRDT- 2008/07/29 09:00
PHST- 2007/10/15 00:00 [received]
PHST- 2008/01/29 00:00 [revised]
PHST- 2008/02/06 00:00 [accepted]
PHST- 2008/07/29 09:00 [pubmed]
PHST- 2009/03/27 09:00 [medline]
PHST- 2008/07/29 09:00 [entrez]
AID - S0955-2863(08)00052-1 [pii]
AID - 10.1016/j.jnutbio.2008.02.004 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2009 Mar;20(3):202-9. doi: 10.1016/j.jnutbio.2008.02.004.
      Epub 2008 Jul 24.

PMID- 18717615
OWN - NLM
STAT- MEDLINE
DCOM- 20090508
LR  - 20211020
IS  - 0730-7268 (Print)
IS  - 0730-7268 (Linking)
VI  - 28
IP  - 1
DP  - 2009 Jan
TI  - Evaluation of the effects of coal fly ash amendments on the toxicity of a
      contaminated marine sediment.
PG  - 26-35
LID - 10.1897/08-050.1 [doi]
AB  - Approaches for cleaning up contaminated sediments range from dredging to
      in situ treatment. In this study, we discuss the effects of amending
      reference and contaminated sediments with coal fly ash to reduce the
      bioavailability and toxicity of a field sediment contaminated with
      polycyclic aromatic hydrocarbons (PAHs). Six fly ashes and a coconut
      charcoal were evaluated in 7-d whole sediment toxicity tests with a
      marine amphipod (Ampelisca abdita) and mysid (Americamysis bahia). Fly
      ashes with high carbon content and the coconut charcoal showed
      proficiency at reducing toxicity. Some of the fly ashes demonstrated
      toxicity in the reference treatments. It is suspected that some of this
      toxicity is related to the presence of ammonia associated with fly ashes
      as a result of postoxidation treatment to reduce nitrous oxide emissions.
      Relatively simple methods exist to remove ammonia from fly ash before
      use, and fly ashes with low ammonia content are available. Fly ashes were
      also shown to effectively reduce overlying water concentrations of
      several PAHs. No evidence was seen of the release of the metals cadmium,
      copper, nickel, or lead from the fly ashes. A preliminary 28-d polychaete
      bioaccumulation study with one of the high-carbon fly ashes and a
      reference sediment was also performed. Although preliminary, no evidence
      was seen of adverse effects to worm growth or lipid content or of
      accumulation of PAHs or mercury from exposure to the fly ash. These data
      show fly ashes with high carbon content could represent viable remedial
      materials for reducing the bioavailability of organic contaminants in
      sediments.
FAU - Burgess, Robert M
AU  - Burgess RM
AD  - U.S. Environmental Protection Agency, Office of Research and Development,
      National Health and Environmental Effects Research Laboratory, 27
      Tarzwell Drive, Narragansett, Rhode Island 02882, USA.
      burgess.robert@epa.gov
FAU - Perron, Monique M
AU  - Perron MM
FAU - Friedman, Carey L
AU  - Friedman CL
FAU - Suuberg, Eric M
AU  - Suuberg EM
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Cantwell, Mark G
AU  - Cantwell MG
FAU - Pelletier, Marguerite C
AU  - Pelletier MC
FAU - Ho, Kay T
AU  - Ho KT
FAU - Serbst, Jonathan R
AU  - Serbst JR
FAU - Ryba, Stephan A
AU  - Ryba SA
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Environ Toxicol Chem
JT  - Environmental toxicology and chemistry
JID - 8308958
RN  - 0 (Coal)
RN  - 0 (Coal Ash)
RN  - 0 (Metals)
RN  - 0 (Particulate Matter)
RN  - 0 (Polycyclic Compounds)
RN  - 0 (Water Pollutants, Chemical)
RN  - 7440-44-0 (Carbon)
SB  - IM
MH  - Biological Availability
MH  - *Carbon
MH  - *Coal
MH  - Coal Ash
MH  - Geologic Sediments/*chemistry
MH  - Metals/toxicity
MH  - *Particulate Matter
MH  - Polycyclic Compounds/pharmacokinetics/*toxicity
MH  - Seawater/*chemistry
MH  - Water Pollutants, Chemical/pharmacokinetics/*toxicity
PMC - PMC3640504
MID - NIHMS461385
EDAT- 2008/08/23 09:00
MHDA- 2009/05/09 09:00
CRDT- 2008/08/23 09:00
PHST- 2008/01/30 00:00 [received]
PHST- 2008/07/08 00:00 [accepted]
PHST- 2008/08/23 09:00 [pubmed]
PHST- 2009/05/09 09:00 [medline]
PHST- 2008/08/23 09:00 [entrez]
AID - 08-050 [pii]
AID - 10.1897/08-050.1 [doi]
PST - ppublish
SO  - Environ Toxicol Chem. 2009 Jan;28(1):26-35. doi: 10.1897/08-050.1.

PMID- 20664816
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211020
IS  - 1069-3629 (Print)
IS  - 1069-3629 (Linking)
VI  - 29
IP  - 1
DP  - 2009 Jan 1
TI  - Simulation of the Vapor Intrusion Process for Non-Homogeneous Soils Using
      a Three-Dimensional Numerical Model.
PG  - 92-104
AB  - This paper presents model simulation results of vapor intrusion into
      structures built atop sites contaminated with volatile or semi-volatile
      chemicals of concern. A three-dimensional finite element model was used
      to investigate the importance of factors that could influence vapor
      intrusion when the site is characterized by non-homogeneous soils. Model
      simulations were performed to examine how soil layers of differing
      properties alter soil gas concentration profiles and vapor intrusion
      rates into structures. The results illustrate difference in soil gas
      concentration profiles and vapor intrusion rates between homogeneous and
      layered soils. The findings support the need for site conceptual models
      to adequately represent the site's geology when conducting site
      characterizations, interpreting field data and assessing the risk of
      vapor intrusion at a given site. For instance, in layered geologies, a
      lower permeability and diffusivity soil layer between the source and
      building often limits vapor intrusion rates, even if a higher
      permeability layer near the foundation permits increased soil gas flow
      rates into the building. In addition, the presence of water-saturated
      clay layers can considerably influence soil gas concentration profiles.
      Therefore, interpreting field data without accounting for clay layers in
      the site conceptual model could result in inaccurate risk calculations.
      Important considerations for developing more accurate conceptual site
      models are discussed in light of the findings.
FAU - Bozkurt, Ozgur
AU  - Bozkurt O
AD  - Brown University, Division of Engineering.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Suuberg, Eric M
AU  - Suuberg EM
LA  - eng
GR  - P42 ES013660/ES/NIEHS NIH HHS/United States
GR  - P42 ES013660-05/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Ground Water Monit Remediat
JT  - Ground water monitoring & remediation
JID - 100911134
PMC - PMC2907115
MID - NIHMS175352
EDAT- 2009/01/01 00:00
MHDA- 2009/01/01 00:01
CRDT- 2010/07/29 06:00
PHST- 2010/07/29 06:00 [entrez]
PHST- 2009/01/01 00:00 [pubmed]
PHST- 2009/01/01 00:01 [medline]
AID - 10.1111/j.1745-6592.2008.01218.x [doi]
PST - ppublish
SO  - Ground Water Monit Remediat. 2009 Jan 1;29(1):92-104. doi:
      10.1111/j.1745-6592.2008.01218.x.

PMID- 18830698
OWN - NLM
STAT- MEDLINE
DCOM- 20090303
LR  - 20181128
IS  - 1557-1904 (Electronic)
IS  - 1557-1890 (Linking)
VI  - 3
IP  - 4
DP  - 2008 Dec
TI  - Manufactured aluminum oxide nanoparticles decrease expression of tight
      junction proteins in brain vasculature.
PG  - 286-95
LID - 10.1007/s11481-008-9131-5 [doi]
AB  - Manufactured nanoparticles of aluminum oxide (nano-alumina) have been
      widely used in the environment; however, their potential toxicity
      provides a growing concern for human health. The present study focuses on
      the hypothesis that nano-alumina can affect the blood-brain barrier and
      induce endothelial toxicity. In the first series of experiments, human
      brain microvascular endothelial cells (HBMEC) were exposed to alumina and
      control nanoparticles in dose- and time-responsive manners. Treatment
      with nano-alumina markedly reduced HBMEC viability, altered mitochondrial
      potential, increased cellular oxidation, and decreased tight junction
      protein expression as compared to control nanoparticles. Alterations of
      tight junction protein levels were prevented by cellular enrichment with
      glutathione. In the second series of experiments, rats were infused with
      nano-alumina at the dose of 29 mg/kg and the brains were stained for
      expression of tight junction proteins. Treatment with nano-alumina
      resulted in a marked fragmentation and disruption of integrity of
      claudin-5 and occludin. These results indicate that cerebral vasculature
      can be affected by nano-alumina. In addition, our data indicate that
      alterations of mitochondrial functions may be the underlying mechanism of
      nano-alumina toxicity.
FAU - Chen, Lei
AU  - Chen L
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky Medical Center, 593 Wethington
      Bldg., 900 S Limestone, Lexington, KY 40536, USA.
FAU - Yokel, Robert A
AU  - Yokel RA
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 CA133257/CA/NCI NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - P42 ES07380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-129005/ES/NIEHS NIH HHS/United States
GR  - R01 MH063022-05/MH/NIMH NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 MH063022-07/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-130009/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20081001
PL  - United States
TA  - J Neuroimmune Pharmacol
JT  - Journal of neuroimmune pharmacology : the official journal of the Society
      on NeuroImmune Pharmacology
JID - 101256586
RN  - 0 (Antioxidants)
RN  - 0 (Claudin-5)
RN  - 0 (Cldn5 protein, rat)
RN  - 0 (Membrane Proteins)
RN  - 0 (OCLN protein, human)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, rat)
RN  - GAN16C9B8O (Glutathione)
RN  - LMI26O6933 (Aluminum Oxide)
SB  - IM
MH  - Aluminum Oxide/*toxicity
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Blood-Brain Barrier/*drug effects
MH  - Brain/blood supply/*drug effects/pathology
MH  - Cerebrovascular Circulation/*drug effects
MH  - Claudin-5
MH  - Cytoskeleton/drug effects/pathology
MH  - Endothelial Cells/drug effects
MH  - Glutathione/pharmacology
MH  - Humans
MH  - Membrane Proteins/drug effects
MH  - Metal Nanoparticles/*toxicity
MH  - Microvessels/drug effects
MH  - Mitochondria/drug effects/pathology
MH  - Occludin
MH  - Oxidative Stress/drug effects
MH  - Rats
MH  - Rats, Inbred F344
MH  - Tight Junctions/*drug effects
PMC - PMC2771674
MID - NIHMS115911
EDAT- 2008/10/03 09:00
MHDA- 2009/03/04 09:00
CRDT- 2008/10/03 09:00
PHST- 2008/05/21 00:00 [received]
PHST- 2008/09/17 00:00 [accepted]
PHST- 2008/10/03 09:00 [pubmed]
PHST- 2009/03/04 09:00 [medline]
PHST- 2008/10/03 09:00 [entrez]
AID - 10.1007/s11481-008-9131-5 [doi]
PST - ppublish
SO  - J Neuroimmune Pharmacol. 2008 Dec;3(4):286-95. doi:
      10.1007/s11481-008-9131-5. Epub 2008 Oct 1.

PMID- 18423858
OWN - NLM
STAT- MEDLINE
DCOM- 20090129
LR  - 20211020
IS  - 0304-3894 (Print)
IS  - 0304-3894 (Linking)
VI  - 159
IP  - 2-3
DP  - 2008 Nov 30
TI  - Reductive dechlorination of 3,3',4,4'-tetrachlorobiphenyl (PCB77) using
      palladium or palladium/iron nanoparticles and assessment of the reduction
      in toxic potency in vascular endothelial cells.
PG  - 483-91
LID - 10.1016/j.jhazmat.2008.02.109 [doi]
AB  - Palladium-based nanoparticles immobilized in polymeric matrices were
      applied to the reductive dechlorination of 3,3',4,4'-tetrachlorobiphenyl
      (PCB77) at room temperature. Two different dechlorination platforms were
      evaluated using (1) Pd nanoparticles within conductive polypyrrole films;
      or (2) immobilized Fe/Pd nanoparticles within polyvinylidene fluoride
      microfiltration membranes. For the first approach, the polypyrrole film
      was electrochemically formed in the presence of perchlorate ions that
      were incorporated into the film to counter-balance the positive charges
      of the polypyrrole chain. The film was then incubated in a solution
      containing tetrachloropalladate ions, which were exchanged with the
      perchlorate ions within the film. During this exchange, reduction of
      tetrachloropalladate by polypyrrole occurred, which led to the formation
      of palladium nanoparticles within the film. For the second approach, the
      membrane-supported Fe/Pd nanoparticles were prepared in three steps:
      polymerization of acrylic acid in polyvinylidene fluoride microfiltration
      membrane pores was followed by ion exchange of Fe(2+), and then chemical
      reduction of the ferrous ions bound to the carboxylate groups. The
      membrane-supported iron nanoparticles were then soaked in a solution of
      tetrachloropalladate resulting in the deposition of Pd on the Fe surface.
      The nanoparticles prepared by both approaches were employed in the
      dechlorination of PCB77. The presence of hydrogen was required when the
      monometallic Pd nanoparticles were employed. The results indicate the
      removal of chlorine atoms from PCB77, which led to the formation of lower
      chlorinated intermediates and ultimately biphenyl. Toxicity associated
      with vascular dysfunction by PCB77 and biphenyl was compared using
      cultured endothelial cells. The data strongly suggest that the
      dechlorination system used in this study markedly reduced the
      proinflammatory activity of PCB77, a persistent organic pollutant.
FAU - Venkatachalam, Karthik
AU  - Venkatachalam K
AD  - Department of Chemistry, University of Kentucky, Lexington, KY 40506,
      United States.
FAU - Arzuaga, Xabier
AU  - Arzuaga X
FAU - Chopra, Nitin
AU  - Chopra N
FAU - Gavalas, Vasilis G
AU  - Gavalas VG
FAU - Xu, Jian
AU  - Xu J
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Bachas, Leonidas G
AU  - Bachas LG
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-12/ES/NIEHS NIH HHS/United States
GR  - P42 ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20080306
PL  - Netherlands
TA  - J Hazard Mater
JT  - Journal of hazardous materials
JID - 9422688
RN  - 0 (Environmental Pollutants)
RN  - 0 (Indicators and Reagents)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 5TWQ1V240M (Palladium)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - E1UOL152H7 (Iron)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Cyclooxygenase 2/metabolism
MH  - Cytochrome P-450 CYP1A1/metabolism
MH  - Electrochemistry
MH  - Endothelial Cells/*drug effects
MH  - Environmental Pollutants/*chemistry/*toxicity
MH  - Gas Chromatography-Mass Spectrometry
MH  - Indicators and Reagents
MH  - Iron/*chemistry
MH  - Microscopy, Electron, Transmission
MH  - Myocytes, Smooth Muscle/*drug effects
MH  - Nanoparticles
MH  - Oxidation-Reduction
MH  - Palladium/*chemistry
MH  - Particle Size
MH  - Polychlorinated Biphenyls/*chemistry/*toxicity
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/metabolism
PMC - PMC3247144
MID - NIHMS76287
EDAT- 2008/04/22 09:00
MHDA- 2009/01/30 09:00
CRDT- 2008/04/22 09:00
PHST- 2007/05/04 00:00 [received]
PHST- 2007/11/16 00:00 [revised]
PHST- 2008/02/18 00:00 [accepted]
PHST- 2008/04/22 09:00 [pubmed]
PHST- 2009/01/30 09:00 [medline]
PHST- 2008/04/22 09:00 [entrez]
AID - S0304-3894(08)00277-X [pii]
AID - 10.1016/j.jhazmat.2008.02.109 [doi]
PST - ppublish
SO  - J Hazard Mater. 2008 Nov 30;159(2-3):483-91. doi:
      10.1016/j.jhazmat.2008.02.109. Epub 2008 Mar 6.

PMID- 18786521
OWN - NLM
STAT- MEDLINE
DCOM- 20090121
LR  - 20211020
IS  - 1872-7786 (Electronic)
IS  - 0009-2797 (Linking)
VI  - 176
IP  - 2-3
DP  - 2008 Nov 25
TI  - Coplanar polychlorinated biphenyl-induced CYP1A1 is regulated through
      caveolae signaling in vascular endothelial cells.
PG  - 71-8
LID - 10.1016/j.cbi.2008.08.007 [doi]
AB  - Polychlorinated biphenyls (PCBs) are persistent environmental
      contaminants that can induce inflammatory processes in the vascular
      endothelium. We hypothesize that the plasma membrane microdomains called
      caveolae are critical in endothelial activation and toxicity induced by
      PCBs. Caveolae are particularly abundant in endothelial cells and play a
      major role in endothelial trafficking and the regulation of signaling
      pathways associated with the pathology of vascular diseases. We focused
      on the role of caveolae and their major protein component, caveolin-1
      (Cav-1), on aryl hydrocarbon receptor (AhR)-mediated induction of
      cytochrome P450 1A1 (CYP1A1) by coplanar PCBs. Endothelial cell exposure
      to PCB77 increased both caveolin-1 and CYP1A1 levels in a time-dependent
      manner in total cell lysates, with a maximum increase at 6h. Furthermore,
      PCB77 accumulated mainly in the caveolae-rich fraction, as determined by
      gas chromatograph-mass spectrometry. Immunoprecipitation analysis
      revealed that PCB77 increased AhR binding to caveolin-1. Silencing of
      caveolin-1 significantly attenuated PCB77-mediated induction of CYP1A1
      and oxidative stress. Similar effects were observed in caveolin-1 null
      mice treated with PCB77. These data suggest that caveolae may play a role
      in regulating vascular toxicity induced by persistent environmental
      pollutants such as coplanar PCBs. This may have implications in
      understanding mechanisms of inflammatory diseases induced by
      environmental pollutants.
FAU - Lim, Eun Jin
AU  - Lim EJ
AD  - Molecular and Cell Nutrition Laboratory, Department of Chemistry, College
      of Agriculture, University of Kentucky, Lexington, KY 40536, USA.
FAU - Majkova, Zuzana
AU  - Majkova Z
FAU - Xu, Shifen
AU  - Xu S
FAU - Bachas, Leonidas
AU  - Bachas L
FAU - Arzuaga, Xabier
AU  - Arzuaga X
FAU - Smart, Eric
AU  - Smart E
FAU - Tseng, Michael T
AU  - Tseng MT
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-11/ES/NIEHS NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080822
PL  - Ireland
TA  - Chem Biol Interact
JT  - Chemico-biological interactions
JID - 0227276
RN  - 0 (Caveolin 1)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Receptors, LDL)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Caveolae/*drug effects/*metabolism
MH  - Caveolin 1/deficiency/metabolism
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/cytology/*drug effects/metabolism
MH  - Enzyme Induction/drug effects
MH  - Female
MH  - Male
MH  - Mice
MH  - Mice, Nude
MH  - Oxidative Stress/drug effects
MH  - Polychlorinated Biphenyls/*pharmacology
MH  - Receptors, Aryl Hydrocarbon/metabolism
MH  - Receptors, LDL/deficiency/metabolism
MH  - Signal Transduction/*drug effects
MH  - Time Factors
PMC - PMC2603293
MID - NIHMS80101
EDAT- 2008/09/13 09:00
MHDA- 2009/01/22 09:00
CRDT- 2008/09/13 09:00
PHST- 2008/05/30 00:00 [received]
PHST- 2008/08/07 00:00 [revised]
PHST- 2008/08/12 00:00 [accepted]
PHST- 2008/09/13 09:00 [pubmed]
PHST- 2009/01/22 09:00 [medline]
PHST- 2008/09/13 09:00 [entrez]
AID - S0009-2797(08)00405-5 [pii]
AID - 10.1016/j.cbi.2008.08.007 [doi]
PST - ppublish
SO  - Chem Biol Interact. 2008 Nov 25;176(2-3):71-8. doi:
      10.1016/j.cbi.2008.08.007. Epub 2008 Aug 22.

PMID- 18671994
OWN - NLM
STAT- MEDLINE
DCOM- 20081106
LR  - 20211020
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 232
IP  - 2
DP  - 2008 Oct 15
TI  - Benzo[a]pyrene induces intercellular adhesion molecule-1 through a
      caveolae and aryl hydrocarbon receptor mediated pathway.
PG  - 309-16
LID - 10.1016/j.taap.2008.07.001 [doi]
AB  - Toxicologic and epidemiologic studies have linked benzo[a]pyrene (B[a]P)
      exposure with cardiovascular diseases such as atherosclerosis. The
      mechanisms of action leading to these diseases have not been fully
      understood. One key step in the development of atherosclerosis is
      vascular endothelial dysfunction, which is characterized by increased
      adhesiveness. To determine if B[a]P could lead to increased endothelial
      adhesiveness, the effects of B[a]P on human endothelial cell
      intercellular adhesion molecule-1 (ICAM-1) expression was investigated.
      B[a]P was able to increase ICAM-1 protein only after pretreatment with
      the aryl hydrocarbon receptor (AhR) agonist beta-naphthoflavone (beta-
      NF). Knockdown of AhR by siRNA or treatment with AhR antagonist alpha-
      naphthoflavone (alpha-NF) eliminated the induction of ICAM-1 from B[a]P,
      confirming the necessity of AhR in this process. Likewise, B[a]P only
      increased monocyte adhesion to the vascular endothelium when cells were
      pretreated with beta-NF. Experiments were done to define a signaling
      mechanism. B[a]P increased phosphorylation of MEK and p38-MAPK, and
      inhibitors to these proteins blunted the ICAM-1 induction. B[a]P was also
      able to increase AP-1 DNA binding and phosphorylation of cJun.
      Phosphorylation of cJun was disrupted by MEK and p38-MAPK inhibitors
      linking the signaling cascade. Finally, the importance of membrane
      microdomains, caveolae, was demonstrated by knockdown of the structural
      protein caveolin-1. Disruption of caveolae eliminated the B[a]P-induced
      ICAM-1 expression. These data suggest a possible pro-inflammatory
      mechanism of action of B[a]P involving caveolae, leading to increased
      vascular endothelial adhesiveness, and this inflammation may be a
      critical step in the development of B[a]P-induced atherosclerosis.
FAU - Oesterling, Elizabeth
AU  - Oesterling E
AD  - Graduate Center for Toxicology, College of Medicine, University of
      Kentucky, Lexington, KY 40536-0200, USA.
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-11/ES/NIEHS NIH HHS/United States
GR  - T32ES07266/ES/NIEHS NIH HHS/United States
GR  - P42ES07380/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080711
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 3417WMA06D (Benzo(a)pyrene)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Benzo(a)pyrene/*toxicity
MH  - Cardiovascular Diseases/chemically induced/enzymology/*metabolism
MH  - Caveolae/drug effects/enzymology/*physiology
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/physiology
MH  - Endothelium, Vascular/drug effects/enzymology/physiology
MH  - Extracellular Signal-Regulated MAP Kinases/drug effects/*physiology
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*biosynthesis/genetics/physiology
MH  - Receptors, Aryl Hydrocarbon/*biosynthesis/genetics/physiology
PMC - PMC2633733
MID - NIHMS73626
EDAT- 2008/08/02 09:00
MHDA- 2008/11/07 09:00
CRDT- 2008/08/02 09:00
PHST- 2008/05/28 00:00 [received]
PHST- 2008/06/30 00:00 [revised]
PHST- 2008/07/01 00:00 [accepted]
PHST- 2008/08/02 09:00 [pubmed]
PHST- 2008/11/07 09:00 [medline]
PHST- 2008/08/02 09:00 [entrez]
AID - S0041-008X(08)00287-1 [pii]
AID - 10.1016/j.taap.2008.07.001 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2008 Oct 15;232(2):309-16. doi:
      10.1016/j.taap.2008.07.001. Epub 2008 Jul 11.

PMID- 18710415
OWN - NLM
STAT- MEDLINE
DCOM- 20081224
LR  - 20211020
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 107
IP  - 2
DP  - 2008 Oct
TI  - PPARalpha and PPARgamma effectively protect against HIV-induced
      inflammatory responses in brain endothelial cells.
PG  - 497-509
LID - 10.1111/j.1471-4159.2008.05626.x [doi]
AB  - Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors
      which down-regulate inflammatory signaling pathways. Therefore, we
      hypothesized that alterations of PPAR functions can contribute to human
      immunodeficiency virus-1 (HIV-1)-induced dysfunction of brain endothelial
      cells. Indeed, treatment with HIV-1 transactivator of transcription (Tat)
      protein decreased PPAR transactivation in brain endothelial cells. We
      next stably over-expressed PPARalpha and PPARgamma in a newly developed
      cell line of human brain endothelial cells (hCMEC/D3 cells). Tat-induced
      up-regulation of inflammatory mediators, such as interleukin (IL)-1beta,
      tumor necrosis factor-alpha, CCL2, and E-selectin were markedly
      attenuated in hCMEC/D3 over-expressing PPARalpha or PPARgamma. These
      results were confirmed in CCL2 and E-selectin promoter activity studies.
      Similar protective effects were observed in hCMEC/D3 after activation of
      PPARgamma by exogenous PPAR agonists (dPGJ(2) and rosiglitazone). PPAR
      over-expression also prevented Tat-induced binding activity and
      transactivation of nuclear factor-kappaB. Importantly, increased PPAR
      activity attenuated induction of IL-1beta, tumor necrosis factor-alpha,
      CCL2, and E-selectin in hCMEC/D3 cells co-cultured with HIV-1-infected
      Jurkat cells. The protective effects of PPAR over-expression were
      reversed by the antagonists of PPARalpha (MK886) or PPARgamma (GW9662).
      The present data suggest that targeting PPAR signaling may provide a
      novel therapeutic approach to attenuate HIV-1-induced local inflammatory
      responses in brain endothelial cells.
FAU - Huang, Wen
AU  - Huang W
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, Kentucky, USA.
FAU - Rha, Geun Bae
AU  - Rha GB
FAU - Han, Min-Joon
AU  - Han MJ
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Zhong, Yu
AU  - Zhong Y
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P20 RR15592/RR/NCRR NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P20 RR015592/RR/NCRR NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - P42 ES007380-090007/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 NS039254-07/NS/NINDS NIH HHS/United States
GR  - R01 MH063022-06A2/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
GR  - MH72567/MH/NIMH NIH HHS/United States
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20080814
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Cytokines)
RN  - 0 (E-Selectin)
RN  - 0 (Gene Products, tat)
RN  - 0 (PPAR alpha)
RN  - 0 (PPAR gamma)
RN  - 60203-57-8 (9-deoxy-delta-9-prostaglandin D2)
RN  - RXY07S6CZ2 (Prostaglandin D2)
SB  - IM
MH  - Antineoplastic Agents/pharmacology
MH  - Brain/anatomy & histology
MH  - Cell Line, Transformed
MH  - Cytokines/metabolism
MH  - Dose-Response Relationship, Drug
MH  - E-Selectin/metabolism
MH  - Endothelial Cells/drug effects/*metabolism/*virology
MH  - Gene Products, tat/pharmacology
MH  - HIV/*physiology
MH  - Humans
MH  - Microvessels/*cytology
MH  - PPAR alpha/*metabolism
MH  - PPAR gamma/*metabolism
MH  - Prostaglandin D2/analogs & derivatives/pharmacology
MH  - Transcriptional Activation/drug effects
MH  - Transfection/methods
MH  - Up-Regulation/drug effects
PMC - PMC2597373
MID - NIHMS70510
EDAT- 2008/08/20 09:00
MHDA- 2008/12/25 09:00
CRDT- 2008/08/20 09:00
PHST- 2008/08/20 09:00 [pubmed]
PHST- 2008/12/25 09:00 [medline]
PHST- 2008/08/20 09:00 [entrez]
AID - JNC5626 [pii]
AID - 10.1111/j.1471-4159.2008.05626.x [doi]
PST - ppublish
SO  - J Neurochem. 2008 Oct;107(2):497-509. doi:
      10.1111/j.1471-4159.2008.05626.x. Epub 2008 Aug 14.

PMID- 18803934
OWN - NLM
STAT- MEDLINE
DCOM- 20081010
LR  - 20181113
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
VI  - 57
IP  - 10
DP  - 2008 Oct
TI  - The role of fatty acids and caveolin-1 in tumor necrosis factor alpha-
      induced endothelial cell activation.
PG  - 1328-39
LID - 10.1016/j.metabol.2008.01.036 [doi]
AB  - Hypertriglyceridemia and associated high circulating free fatty acids are
      important risk factors for atherosclerosis. In contrast to omega-3 fatty
      acids, linoleic acid, the major omega-6 unsaturated fatty acid in the
      American diet, may be atherogenic by amplifying an endothelial
      inflammatory response. We hypothesize that omega-6 and omega-3 fatty
      acids can differentially modulate tumor necrosis factor alpha (TNF-
      alpha)-induced endothelial cell activation and that functional plasma
      membrane microdomains called caveolae are required for endothelial cell
      activation. Caveolae are particularly abundant in endothelial cells and
      play a major role in endothelial trafficking and the regulation of
      signaling pathways associated with the pathology of vascular diseases. To
      test our hypothesis, endothelial cells were preenriched with either
      linoleic acid or alpha-linolenic acid before TNF-alpha-induced
      endothelial activation. Measurements included oxidative stress and
      nuclear factor kappaB-dependent induction of cyclooxygenase-2 (COX-2) and
      prostaglandin E(2) (PGE(2)) under experimental conditions with intact
      caveolae and with cells in which caveolin-1 was silenced by small
      interfering RNA. Exposure to TNF-alpha induced oxidative stress and
      inflammatory mediators, such as p38 mitogen-activated protein kinase
      (MAPK), nuclear factor kappaB, COX-2, and PGE(2), which were all
      amplified by preenrichment with linoleic acid but blocked or reduced by
      alpha-linolenic acid. The p38 MAPK inhibitor SB203580 blocked TNF-alpha-
      mediated induction of COX-2 protein expression, suggesting a regulatory
      mechanism through p38 MAPK signaling. Image overlay demonstrated TNF-
      alpha-induced colocalization of TNF receptor type 1 with caveolin-1.
      Caveolin-1 was significantly induced by TNF-alpha, which was further
      amplified by linoleic acid and blocked by alpha-linolenic acid.
      Furthermore, silencing of the caveolin-1 gene completely blocked TNF-
      alpha-induced production of COX-2 and PGE(2) and significantly reduced
      the amplified response of linoleic acid plus TNF-alpha. These data
      suggest that omega-6 and omega-3 fatty acids can differentially modulate
      TNF-alpha-induced inflammatory stimuli and that caveolae and its fatty
      acid composition play a regulatory role during TNF-alpha-induced
      endothelial cell activation and inflammation.
FAU - Wang, Lei
AU  - Wang L
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington KY 40536, USA.
FAU - Lim, Eun-Jin
AU  - Lim EJ
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Caveolin 1)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (NF-kappa B)
RN  - 0 (Pyridines)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0RBV727H71 (alpha-Linolenic Acid)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - K7Q1JQR04M (Dinoprostone)
RN  - OU13V1EYWQ (SB 203580)
SB  - IM
MH  - Animals
MH  - Caveolae/metabolism
MH  - Caveolin 1/biosynthesis/genetics/metabolism
MH  - Cyclooxygenase 2/biosynthesis
MH  - Cyclooxygenase Inhibitors/pharmacology
MH  - Dinoprostone/immunology
MH  - Endothelial Cells/*drug effects/*metabolism
MH  - Enzyme Activation/drug effects
MH  - Imidazoles/pharmacology
MH  - Linoleic Acid/*pharmacology
MH  - NF-kappa B/metabolism
MH  - Oxidative Stress/drug effects
MH  - Pyridines/pharmacology
MH  - RNA, Small Interfering/pharmacology
MH  - Receptors, Tumor Necrosis Factor, Type I/metabolism
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Up-Regulation/drug effects
MH  - alpha-Linolenic Acid/*pharmacology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC3349996
MID - NIHMS71935
EDAT- 2008/09/23 09:00
MHDA- 2008/10/11 09:00
CRDT- 2008/09/23 09:00
PHST- 2007/11/14 00:00 [received]
PHST- 2008/01/31 00:00 [accepted]
PHST- 2008/09/23 09:00 [pubmed]
PHST- 2008/10/11 09:00 [medline]
PHST- 2008/09/23 09:00 [entrez]
AID - S0026-0495(08)00069-3 [pii]
AID - 10.1016/j.metabol.2008.01.036 [doi]
PST - ppublish
SO  - Metabolism. 2008 Oct;57(10):1328-39. doi: 10.1016/j.metabol.2008.01.036.

PMID- 18667611
OWN - NLM
STAT- MEDLINE
DCOM- 20080828
LR  - 20211020
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 28
IP  - 31
DP  - 2008 Jul 30
TI  - Caveolin-1 regulates human immunodeficiency virus-1 Tat-induced
      alterations of tight junction protein expression via modulation of the
      Ras signaling.
PG  - 7788-96
LID - 10.1523/JNEUROSCI.0061-08.2008 [doi]
AB  - The blood-brain barrier (BBB) is the critical structure for preventing
      human immunodeficiency virus (HIV) trafficking into the brain. Specific
      HIV proteins, such as Tat protein, can contribute to the dysfunction of
      tight junctions at the BBB and HIV entry into the brain. Tat is released
      by HIV-1-infected cells and can interact with a variety of cell surface
      receptors activating several signal transduction pathways, including
      those localized in caveolae. The present study focused on the mechanisms
      of Tat-induced caveolae-associated Ras signaling at the level of the BBB.
      Treatment with Tat activated the Ras pathway in human brain microvascular
      endothelial cells (HBMECs). However, caveolin-1 silencing markedly
      attenuated these effects. Because the integrity of the brain endothelium
      is regulated by intercellular tight junctions, these structural elements
      of the BBB were also evaluated in the present study. Exposure to Tat
      diminished the expression of several tight junction proteins, namely,
      occludin, zonula occludens (ZO)-1, and ZO-2 in the caveolar fraction of
      HBMECs. These effects were effectively protected by pharmacological
      inhibition of the Ras signaling and by silencing of caveolin-1. The
      present data indicate the importance of caveolae-associated signaling in
      the disruption of tight junctions on Tat exposure. They also demonstrate
      that caveolin-1 may constitute an early and critical modulator that
      controls signaling pathways leading to the disruption of tight junction
      proteins. Thus, caveolin-1 may provide an effective target to protect
      against Tat-induced HBMEC dysfunction and the disruption of the BBB in
      HIV-1-infected patients.
FAU - Zhong, Yu
AU  - Zhong Y
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, Kentucky 40536, USA.
FAU - Smart, Eric J
AU  - Smart EJ
FAU - Weksler, Babette
AU  - Weksler B
FAU - Couraud, Pierre-Olivier
AU  - Couraud PO
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - MH063022/MH/NIMH NIH HHS/United States
GR  - R01 MH063022-05/MH/NIMH NIH HHS/United States
GR  - P01 DA019398/DA/NIDA NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P42 ES007380-120009/ES/NIEHS NIH HHS/United States
GR  - P01 DA19398/DA/NIDA NIH HHS/United States
GR  - R01 MH063022-06A2/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 NS039254-09/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for
      Neuroscience
JID - 8102140
RN  - 0 (CAV1 protein, human)
RN  - 0 (Caveolin 1)
RN  - 0 (Membrane Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (TJP1 protein, human)
RN  - 0 (Tjp1 protein, mouse)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Animals
MH  - Caveolin 1/antagonists & inhibitors/deficiency/genetics/*physiology
MH  - Cell Line, Transformed
MH  - *Gene Expression Regulation, Viral
MH  - HIV-1/*physiology
MH  - Humans
MH  - Membrane Proteins/biosynthesis/genetics/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Phosphoproteins/biosynthesis/genetics/*physiology
MH  - *Signal Transduction/genetics
MH  - Zonula Occludens-1 Protein
MH  - ras Proteins/*physiology
MH  - tat Gene Products, Human Immunodeficiency Virus/*physiology
PMC - PMC2635104
MID - NIHMS85657
EDAT- 2008/08/01 09:00
MHDA- 2008/08/30 09:00
CRDT- 2008/08/01 09:00
PHST- 2008/08/01 09:00 [pubmed]
PHST- 2008/08/30 09:00 [medline]
PHST- 2008/08/01 09:00 [entrez]
AID - 28/31/7788 [pii]
AID - 10.1523/JNEUROSCI.0061-08.2008 [doi]
PST - ppublish
SO  - J Neurosci. 2008 Jul 30;28(31):7788-96. doi:
      10.1523/JNEUROSCI.0061-08.2008.

TI  - Sequential Inactivation of Bacillus Subtilis Spores with Ultraviolet Radiation and Iodine
DP  - 2008 07 01
AU  - Pennell,Kelly,G.
AU  - Naunovic,Zorana,
AU  - Blatchley III,Ernest,R.
PG  - 513
DO  - 10.1061/(ASCE)0733-9372(2008)134:7(513)
TA  - Journal of environmental engineering (New York, N.Y.)
VI  - 134
IP  - 7

PMID- 31130775
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 0888-5885 (Print)
IS  - 0888-5885 (Linking)
VI  - 47
IP  - 14
DP  - 2008 Jul 1
TI  - Functionalized Membranes by Layer-By-Layer Assembly of Polyelectrolytes
      and In Situ Polymerization of Acrylic Acid for Applications in Enzymatic
      Catalysis.
PG  - 4586-4597
LID - 10.1021/ie800142d [doi]
AB  - This research work was directed toward the development of highly active,
      stable, and reusable functionalized polymeric membrane domains for
      enzymatic catalysis. Functionalized membranes were created by two
      different approaches. In the first approach, which involved alternative
      attachment of cationic and anionic polyelectrolytes, functionalization
      was performed using a layer-by-layer (LBL) assembly technique within a
      nylon-based microfiltration (MF) membrane. In the second approach, a
      hydrophobic polyvinylidene fluoride (PVDF) MF membrane was functionalized
      by the in situ polymerization of acrylic acid. The enzyme, glucose
      oxidase (GOX), was then electrostatically immobilized inside the
      functionalized membrane domains to study the catalytic oxidation of
      glucose to gluconic acid and H2O2. Characterization of the functionalized
      membranes, in terms of polyelectrolyte/polymer domains and permeate flux,
      was also conducted. The kinetics of H2O2 formation was discussed, along
      with the effects of residence time and pH on the activity of GOX. The
      stability and reusability of the electrostatically immobilized enzymatic
      system were also investigated.
FAU - Datta, Saurav
AU  - Datta S
AD  - Department of Chemical and Materials Engineering, UniVersity of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Cecil, Caitlyn
AU  - Cecil C
AD  - Department of Chemical and Materials Engineering, UniVersity of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Bhattacharyya, D
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, UniVersity of Kentucky,
      Lexington, Kentucky 40506-0046.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20080620
PL  - United States
TA  - Ind Eng Chem Res
JT  - Industrial & engineering chemistry research
JID - 9882836
PMC - PMC6533002
MID - NIHMS997158
EDAT- 2008/07/01 00:00
MHDA- 2008/07/01 00:01
CRDT- 2019/05/28 06:00
PHST- 2019/05/28 06:00 [entrez]
PHST- 2008/07/01 00:00 [pubmed]
PHST- 2008/07/01 00:01 [medline]
AID - 10.1021/ie800142d [doi]
PST - ppublish
SO  - Ind Eng Chem Res. 2008 Jul 1;47(14):4586-4597. doi: 10.1021/ie800142d.
      Epub 2008 Jun 20.

PMID- 31131070
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1932-7447 (Print)
IS  - 1932-7447 (Linking)
VI  - 112
IP  - 25
DP  - 2008 Jun 1
TI  - Modeling of Fe/Pd Nanoparticle-Based Functionalized Membrane Reactor for
      PCB Dechlorination at Room Temperature.
PG  - 9133-9144
LID - 10.1021/jp7097262 [doi]
AB  - This research deals with the modeling and experimental verification of
      polychlorinated biphenyl (PCB) dechlorination using a porous membrane
      reactor embedded with Fe/Pd nanoparticles. We synthesized core/shell
      Fe/Pd nanoparticles in polyvinylidene fluoride (PVDF) microfiltration
      membranes functionalized with poly(acrylic acid) (PAA). PAA
      functionalization was achieved by in situ free radical polymerization of
      acrylic acid in microfiltration membrane pores. Target ferrous ions were
      then introduced into the membranes by the ion exchange process.
      Subsequent reduction resulted in the in situ formation of 20-40 nm Fe
      nanoparticles. Bimetallic nanoparticles can be formed by post-deposition
      of Pd. The membranes and Fe/Pd nanoparticles were characterized by
      thermogravimetric analyzer (TGA), FTIR, scanning electron microscopy
      (SEM), and transmission electron microscopy (TEM). 2,2'-Dichlorobiphenyl
      (PCB4) and 3,3',4,4'-tertrachlorobiphenyl (PCB77) were chosen as the
      model compounds to investigate the catalytic properties of bimetallic
      nanoparticles, the reaction mechanism, and the intrinsic kinetics. A two-
      dimensional steady-state model was developed to correlate and simulate
      mass transfer and reaction in the membrane pores under pressure-driven
      convective flow conditions. The 2D model equations were solved by a
      finite element technique. The influence of changing parameters such as
      reactor geometry (i.e., membrane pore size) and Pd coating composition
      were evaluated by the model and compared well with the experimental data.
FAU - Xu, Jian
AU  - Xu J
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
FAU - Bhattacharyya, Dibakar
AU  - Bhattacharyya D
AD  - Department of Chemical and Materials Engineering, University of Kentucky,
      Lexington, Kentucky 40506-0046.
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20080529
PL  - United States
TA  - J Phys Chem C Nanomater Interfaces
JT  - The journal of physical chemistry. C, Nanomaterials and interfaces
JID - 101299949
PMC - PMC6533007
MID - NIHMS997159
EDAT- 2008/06/01 00:00
MHDA- 2008/06/01 00:01
CRDT- 2019/05/28 06:00
PHST- 2019/05/28 06:00 [entrez]
PHST- 2008/06/01 00:00 [pubmed]
PHST- 2008/06/01 00:01 [medline]
AID - 10.1021/jp7097262 [doi]
PST - ppublish
SO  - J Phys Chem C Nanomater Interfaces. 2008 Jun 1;112(25):9133-9144. doi:
      10.1021/jp7097262. Epub 2008 May 29.

PMID- 18456438
OWN - NLM
STAT- MEDLINE
DCOM- 20080717
LR  - 20211020
IS  - 0378-4274 (Print)
IS  - 0378-4274 (Linking)
VI  - 178
IP  - 3
DP  - 2008 May 30
TI  - Alumina nanoparticles induce expression of endothelial cell adhesion
      molecules.
PG  - 160-6
LID - 10.1016/j.toxlet.2008.03.011 [doi]
AB  - Nanotechnology is a rapidly growing industry that has elicited much
      concern because of the lack of available toxicity data. Exposure to
      ultrafine particles may be a risk for the development of vascular
      diseases due to dysfunction of the vascular endothelium. Increased
      endothelial adhesiveness is a critical first step in the development of
      vascular diseases, such as atherosclerosis. The hypothesis that alumina
      nanoparticles increase inflammatory markers of the endothelium, measured
      by the induction of adhesion molecules as well as the adhesion of
      monocytes to the endothelial monolayer, was tested. Following
      characterization of alumina nanoparticles by transmission electron
      microscopy (TEM), electron diffraction, and particle size distribution
      analysis, endothelial cells were exposed to alumina at various
      concentrations and times. Both porcine pulmonary artery endothelial cells
      and human umbilical vein endothelial cells showed increased mRNA and
      protein expression of VCAM-1, ICAM-1, and ELAM-1. Furthermore, human
      endothelial cells treated with alumina particles showed increased
      adhesion of activated monocytes. The alumina particles tended to
      agglomerate at physiological pH in serum-containing media, which led to a
      range of particle sizes from nano to micron size during treatment
      conditions. These data show that alumina nanoparticles can elicit a
      proinflammatory response and thus present a cardiovascular disease risk.
FAU - Oesterling, Elizabeth
AU  - Oesterling E
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington, KY
      40536, USA.
FAU - Chopra, Nitin
AU  - Chopra N
FAU - Gavalas, Vasileios
AU  - Gavalas V
FAU - Arzuaga, Xabier
AU  - Arzuaga X
FAU - Lim, Eun Jin
AU  - Lim EJ
FAU - Sultana, Rukhsana
AU  - Sultana R
FAU - Butterfield, D Allan
AU  - Butterfield DA
FAU - Bachas, Leonidas
AU  - Bachas L
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080327
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (E-Selectin)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - LMI26O6933 (Aluminum Oxide)
SB  - IM
MH  - Aluminum Oxide/*toxicity
MH  - Animals
MH  - Cell Adhesion/*drug effects
MH  - Cell Adhesion Molecules/genetics/*metabolism
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - E-Selectin/genetics/metabolism
MH  - Endothelium, Vascular/*drug effects/metabolism/ultrastructure
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/genetics/metabolism
MH  - Metal Nanoparticles/*toxicity
MH  - Microscopy, Electron, Transmission/methods
MH  - Monocytes/drug effects/metabolism/ultrastructure
MH  - Particle Size
MH  - RNA, Messenger/metabolism
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
EDAT- 2008/05/06 09:00
MHDA- 2008/07/18 09:00
CRDT- 2008/05/06 09:00
PHST- 2007/10/29 00:00 [received]
PHST- 2008/03/12 00:00 [revised]
PHST- 2008/03/12 00:00 [accepted]
PHST- 2008/05/06 09:00 [pubmed]
PHST- 2008/07/18 09:00 [medline]
PHST- 2008/05/06 09:00 [entrez]
AID - S0378-4274(08)00079-9 [pii]
AID - 10.1016/j.toxlet.2008.03.011 [doi]
PST - ppublish
SO  - Toxicol Lett. 2008 May 30;178(3):160-6. doi:
      10.1016/j.toxlet.2008.03.011. Epub 2008 Mar 27.

PMID- 18276775
OWN - NLM
STAT- MEDLINE
DCOM- 20080506
LR  - 20211020
IS  - 1521-0111 (Electronic)
IS  - 0026-895X (Linking)
VI  - 73
IP  - 5
DP  - 2008 May
TI  - Simvastatin protects against amyloid beta and HIV-1 Tat-induced promoter
      activities of inflammatory genes in brain endothelial cells.
PG  - 1424-33
LID - 10.1124/mol.107.042028 [doi]
AB  - Increased deposition of amyloid beta (Abeta) is characteristic for normal
      aging and human immunodeficiency virus-1 (HIV-1)-associated alterations
      of the central nervous system. In addition, both Abeta and HIV-1 are
      known to induce cellular oxidative stress and disruption of the blood-
      brain barrier (BBB). Therefore, we hypothesize that Abeta and HIV-1
      protein Tat can potentiate their proinflammatory effects at the brain
      endothelium level. To address this hypothesis, we studied promoter
      activity of three proinflammatory genes in an in vitro BBB model of human
      brain microvascular endothelial cells (HBMEC) cocultured with a human
      astrocyte cell line producing Tat (SVGA-Tat cells) and exposed to Abeta.
      Treatment of HBMEC with Abeta(1-40) in the presence of SVGA-Tat cells
      resulted in a significant up-regulation of E-selectin, CC chemokine
      ligand-2, and interleukin-6 promoter activities and protein levels
      compared with the individual effects of Abeta or Tat. In addition, Abeta
      markedly amplified E-selectin promoter activity in HBMEC cocultured with
      HIV-1-infected Jurkat T cells. Simvastatin, the
      3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, effectively
      blocked proinflammatory reactions induced by Abeta in cocultures with
      SVGA-Tat cells or with HIV-1-infected Jurkat cells. The present study
      indicates that a combined exposure to Abeta and Tat or HIV-1 can
      synergistically potentiate the expression of inflammatory genes in brain
      endothelial cells. In addition, simvastatin may provide a beneficial
      influence by reducing these effects at the BBB level.
FAU - Andras, Ibolya E
AU  - Andras IE
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky Medical Center, 593 Wethington
      Bldg., 900 S Limestone, Lexington, KY 40536, USA.
FAU - Rha, Geunbae
AU  - Rha G
FAU - Huang, Wen
AU  - Huang W
FAU - Eum, Sungyong
AU  - Eum S
FAU - Couraud, Pierre-Olivier
AU  - Couraud PO
FAU - Romero, Ignacio A
AU  - Romero IA
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - R01 NS039254-05/NS/NINDS NIH HHS/United States
GR  - R01 MH063022-05/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - P42 ES007380-130009/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - R01 MH072567-04/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-139005/ES/NIEHS NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 MH063022-07/MH/NIMH NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20080214
PL  - United States
TA  - Mol Pharmacol
JT  - Molecular pharmacology
JID - 0035623
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Anticholesteremic Agents)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Peptide Fragments)
RN  - 0 (Selectins)
RN  - 0 (amyloid beta-protein (1-40))
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - AGG2FN16EV (Simvastatin)
SB  - IM
MH  - Amyloid beta-Peptides/*pharmacology
MH  - Anticholesteremic Agents/pharmacology
MH  - Astrocytes/drug effects/metabolism/pathology
MH  - Brain/drug effects/metabolism/*pathology
MH  - Cell Line, Transformed
MH  - Cytoprotection/drug effects
MH  - Endothelial Cells/drug effects/*metabolism/pathology
MH  - Gene Expression Regulation/*drug effects
MH  - HIV-1/pathogenicity/physiology
MH  - Humans
MH  - Inflammation/genetics
MH  - Inflammation Mediators/metabolism
MH  - Jurkat Cells
MH  - Peptide Fragments/*pharmacology
MH  - Promoter Regions, Genetic/*genetics
MH  - Selectins/genetics
MH  - Simvastatin/*pharmacology
MH  - Transcriptional Activation/drug effects
MH  - tat Gene Products, Human Immunodeficiency Virus/genetics/*metabolism
PMC - PMC2731660
MID - NIHMS115914
EDAT- 2008/02/16 09:00
MHDA- 2008/05/07 09:00
CRDT- 2008/02/16 09:00
PHST- 2008/02/16 09:00 [pubmed]
PHST- 2008/05/07 09:00 [medline]
PHST- 2008/02/16 09:00 [entrez]
AID - mol.107.042028 [pii]
AID - 10.1124/mol.107.042028 [doi]
PST - ppublish
SO  - Mol Pharmacol. 2008 May;73(5):1424-33. doi: 10.1124/mol.107.042028. Epub
      2008 Feb 14.

PMID- 18028363
OWN - NLM
STAT- MEDLINE
DCOM- 20080721
LR  - 20111117
IS  - 1365-2672 (Electronic)
IS  - 1364-5072 (Linking)
VI  - 104
IP  - 4
DP  - 2008 Apr
TI  - Phenotypic persistence and external shielding ultraviolet radiation
      inactivation kinetic model.
PG  - 1192-202
AB  - AIM: To develop an inactivation kinetic model to describe ultraviolet
      (UV) dose-response behaviour for micro-organisms that exhibit tailing
      using two commonly referenced causes for tailing: physical shielding of
      micro-organisms and phenotypic persistence. METHODS AND RESULTS: Dose-
      response data for Escherichia coli, Mycobacterium terrae and Bacillus
      subtilis spores exposed to UV radiation were fit to the phenotypic
      persistence and external shielding (PPES) model. The fraction of
      persistent micro-organisms in the original population
      (N(persistent)/N(total)) that exhibited reduced sensitivity to UV
      radiation was estimated by the PPES model as approx. 10(-7), 10(-5) and
      10(-4) for E. coli, B. subtilis spores and Myco. terrae, respectively.
      Particle shielding effects were evaluated for Myco. terrae and resulted
      in additional reduction in UV sensitivity. CONCLUSIONS: Tailing occurred
      in laboratory experiments even when clumping and shielding were
      eliminated as major factors in UV resistance, suggesting that phenotypic
      persistence in addition to shielding may be important to consider when
      evaluating dose-response curves for disinfection applications.
      SIGNIFICANCE AND IMPACT OF THE STUDY: The PPES model provides a
      mechanistically plausible tool for estimating the dose-response behaviour
      for micro-organisms that exhibit tailing in dispersed and aggregated
      settings. Accurate dose-response behaviour (including the tailing region)
      is critical to the analysis and validation of all UV disinfection
      systems.
FAU - Pennell, K G
AU  - Pennell KG
AD  - Division of Engineering, Brown University, Providence, RI, USA.
FAU - Aronson, A I
AU  - Aronson AI
FAU - Blatchley, E R 3rd
AU  - Blatchley ER 3rd
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20071120
PL  - England
TA  - J Appl Microbiol
JT  - Journal of applied microbiology
JID - 9706280
SB  - IM
MH  - Bacillus subtilis/radiation effects
MH  - Disinfection/*methods
MH  - Dose-Response Relationship, Radiation
MH  - Escherichia coli/radiation effects
MH  - Microbial Viability/radiation effects
MH  - Models, Biological
MH  - Nontuberculous Mycobacteria/radiation effects
MH  - Phenotype
MH  - Spores, Bacterial/radiation effects
MH  - *Ultraviolet Rays
MH  - *Water Microbiology
MH  - Water Purification/*methods
EDAT- 2007/11/22 09:00
MHDA- 2008/07/22 09:00
CRDT- 2007/11/22 09:00
PHST- 2007/11/22 09:00 [pubmed]
PHST- 2008/07/22 09:00 [medline]
PHST- 2007/11/22 09:00 [entrez]
AID - JAM3645 [pii]
AID - 10.1111/j.1365-2672.2007.03645.x [doi]
PST - ppublish
SO  - J Appl Microbiol. 2008 Apr;104(4):1192-202. doi:
      10.1111/j.1365-2672.2007.03645.x. Epub 2007 Nov 20.

PMID- 18155686
OWN - NLM
STAT- MEDLINE
DCOM- 20080509
LR  - 20181113
IS  - 0009-2797 (Print)
IS  - 0009-2797 (Linking)
VI  - 172
IP  - 1
DP  - 2008 Mar 10
TI  - Changing ratios of omega-6 to omega-3 fatty acids can differentially
      modulate polychlorinated biphenyl toxicity in endothelial cells.
PG  - 27-38
AB  - Exposure to persistent organic pollutants, such as polychlorinated
      biphenyls (PCBs) can cause endothelial cell (EC) activation by inducing
      pro-inflammatory signaling pathways. Our previous studies indicated that
      linoleic acid (LA, 18:2), a major omega-6 unsaturated fatty acid in the
      American diet, can potentiate PCB77-mediated inflammatory responses in
      EC. In addition, omega-3 fatty acids (such as alpha-linolenic acid, ALA
      and 18:3) are known for their anti-inflammatory properties. We tested the
      hypothesis that mechanisms of PCB-induced endothelial cell activation and
      inflammation can be modified by different ratios of omega-6 to omega-3
      fatty acids. EC were pretreated with LA, ALA, or different ratios of
      these fatty acids, followed by exposure to PCB77. PCB77-induced oxidative
      stress and activation of the oxidative stress sensitive transcription
      factor nuclear factor kappaB (NF-kappaB) were markedly increased in the
      presence of LA and diminished by increasing the relative amount of ALA to
      LA. Similar protective effects by increasing ALA were observed by
      measuring NF-kappaB-responsive genes, such as vascular cell adhesion
      molecule-1 (VCAM-1) and cyclooxygenase-2 (COX-2). COX-2 catalyzes the
      rate limiting step of the biosynthesis of prostaglandin E(2) (PGE(2)).
      PCB77 exposure also increased PGE(2) levels, which were down-regulated
      with relative increasing amounts of ALA to LA. The present studies
      suggest that NF-kappaB is a critical player in the regulation of PCB-
      induced inflammatory markers as modulated by omega-6 and omega-3 fatty
      acids.
FAU - Wang, Lei
AU  - Wang L
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington 40536, USA.
FAU - Reiterer, Gudrun
AU  - Reiterer G
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES07380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - T32 ES 07266/ES/NIEHS NIH HHS/United States
GR  - T32 ES007266/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-10/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20071119
PL  - Ireland
TA  - Chem Biol Interact
JT  - Chemico-biological interactions
JID - 0227276
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Fatty Acids, Omega-3)
RN  - 0 (Fatty Acids, Omega-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - K7Q1JQR04M (Dinoprostone)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Cells, Cultured
MH  - Cyclooxygenase 2/genetics/metabolism
MH  - Dinoprostone/biosynthesis
MH  - Endothelial Cells/*drug effects/*pathology
MH  - Fatty Acids, Omega-3/*pharmacology
MH  - Fatty Acids, Omega-6/*pharmacology
MH  - Gene Expression Regulation/drug effects
MH  - Inflammation
MH  - Linoleic Acid/pharmacology
MH  - NF-kappa B/antagonists & inhibitors
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Pulmonary Artery/cytology
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
PMC - PMC2277485
MID - NIHMS42795
EDAT- 2007/12/25 09:00
MHDA- 2008/05/10 09:00
CRDT- 2007/12/25 09:00
PHST- 2007/08/17 00:00 [received]
PHST- 2007/11/05 00:00 [revised]
PHST- 2007/11/09 00:00 [accepted]
PHST- 2007/12/25 09:00 [pubmed]
PHST- 2008/05/10 09:00 [medline]
PHST- 2007/12/25 09:00 [entrez]
AID - S0009-2797(07)00317-1 [pii]
AID - 10.1016/j.cbi.2007.11.003 [doi]
PST - ppublish
SO  - Chem Biol Interact. 2008 Mar 10;172(1):27-38. doi:
      10.1016/j.cbi.2007.11.003. Epub 2007 Nov 19.

PMID- 18441810
OWN - NLM
STAT- MEDLINE
DCOM- 20080731
LR  - 20190715
IS  - 0013-936X (Print)
IS  - 0013-936X (Linking)
VI  - 42
IP  - 5
DP  - 2008 Mar 1
TI  - Development and performance of a fluence rate distribution model for a
      cylindrical excimer lamp.
PG  - 1605-14
AB  - Ultraviolet disinfection systems employing excimer lamp technology
      represent a suitable choice in situations where lamp mercury content is
      restricted, or otherwise undesirable. The XeBr* excimer lamp emits nearly
      monochromatic radiation at 282 nm, and dose-response experiments with
      Bacillus subtilis spores have shown that it is germicidally effective. A
      numerical model was developed to describe the fluence rate (E')
      distribution emanating from a cylindrical XeBr* excimer lamp, based on
      liquid water or air as the surrounding medium. The E' distribution model
      is based on physical phenomena that are known to govern excimer lamps;
      the model also accounts for refraction, reflection, and absorbance
      effects of the quartz lamp envelope and the media surrounding the lamp.
      Measurements of the E' distribution by local actinometry supported the
      validity of the numerical model. This model can be used as a component
      (submodel) of a more general model to simulate the behavior of
      photochemical reactors that employ excimer lamps as their source of
      electromagnetic radiation.
FAU - Naunovic, Zorana
AU  - Naunovic Z
AD  - School of Civil Engineering, Purdue University, West Lafayette, Indiana
      47907-2051, USA.
FAU - Pennell, Kelly G
AU  - Pennell KG
FAU - Blatchley, Ernest R 3rd
AU  - Blatchley ER 3rd
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Environ Sci Technol
JT  - Environmental science & technology
JID - 0213155
SB  - IM
MH  - Bacillus subtilis/physiology
MH  - *Lasers
MH  - *Models, Theoretical
MH  - Spores, Bacterial
EDAT- 2008/04/30 09:00
MHDA- 2008/08/01 09:00
CRDT- 2008/04/30 09:00
PHST- 2008/04/30 09:00 [pubmed]
PHST- 2008/08/01 09:00 [medline]
PHST- 2008/04/30 09:00 [entrez]
AID - 10.1021/es070968w [doi]
PST - ppublish
SO  - Environ Sci Technol. 2008 Mar 1;42(5):1605-14. doi: 10.1021/es070968w.

PMID- 18438459
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211020
IS  - 1382-6689 (Print)
IS  - 1382-6689 (Linking)
VI  - 25
IP  - 2
DP  - 2008 Mar
TI  - ORAL ADMINISTRATION OF PCBs INDUCES PROINFLAMMATORY AND PROMETASTATIC
      RESPONSES.
PG  - 251-9
LID - 10.1016/j.etap.2007.10.020 [doi]
AB  - Exposure to specific congeners of polychlorinated biphenyls (PCBs) can
      induce proinflammatory alterations, which may contribute to the formation
      of blood-borne tumor metastasis. The main aim of the present study was to
      establish an experimental model of PCB exposure in which PCBs are
      administered by oral gavage, which resembles the human exposure through
      the food chain. To determine structure-function relationship, we studied
      induction of inflammatory responses in the livers, lungs and brains of
      mice treated with PCB77 (a major coplanar PCB), PCB104 (a non-coplanar
      PCB with multiple ortho-chlorine substituents), and PCB153 (a major non-
      coplanar PCB) after a single gavage dose (150 micromol/kg body weight).
      The strongest expression of proinflammatory proteins occurred 24 h
      following the PCB administration independent of the class of PCB
      congeners. These data indicate that food-chain exposure to PCBs can
      induce proinflammatory mediators in organs that are potential targets for
      PCB-induced toxicity.
FAU - Sipka, Sandor
AU  - Sipka S
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, KY 40536.
FAU - Eum, Sung-Yong
AU  - Eum SY
FAU - Son, Kwang Won
AU  - Son KW
FAU - Xu, Shifen
AU  - Xu S
FAU - Gavalas, Vasileios G
AU  - Gavalas VG
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-090007/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-109005/ES/NIEHS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - Environ Toxicol Pharmacol
JT  - Environmental toxicology and pharmacology
JID - 9612020
PMC - PMC2346434
MID - NIHMS40245
OTO - NOTNLM
OT  - Polychlorinated biphenyls
OT  - inflammation
OT  - tumor metastasis
EDAT- 2008/04/29 09:00
MHDA- 2008/04/29 09:01
CRDT- 2008/04/29 09:00
PHST- 2008/04/29 09:00 [pubmed]
PHST- 2008/04/29 09:01 [medline]
PHST- 2008/04/29 09:00 [entrez]
AID - 10.1016/j.etap.2007.10.020 [doi]
AID - S1382-6689(07)00157-3 [pii]
PST - ppublish
SO  - Environ Toxicol Pharmacol. 2008 Mar;25(2):251-9. doi:
      10.1016/j.etap.2007.10.020.

PMID- 18438464
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211020
IS  - 1382-6689 (Print)
IS  - 1382-6689 (Linking)
VI  - 25
IP  - 2
DP  - 2008 Mar
TI  - Pcbs and tight junction expression.
PG  - 234-40
LID - 10.1016/j.etap.2007.10.019 [doi]
AB  - Polychlorinated biphenyl (PCB) congeners exhibit a broad range of adverse
      biological effects including neurotoxicity. The mechanisms by which PCBs
      cause neurotoxic effects are still not completely understood. The blood-
      brain barrier (BBB) is a physical and metabolic barrier separating brain
      microenvironment from the peripheral circulation and is mainly composed
      of endothelial cells connected by tight junctions. We examined the
      effects of several highly-chlorinated PCB congeners on expression of
      tight junction proteins in human brain endothelial cells. Treatment for
      24 h with selective PCB congeners disrupted expression of the cytosolic
      scaffold proteins of tight junctions, such as zonula occludens (ZO)-1,
      ZO-2, and AF6. In contrast, PCB exposure did not alter expression of
      integral membrane proteins, junctional adhesion molecule-A (JAM-A), and
      claudin-1. Based on these data, we suggest that PCB-mediated selective
      alterations of tight junction protein expression may contribute to their
      neurotoxic effects in the central nervous system.
FAU - Eum, Sung Yong
AU  - Eum SY
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, KY 40536.
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Couraud, Pierre-Olivier
AU  - Couraud PO
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - R01 MH063022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-119005/ES/NIEHS NIH HHS/United States
GR  - R01 DA027569/DA/NIDA NIH HHS/United States
GR  - R01 NS039254/NS/NINDS NIH HHS/United States
GR  - R01 MH098891/MH/NIMH NIH HHS/United States
GR  - R01 MH072567/MH/NIMH NIH HHS/United States
GR  - P42 ES007380-110007/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - Environ Toxicol Pharmacol
JT  - Environmental toxicology and pharmacology
JID - 9612020
PMC - PMC2346445
MID - NIHMS40246
OTO - NOTNLM
OT  - Polychlorinated biphenyls
OT  - blood-brain barrier
OT  - tight junctions
OT  - zonula occludens
EDAT- 2008/04/29 09:00
MHDA- 2008/04/29 09:01
CRDT- 2008/04/29 09:00
PHST- 2008/04/29 09:00 [pubmed]
PHST- 2008/04/29 09:01 [medline]
PHST- 2008/04/29 09:00 [entrez]
AID - 10.1016/j.etap.2007.10.019 [doi]
AID - S1382-6689(07)00160-3 [pii]
PST - ppublish
SO  - Environ Toxicol Pharmacol. 2008 Mar;25(2):234-40. doi:
      10.1016/j.etap.2007.10.019.

PMID- 19255596
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211020
IS  - 1382-6689 (Print)
IS  - 1382-6689 (Linking)
VI  - 25
IP  - 2
DP  - 2008 Mar
TI  - Zinc nutritional status modulates expression of ahr-responsive p450
      enzymes in vascular endothelial cells.
PG  - 197-201
LID - 10.1016/j.etap.2007.10.016 [doi]
AB  - Zinc has anti-inflammatory properties and is crucial for the integrity of
      vascular endothelial cells, and the development and homeostasis of the
      cardiovascular system. The aryl hydrocarbon receptor (AhR) which is
      expressed in the vascular endothelium also plays an important role in
      responses to xenobiotic exposure and cardiovascular development. We
      hypothesize that cellular zinc can modulate induction of AhR responsive
      genes in endothelial cells. To determine if zinc deficiency can alter
      responses to AhR ligands, aortic endothelial cells were exposed to the
      AhR ligands 3,3',4,4'-tetrachlorobiphenyl (PCB77) or beta-naphthoflavone
      (beta-NF) alone or in combination with the membrane permeable zinc
      chelator TPEN, followed by measurements of the AhR responsive cytochrome
      P450 enzymes CYP1A1 and 1B1. Compared to vehicle treated cells, both
      PCB77-induced CYP1A1 activity (EROD) and mRNA expression were
      significantly reduced during zinc deficiency. In addition, PCB77 and
      beta-NF-mediated upregulation of CYP1A1 and CYP1B1 protein expression was
      significantly reduced in zinc-deficient endothelial cells. The inhibition
      of CYP1A1 and CYP1B1 protein expression caused by zinc deficiency was
      reversible by cellular zinc supplementation. Overall, our results
      strongly suggest that nutrition can modulate an environmental toxicant-
      induced biological outcome and that adequate levels of individual
      nutrients such as zinc are necessary for induction of AhR responsive
      genes in vascular endothelial cells.
FAU - Shen, Huiyun
AU  - Shen H
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY, 40536.
FAU - Arzuaga, Xabier
AU  - Arzuaga X
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES007380-11/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - Netherlands
TA  - Environ Toxicol Pharmacol
JT  - Environmental toxicology and pharmacology
JID - 9612020
PMC - PMC2346446
MID - NIHMS40240
OTO - NOTNLM
OT  - AhR
OT  - CYP1A1
OT  - CYP1B1
OT  - EROD
OT  - Zinc deficiency
EDAT- 2009/03/04 09:00
MHDA- 2009/03/04 09:01
CRDT- 2009/03/04 09:00
PHST- 2009/03/04 09:00 [entrez]
PHST- 2009/03/04 09:00 [pubmed]
PHST- 2009/03/04 09:01 [medline]
AID - 10.1016/j.etap.2007.10.016 [doi]
AID - S1382-6689(07)00146-9 [pii]
PST - ppublish
SO  - Environ Toxicol Pharmacol. 2008 Mar;25(2):197-201. doi:
      10.1016/j.etap.2007.10.016.

PMID- 21783859
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211020
IS  - 1382-6689 (Print)
IS  - 1382-6689 (Linking)
VI  - 25
IP  - 2
DP  - 2008 Mar
TI  - Impact of nutrition on PCB toxicity.
PG  - 192-6
LID - 10.1016/j.etap.2007.10.015 [doi]
AB  - Studies are evolving which suggest that nutritional intervention can
      modify pathologies of diseases associated with environmental toxic
      insults. The diet is a major route of exposure to environmental toxins,
      such as persistent organic pollutants and heavy metals. Many persistent
      organics, such as polychlorinated biphenyls (PCBs), bioaccumulate in our
      bodies and "bioremediation" is extremely difficult. Furthermore, many
      environmental toxins induce signaling pathways that are oxidative stress-
      sensitive and similar or the same as the ones associated with the
      etiology and early pathology of many chronic diseases. There is now
      increasing evidence that exposure to PCBs can contribute to the
      development of inflammatory diseases such as atherosclerosis. Activation,
      chronic inflammation, and dysfunction of the vascular endothelium are
      critical events in the initiation and acceleration of atherosclerotic
      lesion formation. Our studies indicate that an increase in cellular
      oxidative stress and an imbalance in antioxidant status are critical
      events in PCB-mediated induction of inflammatory genes and endothelial
      cell dysfunction. We also have evidence that the plasma membrane
      microdomains called caveolae play an important role in endothelial
      activation and toxicity mediated by coplanar PCBs. Caveolae are
      particularly abundant in endothelial cells and play a major role in
      endothelial trafficking and the regulation of signaling pathways
      associated with the pathology of vascular diseases. There is a great need
      to further explore this nutritional paradigm in environmental toxicology
      and to improve our understanding of the relationship between nutrition
      and lifestyle, exposure to environmental toxins and disease. Our studies
      suggest that certain dietary fats can increase the risk of environmental
      insult induced by PCBs, while other dietary factors may provide
      protection. Nutrition may provide the most sensible means to develop
      primary intervention and prevention strategies of diseases associated
      with many environmental toxic insults.
CI  - Copyright (c) 2007. Published by Elsevier B.V.
FAU - Majkova, Zuzana
AU  - Majkova Z
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington, KY
      40536-0200, United States.
FAU - Oesterling, Elizabeth
AU  - Oesterling E
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20071013
PL  - Netherlands
TA  - Environ Toxicol Pharmacol
JT  - Environmental toxicology and pharmacology
JID - 9612020
EDAT- 2008/03/01 00:00
MHDA- 2008/03/01 00:01
CRDT- 2011/07/26 06:00
PHST- 2011/07/26 06:00 [entrez]
PHST- 2008/03/01 00:00 [pubmed]
PHST- 2008/03/01 00:01 [medline]
AID - S1382-6689(07)00145-7 [pii]
AID - 10.1016/j.etap.2007.10.015 [doi]
PST - ppublish
SO  - Environ Toxicol Pharmacol. 2008 Mar;25(2):192-6. doi:
      10.1016/j.etap.2007.10.015. Epub 2007 Oct 13.

PMID- 17976544
OWN - NLM
STAT- MEDLINE
DCOM- 20080408
LR  - 20211020
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1184
DP  - 2007 Dec 12
TI  - Limited role of COX-2 in HIV Tat-induced alterations of tight junction
      protein expression and disruption of the blood-brain barrier.
PG  - 333-44
AB  - Tat protein released from HIV-infected blood-borne leukocytes can
      contribute to the breakdown of the blood-brain barrier (BBB) and
      induction of inflammatory responses and can provide entry for HIV into
      the brain. To mimic this pathology, Tat was injected into the tail vein
      of C57BL/6 mice. Treatment with Tat markedly upregulated expression of
      cyclooxygenase-2 (COX-2) and decreased expression of tight junction
      proteins, occludin and zonula occludens-1 (ZO-1). These alterations were
      associated with the disruption of the BBB integrity as quantified by
      extravasation of Evans blue dye into the brain tissue. In addition,
      direct treatment of brain microvessels with prostaglandin E(2), a product
      of COX-2 activity, resulted in decreased expression of both occludin and
      ZO-1. To determine if upregulation of COX-2 is involved in the disruption
      of tight junction proteins and BBB integrity, mice were pretreated with
      rofecoxib, a specific inhibitor of COX-2, prior to Tat treatment. COX-2
      inhibition attenuated Tat-induced alterations of occludin expression.
      However, rofecoxib was ineffective in preventing downregulation of ZO-1
      expression and increased BBB permeability. These results suggest only a
      limited role of COX-2 overexpression in the loss of tight junction
      integrity and the BBB breakdown in HIV-related brain diseases.
FAU - Pu, Hong
AU  - Pu H
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Neurosurgery, University of Kentucky, Lexington, KY 40536, USA.
FAU - Hayashi, Kentaro
AU  - Hayashi K
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES07380/ES/NIEHS NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20071002
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Lactones)
RN  - 0 (Membrane Proteins)
RN  - 0 (OCLN protein, human)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, mouse)
RN  - 0 (Phosphoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sulfones)
RN  - 0 (TJP1 protein, human)
RN  - 0 (Tjp1 protein, mouse)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 0 (tat peptide (1-72), Human immunodeficiency virus 1)
RN  - 0QTW8Z7MCR (rofecoxib)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/*drug effects
MH  - Cyclooxygenase 2/genetics/*metabolism
MH  - Dinoprostone/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Drug Interactions
MH  - Enzyme Inhibitors/pharmacology
MH  - Gene Expression Regulation/*drug effects
MH  - Lactones/pharmacology
MH  - Male
MH  - Membrane Proteins/genetics/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Occludin
MH  - Phosphoproteins/genetics/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Sulfones/pharmacology
MH  - Zonula Occludens-1 Protein
MH  - tat Gene Products, Human Immunodeficiency Virus/*pharmacology
EDAT- 2007/11/03 09:00
MHDA- 2008/04/09 09:00
CRDT- 2007/11/03 09:00
PHST- 2007/08/12 00:00 [received]
PHST- 2007/09/21 00:00 [revised]
PHST- 2007/09/24 00:00 [accepted]
PHST- 2007/11/03 09:00 [pubmed]
PHST- 2008/04/09 09:00 [medline]
PHST- 2007/11/03 09:00 [entrez]
AID - S0006-8993(07)02270-6 [pii]
AID - 10.1016/j.brainres.2007.09.063 [doi]
PST - ppublish
SO  - Brain Res. 2007 Dec 12;1184:333-44. doi: 10.1016/j.brainres.2007.09.063.
      Epub 2007 Oct 2.

PMID- 17933968
OWN - NLM
STAT- MEDLINE
DCOM- 20080131
LR  - 20211020
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 293
IP  - 6
DP  - 2007 Dec
TI  - The role of caveolin-1 in PCB77-induced eNOS phosphorylation in human-
      derived endothelial cells.
PG  - H3340-7
AB  - Polychlorinated biphenyls (PCBs) may contribute to the pathology of
      atherosclerosis by activating inflammatory responses in vascular
      endothelial cells. Endothelial nitric oxide synthase (eNOS) is
      colocalized with caveolae and is a critical regulator of vascular
      homeostasis. PCBs may be proatherogenic by causing dysfunctional eNOS
      signaling. The objective of this study was to investigate the role of
      caveolin-1 in PCB-induced endothelial dysfunction with a focus on
      mechanisms associated with eNOS signaling. Cells derived from an
      immortalized human vascular endothelial cell line were treated with PCB77
      to study nitrotyrosine formation through eNOS signaling. Phosphorylation
      studies of eNOS, caveolin-1, and kinases, such as Src,
      phosphatidylinositol 3-kinase (PI3K), and Akt, were conducted in cells
      containing either functional or small-interfering RNA-silenced caveolin-1
      protein. We also investigated caveolin-1-regulated mechanisms associated
      with PCB-induced markers of peroxynitrite formation and DNA binding of
      NF-kappaB. Cellular exposure to PCB77 increased eNOS phosphorylation and
      nitric oxide production, as well as peroxynitrite levels. A subsequent
      PCB-induced increase in NF-kappaB DNA binding may have implications in
      oxidative stress-mediated inflammatory mechanisms. The activation of eNOS
      by PCB77 treatment was blocked by inhibitors of the Src/PI3K/Akt pathway.
      PCB77 also increased phosphorylation of caveolin-1, indicating caveolae-
      dependent endocytosis. Caveolin-1 silencing abolished both the PCB-
      stimulated Akt and eNOS phosphorylation, suggesting a regulatory role of
      caveolae in PCB-induced eNOS signaling. These findings suggest that PCB77
      induces eNOS phosphorylation in endothelial cells through a Src/PI3K/Akt-
      dependent mechanism, events regulated by functional caveolin-1. Our data
      provide evidence that caveolae may play a critical role in regulating
      vascular endothelial cell activation and toxicity induced by persistent
      environmental pollutants such as coplanar PCBs.
FAU - Lim, Eun Jin
AU  - Lim EJ
AD  - Molecular and Cell Nutrition Laboratory, University of Kentucky,
      Lexington, KY 40536-0200, USA.
FAU - Smart, Eric J
AU  - Smart EJ
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20071012
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Caveolin 1)
RN  - 0 (Environmental Pollutants)
RN  - 0 (NF-kappa B)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (RNA, Small Interfering)
RN  - 14691-52-2 (Peroxynitrous Acid)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 2.7.10.2 (src-Family Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/chemically induced/metabolism
MH  - Caveolae/*drug effects/metabolism
MH  - Caveolin 1/genetics/*metabolism
MH  - Cell Line
MH  - Cells, Cultured
MH  - Endothelial Cells/*drug effects/enzymology/metabolism
MH  - Environmental Pollutants/*toxicity
MH  - Enzyme Activation
MH  - Humans
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase Type III/*metabolism
MH  - Peroxynitrous Acid/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Phosphorylation
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Proto-Oncogene Proteins c-akt/antagonists & inhibitors/metabolism
MH  - RNA Interference
MH  - RNA, Small Interfering/metabolism
MH  - Signal Transduction/*drug effects
MH  - Swine
MH  - Time Factors
MH  - Tyrosine/analogs & derivatives/metabolism
MH  - src-Family Kinases/antagonists & inhibitors/metabolism
EDAT- 2007/10/16 09:00
MHDA- 2008/02/01 09:00
CRDT- 2007/10/16 09:00
PHST- 2007/10/16 09:00 [pubmed]
PHST- 2008/02/01 09:00 [medline]
PHST- 2007/10/16 09:00 [entrez]
AID - 00921.2007 [pii]
AID - 10.1152/ajpheart.00921.2007 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2007 Dec;293(6):H3340-7. doi:
      10.1152/ajpheart.00921.2007. Epub 2007 Oct 12.

PMID- 17951467
OWN - NLM
STAT- MEDLINE
DCOM- 20080312
LR  - 20211020
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 137
IP  - 11
DP  - 2007 Nov
TI  - Zinc deficiency alters lipid metabolism in LDL receptor deficient mice
      treated with rosiglitazone.
PG  - 2339-45
AB  - Zinc is a structural and functional component of PPAR and zinc deficiency
      may be associated with an increased risk for cardiovascular diseases. We
      tested the hypothesis that zinc deficiency compromises lipid metabolism
      in rosiglitazone (RSG)-treated mice lacking the LDL-receptor (LDL-R)
      gene. LDL-R-deficient mice were maintained for 3 wk on low-fat (7 g/100
      g) diets that were either zinc deficient or zinc adequate. Subsequently,
      diets were adjusted to a high-fat (HF) (15 g/100 g) regimen for 1 wk to
      produce a biological environment of mild oxidative and inflammatory
      stress. One-half of the mice within each zinc group was gavaged daily
      with the PPARgamma agonist RSG starting 2 d prior to the HF feeding.
      Selected lipid parameters were studied. Zinc deficiency increased plasma
      total cholesterol, which was also elevated by RSG. Zinc deficiency also
      caused an increased lipoprotein-cholesterol distribution toward the non-
      HDL fraction (VLDL, intermediate density lipoprotein, LDL). Plasma total
      fatty acids tended to increase during zinc deficiency and RSG treatment
      resulted in similar changes in the fatty acid profile in zinc-deficient
      mice. Fatty acid translocase (FAT/CD36) expression in abdominal aorta was
      upregulated by RSG only in zinc-deficient mice. In contrast, RSG
      treatment markedly increased lipoprotein lipase (LPL) expression only in
      zinc-adequate mice. In vitro studies confirmed that adequate zinc is
      required for RSG-induced PPARgamma activity to transactivate target
      genes. These data suggest that in this atherogenic mouse model treated
      with RSG, lipid metabolism can be compromised during zinc deficiency and
      that adequate dietary zinc may be considered during therapy with the
      antidiabetic medicine RSG.
FAU - Shen, Huiyun
AU  - Shen H
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40536, USA.
FAU - MacDonald, Ruth
AU  - MacDonald R
FAU - Bruemmer, Dennis
AU  - Bruemmer D
FAU - Stromberg, Arnold
AU  - Stromberg A
FAU - Daugherty, Alan
AU  - Daugherty A
FAU - Li, Xiang-an
AU  - Li XA
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42ES 07380/ES/NIEHS NIH HHS/United States
GR  - P20RR16481/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Lipids)
RN  - 0 (Lipoproteins)
RN  - 0 (Receptors, LDL)
RN  - 0 (Thiazolidinediones)
RN  - 05V02F2KDG (Rosiglitazone)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Cholesterol/blood
MH  - Energy Intake
MH  - Fatty Acids, Nonesterified/blood
MH  - Lipids/*physiology
MH  - Lipoproteins/blood
MH  - Liver/drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Receptors, LDL/*deficiency/metabolism
MH  - Rosiglitazone
MH  - Thiazolidinediones/*pharmacology
MH  - Zinc/*deficiency/*pharmacology
EDAT- 2007/10/24 09:00
MHDA- 2008/03/13 09:00
CRDT- 2007/10/24 09:00
PHST- 2007/10/24 09:00 [pubmed]
PHST- 2008/03/13 09:00 [medline]
PHST- 2007/10/24 09:00 [entrez]
AID - 137/11/2339 [pii]
AID - 10.1093/jn/137.11.2339 [doi]
PST - ppublish
SO  - J Nutr. 2007 Nov;137(11):2339-45. doi: 10.1093/jn/137.11.2339.

PMID- 17955387
OWN - NLM
STAT- MEDLINE
DCOM- 20080214
LR  - 20211020
IS  - 1530-7905 (Print)
IS  - 1530-7905 (Linking)
VI  - 7
IP  - 4
DP  - 2007
TI  - PPARalpha ligands reduce PCB-induced endothelial activation: possible
      interactions in inflammation and atherosclerosis.
PG  - 264-72
AB  - Exposure to polychlorinated biphenyls (PCBs) can activate inflammatory
      responses in vascular endothelial cells. Activation of peroxisome
      proliferator-activated receptors (PPARs) by nutrients or synthetic
      agonists has been shown to block pro-inflammatory responses both in vitro
      and in vivo. Here we demonstrate that activation of PPARalpha by
      synthetic agonists can reduce 3,3'4,4'-tetrachlorobiphenyl
      (PCB77)-induced endothelial cell activation. Primary vascular endothelial
      cells were pretreated with the PPARalpha ligands fenofibrate or WY14643
      followed by exposure to PCB77. PPARalpha activation protected endothelial
      cells against PCB77-induced expression of the pro-inflammatory proteins
      vascular cell adhesion molecule-1 (VCAM-1), cycloxygenase-2 (COX-2), and
      PCB77-induced expression and activity of the aryl hydrocarbon receptor
      (AHR) responsive cytochrome P450 1A1 (CYP1A1). Furthermore, basal AHR
      expression was downregulated by fenofibrate and WY14643. We also
      investigated the possible interactions between PCBs, and basal PPAR
      activity and protein expression. Treatment with PCB77 significantly
      reduced basal mRNA expression of PPARalpha and the PPAR responsive gene
      CYP4A1, as well as PPARalpha protein expression. Also, PCB77 exposure
      caused a significant decrease in basal PPAR-dependent reporter gene
      expression in MCF-7 cells. Overall, these findings suggest that PPARalpha
      agonists can reduce PCB77 induction of endothelial cell activation by
      inhibition of the AHR pathway, and that coplanar PCB induced pro-
      inflammatory effects could be mediated, in part, by inhibition of
      PPARalpha expression and function.
FAU - Arzuaga, Xabier
AU  - Arzuaga X
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40536-0200, USA.
FAU - Reiterer, Gudrun
AU  - Reiterer G
FAU - Majkova, Zuzana
AU  - Majkova Z
FAU - Kilgore, Michael W
AU  - Kilgore MW
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20071023
PL  - United States
TA  - Cardiovasc Toxicol
JT  - Cardiovascular toxicology
JID - 101135818
RN  - 0 (Environmental Pollutants)
RN  - 0 (Ligands)
RN  - 0 (PPAR alpha)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Coronary Artery Disease/*chemically induced/*pathology
MH  - Cyclooxygenase 2/biosynthesis
MH  - Cytochrome P-450 CYP1A1/antagonists & inhibitors/metabolism
MH  - Endothelial Cells/drug effects
MH  - Endothelium, Vascular/*drug effects/pathology
MH  - Environmental Pollutants/*antagonists & inhibitors/*toxicity
MH  - Genes, Reporter/drug effects
MH  - Inflammation/*chemically induced/*pathology
MH  - Ligands
MH  - PPAR alpha/agonists/antagonists & inhibitors/*drug effects
MH  - Polychlorinated Biphenyls/*antagonists & inhibitors/*toxicity
MH  - Receptors, Aryl Hydrocarbon/biosynthesis/drug effects/physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/physiology
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/biosynthesis
EDAT- 2007/10/24 09:00
MHDA- 2008/02/15 09:00
CRDT- 2007/10/24 09:00
PHST- 2007/06/11 00:00 [received]
PHST- 2007/10/03 00:00 [accepted]
PHST- 2007/10/24 09:00 [pubmed]
PHST- 2008/02/15 09:00 [medline]
PHST- 2007/10/24 09:00 [entrez]
AID - 10.1007/s12012-007-9005-8 [doi]
PST - ppublish
SO  - Cardiovasc Toxicol. 2007;7(4):264-72. doi: 10.1007/s12012-007-9005-8.
      Epub 2007 Oct 23.

PMID- 17245419
OWN - NLM
STAT- MEDLINE
DCOM- 20071002
LR  - 20161124
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 27
IP  - 8
DP  - 2007 Aug
TI  - The NMDA and AMPA/KA receptors are involved in glutamate-induced
      alterations of occludin expression and phosphorylation in brain
      endothelial cells.
PG  - 1431-43
AB  - Glutamate levels increase dramatically in cerebral ischemia and stroke.
      This may lead to opening of the blood-brain barrier (BBB) and induce
      further brain damage. Because endothelial tight junctions are critical
      elements of the BBB integrity, the aim of this study was to investigate
      the mechanisms of glutamate-induced alterations of the tight-junction
      protein occludin in cultured brain microvascular endothelial cells
      (BMECs). Transient exposure to glutamate resulted in cellular
      redistribution of occludin, followed by a decrease in the total level of
      this protein and diminished barrier function of BMECs. Inhibition of the
      N-methyl-D-aspartate (NMDA) or alpha-
      amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate (AMPA/KA)
      receptors attenuated glutamate-induced changes in occludin redistribution
      but not in the total protein levels. Treatment with glutamate also
      increased tyrosine phosphorylation and decreased threonine
      phosphorylation of occludin. Inhibition of the NMDA receptors by MK-801
      partially protected against glutamate-induced elevation of occludin
      tyrosine phosphorylation. In addition, pretreatment with
      MK-801-attenuated glutamate-mediated disruption of endothelial barrier
      function. Blocking of the AMPA/KA receptors by
      6,7-dinitroquinoxaline-2.3-dione (DNQX) protected against
      hypophosphorylation of threonine residues of occludin; however, it did
      not affect disruption of endothelial integrity. These findings indicate
      the opposite effects of the NMDA and AMPA/KA receptors on occludin
      phosphorylation and disruption of the BBB functions.
FAU - Andras, Ibolya E
AU  - Andras IE
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Surgery, University of Kentucky Medical Center, Lexington, Kentucky
      40536, USA.
FAU - Deli, Maria A
AU  - Deli MA
FAU - Veszelka, Szilvia
AU  - Veszelka S
FAU - Hayashi, Kentaro
AU  - Hayashi K
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20070124
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Membrane Proteins)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, rat)
RN  - 0 (Quinoxalines)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, Kainic Acid)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 2ZD004190S (Threonine)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 42HK56048U (Tyrosine)
RN  - 62T278S1MX (FG 9041)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/physiology
MH  - Brain/blood supply/cytology/metabolism
MH  - Cells, Cultured
MH  - Dizocilpine Maleate/metabolism
MH  - Endothelial Cells/cytology/*metabolism
MH  - Excitatory Amino Acid Antagonists/metabolism
MH  - Glutamic Acid/*metabolism
MH  - Membrane Proteins/*metabolism
MH  - Occludin
MH  - Phosphorylation
MH  - Quinoxalines/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, AMPA/*metabolism
MH  - Receptors, Kainic Acid/*metabolism
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Threonine/metabolism
MH  - Tyrosine/metabolism
EDAT- 2007/01/25 09:00
MHDA- 2007/10/03 09:00
CRDT- 2007/01/25 09:00
PHST- 2007/01/25 09:00 [pubmed]
PHST- 2007/10/03 09:00 [medline]
PHST- 2007/01/25 09:00 [entrez]
AID - 9600445 [pii]
AID - 10.1038/sj.jcbfm.9600445 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2007 Aug;27(8):1431-43. doi:
      10.1038/sj.jcbfm.9600445. Epub 2007 Jan 24.

PMID- 17450213
OWN - NLM
STAT- MEDLINE
DCOM- 20070522
LR  - 20181113
IS  - 0091-6765 (Print)
IS  - 0091-6765 (Linking)
VI  - 115
IP  - 4
DP  - 2007 Apr
TI  - Using nutrition for intervention and prevention against environmental
      chemical toxicity and associated diseases.
PG  - 493-5
AB  - BACKGROUND: Nutrition and lifestyle are well-defined modulators of
      chronic diseases. Poor dietary habits (such as high intake of processed
      foods rich in fat and low intake of fruits and vegetables), as well as a
      sedentary lifestyle clearly contribute to today's compromised quality of
      life in the United States. It is becoming increasingly clear that
      nutrition can modulate the toxicity of environmental pollutants.
      OBJECTIVES: Our goal in this commentary is to discuss the recommendation
      that nutrition should be considered a necessary variable in the study of
      human disease associated with exposure to environmental pollutants.
      DISCUSSION: Certain diets can contribute to compromised health by being a
      source of exposure to environmental toxic pollutants. Many of these
      pollutants are fat soluble, and thus fatty foods often contain higher
      levels of persistent organics than does vegetable matter. Nutrition can
      dictate the lipid milieu, oxidative stress, and antioxidant status within
      cells. The modulation of these parameters by an individual's nutritional
      status may have profound affects on biological processes, and in turn
      influence the effects of environmental pollutants to cause disease or
      dysfunction. For example, potential adverse health effects associated
      with exposure to polychlorinated biphenyls may increase as a result of
      ingestion of certain dietary fats, whereas ingestion of fruits and
      vegetables, rich in antioxidant and anti-inflammatory nutrients or
      bioactive compounds, may provide protection. CONCLUSIONS: We recommend
      that future directions in environmental health research explore this
      nutritional paradigm that incorporates a consideration of the
      relationships between nutrition and lifestyle, exposure to environmental
      toxicants, and disease. Nutritional interventions may provide the most
      sensible means to develop primary prevention strategies of diseases
      associated with many environmental toxic insults.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, 900 S. Limestone, Lexington, KY 40536, USA.
      bhennig@uky.edu
FAU - Ettinger, Adrienne S
AU  - Ettinger AS
FAU - Jandacek, Ronald J
AU  - Jandacek RJ
FAU - Koo, Sung
AU  - Koo S
FAU - McClain, Craig
AU  - McClain C
FAU - Seifried, Harold
AU  - Seifried H
FAU - Silverstone, Allen
AU  - Silverstone A
FAU - Watkins, Bruce
AU  - Watkins B
FAU - Suk, William A
AU  - Suk WA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20070116
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Antioxidants)
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - Antioxidants/physiology
MH  - *Diet
MH  - Dietary Fats/adverse effects
MH  - Environmental Exposure
MH  - Environmental Health/*trends
MH  - Environmental Pollutants/*adverse effects/metabolism
MH  - Humans
MH  - Life Style
MH  - *Nutritional Status
MH  - Research/trends
PMC - PMC1852675
EDAT- 2007/04/24 09:00
MHDA- 2007/05/23 09:00
CRDT- 2007/04/24 09:00
PHST- 2006/07/26 00:00 [received]
PHST- 2007/01/16 00:00 [accepted]
PHST- 2007/04/24 09:00 [pubmed]
PHST- 2007/05/23 09:00 [medline]
PHST- 2007/04/24 09:00 [entrez]
AID - 10.1289/ehp.9549 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2007 Apr;115(4):493-5. doi: 10.1289/ehp.9549.
      Epub 2007 Jan 16.

PMID- 17296487
OWN - NLM
STAT- MEDLINE
DCOM- 20070420
LR  - 20181201
IS  - 0955-2863 (Print)
IS  - 0955-2863 (Linking)
VI  - 18
IP  - 3
DP  - 2007 Mar
TI  - Introductory comments: nutrition, environmental toxins and implications
      in prevention and intervention of human diseases.
PG  - 161-2
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture and
      Graduate Centers for Nutritional Sciences and Toxicology, University of
      Kentucky, Lexington, KY 40536, USA. bhennig@uky.edu
FAU - Ormsbee, Lindell
AU  - Ormsbee L
FAU - Bachas, Leonidas
AU  - Bachas L
FAU - Silverstone, Allen
AU  - Silverstone A
FAU - Milner, John
AU  - Milner J
FAU - Carpenter, David
AU  - Carpenter D
FAU - Thompson, Claudia
AU  - Thompson C
FAU - Suk, William A
AU  - Suk WA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Congress
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - Diet/*adverse effects
MH  - Disease/*etiology
MH  - Environmental Pollutants/*adverse effects
MH  - Humans
MH  - *Preventive Medicine
EDAT- 2007/02/14 09:00
MHDA- 2007/04/21 09:00
CRDT- 2007/02/14 09:00
PHST- 2006/12/13 00:00 [received]
PHST- 2006/12/13 00:00 [accepted]
PHST- 2007/02/14 09:00 [pubmed]
PHST- 2007/04/21 09:00 [medline]
PHST- 2007/02/14 09:00 [entrez]
AID - S0955-2863(06)00272-5 [pii]
AID - 10.1016/j.jnutbio.2006.12.004 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2007 Mar;18(3):161-2. doi: 10.1016/j.jnutbio.2006.12.004.

PMID- 17306736
OWN - NLM
STAT- MEDLINE
DCOM- 20070306
LR  - 20161019
IS  - 1590-3729 (Electronic)
IS  - 0939-4753 (Linking)
VI  - 17
IP  - 2
DP  - 2007 Feb
TI  - Environmental toxicity, nutrition, and gene interactions in the
      development of atherosclerosis.
PG  - 162-9
AB  - There is substantial evidence from epidemiological studies that the
      pathology of cardiovascular diseases is linked in part to environmental
      pollution. Many environmental contaminants, and especially persistent
      organic pollutants, are risk factors for atherosclerosis because they may
      exacerbate an underlying disease by altering gene expression patterns.
      Many mechanisms and signaling pathways associated with the pathology of
      "modern" diseases are similarly modulated by poor dietary habits and
      environmental pollutants. Many genes induced in diseases associated with
      vascular dysfunction such as atherosclerosis are oxidative stress-
      sensitive, suggesting that an imbalance in cellular oxidative stress and
      antioxidant status is a critical underlying factor. One of the emerging
      issues in modern toxicological sciences is the modification of
      environmental toxicity by nutrients. Evidence is emerging which suggests
      that antioxidant nutrients and related bioactive compounds common in
      fruits and vegetables protect against environmental toxic insult to the
      vascular endothelium by down-regulation of signaling pathways involved in
      inflammatory responses associated with vascular diseases such as
      atherosclerosis. Thus, the concept that nutrition may modify or
      ameliorate the toxicity of environmental chemicals may have implications
      for understanding the complex interaction of environmental toxicity and
      disease development.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Room 591, Wethington Health Sciences Bldg., 900
      S. Limestone, Lexington, KY 40536-0200, USA. bhennig@uky.edu
      <bhennig@uky.edu>
FAU - Oesterling, Elizabeth
AU  - Oesterling E
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20060331
PL  - Netherlands
TA  - Nutr Metab Cardiovasc Dis
JT  - Nutrition, metabolism, and cardiovascular diseases : NMCD
JID - 9111474
RN  - 0 (Air Pollutants)
SB  - IM
MH  - Air Pollutants/adverse effects
MH  - Atherosclerosis/*epidemiology/*genetics/physiopathology
MH  - Environmental Exposure/*adverse effects
MH  - Female
MH  - Gene Expression
MH  - Genetic Predisposition to Disease/*epidemiology
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Nutritional Physiological Phenomena/*genetics
MH  - Nutritional Requirements
MH  - Prognosis
MH  - Risk Assessment
MH  - Sex Characteristics
RF  - 71
EDAT- 2007/02/20 09:00
MHDA- 2007/03/07 09:00
CRDT- 2007/02/20 09:00
PHST- 2005/12/20 00:00 [received]
PHST- 2006/01/06 00:00 [revised]
PHST- 2006/01/09 00:00 [accepted]
PHST- 2007/02/20 09:00 [pubmed]
PHST- 2007/03/07 09:00 [medline]
PHST- 2007/02/20 09:00 [entrez]
AID - S0939-4753(06)00015-9 [pii]
AID - 10.1016/j.numecd.2006.01.003 [doi]
PST - ppublish
SO  - Nutr Metab Cardiovasc Dis. 2007 Feb;17(2):162-9. doi:
      10.1016/j.numecd.2006.01.003. Epub 2006 Mar 31.

PMID- 16563718
OWN - NLM
STAT- MEDLINE
DCOM- 20061130
LR  - 20161019
IS  - 0955-2863 (Print)
IS  - 0955-2863 (Linking)
VI  - 17
IP  - 11
DP  - 2006 Nov
TI  - Linoleic acid induces proinflammatory events in vascular endothelial
      cells via activation of PI3K/Akt and ERK1/2 signaling.
PG  - 766-72
AB  - Linoleic acid (18:2n-6), is a major unsaturated fatty acid in the
      American diet. Linoleic acid is considered to be atherogenic because of
      its pro-oxidative and proinflammatory properties. There is substantial
      evidence that linoleic acid (LA) can activate vascular endothelial cells
      and contribute to an inflammatory response. To explore the mechanisms of
      LA-induced proinflammatory signaling pathways, the present study
      addresses the role of the phosphatidylinositol 3-kinase/amino kinase
      terminal (PI3K/Akt), extracellular signal regulated kinase 1/2 (ERK1/2)
      and p38 mitogen-activated protein kinase (MAPK) pathways during vascular
      endothelial cell activation. After a 3- to 6-h exposure, LA significantly
      activated both Akt and ERK in endothelial cells, as assessed by western
      blot and immunofluorescence. In contrast, LA activated p38 MAPK already
      at 10 min, suggesting that p38 MAPK signaling occurred upstream of the
      ERK1/2 pathway. Furthermore, inhibition of ERK activity by PD98059 and
      PI3K/Akt activity by LY294002 or wortmannin significantly reduced the LA-
      induced activation of nuclear factor kappa B (NF-kappaB). These results
      suggest a contribution of both the ERK1/2 and PI3K/Akt pathways to the
      effect of LA on NF-kappaB-dependent transcription. Indeed, LA-mediated
      gene expression of the vascular cell adhesion molecule 1 was suppressed
      by PD98059, wortmannin and LY294002. These data indicate that both
      PI3K/Akt- and ERK1/2-mediated proinflammatory signaling events are
      critical in LA-induced endothelial cell activation and vascular
      inflammation.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40536-0200, USA. bhennig@uky.edu
FAU - Lei, Wang
AU  - Lei W
FAU - Arzuaga, Xabier
AU  - Arzuaga X
FAU - Ghosh, Debjani Das
AU  - Ghosh DD
FAU - Saraswathi, Viswanathan
AU  - Saraswathi V
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20060324
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (NF-kappa B)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Endothelial Cells/*drug effects/*enzymology
MH  - Enzyme Activation/drug effects
MH  - Inflammation/chemically induced/enzymology
MH  - Linoleic Acid/*pharmacology
MH  - Mitogen-Activated Protein Kinase 1/*metabolism
MH  - Mitogen-Activated Protein Kinase 3/*metabolism
MH  - NF-kappa B/metabolism
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction/drug effects
MH  - Swine
MH  - Vascular Cell Adhesion Molecule-1/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2006/03/28 09:00
MHDA- 2006/12/09 09:00
CRDT- 2006/03/28 09:00
PHST- 2005/11/22 00:00 [received]
PHST- 2006/01/04 00:00 [revised]
PHST- 2006/01/09 00:00 [accepted]
PHST- 2006/03/28 09:00 [pubmed]
PHST- 2006/12/09 09:00 [medline]
PHST- 2006/03/28 09:00 [entrez]
AID - S0955-2863(06)00022-2 [pii]
AID - 10.1016/j.jnutbio.2006.01.005 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2006 Nov;17(11):766-72. doi:
      10.1016/j.jnutbio.2006.01.005. Epub 2006 Mar 24.

PMID- 16395283
OWN - NLM
STAT- MEDLINE
DCOM- 20060830
LR  - 20181201
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 26
IP  - 8
DP  - 2006 Aug
TI  - HIV-TAT protein upregulates expression of multidrug resistance protein 1
      in the blood-brain barrier.
PG  - 1052-65
AB  - Central nervous system (CNS) complications of human immunodeficiency
      virus (HIV) infection remain a serious health risk in HIV/acquired
      immunodeficiency syndrome despite significant advances in highly active
      antiretroviral therapy (HAART). Specific drugs used for HAART are
      substrates for the efflux transport systems, such as the multidrug
      resistance-associated proteins (MRPs), which are present on brain
      microvascular endothelial cells (BMEC) and astrocytes, that is, the main
      cell types that form the blood-brain barrier (BBB). Thus, drugs employed
      in HAART are actively removed from the CNS and do not efficiently inhibit
      HIV replication in the brain. To study the potential mechanisms of this
      process, the aim of the present research was to address the hypothesis
      that HIV Tat protein can contribute to upregulation of MRP expression at
      the BBB level. Tat is a protein produced and released by HIV-infected
      cells, which may play an important role in brain vascular pathology in
      the course of HIV infection. Among the family of MRPs, exposure to Tat
      specifically induced MRP1 messenger ribonucleic acid and protein
      expression both in BMEC and astrocytes. These alterations were
      accompanied by enhanced MRP1-mediated efflux functions. Furthermore,
      activation of the mitogen-activated protein kinase signaling cascade was
      identified as the mechanism involved in Tat-mediated overexpression of
      MRP1. These results indicate that Tat exposure can lead to alterations of
      the BBB functions and decrease HAART efficacy in the CNS through
      overexpression of drug efflux transporters.
FAU - Hayashi, Kentaro
AU  - Hayashi K
AD  - Department of Surgery, University of Kentucky, Lexington, Kentucky 40536,
      USA.
FAU - Pu, Hong
AU  - Pu H
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Yamauchi, Atsushi
AU  - Yamauchi A
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20051214
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (Gene Products, tat)
RN  - 0 (RNA, Messenger)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member
      1/*biosynthesis/genetics
MH  - Acquired Immunodeficiency Syndrome/complications/drug
      therapy/genetics/*metabolism
MH  - Animals
MH  - Antiretroviral Therapy, Highly Active
MH  - Astrocytes/cytology/metabolism/virology
MH  - Blood-Brain Barrier/*metabolism/virology
MH  - Cells, Cultured
MH  - Central Nervous System Viral Diseases/drug
      therapy/etiology/genetics/*metabolism
MH  - Endothelial Cells/metabolism/virology
MH  - Gene Products, tat/genetics/*metabolism
MH  - HIV-1/genetics/*metabolism
MH  - Humans
MH  - Male
MH  - Mice
MH  - Protein Biosynthesis/drug effects/genetics
MH  - RNA, Messenger/biosynthesis/genetics
MH  - *Up-Regulation/drug effects/genetics
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2006/01/06 09:00
MHDA- 2006/08/31 09:00
CRDT- 2006/01/06 09:00
PHST- 2006/01/06 09:00 [pubmed]
PHST- 2006/08/31 09:00 [medline]
PHST- 2006/01/06 09:00 [entrez]
AID - 9600254 [pii]
AID - 10.1038/sj.jcbfm.9600254 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2006 Aug;26(8):1052-65. doi:
      10.1038/sj.jcbfm.9600254. Epub 2005 Dec 14.

PMID- 16611624
OWN - NLM
STAT- MEDLINE
DCOM- 20060830
LR  - 20211020
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 92
IP  - 1
DP  - 2006 Jul
TI  - c-Src is the primary signaling mediator of polychlorinated biphenyl-
      induced interleukin-8 expression in a human microvascular endothelial
      cell line.
PG  - 311-20
AB  - Interleukin-8/CXCL8 (IL-8) is a prominent factor that modulates
      endothelial cell proliferation, migration, and angiogenesis. Therefore,
      the present study focused on the regulatory mechanisms of IL-8 expression
      induced by environmental pollutants such as polychlorinated biphenyls
      (PCBs). Treatment of human microvascular endothelial cells (HMECs) with
      specific PCB congener, 2,2',4,6,6'-pentachlorobiphenyl (PCB 104), dose
      dependently increased levels of IL-8 mRNA and secreted protein.
      IL-8-neutralizing antibody inhibited migration of endothelial cells
      stimulated by conditioned media derived from PCB 104-treated HMECs. Site-
      directed mutagenesis of the IL-8 promoter- and DNA-binding assays
      revealed that activator protein 1 (AP-1) and nuclear factor kappaB (NF-
      kappaB) sites are required for PCB 104-induced IL-8 transcription. Most
      importantly, pharmacological inhibition of Src kinase activity or
      overexpression of dominant-negative c-src in HMECs resulted in a
      significant decrease in IL-8 expression and promoter activity. In
      contrast, ectopic expression of activated c-Src markedly increased
      promoter activity of IL-8. These stimulatory effects of dominant-positive
      c-src were abrogated by mutagenesis of AP-1- and NF-kappaB-binding sites
      in the IL-8 promoter.
FAU - Eum, Sung Yong
AU  - Eum SY
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Surgery and College of Agriculture, University of Kentucky, 900 South
      Limestone, Lexington, KY 40536, USA.
FAU - Rha, Geun Bae
AU  - Rha GB
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20060411
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (DNA Primers)
RN  - 0 (Interleukin-8)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.10.2 (Proto-Oncogene Proteins pp60(c-src))
SB  - IM
MH  - Base Sequence
MH  - Cell Line
MH  - DNA Primers
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Humans
MH  - Interleukin-8/*genetics
MH  - Mutagenesis, Site-Directed
MH  - NF-kappa B/physiology
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Promoter Regions, Genetic
MH  - Proto-Oncogene Proteins pp60(c-src)/*physiology
MH  - RNA, Messenger/genetics
MH  - Signal Transduction/*physiology
MH  - Transcription Factor AP-1/physiology
EDAT- 2006/04/14 09:00
MHDA- 2006/08/31 09:00
CRDT- 2006/04/14 09:00
PHST- 2006/04/14 09:00 [pubmed]
PHST- 2006/08/31 09:00 [medline]
PHST- 2006/04/14 09:00 [entrez]
AID - kfj194 [pii]
AID - 10.1093/toxsci/kfj194 [doi]
PST - ppublish
SO  - Toxicol Sci. 2006 Jul;92(1):311-20. doi: 10.1093/toxsci/kfj194. Epub 2006
      Apr 11.

PMID- 16778083
OWN - NLM
STAT- MEDLINE
DCOM- 20060721
LR  - 20181201
IS  - 1541-7786 (Print)
IS  - 1541-7786 (Linking)
VI  - 4
IP  - 6
DP  - 2006 Jun
TI  - Interplay between epidermal growth factor receptor and Janus kinase 3
      regulates polychlorinated biphenyl-induced matrix metalloproteinase-3
      expression and transendothelial migration of tumor cells.
PG  - 361-70
AB  - We hypothesize that environmental toxicants, such as polychlorinated
      biphenyl congeners, can activate vascular endothelial cells and thus
      increase formation of blood-borne metastases. This study indicates that
      exposure of human microvascular endothelial cells to
      2,2',4,6,6'-pentachlorobiphenyl can stimulate transendothelial migration
      of tumor cells through up-regulation of matrix metalloproteinase (MMP)-3.
      In a series of experiments with specific small interfering RNA and
      pharmacologic inhibitors, we provide evidence that
      2,2',4,6,6'-pentachlorobiphenyl can activate epidermal growth factor
      receptor (EGFR) and Janus kinase 3 (JAK3) in a closely coordinated and
      cross-dependent fashion. Activated EGFR and JAK3 stimulate in concert
      c-Jun NH(2)-terminal kinase and extracellular signal-regulated kinase 1/2
      as well as increase DNA-binding activity of transcription factors
      activator protein-1 and polyomavirus enhancer activator protein 3,
      leading to transcriptional up-regulation of MMP-3 expression. These
      results indicate that the interplay among EGFR, JAK3, and mitogen-
      activated protein kinases, such as c-Jun NH(2)-terminal kinase and
      extracellular signal-regulated kinase 1/2, is critical for
      polychlorinated biphenyl-induced MMP-3 expression and accelerated
      transendothelial migration of tumor cells.
FAU - Eum, Sung Yong
AU  - Eum SY
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Surgery, University of Kentucky, Lexington, USA.
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Cancer Res
JT  - Molecular cancer research : MCR
JID - 101150042
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 0 (enhancer-binding protein AP-3)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (JAK3 protein, human)
RN  - EC 2.7.10.2 (Janus Kinase 3)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - Z4YYF101N3 (2,2',4,6,6'-pentachlorobiphenyl)
SB  - IM
MH  - Breast Neoplasms/metabolism/*pathology
MH  - Capillary Permeability
MH  - Cell Adhesion
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - DNA-Binding Proteins/metabolism
MH  - Endothelial Cells/drug effects/enzymology
MH  - Endothelium, Vascular/*drug effects
MH  - ErbB Receptors/*metabolism
MH  - Humans
MH  - Janus Kinase 3
MH  - Matrix Metalloproteinase 3/*genetics
MH  - Mitogen-Activated Protein Kinases
MH  - Neoplasm Metastasis
MH  - Polychlorinated Biphenyls/metabolism/*toxicity
MH  - Protein-Tyrosine Kinases/*metabolism
MH  - Transcription Factor AP-1/metabolism
MH  - Transcription Factors/metabolism
MH  - Up-Regulation
EDAT- 2006/06/17 09:00
MHDA- 2006/07/22 09:00
CRDT- 2006/06/17 09:00
PHST- 2006/06/17 09:00 [pubmed]
PHST- 2006/07/22 09:00 [medline]
PHST- 2006/06/17 09:00 [entrez]
AID - 4/6/361 [pii]
AID - 10.1158/1541-7786.MCR-05-0119 [doi]
PST - ppublish
SO  - Mol Cancer Res. 2006 Jun;4(6):361-70. doi: 10.1158/1541-7786.MCR-05-0119.

PMID- 16775385
OWN - NLM
STAT- MEDLINE
DCOM- 20070322
LR  - 20181113
IS  - 1535-1084 (Print)
IS  - 1535-1084 (Linking)
VI  - 8
IP  - 3
DP  - 2006
TI  - Cyclooxygenase-2 is involved in HIV-1 Tat-induced inflammatory responses
      in the brain.
PG  - 337-52
AB  - Cyclooxygenase (COX)-2, a rate-limiting enzyme for prostanoid synthesis,
      can be involved in inflammatory-mediated cytotoxicity. Although the
      contribution of COX-2 to peripheral inflammation is well understood, its
      role in brain inflammation is not fully recognized. In particular, COX-2
      involvement in inflammatory responses induced by HIV proteins in the
      central nervous system is not known. Therefore, the present study focused
      on COX-2 expression and its role in modulating the expression of brain
      inflammatory-related genes following exposure to the HIV-1
      transactivating protein Tat. Intrahippocampal injections of Tat induced
      dose-dependent upregulation of COX-2 mRNA and protein levels in C57BL/6
      mice. COX-2 immunoreactivity was primarily localized in microglial cells
      and astrocytes. Tat-induced COX-2 expression was partially prevented by
      pyrrolidine dithiocarbamate, a potent antioxidant and an inhibitor of the
      transcription factor, nuclear factor kappaB. Most importantly,
      administration of the COX-2 inhibitor NS-398 attenuated Tat-mediated
      upregulation of mRNA and protein expression of inflammatory mediators,
      such as monocyte chemoattractant protein-1, interleukin-1beta, tumor
      necrosis factor-alpha, and inducible nitric oxide synthase. Moreover,
      treatment with NS-398 significantly attenuated Tat-induced activation of
      microglial cells. These results provide evidence that COX-2
      overexpression can modulate induction of brain inflammatory mediators in
      response to HIV-1 Tat protein. Such alterations may play an important
      role in the development of brain inflammatory reactions in HIV-infected
      patients and contribute to the development of neurological complications
      in the course of HIV-1 infection.
FAU - Flora, Govinder
AU  - Flora G
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Surgery, University of Kentucky, Lexington KY 40536, USA.
FAU - Pu, Hong
AU  - Pu H
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
GR  - MH072567/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Neuromolecular Med
JT  - Neuromolecular medicine
JID - 101135365
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Gene Products, tat)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitrobenzenes)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sulfonamides)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 123653-11-2 (N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Animals
MH  - Astrocytes/cytology/metabolism
MH  - *Brain/enzymology/immunology
MH  - Cyclooxygenase 2/genetics/*metabolism
MH  - Cyclooxygenase Inhibitors/metabolism
MH  - Dose-Response Relationship, Immunologic
MH  - Gene Expression Regulation, Enzymologic
MH  - Gene Products, tat/*immunology
MH  - HIV-1/*immunology
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microglia/cytology/metabolism
MH  - NF-kappa B/metabolism
MH  - Nitrobenzenes/metabolism
MH  - Oxidation-Reduction
MH  - RNA, Messenger/metabolism
MH  - Sulfonamides/metabolism
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2006/06/16 09:00
MHDA- 2007/03/23 09:00
CRDT- 2006/06/16 09:00
PHST- 2005/07/22 00:00 [received]
PHST- 2005/11/07 00:00 [revised]
PHST- 2005/12/05 00:00 [accepted]
PHST- 2006/06/16 09:00 [pubmed]
PHST- 2007/03/23 09:00 [medline]
PHST- 2006/06/16 09:00 [entrez]
AID - NMM:8:3:337 [pii]
AID - 10.1385/NMM:8:3:337 [doi]
PST - ppublish
SO  - Neuromolecular Med. 2006;8(3):337-52. doi: 10.1385/NMM:8:3:337.

PMID- 15829913
OWN - NLM
STAT- MEDLINE
DCOM- 20051130
LR  - 20161019
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 25
IP  - 10
DP  - 2005 Oct
TI  - HIV-1 Tat protein-induced alterations of ZO-1 expression are mediated by
      redox-regulated ERK 1/2 activation.
PG  - 1325-35
AB  - HIV-1 Tat protein plays an important role in inducing monocyte
      infiltration into the brain and may alter the structure and functions of
      the blood-brain barrier (BBB). The BBB serves as a frontline defense
      system, protecting the central nervous system from infected monocytes
      entering the brain. Therefore, the aim of the present study was to
      examine the mechanisms of Tat effect on the integrity of the BBB in the
      mouse brain. Tat was injected into the right hippocampi of C57BL/6 mice
      and expression of tight junction protein zonula occludens-1 (ZO-1) was
      determined in control and treated mice. Tat administration resulted in
      decreased mRNA levels of ZO-1 and marked disruption of ZO-1 continuity.
      These changes were associated with accumulation of inflammatory cells in
      brain tissue of Tat-treated mice. Further experiments indicated that Tat-
      mediated alterations of redox-related signaling may be responsible for
      decreased ZO-1 expression. Specifically, injections with Tat resulted in
      activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and
      pretreatment with U 0126, a specific inhibitor of ERK kinase, effectively
      ameliorated the Tat-induced diminished ZO-1 levels. In addition,
      administration of N-acetylcysteine (NAC), a precursor of glutathione and
      a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and
      alterations in ZO-1 expression. These results indicate that Tat-induced
      oxidative stress can play an important role in affecting the integrity of
      the BBB through the ERK 1/2 pathway.
FAU - Pu, Hong
AU  - Pu H
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Surgery, University of Kentucky Medical Center, Kentucky 40536, USA.
FAU - Tian, Jing
AU  - Tian J
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Hayashi, Kentaro
AU  - Hayashi K
FAU - Flora, Govinder
AU  - Flora G
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Gene Products, tat)
RN  - 0 (Membrane Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tjp1 protein, mouse)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/drug effects
MH  - Gene Expression Regulation/*drug effects
MH  - Gene Products, tat/administration & dosage/*pharmacology
MH  - Hippocampus
MH  - Inflammation
MH  - Membrane Proteins/*genetics
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mitogen-Activated Protein Kinase 3/*metabolism/physiology
MH  - Oxidation-Reduction
MH  - Oxidative Stress/drug effects
MH  - Phosphoproteins/*genetics
MH  - RNA, Messenger/analysis
MH  - Signal Transduction
MH  - Zonula Occludens-1 Protein
EDAT- 2005/04/15 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/04/15 09:00
PHST- 2005/04/15 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/04/15 09:00 [entrez]
AID - 9600125 [pii]
AID - 10.1038/sj.jcbfm.9600125 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2005 Oct;25(10):1325-35. doi:
      10.1038/sj.jcbfm.9600125.

PMID- 15815581
OWN - NLM
STAT- MEDLINE
DCOM- 20050921
LR  - 20161019
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 25
IP  - 9
DP  - 2005 Sep
TI  - Signaling mechanisms of HIV-1 Tat-induced alterations of claudin-5
      expression in brain endothelial cells.
PG  - 1159-70
AB  - Exposure of brain microvascular endothelial cells (BMEC) to human
      immunodeficiency virus-1 (HIV-1) Tat protein can decrease expression and
      change distribution of tight junction proteins, including claudin-5.
      Owing to the importance of claudin-5 in maintaining the blood-brain
      barrier (BBB) integrity, the present study focused on the regulatory
      mechanisms of Tat-induced alterations of claudin-5 mRNA and protein
      levels. Real-time reverse-transcription-polymerase chain reaction
      revealed that claudin-5 mRNA was markedly diminished in BMEC exposed to
      Tat. However, U0126 (an inhibitor of mitogen-activated protein kinase
      kinase1/2, MEK1/2) protected against this effect. In addition, inhibition
      of the vascular endothelial growth factor receptor type 2 (VEGFR-2) by
      SU1498, phosphatidylinositol-3 kinase (PI-3 K) by LY294002, nuclear
      factor-kappaB (NF-kappaB) by peptide SN50, and intracellular calcium by
      BAPTA/AM partially prevented Tat-mediated alterations in claudin-5
      protein levels and immunoreactivity patterns. In contrast, inhibition of
      protein kinase C did not affect claudin-5 expression in Tat-treated
      cells. The present findings indicate that activation of VEGFR-2 and
      multiple redox-regulated signal transduction pathways are involved in
      Tat-induced alterations of claudin-5 expression. Because claudins
      constitute the major backbone of tight junctions, the present data are
      relevant to the disturbances of the BBB in the course of HIV-1 infection.
FAU - Andras, Ibolya E
AU  - Andras IE
AD  - Department of Surgery, University of Kentucky, Lexington, Kentucky 40536,
      USA.
FAU - Pu, Hong
AU  - Pu H
FAU - Tian, Jing
AU  - Tian J
FAU - Deli, Maria A
AU  - Deli MA
FAU - Nath, Avindra
AU  - Nath A
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Chelating Agents)
RN  - 0 (Claudin-5)
RN  - 0 (Cldn5 protein, rat)
RN  - 0 (Gene Products, tat)
RN  - 0 (Membrane Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Brain Chemistry/*drug effects
MH  - Calcium/pharmacology
MH  - Cells, Cultured
MH  - Chelating Agents/pharmacology
MH  - Claudin-5
MH  - Down-Regulation/physiology
MH  - Endothelial Cells/*drug effects
MH  - Gene Products, tat/*pharmacology
MH  - Genes, ras/genetics
MH  - HIV-1/*metabolism
MH  - Membrane Proteins/*biosynthesis
MH  - Microscopy, Fluorescence
MH  - NF-kappa B/drug effects/physiology
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/*physiology
MH  - Vascular Endothelial Growth Factor Receptor-2/metabolism
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2005/04/09 09:00
MHDA- 2005/09/22 09:00
CRDT- 2005/04/09 09:00
PHST- 2005/04/09 09:00 [pubmed]
PHST- 2005/09/22 09:00 [medline]
PHST- 2005/04/09 09:00 [entrez]
AID - 9600115 [pii]
AID - 10.1038/sj.jcbfm.9600115 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2005 Sep;25(9):1159-70. doi:
      10.1038/sj.jcbfm.9600115.

PMID- 16140885
OWN - NLM
STAT- MEDLINE
DCOM- 20051121
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 135
IP  - 9
DP  - 2005 Sep
TI  - Zinc deficiency increases plasma lipids and atherosclerotic markers in
      LDL-receptor-deficient mice.
PG  - 2114-8
AB  - Low zinc concentration can be associated with an increased risk of
      cardiovascular diseases. In the current study, we hypothesize that zinc
      deficiency can increase and zinc supplementation can decrease
      proatherosclerotic events in LDL receptor knock-out (LDL-R-/-) mice fed a
      moderate-fat diet. Mice were fed either a zinc-deficient (0 micromol
      Zn/g), a control (0.45 micromol Zn/g), or a zinc-supplemented (1.529
      micromol Zn/g) diet for 4 wk. Mice fed the zinc-deficient diet had
      significantly increased concentrations of cholesterol and
      triacylglycerides in the VLDL and HDL fractions. Zinc supplementation
      decreased these lipid variables compared with control mice. We detected
      significantly higher concentrations of glutathione reductase mRNA in the
      thoracic aortae of zinc-deficient mice. Furthermore, inflammatory
      markers, such as nuclear factor-kappaB and vascular cell adhesion
      molecule-1, were significantly increased in zinc-deficient mice compared
      with mice of the control or supplemented groups. In addition, zinc
      deficiency significantly reduced the DNA binding activity of peroxisome
      proliferator activate receptors (PPARs) in liver extracts. Interestingly,
      mRNA expression levels of PPARgamma were significantly increased in
      thoracic aortae of zinc-deficient mice, indicating an adaptation process
      to decreased PPAR signaling. These data provide in vivo evidence of zinc
      deficiency inducing proinflammatory events in an atherogenic mouse model.
      These data also suggest that adequate zinc may be a critical component in
      protective PPAR signaling during atherosclerosis.
FAU - Reiterer, Gudrun
AU  - Reiterer G
AD  - Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, 40546, USA.
FAU - MacDonald, Ruth
AU  - MacDonald R
FAU - Browning, Jim D
AU  - Browning JD
FAU - Morrow, Jason
AU  - Morrow J
FAU - Matveev, Sergey V
AU  - Matveev SV
FAU - Daugherty, Alan
AU  - Daugherty A
FAU - Smart, Eric
AU  - Smart E
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Biomarkers)
RN  - 0 (Lipids)
RN  - 0 (PPAR gamma)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, LDL)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - EC 1.8.1.7 (Glutathione Reductase)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/*metabolism
MH  - Biomarkers/*metabolism
MH  - Body Weight
MH  - Glutathione Reductase/genetics
MH  - Lipids/*blood
MH  - Liver/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Osmolar Concentration
MH  - PPAR gamma/genetics
MH  - RNA, Messenger/metabolism
MH  - Receptors, LDL/*deficiency
MH  - Transcription Factors/metabolism
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
MH  - Zinc/*deficiency/metabolism
EDAT- 2005/09/06 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/09/06 09:00
PHST- 2005/09/06 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/09/06 09:00 [entrez]
AID - 135/9/2114 [pii]
AID - 10.1093/jn/135.9.2114 [doi]
PST - ppublish
SO  - J Nutr. 2005 Sep;135(9):2114-8. doi: 10.1093/jn/135.9.2114.

PMID- 15934943
OWN - NLM
STAT- MEDLINE
DCOM- 20050624
LR  - 20181201
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 93
IP  - 5
DP  - 2005 Jun
TI  - HIV-Tat protein induces P-glycoprotein expression in brain microvascular
      endothelial cells.
PG  - 1231-41
AB  - Among the different factors which can contribute to CNS alterations
      associated with HIV infection, Tat protein is considered to play a
      critical role. Evidence indicates that Tat can contribute to brain
      vascular pathology through induction of endothelial cell activation. In
      the present study, we hypothesized that Tat can affect expression of
      P-glycoprotein (P-gp) in brain microvascular endothelial cells (BMEC).
      P-gp is an ATP-dependent cellular efflux transporter which is involved in
      the removal of specific non-polar molecules, including drugs used for
      highly active antiretroviral therapy (HAART). Treatment of BMEC with
      Tat(1-72) resulted in P-gp overexpression both at mRNA and protein
      levels. These alterations were confirmed in vivo in brain vessels of mice
      injected with Tat(1-72) into the hippocampus. Furthermore, pre-treatment
      of BMEC with SN50, a specific NF-kappaB inhibitor, protected against
      Tat(1-72)-stimulated expression of mdr1a gene, i.e. the gene which
      encodes for P-gp in rodents. Tat(1-72)-mediated changes in P-gp
      expression were correlated with increased rhodamine 123 efflux,
      indicating the up-regulation of transporter functions of P-gp. These
      results suggest that Tat-induced overexpression of P-gp in brain
      microvessels may have significant implications for the development of
      resistance to HAART and may be a contributing factor for low efficacy of
      HAART in the CNS.
FAU - Hayashi, Kentaro
AU  - Hayashi K
AD  - Molecular Neuroscience and Vascular Biology Laboratory, Department of
      Surgery, University of Kentucky Medical Center, Lexington, Kentucky
      40536, USA.
FAU - Pu, Hong
AU  - Pu H
FAU - Tian, Jing
AU  - Tian J
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B)
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (ATP-Binding Cassette Transporters)
RN  - 0 (Gene Products, tat)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 0 (tat peptide (1-72), Human immunodeficiency virus 1)
RN  - 9EI49ZU76O (multidrug resistance protein 3)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B/genetics
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/*metabolism
MH  - ATP-Binding Cassette Transporters/genetics
MH  - Animals
MH  - Astrocytes/metabolism
MH  - Brain/*blood supply/cytology
MH  - Cells, Cultured
MH  - Endothelial Cells/*metabolism
MH  - Gene Products, tat/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microcirculation
MH  - NF-kappa B/physiology
MH  - RNA, Messenger/metabolism
MH  - Up-Regulation
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2005/06/07 09:00
MHDA- 2005/06/25 09:00
CRDT- 2005/06/07 09:00
PHST- 2005/06/07 09:00 [pubmed]
PHST- 2005/06/25 09:00 [medline]
PHST- 2005/06/07 09:00 [entrez]
AID - JNC3114 [pii]
AID - 10.1111/j.1471-4159.2005.03114.x [doi]
PST - ppublish
SO  - J Neurochem. 2005 Jun;93(5):1231-41. doi:
      10.1111/j.1471-4159.2005.03114.x.

PMID- 15962513
OWN - NLM
STAT- MEDLINE
DCOM- 20050715
LR  - 20191026
IS  - 0272-4340 (Print)
IS  - 0272-4340 (Linking)
VI  - 25
IP  - 1
DP  - 2005 Feb
TI  - Mechanisms of the blood-brain barrier disruption in HIV-1 infection.
PG  - 181-99
AB  - (1) Alterations of brain microvasculature and the disruption of the
      blood-brain barrier (BBB) integrity are commonly associated with human
      immunodeficiency virus type 1 (HIV-1) infection. These changes are most
      frequently found in human immunodeficiency virus-related encephalitis
      (HIVE) and in human immunodeficiency virus-associated dementia (HAD). (2)
      It has been hypothesized that the disruption of the BBB occurs early in
      the course of HIV-1 infection and can be responsible for HIV-1 entry into
      the CNS. (3) The current review discusses the mechanisms of injury to
      brain endothelial cells and alterations of the BBB integrity in HIV-
      infection with focus on the vascular effects of HIV Tat protein. In
      addition, this review describes the mechanisms of the BBB disruption due
      to HIV-1 or Tat protein interaction with selected risk factors for HIV
      infection, such as substance abuse and aging.
FAU - Toborek, Michal
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky, Lexington, Kentucky 40536,
      USA. mjtobo00@uky.edu
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Flora, Govinder
AU  - Flora G
FAU - Pu, Hong
AU  - Pu H
FAU - Andras, Ibolya E
AU  - Andras IE
FAU - Wylegala, Edward
AU  - Wylegala E
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Nath, Avindra
AU  - Nath A
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
SB  - IM
MH  - AIDS Dementia Complex/immunology/*physiopathology
MH  - Blood-Brain Barrier/immunology/*physiopathology/*virology
MH  - *HIV-1
MH  - Humans
RF  - 139
EDAT- 2005/06/21 09:00
MHDA- 2005/07/16 09:00
CRDT- 2005/06/21 09:00
PHST- 2005/06/21 09:00 [pubmed]
PHST- 2005/07/16 09:00 [medline]
PHST- 2005/06/21 09:00 [entrez]
AID - 10.1007/s10571-004-1383-x [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2005 Feb;25(1):181-99. doi:
      10.1007/s10571-004-1383-x.

PMID- 15589507
OWN - NLM
STAT- MEDLINE
DCOM- 20050218
LR  - 20161019
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 191
IP  - 1
DP  - 2005 Jan
TI  - Proinflammatory synergism of ethanol and HIV-1 Tat protein in brain
      tissue.
PG  - 2-12
AB  - Human immunodeficiency virus type 1 (HIV-1) Tat protein is a potent
      transactivator of viral replication. It is actively released from HIV-
      infected cells and has been shown to induce cell injury effects. Alcohol
      abuse is a risk factor of HIV infection and we hypothesize that alcohol
      and Tat may interact in an additive or synergistic fashion to influence
      molecular processes which can contribute to their toxic effects. To study
      this possibility, we investigated the effects of two intraperitoneal
      injections of ethanol (EtOH, 3 g/kg each, 16 h apart) and a single
      intracerebral injection of Tat (25 microg/microl into the right
      hippocampus, injected 12 h after the first EtOH injection) on generation
      of cellular oxidative stress, DNA binding activity of redox-responsive
      transcription factors, and induction of inflammatory genes in the
      hippocampus and corpus striatum of mouse brain. As compared to control
      animals, treatment with EtOH plus Tat resulted in increased production of
      reactive oxygen species in both brain regions. In addition, DNA binding
      activities of nuclear factor-kappaB (NF-kappaB) and CREB in both brain
      regions and SP-1 in the hippocampus were more pronounced in mice injected
      with Tat plus EtOH as compared to the effects of Tat or EtOH alone. Among
      studied inflammatory genes, induction of IL-1beta and MCP-1 was
      potentiated in animals injected with EtOH plus Tat. These results
      indicate that Tat and EtOH can cross-amplify their cellular effects,
      leading to alterations of redox-regulated inflammatory pathways in the
      brain. Such potentiation of proinflammatory stimulation may further
      contribute to CNS pathology in HIV-infected patients who are alcohol
      abusers.
FAU - Flora, Govinder
AU  - Flora G
AD  - Department of Surgery, University of Kentucky, Lexington, KY 40536, USA.
FAU - Pu, Hong
AU  - Pu H
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Ravikumar, R
AU  - Ravikumar R
FAU - Nath, Avindra
AU  - Nath A
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Gene Products, tat)
RN  - 0 (Inflammation Mediators)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Animals
MH  - Brain/drug effects/*metabolism/*pathology
MH  - Drug Synergism
MH  - Ethanol/*pharmacology
MH  - Gene Products, tat/biosynthesis/genetics/*physiology
MH  - HIV-1/*drug effects/*physiology
MH  - Inflammation Mediators/*pharmacology/physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2004/12/14 09:00
MHDA- 2005/02/19 09:00
CRDT- 2004/12/14 09:00
PHST- 2004/02/22 00:00 [received]
PHST- 2004/06/01 00:00 [revised]
PHST- 2004/06/07 00:00 [accepted]
PHST- 2004/12/14 09:00 [pubmed]
PHST- 2005/02/19 09:00 [medline]
PHST- 2004/12/14 09:00 [entrez]
AID - S0014488604002377 [pii]
AID - 10.1016/j.expneurol.2004.06.007 [doi]
PST - ppublish
SO  - Exp Neurol. 2005 Jan;191(1):2-12. doi: 10.1016/j.expneurol.2004.06.007.

PMID- 15626652
OWN - NLM
STAT- MEDLINE
DCOM- 20050322
LR  - 20181113
IS  - 0091-6765 (Print)
IS  - 0091-6765 (Linking)
VI  - 113
IP  - 1
DP  - 2005 Jan
TI  - Dietary fat interacts with PCBs to induce changes in lipid metabolism in
      mice deficient in low-density lipoprotein receptor.
PG  - 83-7
AB  - There is evidence that dietary fat can modify the cytotoxicity of
      polychlorinated biphenyls (PCBs) and that coplanar PCBs can induce
      inflammatory processes critical in the pathology of vascular diseases. To
      test the hypothesis that the interaction of PCBs with dietary fat is
      dependent on the type of fat, low-density lipoprotein receptor-deficient
      (LDL-R(-/-)) mice were fed diets enriched with either olive oil or corn
      oil for 4 weeks. Half of the animals from each group were injected with
      PCB-77. Vascular cell adhesion molecule-1 (VCAM-1) expression in aortic
      arches was nondetectable in the olive-oil-fed mice but was highly
      expressed in the presence of PCB-77. PCB treatment increased liver
      neutral lipids and decreased serum fatty acid levels only in mice fed the
      corn-oil-enriched diet. PCB treatment increased mRNA expression of genes
      involved in inflammation, apoptosis, and oxidative stress in all mice.
      Upon PCB treatment, mice in both olive- and corn-oil-diet groups showed
      induction of genes involved in fatty acid degradation but with up-
      regulation of different key enzymes. Genes involved in fatty acid
      synthesis were reduced only upon PCB treatment in corn-oil-fed mice,
      whereas lipid transport/export genes were altered in olive-oil-fed mice.
      These data suggest that dietary fat can modify changes in lipid
      metabolism induced by PCBs in serum and tissues. These findings have
      implications for understanding the interactions of nutrients with
      environmental contaminants on the pathology of inflammatory diseases such
      as atherosclerosis.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture and
      Graduate Center for Nutritional Sciences, University of Kentucky,
      Lexington, Kentucky 40536-0200, USA. bhenning@uky.edu
FAU - Reiterer, Gudrun
AU  - Reiterer G
FAU - Toborek, Michal
AU  - Toborek M
FAU - Matveev, Sergey V
AU  - Matveev SV
FAU - Daugherty, Alan
AU  - Daugherty A
FAU - Smart, Eric
AU  - Smart E
FAU - Robertson, Larry W
AU  - Robertson LW
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES013661/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Receptors, LDL)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Diet
MH  - Dietary Fats/*pharmacology
MH  - Drug Interactions
MH  - Environmental Pollutants/*pharmacology/*poisoning
MH  - Mice
MH  - Polychlorinated Biphenyls/*pharmacology/*poisoning
MH  - Receptors, LDL/*drug effects/*physiology
PMC - PMC1253714
EDAT- 2005/01/01 09:00
MHDA- 2005/03/23 09:00
CRDT- 2005/01/01 09:00
PHST- 2005/01/01 09:00 [pubmed]
PHST- 2005/03/23 09:00 [medline]
PHST- 2005/01/01 09:00 [entrez]
AID - 10.1289/ehp.7280 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2005 Jan;113(1):83-7. doi: 10.1289/ehp.7280.

PMID- 16046791
OWN - NLM
STAT- MEDLINE
DCOM- 20051026
LR  - 20191109
IS  - 1530-7905 (Print)
IS  - 1530-7905 (Linking)
VI  - 5
IP  - 2
DP  - 2005
TI  - Modification of environmental toxicity by nutrients: implications in
      atherosclerosis.
PG  - 153-60
AB  - We hypothesize that nutrition can modulate the toxicity of environmental
      pollutants and thus modulate health and disease outcome associated with
      chemical insult. There is now increasing evidence that exposure to
      persistent organic pollutants, such as PCBs, can contribute to the
      development of inflammatory diseases such as atherosclerosis. Activation,
      chronic inflammation, and dysfunction of the vascular endothelium are
      critical events in the initiation and acceleration of atherosclerotic
      lesion formation. Our studies indicate that an increase in cellular
      oxidative stress and an imbalance in antioxidant status are critical
      events in PCB-mediated induction of inflammatory genes and endothelial
      cell dysfunction. Furthermore, we have found that specific dietary fats
      can further compromise endothelial dysfunction induced by selected PCBs
      and that antioxidant nutrients (such as vitamin E and dietary flavonoids)
      can protect against endothelial cell damage mediated by these persistent
      organic pollutants. Our recent data suggest that membrane lipid rafts
      such as caveolae may play a major role in the regulation of PCB-induced
      inflammatory signaling in endothelial cells. In addition, PCB- and lipid-
      induced inflammation can be down-regulated by ligands of anti-atherogenic
      peroxisome proliferator-activated receptors (PPARs). We hypothesize that
      PCBs contribute to an endothelial inflammatory response in part by down-
      regulating PPAR signaling. Our data so far support our hypothesis that
      antioxidant nutrients and related bioactive compounds common in fruits
      and vegetables protect against environmental toxic insult to the vascular
      endothelium by down-regulation of signaling pathways involved in
      inflammatory responses and atherosclerosis. Even though the concept that
      nutrition may modify or ameliorate the toxicity of environmental
      chemicals is provocative and warrants further study, the implications for
      human health could be significant. More research is needed to understand
      observed interactions of PCB toxicity with nutritional interventions.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture, Graduate
      Center for Nutritional Sciences, University of Kentucky, Lexington, KY
      40536-0200, USA. bhennig@uky.edu
FAU - Reiterer, Gudrun
AU  - Reiterer G
FAU - Majkova, Zuzana
AU  - Majkova Z
FAU - Oesterling, Elizabeth
AU  - Oesterling E
FAU - Meerarani, Purushothaman
AU  - Meerarani P
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Cardiovasc Toxicol
JT  - Cardiovascular toxicology
JID - 101135818
RN  - 0 (Antioxidants)
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Peroxisome Proliferator-Activated Receptors)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Arteriosclerosis/chemically induced/*prevention & control
MH  - Caveolae/drug effects
MH  - Diet
MH  - Dietary Fats/pharmacology
MH  - Endothelial Cells/drug effects
MH  - Environmental Pollutants/*antagonists & inhibitors/*toxicity
MH  - Humans
MH  - *Nutritional Physiological Phenomena
MH  - Peroxisome Proliferator-Activated Receptors/genetics/physiology
MH  - Polychlorinated Biphenyls/toxicity
RF  - 64
EDAT- 2005/07/28 09:00
MHDA- 2005/10/27 09:00
CRDT- 2005/07/28 09:00
PHST- 2005/07/28 09:00 [pubmed]
PHST- 2005/10/27 09:00 [medline]
PHST- 2005/07/28 09:00 [entrez]
AID - CT:5:2:153 [pii]
AID - 10.1385/ct:5:2:153 [doi]
PST - ppublish
SO  - Cardiovasc Toxicol. 2005;5(2):153-60. doi: 10.1385/ct:5:2:153.

PMID- 15255940
OWN - NLM
STAT- MEDLINE
DCOM- 20040910
LR  - 20161124
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 90
IP  - 3
DP  - 2004 Aug
TI  - Arachidonic acid increases choline acetyltransferase activity in spinal
      cord neurons through a protein kinase C-mediated mechanism.
PG  - 629-36
AB  - Arachidonic acid (AA) plays an important role as a signaling factor in
      the CNS. Therefore, exposure to AA may affect cholinergic neurons in the
      spinal cord. To test this hypothesis, mRNA expression and activity of
      choline acetyltransferase (ChAT) was measured in cultured spinal cord
      neurons treated with increasing concentrations (0.1-10 microm) of AA.
      Exposure to AA increased mRNA levels and activity of ChAT in dose- and
      time-dependent manners. The most marked effect of AA on ChAT expression
      was observed in spinal cord neurons treated with 10 microm AA for 1 h. To
      study the mechanisms associated with these effects, ChAT mRNA levels and
      activity were measured in cultured spinal cord neurons exposed to AA and
      inhibitors of protein kinase C (PKC), such as
      1-(5-isoquinolinesulfonyl)-2-methylpiperazine dichloride (H-7) and
      chelerythrine. Inhibition of PKC completely prevented an AA-induced
      increase in ChAT expression. In addition, exposure of spinal cord neurons
      to phorbol-12-myristate-13-acetate (PMA), an activator of PKC, mimicked
      AA-induced stimulation of ChAT activity. The AA-mediated increase in ChAT
      mRNA levels and activity was also prevented by treatments with EGTA,
      indicating the role of calcium metabolism in induction of this enzyme. In
      contrast, treatments with 7-nitroindazole (7-NI, a specific inhibitor of
      neuronal nitric oxide synthase), sodium vanadate (NaV, a non-specific
      inhibitor of phosphatases), and N-acetyl-cysteine (NAC, an antioxidant)
      had no effect on AA-induced changes in ChAT activity. The protein
      synthesis inhibitor cycloheximide completely blocked AA-mediated increase
      in ChAT activity. These results indicate that the AA-evoked increase in
      ChAT activity in spinal cord neurons is mediated by PKC, presumably at
      the transcriptional level.
FAU - Chalimoniuk, Malgorzata
AU  - Chalimoniuk M
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      Kentucky 40536, USA.
FAU - King-Pospisil, Kelley
AU  - King-Pospisil K
FAU - Pedersen, Ward A
AU  - Pedersen WA
FAU - Malecki, Andrzej
AU  - Malecki A
FAU - Wylegala, Edward
AU  - Wylegala E
FAU - Mattson, Mark P
AU  - Mattson MP
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Antioxidants)
RN  - 0 (Chelating Agents)
RN  - 0 (Enzyme Activators)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 1.14.13.39 (Nos1 protein, mouse)
RN  - EC 2.3.1.6 (Choline O-Acetyltransferase)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
SB  - IM
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Arachidonic Acid/*pharmacology
MH  - Cells, Cultured
MH  - Chelating Agents/pharmacology
MH  - Choline O-Acetyltransferase/drug effects/genetics/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Enzyme Activation/drug effects
MH  - Enzyme Activators/pharmacology
MH  - Enzyme Inhibitors/pharmacology
MH  - Mice
MH  - Neurons/drug effects/*enzymology
MH  - Nitric Oxide Synthase/antagonists & inhibitors
MH  - Nitric Oxide Synthase Type I
MH  - Oxidative Stress/drug effects
MH  - Phosphoric Monoester Hydrolases/antagonists & inhibitors
MH  - Protein Kinase C/drug effects/*metabolism
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - Spinal Cord/*cytology/embryology
EDAT- 2004/07/17 05:00
MHDA- 2004/09/11 05:00
CRDT- 2004/07/17 05:00
PHST- 2004/07/17 05:00 [pubmed]
PHST- 2004/09/11 05:00 [medline]
PHST- 2004/07/17 05:00 [entrez]
AID - 10.1111/j.1471-4159.2004.02535.x [doi]
AID - JNC2535 [pii]
PST - ppublish
SO  - J Neurochem. 2004 Aug;90(3):629-36. doi:
      10.1111/j.1471-4159.2004.02535.x.

PMID- 15226458
OWN - NLM
STAT- MEDLINE
DCOM- 20040810
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 134
IP  - 7
DP  - 2004 Jul
TI  - Peroxisome proliferator activated receptors alpha and gamma require zinc
      for their anti-inflammatory properties in porcine vascular endothelial
      cells.
PG  - 1711-5
AB  - Zinc is an essential structural component of various proteins and is
      crucial for the integrity of the vascular endothelium. The present study
      focused on the effect of zinc deficiency on the anti-inflammatory
      properties of peroxisome proliferator activated receptor (PPAR) alpha and
      gamma agonists. Porcine pulmonary-arterial endothelial cells were
      deprived from zinc by chelator N,N,N',N'-tetrakis
      (2-pyridylmethyl)ethylene diamine. Cells were exposed to TNF-alpha for 2
      h following pretreament with the PPARalpha agonists fenofibrate or
      ciprofibrate or the PPARgamma agonists thiazolidinedione or troglitazone.
      The inflammatory response was tested by measuring nuclear factor-kappaB
      (NF-kappaB) and activator protein-1 (AP-1) binding activities as well as
      by measuring mRNA expression levels of inflammatory genes, such as
      vascular cell adhesion molecule-1 (VCAM-1) and IL-6. All PPAR agonists
      tested lost their potency to downregulate the TNF-alpha-induced
      inflammatory response in zinc-deficient cells. However, if zinc was added
      back, all PPAR agonists significantly downregulated the TNF-alpha-
      mediated induction of inflammatory transcription factors NF-kappaB and
      AP-1 and significantly reduced the expression of their target genes,
      VCAM-1 and IL-6. We therefore hypothesize that zinc is required for the
      PPARalpha and -gamma DNA binding activity. Indeed, zinc deficiency
      significantly reduced the agonist-induced binding activity of PPARalpha
      and -gamma to the PPAR response element. Our data demonstrate the
      importance of zinc in PPAR signaling and the requirement of zinc for the
      anti-inflammatory properties of PPARalpha and -gamma agonists.
FAU - Reiterer, Gudrun
AU  - Reiterer G
AD  - Graduate Center for Nutritional Sciences, College of Agriculture,
      University of Kentucky, Lexington, KY 40546-0215, USA.
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Interleukin-6)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Inflammation/*prevention & control
MH  - Interleukin-6/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/agonists/*drug effects/physiology
MH  - Swine
MH  - Transcription Factors/agonists/*drug effects/physiology
MH  - Vascular Cell Adhesion Molecule-1/metabolism
MH  - Zinc/deficiency/*pharmacology
EDAT- 2004/07/01 05:00
MHDA- 2004/08/11 05:00
CRDT- 2004/07/01 05:00
PHST- 2004/07/01 05:00 [pubmed]
PHST- 2004/08/11 05:00 [medline]
PHST- 2004/07/01 05:00 [entrez]
AID - 10.1093/jn/134.7.1711 [doi]
PST - ppublish
SO  - J Nutr. 2004 Jul;134(7):1711-5. doi: 10.1093/jn/134.7.1711.

PMID- 15149853
OWN - NLM
STAT- MEDLINE
DCOM- 20040728
LR  - 20171116
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 296
IP  - 2
DP  - 2004 Jun 10
TI  - VEGF regulates PCB 104-mediated stimulation of permeability and
      transmigration of breast cancer cells in human microvascular endothelial
      cells.
PG  - 231-44
AB  - Polychlorinated biphenyl (PCB) congeners, a group of worldwide,
      persistent environmental contaminants, are known to cause carcinogenesis
      and tumor promotion, and may also affect the development of cancer
      metastasis. Because vascular endothelial cells create a selective barrier
      to the passage of cancer cells, we hypothesize that specific PCB
      congeners can disrupt endothelial integrity and increase the
      transendothelial migration of tumor cells. To examine this hypothesis, we
      elucidated the effects of 2,2',4,6,6'-pentachlorobiphenyl (PCB 104), a
      representative of highly ortho-substituted non-coplanar PCB congeners, on
      the endothelial permeability and transendothelial migration of MDA-MB-231
      breast cancer cells. Exposure of human microvascular endothelial cell 1
      (HMEC-1) to PCB 104 induced endothelial hyperpermeability and markedly
      increased transendothelial migration of MDA-MB-231 cells. These effects
      were associated with overexpression of vascular endothelial growth factor
      (VEGF). PCB 104-mediated elevation of VEGF expression was induced by
      phosphatidylinositol 3-kinase (PI3K) but not affected by co-treatments
      with antioxidants or the NF-kappaB inhibitor SN50. In addition, the
      PI3K-dependent pathway was involved in PCB 104-induced activation of
      AP-1, a transcription factor implicated in the regulation of VEGF gene
      expression. The VEGF receptor (KDR/Flk-1) antagonist SU1498 and the PI3K
      inhibitor LY294002 inhibited PCB 104-induced hyperpermeability. These
      results indicate that PCB 104 may contribute to tumor metastasis by
      inducing VEGF overexpression that stimulates endothelial
      hyperpermeability and transendothelial migration of cancer cells.
FAU - Eum, Sung Yong
AU  - Eum SY
AD  - Department of Surgery, University of Kentucky, Lexington, KY 40536, USA.
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - Z4YYF101N3 (2,2',4,6,6'-pentachlorobiphenyl)
SB  - IM
MH  - Breast Neoplasms/*pathology
MH  - Capillary Permeability
MH  - Cell Adhesion/drug effects
MH  - Cell Movement/drug effects
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*cytology/drug effects
MH  - Humans
MH  - Neoplasm Invasiveness/*pathology
MH  - Neoplasm Metastasis/pathology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Polychlorinated Biphenyls/*pharmacology
MH  - Transcription, Genetic/drug effects
MH  - Up-Regulation/drug effects
MH  - Vascular Endothelial Growth Factor A/biosynthesis/*physiology
EDAT- 2004/05/20 05:00
MHDA- 2004/07/29 05:00
CRDT- 2004/05/20 05:00
PHST- 2003/09/15 00:00 [received]
PHST- 2004/01/23 00:00 [revised]
PHST- 2004/05/20 05:00 [pubmed]
PHST- 2004/07/29 05:00 [medline]
PHST- 2004/05/20 05:00 [entrez]
AID - 10.1016/j.yexcr.2004.01.030 [doi]
AID - S0014482704000667 [pii]
PST - ppublish
SO  - Exp Cell Res. 2004 Jun 10;296(2):231-44. doi:
      10.1016/j.yexcr.2004.01.030.

PMID- 15135227
OWN - NLM
STAT- MEDLINE
DCOM- 20040826
LR  - 20161025
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 124
IP  - 2
DP  - 2004 May 19
TI  - Nicotine attenuates oxidative stress, activation of redox-regulated
      transcription factors and induction of proinflammatory genes in
      compressive spinal cord trauma.
PG  - 188-98
AB  - Pathophysiology of neurodegeneration following spinal cord injury (SCI)
      involves alterations of cellular redox status, activation of
      transcription factors and induction of proinflammatory genes. In
      addition, recent evidence indicates that nicotine can induce potent
      neuroprotective effects. To study the influence of nicotine on the redox
      signaling pathways in relationship to SCI, moderate contusions of spinal
      cords at the level of T-10 were induced in rats treated or untreated with
      nicotine. Cellular oxidative stress, DNA binding activity of redox-
      responsive transcription factors (AP-1, NF-kappaB and CREB) as well as
      mRNA levels of inflammatory genes (MCP-1 and TNF-alpha) were determined
      in the thoracic and lumbar regions of the spinal cords. Nicotine was
      administrated 2 h after the SCI in a single i.p. injection at the dose of
      0.35, 3.5 or 7 mg/kg, and rats were sacrificed 3 h following such an
      injection. Spinal cord trauma was associated with a significant increase
      in oxidative stress, and activation of NF-kappaB, AP-1 and CREB, as well
      as overexpression of MCP-1 and TNF-alpha in both the thoracic and lumbar
      regions. Nicotine administration following the SCI markedly attenuated,
      especially in the lumbar region, these oxidative and proinflammatory
      responses. These protective effects of nicotine were fully reversed by
      inhibition of neuronal nicotinic receptors by mecamylamine. The present
      results indicate that nicotine administration can attenuate the oxidative
      injury to spinal cords and suggest that neuronal nicotinic receptors can
      be attractive targets for neuroprotective therapy.
FAU - Ravikumar, R
AU  - Ravikumar R
AD  - Department of Surgery, University of Kentucky, Lexington, KY 40536, USA.
FAU - Flora, Govinder
AU  - Flora G
FAU - Geddes, James W
AU  - Geddes JW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-kappa B)
RN  - 0 (Nicotinic Antagonists)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Nicotinic)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Animals
MH  - Binding, Competitive/drug effects/genetics
MH  - Chemokine CCL2/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression Regulation/drug effects/genetics
MH  - Inflammation/*drug therapy/genetics/metabolism
MH  - Inflammation Mediators/*metabolism
MH  - Male
MH  - NF-kappa B/drug effects/metabolism
MH  - Nicotine/*pharmacology/therapeutic use
MH  - Nicotinic Antagonists/pharmacology
MH  - Oxidation-Reduction
MH  - Oxidative Stress/*drug effects/physiology
MH  - RNA, Messenger/drug effects/metabolism
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptors, Nicotinic/drug effects/metabolism
MH  - Spinal Cord Compression/*drug therapy/genetics/metabolism
MH  - Transcription Factor AP-1/metabolism
MH  - Transcription Factors/*drug effects/genetics
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/drug effects/metabolism
MH  - Up-Regulation/drug effects/genetics
EDAT- 2004/05/12 05:00
MHDA- 2004/08/27 05:00
CRDT- 2004/05/12 05:00
PHST- 2004/02/15 00:00 [accepted]
PHST- 2004/05/12 05:00 [pubmed]
PHST- 2004/08/27 05:00 [medline]
PHST- 2004/05/12 05:00 [entrez]
AID - 10.1016/j.molbrainres.2004.02.018 [doi]
AID - S0169328X0400097X [pii]
PST - ppublish
SO  - Brain Res Mol Brain Res. 2004 May 19;124(2):188-98. doi:
      10.1016/j.molbrainres.2004.02.018.

PMID- 14993245
OWN - NLM
STAT- MEDLINE
DCOM- 20050318
LR  - 20210217
IS  - 0022-2275 (Print)
IS  - 0022-2275 (Linking)
VI  - 45
IP  - 5
DP  - 2004 May
TI  - Linoleic acid-induced endothelial activation: role of calcium and
      peroxynitrite signaling.
PG  - 794-804
AB  - Hypertriglyceridemia, an important risk factor of atherosclerosis, is
      associated with increased circulating free fatty acids. Research to date
      indicates that linoleic acid (LA), the major fatty acid in the American
      diet, may be atherogenic by activating vascular endothelial cells.
      However, the exact signaling mechanisms involved in LA-mediated
      proinflammatory events in endothelial cells still remain unclear. We
      previously reported increased superoxide formation after LA exposure in
      endothelial cells. The objective of the present investigation is to
      determine the role of calcium and peroxynitrite in mediating the
      proinflammatory effect of LA in vascular endothelial cells. LA exposure
      increased intracellular calcium, nitric oxide, and tetrahydrodiopterin
      levels as well as the expression of E-selectin. Inhibiting calcium
      signaling using 1,2-bis(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid
      and heparin decreased the expression of E-selectin. Also, LA-mediated
      nuclear factor kappa B activation and E-selectin gene expression were
      suppressed by Mn (III) tetrakis (1-methyl-4-pyridyl) porphyrin
      pentachloride (a superoxide scavenger), N(G)-monomethyl-l-arginine (an
      endothelial nitric oxide synthase inhibitor), and 5,10,15,20-tetrakis
      (4-sulfonatophenyl) porphyrinato iron (III) chloride (a peroxynitrite
      scavenger). LA exposure resulted in increased nitrotyrosine levels, as
      observed by Western blotting and immunofluorescence. Our data suggest
      that the proinflammatory effects of LA can be mediated through calcium
      and peroxynitrite signaling.
FAU - Saraswathi, Viswanathan
AU  - Saraswathi V
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40546, USA.
FAU - Wu, Guoyao
AU  - Wu G
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES-07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20040301
PL  - United States
TA  - J Lipid Res
JT  - Journal of lipid research
JID - 0376606
RN  - 0 (Borohydrides)
RN  - 0 (E-Selectin)
RN  - 0 (NF-kappa B)
RN  - 14691-52-2 (Peroxynitrous Acid)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Borohydrides/metabolism
MH  - Calcium/analysis/*metabolism
MH  - Calcium Signaling/drug effects
MH  - Cells, Cultured
MH  - E-Selectin/biosynthesis/genetics
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Linoleic Acid/*pharmacology
MH  - Models, Biological
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide/metabolism
MH  - Peroxynitrous Acid/*metabolism
MH  - Pulmonary Artery/cytology
MH  - Swine
MH  - Tyrosine/*analogs & derivatives/metabolism
EDAT- 2004/03/03 05:00
MHDA- 2005/03/19 09:00
CRDT- 2004/03/03 05:00
PHST- 2004/03/03 05:00 [pubmed]
PHST- 2005/03/19 09:00 [medline]
PHST- 2004/03/03 05:00 [entrez]
AID - 10.1194/jlr.M300497-JLR200 [doi]
AID - S0022-2275(20)31819-8 [pii]
PST - ppublish
SO  - J Lipid Res. 2004 May;45(5):794-804. doi: 10.1194/jlr.M300497-JLR200.
      Epub 2004 Mar 1.

PMID- 15051824
OWN - NLM
STAT- MEDLINE
DCOM- 20040506
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 134
IP  - 4
DP  - 2004 Apr
TI  - Quercetin protects against linoleic acid-induced porcine endothelial cell
      dysfunction.
PG  - 771-5
AB  - Consumption of plant phenolics, such as quercetin, may be associated with
      decreased risk of cardiovascular disease by stabilizing and protecting
      vascular endothelial cells against oxidative and proinflammatory insults.
      The present study focused on the effect of quercetin on linoleic acid-
      induced oxidative stress and the inflammatory pathways of nuclear factor-
      kappaB (NF-kappaB) and activator protein-1 (AP-1). Because the
      transcription factor peroxisome proliferator activated receptor gamma
      (PPARgamma) was reported to downregulate inflammatory pathways, we
      further investigated the effect of quercetin on PPARgamma. Porcine
      pulmonary-arterial endothelial cells were activated with linoleic acid in
      the presence or absence of quercetin. Oxidative stress was markedly
      induced by endothelial cell exposure to linoleic acid and diminished by
      treatment with quercetin as measured via the oxidation of
      2',7'-dichlorofluorescin. Quercetin reduced linoleic acid-mediated
      binding activity of NF-kappaB and AP-1 and mRNA levels of inflammatory
      genes such as interleukin-6 (IL-6) and vascular cell adhesion molecule-1
      (VCAM-1). Cotreatment of linoleic acid plus quercetin or vitamin E also
      decreased linoleic acid-induced binding activity of PPARgamma. These data
      suggest that quercetin has potent antioxidative and anti-inflammatory
      properties and protects endothelial cells against linoleic acid-mediated
      cell dysfunction.
FAU - Reiterer, Gudrun
AU  - Reiterer G
AD  - Department of. Surgery, College of Agriculture, University of Kentucky,
      Lexington, KY 40546-0215, USA.
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Antioxidants)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 1406-18-4 (Vitamin E)
RN  - 9IKM0I5T1E (Quercetin)
RN  - 9KJL21T0QJ (Linoleic Acid)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Endothelial Cells/*drug effects/*physiology
MH  - Interleukin-6/genetics
MH  - Linoleic Acid/*pharmacology
MH  - NF-kappa B/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/drug effects
MH  - Quercetin/*pharmacology
MH  - RNA, Messenger/analysis
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
MH  - Swine
MH  - Transcription Factor AP-1/metabolism
MH  - Transcription Factors/metabolism
MH  - Vascular Cell Adhesion Molecule-1/genetics
MH  - Vitamin E/pharmacology
EDAT- 2004/03/31 05:00
MHDA- 2004/05/07 05:00
CRDT- 2004/03/31 05:00
PHST- 2004/03/31 05:00 [pubmed]
PHST- 2004/05/07 05:00 [medline]
PHST- 2004/03/31 05:00 [entrez]
AID - 10.1093/jn/134.4.771 [doi]
PST - ppublish
SO  - J Nutr. 2004 Apr;134(4):771-5. doi: 10.1093/jn/134.4.771.

PMID- 15068811
OWN - NLM
STAT- MEDLINE
DCOM- 20050624
LR  - 20161025
IS  - 0955-2863 (Print)
IS  - 0955-2863 (Linking)
VI  - 15
IP  - 4
DP  - 2004 Apr
TI  - Emerging issues: nutritional awareness in environmental toxicology.
PG  - 194-5
AB  - Based on recent evidence, we hypothesize that nutrition can modulate the
      toxicity of environmental pollutants and thus modulate health and disease
      outcome associated with chemical insults. For example, certain dietary
      fats may increase the risk to environmental insult induced by
      polychlorinated biphenyls (PCBs), and fruits and vegetables, rich in
      antioxidant and anti-inflammatory nutrients or bioactive compounds, may
      provide protection. Nutritional awareness in environmental toxicology is
      critical, because of opportunities to develop dietary guidelines which
      specifically target exposed populations. Nutrition may provide the most
      sensible means to develop primary prevention strategies of diseases
      associated with environmental toxicology.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, 200 W.P. Garrigus Building, Lexington, KY
      40546-0215, USA. bhenning@uky.edu
FAU - Toborek, Michal
AU  - Toborek M
FAU - Bachas, Leonidas G
AU  - Bachas LG
FAU - Suk, William A
AU  - Suk WA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - *Awareness
MH  - Diet
MH  - Environmental Pollutants/*toxicity
MH  - Humans
MH  - *Nutritional Physiological Phenomena
MH  - Preventive Medicine
MH  - Risk Factors
EDAT- 2004/04/08 05:00
MHDA- 2005/06/25 09:00
CRDT- 2004/04/08 05:00
PHST- 2004/04/08 05:00 [pubmed]
PHST- 2005/06/25 09:00 [medline]
PHST- 2004/04/08 05:00 [entrez]
AID - 10.1016/j.jnutbio.2004.01.002 [doi]
AID - S0955286304000221 [pii]
PST - ppublish
SO  - J Nutr Biochem. 2004 Apr;15(4):194-5. doi: 10.1016/j.jnutbio.2004.01.002.

PMID- 15502879
OWN - NLM
STAT- MEDLINE
DCOM- 20051019
LR  - 20191109
IS  - 1076-1551 (Print)
IS  - 1076-1551 (Linking)
VI  - 10
IP  - 1-6
DP  - 2004 Jan-Jun
TI  - Gene expression profile in interleukin-4-stimulated human vascular
      endothelial cells.
PG  - 19-27
AB  - Interleukin-4 (IL-4)-mediated pro-oxidative and pro-inflammatory vascular
      environments have been implicated in the pathogenesis of atherosclerosis.
      The cellular and molecular regulatory mechanisms underlying this process,
      however, are not fully understood. In the present study, we employed
      GeneChip microarray analysis to investigate global gene expression
      patterns in human vascular endothelial cells after treatment with IL-4.
      Our results showed that mRNA levels of a total of 106 genes were
      significantly up-regulated and 41 genes significantly down-regulated with
      more than a 2-fold change. The majority of these genes are critically
      involved in the regulation of inflammatory responses, apoptosis, signal
      transduction, transcription factors, and metabolism; functions of the
      remaining genes are unknown. The changes in gene expression of selected
      genes related to inflammatory reactions, such as vascular cell adhesion
      molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant protein-1
      (MCP-1), and interleukin-6 (IL-6), were verified by quantitative real-
      time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-
      linked immunosorbent assay (ELISA) analyses. IL-4 treatment also
      significantly increased the adherence of inflammatory cells to
      endothelial cell monolayers in a dose-dependent manner. These results may
      help determine the molecular mechanisms of action of IL-4 in human
      vascular endothelium. In addition, a better understanding of IL-4-induced
      vascular injury at the level of gene expression could lead to the
      identification of new therapeutic strategies for atherosclerosis.
FAU - Lee, Yong Woo
AU  - Lee YW
AD  - Department of Surgery/Division of Neurosurgery, University of Kentucky
      College of Medicine, 800 Rose Street, Lexington, Kentucky 40536, USA.
      ylee2@uky.edu
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Chen, Kuey Chu
AU  - Chen KC
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Mol Med
JT  - Molecular medicine (Cambridge, Mass.)
JID - 9501023
RN  - 0 (Inflammation Mediators)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Apoptosis/genetics
MH  - Cell Line, Tumor
MH  - Endothelial Cells/*drug effects/metabolism
MH  - *Gene Expression Profiling
MH  - Gene Expression Regulation/*drug effects
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Interleukin-4/*pharmacology
MH  - Oligonucleotide Array Sequence Analysis
MH  - RNA, Messenger/metabolism
MH  - Signal Transduction/genetics
MH  - Transcription Factors/genetics
PMC - PMC1431351
EDAT- 2004/10/27 09:00
MHDA- 2005/10/20 09:00
CRDT- 2004/10/27 09:00
PHST- 2004/10/27 09:00 [pubmed]
PHST- 2005/10/20 09:00 [medline]
PHST- 2004/10/27 09:00 [entrez]
AID - 10.2119/2004-00024.lee [doi]
PST - ppublish
SO  - Mol Med. 2004 Jan-Jun;10(1-6):19-27. doi: 10.2119/2004-00024.lee.

PMID- 14684755
OWN - NLM
STAT- MEDLINE
DCOM- 20060426
LR  - 20190911
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 22
IP  - 6
DP  - 2003 Dec
TI  - Involvement of CYP 2C9 in mediating the proinflammatory effects of
      linoleic acid in vascular endothelial cells.
PG  - 502-10
AB  - OBJECTIVE: Polyunsaturated fatty acids such as linoleic acid are well
      known dietary lipids that may be atherogenic by activating vascular
      endothelial cells. In the liver, fatty acids can be metabolized by
      cytochrome P450 (CYP) enzymes, but little is known about the role of
      these enzymes in the vascular endothelium. CYP 2C9 is involved in
      linoleic acid epoxygenation, and the major product of this reaction is
      leukotoxin (LTX). We investigated the role of CYP-mediated mechanisms of
      linoleic acid metabolism in endothelial cell activation by examining the
      effects of linoleic acid or its oxidized metabolites such as LTX and
      leukotoxin diol (LTD). METHODS: The effect of linoleic acid on CYP 2C9
      gene expression was studied by RT-PCR. Oxidative stress was monitored by
      measuring DCF fluorescence and intracellular glutathione levels, and
      electrophoretic mobility shift assay was carried out to study the
      activation of oxidative stress sensitive transcription factors. Analysis
      of oxidized lipids was carried out by liquid chromatography/mass
      spectrometry. RESULTS: Linoleic acid treatment for six hours increased
      the expression of CYP 2C9 in endothelial cells. Linoleic acid-mediated
      increase in oxidative stress and activation of AP-1 were blocked by
      sulfaphenazole, a specific inhibitor of CYP 2C9. The linoleic acid
      metabolites LTX and LTD increased oxidative stress and activation of
      transcription factors only at high concentrations. CONCLUSION: Our data
      show that CYP 2C9 plays a key role in linoleic acid-induced oxidative
      stress and subsequent proinflammatory events in vascular endothelial
      cells by possibly causing superoxide generation through uncoupling
      processes.
FAU - Viswanathan, Saraswathi
AU  - Viswanathan S
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40546-0215, USA.
FAU - Hammock, Bruce D
AU  - Hammock BD
FAU - Newman, John W
AU  - Newman JW
FAU - Meerarani, Purushothaman
AU  - Meerarani P
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P01 ES 11269/ES/NIEHS NIH HHS/United States
GR  - P42 ES 04699/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (9,10-dihydroxy-12-octadecenoic acid)
RN  - 0 (Exotoxins)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Stearic Acids)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (leukotoxin)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 1.14.13.- (CYP2C9 protein, human)
RN  - EC 1.14.13.- (Cytochrome P-450 CYP2C9)
RN  - EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Aryl Hydrocarbon Hydroxylases/*metabolism
MH  - Cytochrome P-450 CYP2C9
MH  - Dose-Response Relationship, Immunologic
MH  - Electrophoretic Mobility Shift Assay
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Exotoxins/metabolism/pharmacology
MH  - Gas Chromatography-Mass Spectrometry
MH  - Gene Expression Regulation/drug effects
MH  - Glutathione/metabolism
MH  - Humans
MH  - Immunosuppressive Agents/pharmacology
MH  - Inflammation Mediators/*metabolism
MH  - Linoleic Acid/*metabolism/*pharmacology
MH  - NF-kappa B/drug effects/metabolism
MH  - Oxidative Stress/drug effects
MH  - Pulmonary Artery/cytology
MH  - Reactive Oxygen Species/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Stearic Acids/metabolism/pharmacology
MH  - Swine
MH  - Transcription Factor AP-1/drug effects/metabolism
MH  - Umbilical Veins/cytology
EDAT- 2003/12/20 05:00
MHDA- 2006/04/28 09:00
CRDT- 2003/12/20 05:00
PHST- 2003/12/20 05:00 [pubmed]
PHST- 2006/04/28 09:00 [medline]
PHST- 2003/12/20 05:00 [entrez]
AID - 10.1080/07315724.2003.10719328 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 2003 Dec;22(6):502-10. doi:
      10.1080/07315724.2003.10719328.

PMID- 12970578
OWN - NLM
STAT- MEDLINE
DCOM- 20040614
LR  - 20161124
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 76
IP  - 1
DP  - 2003 Nov
TI  - Dietary flavonoids modulate PCB-induced oxidative stress, CYP1A1
      induction, and AhR-DNA binding activity in vascular endothelial cells.
PG  - 212-9
AB  - Polychlorinated biphenyls (PCBs), especially the more coplanar PCBs, have
      been shown to induce oxidative stress, various transcription factors, and
      subsequent inflammatory processes critical to atherosclerosis in vascular
      endothelial cells. Dietary flavonoids such as catechins and quercetin
      possess antioxidant and anti-inflammatory properties. To test the
      hypothesis that flavonoids can modify PCB-mediated endothelial
      cytotoxicity, endothelial cells were treated with
      epigallocatechin-3-gallate (EGCG; 5 to 50 muM) or quercetin (10 to 100
      muM) with or without PCB 77 (3,3',4,4'-tetrachlorobiphenyl, 3.4 muM) for
      6 h. EGCG and quercetin strongly, and in a concentration-dependent
      manner, inhibited oxidative stress induced by PCB 77 as measured by DCF
      fluorescence. The role of cytochrome P450 1A1 (CYP1A1) in the PCB-induced
      toxicity was investigated. EGCG at 50 muM and quercetin at 100 muM
      concentrations markedly inhibited CYP1A1 mRNA levels and enzyme activity.
      Furthermore, EGCG and quercetin downregulated the PCB 77-mediated
      increase in aryl hydrocarbon receptor (AhR)-DNA binding activity. These
      data suggest that protective effects of EGCG and quercetin are initiated
      upstream from CYP1A1 and that these flavonoids may be of value for
      inhibiting the toxic effects of PCBs on vascular endothelial cells.
FAU - Ramadass, Pachaikani
AU  - Ramadass P
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington 40546-0215, USA.
FAU - Meerarani, Purushothaman
AU  - Meerarani P
FAU - Toborek, Michal
AU  - Toborek M
FAU - Robertson, Larry W
AU  - Robertson LW
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20030911
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (Flavonoids)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 8R1V1STN48 (Catechin)
RN  - 9007-49-2 (DNA)
RN  - 9IKM0I5T1E (Quercetin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/*biosynthesis
MH  - DNA/metabolism
MH  - Endothelial Cells/*drug effects/enzymology/metabolism
MH  - Enzyme Induction/drug effects
MH  - Flavonoids/*pharmacology
MH  - Oxidative Stress/*drug effects
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Protein Binding/drug effects
MH  - Pulmonary Artery/cytology
MH  - Quercetin/pharmacology
MH  - Receptors, Aryl Hydrocarbon/*metabolism
MH  - Swine
EDAT- 2003/09/13 05:00
MHDA- 2004/06/15 05:00
CRDT- 2003/09/13 05:00
PHST- 2003/09/13 05:00 [pubmed]
PHST- 2004/06/15 05:00 [medline]
PHST- 2003/09/13 05:00 [entrez]
AID - 10.1093/toxsci/kfg227 [doi]
AID - kfg227 [pii]
PST - ppublish
SO  - Toxicol Sci. 2003 Nov;76(1):212-9. doi: 10.1093/toxsci/kfg227. Epub 2003
      Sep 11.

PMID- 14568117
OWN - NLM
STAT- MEDLINE
DCOM- 20040105
LR  - 20190917
IS  - 0168-0102 (Print)
IS  - 0168-0102 (Linking)
VI  - 47
IP  - 3
DP  - 2003 Nov
TI  - Nicotine upregulates nerve growth factor expression and prevents
      apoptosis of cultured spinal cord neurons.
PG  - 349-55
AB  - Modulation of neurotrophic factor expression may constitute an important
      part of neuroprotective effects of nicotine. Therefore, the effects of
      nicotine on expression of nerve growth factor (NGF) and its receptor,
      tyrosine receptor kinase A (trkA), were studied in cultured spinal cord
      neurons treated with arachidonic acid. Because injury to spinal cord is
      associated with elevated levels of arachidonic acid, this cell culture
      system has been developed in our laboratory as an in vitro model of
      neuronal injury in spinal cord trauma. Treatment with nicotine markedly
      upregulated NGF mRNA and protein expression in spinal cord neurons. In
      addition, a 12h treatment with nicotine increased mRNA levels of trkA.
      Both nicotine and exogenous NGF inhibited arachidonic acid induced
      apoptosis of spinal cord neurons. However, the blockage of the trkA
      receptor prevented nicotine-mediated anti-apoptotic effects. The present
      results indicate that increased expression of NGF may be an important
      element of the neuroprotective effects of nicotine in injured spinal cord
      neurons.
FAU - Garrido, Rosario
AU  - Garrido R
AD  - Department of Surgery, University of Kentucky Medical Center, 800 Rose
      Street, Lexington, KY 40536, USA.
FAU - King-Pospisil, Kelley
AU  - King-Pospisil K
FAU - Son, Kwang Won
AU  - Son KW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Neurosci Res
JT  - Neuroscience research
JID - 8500749
RN  - 6M3C89ZY6R (Nicotine)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects/physiology
MH  - Cells, Cultured
MH  - Gene Expression Regulation/drug effects/physiology
MH  - Mice
MH  - Nerve Growth Factor/*biosynthesis/genetics
MH  - Neurons/*drug effects/metabolism
MH  - Nicotine/*pharmacology
MH  - Receptor, trkA/antagonists & inhibitors/metabolism
MH  - Spinal Cord/drug effects/metabolism
MH  - Up-Regulation/*drug effects/physiology
EDAT- 2003/10/22 05:00
MHDA- 2004/01/06 05:00
CRDT- 2003/10/22 05:00
PHST- 2003/10/22 05:00 [pubmed]
PHST- 2004/01/06 05:00 [medline]
PHST- 2003/10/22 05:00 [entrez]
AID - S0168010203002220 [pii]
AID - 10.1016/s0168-0102(03)00222-0 [doi]
PST - ppublish
SO  - Neurosci Res. 2003 Nov;47(3):349-55. doi: 10.1016/s0168-0102(03)00222-0.

PMID- 14651807
OWN - NLM
STAT- MEDLINE
DCOM- 20040116
LR  - 20161025
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 20
IP  - 11
DP  - 2003 Nov
TI  - Apoptosis of spinal cord neurons by preventing depletion nicotine
      attenuates arachidonic acid-induced of neurotrophic factors.
PG  - 1201-13
AB  - Increased levels of free fatty acids and, in particular, arachidonic acid
      can lead to induction of apoptosis of spinal cord neurons. Because of the
      importance of neurotrophic factors in cell survival and death, mRNA and
      protein levels of brain-derived neurotrophic factor (BDNF) and basic
      fibroblast growth factor (FGF-2) were studied in cultured spinal cord
      neurons treated with arachidonic acid. In addition, the present study
      focused on the effects of nicotine and neuronal nicotinic acetylcholine
      receptors (nAChRs) on these processes. A 2-h exposure to arachidonic acid
      markedly diminished expression of BDNF and FGF-2. These effects were
      fully prevented by pretreatment with 10 microM nicotine. Mecamylamine (a
      non-specific antagonist of nAChRs) and alpha-bungarotoxin (a specific
      antagonist of the nAChRalpha7) completely inhibited nicotine-mediated
      protection against arachidonic acid-induced alterations of BDNF and
      FGF-2. In addition, nicotine, BDNF and FGF-2 fully protected against
      arachidonic acid-induced apoptosis of spinal cord neurons. BDNF and FGF-2
      were effective in prevention of apoptotic cell death even when applied 2
      h after the beginning of arachidonic acid treatment. These results
      suggest that arachidonic acid can induce apoptosis of spinal cord neurons
      by depletion of neurotrophic factors and that nicotine can protect
      against these effects through the nAChRalpha7-mediated pathway.
FAU - Garrido, Rosario
AU  - Garrido R
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      Kentucky 40536, USA.
FAU - Springer, Joe E
AU  - Springer JE
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Nicotinic Antagonists)
RN  - 0 (Receptors, Nicotinic)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Arachidonic Acid/toxicity
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/drug effects
MH  - Cells, Cultured
MH  - Embryo, Mammalian
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fibroblast Growth Factor 2/biosynthesis/drug effects
MH  - Mice
MH  - Nerve Growth Factors/biosynthesis/*drug effects
MH  - Neurons/*drug effects/pathology
MH  - Neuroprotective Agents/*pharmacology
MH  - Nicotine/*pharmacology
MH  - Nicotinic Antagonists/pharmacology
MH  - Receptors, Nicotinic/drug effects/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Spinal Cord/drug effects
EDAT- 2003/12/04 05:00
MHDA- 2004/01/17 05:00
CRDT- 2003/12/04 05:00
PHST- 2003/12/04 05:00 [pubmed]
PHST- 2004/01/17 05:00 [medline]
PHST- 2003/12/04 05:00 [entrez]
AID - 10.1089/089771503322584628 [doi]
PST - ppublish
SO  - J Neurotrauma. 2003 Nov;20(11):1201-13. doi: 10.1089/089771503322584628.

PMID- 14515355
OWN - NLM
STAT- MEDLINE
DCOM- 20031216
LR  - 20161019
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 74
IP  - 2
DP  - 2003 Oct 15
TI  - HIV-1 Tat protein alters tight junction protein expression and
      distribution in cultured brain endothelial cells.
PG  - 255-65
AB  - Disruption of the blood-brain barrier (BBB) is widely believed to be the
      main route of human immunodeficiency virus (HIV) entry into the central
      nervous system (CNS). Although mechanisms of this process are not fully
      understood, alterations of tight junction protein expression can
      contribute, at least in part, to this phenomenon. Tight junctions are
      critical structural and functional elements of cerebral microvascular
      endothelial cells and the BBB. The aim of the present study was to
      examine the effects of HIV-1 Tat protein on expression of tight junction
      proteins. Primary cultures of brain microvascular endothelial cells
      (BMEC) were employed in these experiments. A 24-hr exposure of BMEC to
      Tat(1-72) resulted in a decrease of claudin-1, claudin-5, and zonula
      occludens (ZO)-2 expression, whereas total levels of occludin and ZO-1
      remained unchanged. In addition, a short (3-hr) exposure of BMEC to
      Tat(1-72) induced cellular redistribution of claudin-5 immunoreactivity.
      Tat(1-72)-induced alterations of claudin-5 expression also were confirmed
      in vivo where Tat(1-72) was injected into the right hippocampus of mice.
      These findings indicate that HIV-1 Tat protein can markedly affect
      expression and distribution of specific tight junction proteins in brain
      endothelium. Alterations of only distinct tight junction proteins suggest
      a finely tuned effect of Tat(1-72) on the BBB. Because tight junction
      proteins are critical for the barrier function of the BBB, such
      alterations can lead to disturbances of the BBB integrity and contribute
      to HIV trafficking into the brain.
CI  - Copyright 2003 Wiley-Liss, Inc.
FAU - Andras, Ibolya E
AU  - Andras IE
AD  - Department of Surgery, University of Kentucky, Lexington, Kentucky, USA.
FAU - Pu, Hong
AU  - Pu H
FAU - Deli, Maria A
AU  - Deli MA
FAU - Nath, Avindra
AU  - Nath A
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (CLDN1 protein, human)
RN  - 0 (Claudin-1)
RN  - 0 (Claudin-5)
RN  - 0 (Cldn1 protein, mouse)
RN  - 0 (Cldn1 protein, rat)
RN  - 0 (Cldn5 protein, mouse)
RN  - 0 (Cldn5 protein, rat)
RN  - 0 (Gene Products, tat)
RN  - 0 (Membrane Proteins)
RN  - 0 (OCLN protein, human)
RN  - 0 (Occludin)
RN  - 0 (Ocln protein, mouse)
RN  - 0 (Ocln protein, rat)
RN  - 0 (Peptide Fragments)
RN  - 0 (TJP2 protein, human)
RN  - 0 (Tjp2 protein, mouse)
RN  - 0 (Zonula Occludens-2 Protein)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - AIDS Dementia Complex/*metabolism
MH  - Animals
MH  - Blood-Brain Barrier/*drug effects/immunology
MH  - Claudin-1
MH  - Claudin-5
MH  - Down-Regulation/drug effects/physiology
MH  - Endothelium, Vascular/physiopathology
MH  - Gene Products, tat/metabolism/*pharmacology
MH  - *HIV-1
MH  - Male
MH  - Membrane Proteins/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Occludin
MH  - Peptide Fragments/metabolism/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Tight Junctions/*drug effects/metabolism
MH  - Virus Replication/physiology
MH  - Zonula Occludens-2 Protein
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2003/09/30 05:00
MHDA- 2003/12/17 05:00
CRDT- 2003/09/30 05:00
PHST- 2003/09/30 05:00 [pubmed]
PHST- 2003/12/17 05:00 [medline]
PHST- 2003/09/30 05:00 [entrez]
AID - 10.1002/jnr.10762 [doi]
PST - ppublish
SO  - J Neurosci Res. 2003 Oct 15;74(2):255-65. doi: 10.1002/jnr.10762.

PMID- 14519784
OWN - NLM
STAT- MEDLINE
DCOM- 20031201
LR  - 20211025
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 133
IP  - 10
DP  - 2003 Oct
TI  - Zinc modulates PPARgamma signaling and activation of porcine endothelial
      cells.
PG  - 3058-64
AB  - Dietary zinc has potent antioxidant and anti-inflammatory properties and
      is a critical component of peroxisome proliferator-activated receptor
      (PPAR) gene expression and regulation. To assess the protective
      mechanisms of PPARgamma in endothelial cell dysfunction and the role of
      zinc in the modulation of PPARgamma signaling, cultured porcine pulmonary
      artery endothelial cells were exposed to the membrane-permeable zinc
      chelator N,N,N'N'-tetrakis (2-pyridylmethyl)-ethylene diamine (TPEN),
      thiazolidinedione (TZD; PPARgamma agonist) or bisphenol A diglycidyl
      ether (BADGE; PPARgamma antagonist). Subsequently, endothelial cells were
      activated by treatment with linoleic acid (90 micro mol/L) for 6 h. Zinc
      chelation by TPEN increased the DNA binding activity of nuclear factor
      (NF)-kappaB and activator protein (AP)-1, decreased PPARgamma expression
      and activation as well as up-regulated interleukin (IL)-6 expression and
      production. These effects were fully reversed by zinc supplementation. In
      addition, exposure to TZD down-regulated linoleic acid-induced DNA
      binding activity of NF-kappaB and AP-1, whereas BADGE further induced
      activation of these oxidative stress-sensitive transcription factors.
      Most importantly, the TZD-mediated down-regulation of NF-kappaB and AP-1
      and reduced inflammatory response were impaired during zinc chelation.
      These data suggest that zinc plays a critical role in PPARgamma signaling
      in linoleic acid-induced endothelial cell activation and indicate that
      PPARgamma signaling is impaired during zinc deficiency.
FAU - Meerarani, Purushothaman
AU  - Meerarani P
AD  - Molecular and Cell Nutrition Laboratory, College of Agriculture,
      University of Kentucky, Lexington, KY 40546-0215, USA.
FAU - Reiterer, Gudrun
AU  - Reiterer G
FAU - Toborek, Michal
AU  - Toborek M
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Benzhydryl Compounds)
RN  - 0 (Chelating Agents)
RN  - 0 (Epoxy Compounds)
RN  - 0 (Ethylenediamines)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Thiazolidinediones)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 9007-49-2 (DNA)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - AA68LXK93C (2,4-thiazolidinedione)
RN  - F3XRM1NX4H (2,2-bis(4-glycidyloxyphenyl)propane)
RN  - J41CSQ7QDS (Zinc)
RN  - R9PTU1U29I (N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine)
SB  - IM
MH  - Animals
MH  - Benzhydryl Compounds
MH  - Cells, Cultured
MH  - Chelating Agents/pharmacology
MH  - DNA/metabolism
MH  - Diet
MH  - Electrophoretic Mobility Shift Assay
MH  - Endothelium, Vascular/*drug effects/*physiology
MH  - Epoxy Compounds
MH  - Ethylenediamines/pharmacology
MH  - Interleukin-6/metabolism
MH  - Linoleic Acid/pharmacology
MH  - NF-kappa B/metabolism
MH  - Pulmonary Artery
MH  - Receptors, Cytoplasmic and Nuclear/agonists/antagonists &
      inhibitors/*metabolism
MH  - Signal Transduction/*drug effects
MH  - Swine
MH  - Thiazolidinediones/pharmacology
MH  - Transcription Factor AP-1/metabolism
MH  - Transcription Factors/agonists/antagonists & inhibitors/*metabolism
MH  - Zinc/*pharmacology
EDAT- 2003/10/02 05:00
MHDA- 2003/12/03 05:00
CRDT- 2003/10/02 05:00
PHST- 2003/10/02 05:00 [pubmed]
PHST- 2003/12/03 05:00 [medline]
PHST- 2003/10/02 05:00 [entrez]
AID - 10.1093/jn/133.10.3058 [doi]
PST - ppublish
SO  - J Nutr. 2003 Oct;133(10):3058-64. doi: 10.1093/jn/133.10.3058.

PMID- 12805654
OWN - NLM
STAT- MEDLINE
DCOM- 20040802
LR  - 20171116
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 75
IP  - 1
DP  - 2003 Sep
TI  - PCB 104-induced proinflammatory reactions in human vascular endothelial
      cells: relationship to cancer metastasis and atherogenesis.
PG  - 47-56
AB  - Polychlorinated biphenyls (PCBs) are widespread environmental
      contaminants that are known to induce carcinogenic and possibly
      atherogenic events. Recent evidence suggests that selected PCBs may be
      potent developmental agents of vascular inflammatory responses by
      inducing cellular oxidative stress and activating redox-responsive
      transcription factors. Therefore, the aim of this paper is to investigate
      PCB-induced proinflammatory reactions in human vascular endothelial
      cells. To determine the proinflammatory effects, cellular oxidative
      stress and expression of genes encoding for monocyte chemoattractant
      protein-1 (MCP-1) and adhesion molecules, such as E-selectin and
      intercellular adhesion molecule-1 (ICAM-1), were assessed in human
      umbilical vein endothelial cells (HUVEC) exposed to
      2,2',4,6,6'-pentachlorobiphenyl (PCB 104), a representative of ortho-
      substituted, non-coplanar PCB congeners. PCB 104 increased the oxidative
      stress in endothelial cells, as determined by the increased
      2',7'-dichlorofluorescein (DCF) and rhodamine 123 fluorescence. In
      addition, PCB 104 markedly upregulated the expression of MCP-1,
      E-selectin, and ICAM-1 at both the mRNA and protein levels. These effects
      were time- and concentration-dependent. The maximum expression of
      inflammatory genes was observed in endothelial cells exposed to 20 microM
      of PCB 104 for 1 or 2 h, depending on the specific gene. In addition, PCB
      104 elevated the adhesion of THP-1 cells (a human acute monocytic
      leukemia cell line) to endothelial cell monolayers. These results
      indicate that PCB 104 is a potent stimulant of inflammatory mediators in
      human vascular endothelial cells. We hypothesize that these
      proinflammatory processes may contribute to the development of cancer
      metastasis and/or atherogenesis in patients exposed to PCBs.
FAU - Choi, Wangsun
AU  - Choi W
AD  - Department of Surgery, University of Kentucky, Lexington, Kentucky 40536,
      USA.
FAU - Eum, Sung Yong
AU  - Eum SY
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Robertson, Larry W
AU  - Robertson LW
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20030612
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (Chemokine CCL2)
RN  - 0 (E-Selectin)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Reactive Oxygen Species)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - Z4YYF101N3 (2,2',4,6,6'-pentachlorobiphenyl)
SB  - IM
MH  - Cell Adhesion/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - E-Selectin/biosynthesis/genetics
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Environmental Pollutants/*toxicity
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Inflammation/chemically induced/metabolism
MH  - Intercellular Adhesion Molecule-1/biosynthesis/genetics
MH  - Oxidative Stress
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Reactive Oxygen Species/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Up-Regulation
EDAT- 2003/06/14 05:00
MHDA- 2004/08/03 05:00
CRDT- 2003/06/14 05:00
PHST- 2003/06/14 05:00 [pubmed]
PHST- 2004/08/03 05:00 [medline]
PHST- 2003/06/14 05:00 [entrez]
AID - 10.1093/toxsci/kfg149 [doi]
AID - kfg149 [pii]
PST - ppublish
SO  - Toxicol Sci. 2003 Sep;75(1):47-56. doi: 10.1093/toxsci/kfg149. Epub 2003
      Jun 12.

PMID- 14550782
OWN - NLM
STAT- MEDLINE
DCOM- 20040120
LR  - 20191108
IS  - 1044-7431 (Print)
IS  - 1044-7431 (Linking)
VI  - 24
IP  - 1
DP  - 2003 Sep
TI  - HIV-1 Tat protein upregulates inflammatory mediators and induces monocyte
      invasion into the brain.
PG  - 224-37
AB  - Impaired inflammatory functions may be critical factors in the mechanisms
      by which HIV-1 enters the CNS. Evidence indicates that a viral gene
      product, the protein Tat, can markedly contribute to these effects. In
      the present study we tested the hypothesis that Tat can upregulate the
      expression of inflammatory cytokines and adhesion molecules and
      facilitate the entry of monocytes into the brain. Expression of
      inflammatory mediators such as monocyte chemoattractant protein-1
      (MCP-1), tumor necrosis factor-alpha (TNF-alpha), vascular cell adhesion
      molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) was
      assessed in C57BL/6 mice injected with Tat(1-72) into the right
      hippocampus. In the Tat(1-72)-injected groups, mRNA and protein levels of
      MCP-1, TNF-alpha, VCAM-1, and ICAM-1 were markedly elevated compared to
      those in control animals. The most pronounced changes were observed in
      and around the injected hippocampus. Double-labeling immunohistochemistry
      demonstrated that inflammatory proteins were primarily expressed in
      activated microglial cells and perivascular cells. In addition,
      astrocytes and endothelial cells were susceptible to Tat(1-72)-induced
      inflammatory responses. These changes were associated with a substantial
      infiltration of monocytes into the brain. These data demonstrate that
      intracerebral administration of Tat can induce profound proinflammatory
      effects in the brain, leading to monocyte infiltration.
FAU - Pu, Hong
AU  - Pu H
AD  - Department of Surgery/Neurosurgery, University of Kentucky Medical
      Center, 800 Rose Street, Lexington, KY 40536, USA.
FAU - Tian, Jing
AU  - Tian J
FAU - Flora, Govinder
AU  - Flora G
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Nath, Avindra
AU  - Nath A
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA 013843/AA/NIAAA NIH HHS/United States
GR  - MH 63022/MH/NIMH NIH HHS/United States
GR  - NS 39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Cell Neurosci
JT  - Molecular and cellular neurosciences
JID - 9100095
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Gene Products, tat)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Peptide Fragments)
RN  - 0 (RNA, Messenger)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - AIDS Dementia Complex/immunology/*metabolism/physiopathology
MH  - Animals
MH  - Blood-Brain Barrier/drug effects/immunology
MH  - Brain/immunology/metabolism
MH  - Cell Adhesion Molecules/genetics/immunology/metabolism
MH  - Chemotaxis, Leukocyte/*drug effects/immunology
MH  - Encephalitis/immunology/*metabolism
MH  - Endothelium, Vascular/immunology/metabolism
MH  - Gene Expression Regulation/drug effects/immunology
MH  - Gene Products, tat/immunology/metabolism/*pharmacology
MH  - HIV-1/immunology/*metabolism
MH  - Inflammation Mediators/immunology/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/immunology
MH  - Neuroglia/drug effects/immunology/metabolism
MH  - Peptide Fragments/immunology/metabolism/pharmacology
MH  - RNA, Messenger/drug effects/metabolism
MH  - Up-Regulation/immunology
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2003/10/11 05:00
MHDA- 2004/01/21 05:00
CRDT- 2003/10/11 05:00
PHST- 2003/10/11 05:00 [pubmed]
PHST- 2004/01/21 05:00 [medline]
PHST- 2003/10/11 05:00 [entrez]
AID - S1044743103001714 [pii]
AID - 10.1016/s1044-7431(03)00171-4 [doi]
PST - ppublish
SO  - Mol Cell Neurosci. 2003 Sep;24(1):224-37. doi:
      10.1016/s1044-7431(03)00171-4.

PMID- 12758055
OWN - NLM
STAT- MEDLINE
DCOM- 20030708
LR  - 20190727
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 189
IP  - 1
DP  - 2003 May 15
TI  - 2,2',4,6,6'-pentachlorobiphenyl (PCB 104) induces apoptosis of human
      microvascular endothelial cells through the caspase-dependent activation
      of CREB.
PG  - 1-10
AB  - It has been proposed that endothelial integrity can play an active
      regulatory role in the extravasation of tumor cells during cancer
      metastasis. Since polychlorinated biphenyls (PCBs) have been shown to
      cause endothelial cell activation or injury and to lead to various
      diseases that involve dysfunction of the vascular endothelium, the
      present study was designed to determine the cellular and molecular
      signaling mechanisms of PCB-induced apoptosis in human microvascular
      endothelial cells (HMEC-1). A significant and marked decrease in cell
      viability was observed in HMEC-1 treated with
      2,2',4,6,6'-pentachlorobiphenyl (PCB 104) in a time- and dose-dependent
      manner. Exposure of HMEC-1 to PCB 104 also dramatically induced
      internucleosomal DNA fragmentation. However, the caspase inhibitor zVAD-
      fmk significantly reversed the PCB 104-induced DNA fragmentation in
      HMEC-1, suggesting that endothelial cell death induced by PCB 104
      exposure is, at least in part, due to caspase-dependent apoptotic
      pathways. To elucidate the molecular signaling mechanisms of PCB
      104-induced apoptotic cell death in human microvascular endothelial
      cells, the present study focused on the effects of acute exposure of PCB
      104 on the activation of several transcription factors, such as cAMP
      responsive element-binding protein (CREB), activator protein-1 (AP-1),
      nuclear factor-kappaB (NF-kappaB), and signal transducers and activators
      of transcription (STAT1), which have been known to play a pivotal role in
      the molecular signaling cascades for the induction of apoptosis. A series
      of electrophoretic mobility shift assay showed that PCB 104 specifically
      increased only CREB DNA-binding activity in a dose-dependent manner.
      AP-1, NF-kappaB, and STAT1, however, were not activated. In addition,
      zVAD-fmk significantly and dose-dependently blocked the CREB activation
      enhanced by PCB 104 exposure. These results suggest that PCB-induced
      death of human microvascular endothelial cells is mediated, at least in
      part, via the caspase-dependent apoptotic pathways and that the selective
      activation of CREB is involved in this process.
FAU - Lee, Yong Woo
AU  - Lee YW
AD  - Department of Surgery, University of Kentucky, Lexington, KY 40536, USA.
FAU - Park, Hyen Joo
AU  - Park HJ
FAU - Son, Kwang Won
AU  - Son KW
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Robertson, Larry W
AU  - Robertson LW
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Apoptosis/*drug effects/physiology
MH  - Caspases/*metabolism
MH  - Cell Line
MH  - Cell Survival/drug effects/physiology
MH  - Cyclic AMP Response Element-Binding Protein/*metabolism
MH  - Endothelium, Vascular/cytology/*drug effects/enzymology
MH  - Enzyme Activation/drug effects/physiology
MH  - Humans
MH  - Microcirculation/cytology/drug effects/enzymology
MH  - Polychlorinated Biphenyls/chemistry/*pharmacology
EDAT- 2003/05/22 05:00
MHDA- 2003/07/09 05:00
CRDT- 2003/05/22 05:00
PHST- 2003/05/22 05:00 [pubmed]
PHST- 2003/07/09 05:00 [medline]
PHST- 2003/05/22 05:00 [entrez]
AID - S0041008X0300084X [pii]
AID - 10.1016/s0041-008x(03)00084-x [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2003 May 15;189(1):1-10. doi:
      10.1016/s0041-008x(03)00084-x.

PMID- 12701065
OWN - NLM
STAT- MEDLINE
DCOM- 20030519
LR  - 20161019
IS  - 0026-0495 (Print)
IS  - 0026-0495 (Linking)
VI  - 52
IP  - 4
DP  - 2003 Apr
TI  - Cholesterol attenuates linoleic acid-induced endothelial cell activation.
PG  - 493-500
AB  - Vascular endothelial cell activation and dysfunction are critical early
      events in atherosclerosis. Even though very low or high levels of
      cholesterol can compromise cellular functions, cholesterol is a critical
      membrane component and may protect the vascular endothelium from
      oxidative stress and polyunsaturated fatty acid-mediated inflammatory
      responses. We have previously shown that the parent omega-6 fatty acid
      linoleic acid can markedly activate vascular endothelial cells. We now
      propose that membrane cholesterol can modify and inhibit linoleic acid-
      mediated endothelial cell dysfunction. To test this hypothesis, pulmonary
      artery endothelial cells were incubated with cholesterol (0 to 100
      micromol/L) for 24 hours and then treated with 90 micromol/L of linoleic
      acid (18:2n-6) for 6 to 24 hours. In control cells, treatment with
      linoleic acid reduced intracellular glutathione levels and induced the
      DNA binding activity of nuclear factor-kappaB (NF-kappaB) leading to the
      upregulation of interleukin-6 (IL-6). In addition, the expression of
      endothelial nitric oxide synthase (eNOS) was altered, with linoleic acid
      increasing eNOS activity. In contrast, enrichment with cholesterol
      enhanced glutathione levels and reduced the linoleic acid-induced
      activation of NF-kappaBand the production of IL-6. Prior exposure to 50
      micromol/L cholesterol also prevented the fatty acid-induced increase in
      eNOS activation. Cholesterol loading activated peroxisome proliferator-
      activated receptor-gamma (PPAR-gamma), a nuclear receptor that can
      decrease inflammatory responses. Furthermore, the PPAR-gamma agonist
      thiazolidinedione markedly downregulated the NF-kappaB activation
      mediated by linoleic acid. Our data suggest that signaling pathways
      linked to endothelial cell activation by prooxidant and proinflammatory
      insults may be influenced by cellular cholesterol levels.
CI  - Copyright 2003 Elsevier, Inc. All rights reserved.
FAU - Meerarani, Purushothaman
AU  - Meerarani P
AD  - Department of Animal Sciences, the Graduate Center for Nutritional
      Sciences, University of Kentucky, Lexington 40546-0215, USA.
FAU - Smart, Eric J
AU  - Smart EJ
FAU - Toborek, Michal
AU  - Toborek M
FAU - Boissonneault, Gilbert A
AU  - Boissonneault GA
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Culture Media)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Oxidants)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factors)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cholesterol/*pharmacology
MH  - Culture Media
MH  - Electrophoretic Mobility Shift Assay
MH  - Endothelium, Vascular/*cytology/drug effects
MH  - Glutathione/metabolism
MH  - Inflammation/pathology
MH  - Interleukin-6/biosynthesis
MH  - Linoleic Acid/*pharmacology
MH  - NF-kappa B/drug effects/metabolism
MH  - Nitric Oxide Synthase/biosynthesis/genetics
MH  - Nitric Oxide Synthase Type III
MH  - Oxidants/pharmacology
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/drug effects/physiology
MH  - Swine
MH  - Transcription Factors/metabolism
EDAT- 2003/04/18 05:00
MHDA- 2003/05/20 05:00
CRDT- 2003/04/18 05:00
PHST- 2003/04/18 05:00 [pubmed]
PHST- 2003/05/20 05:00 [medline]
PHST- 2003/04/18 05:00 [entrez]
AID - 10.1053/meta.2003.50087 [doi]
AID - S0026049502052964 [pii]
PST - ppublish
SO  - Metabolism. 2003 Apr;52(4):493-500. doi: 10.1053/meta.2003.50087.

PMID- 12388243
OWN - NLM
STAT- MEDLINE
DCOM- 20030117
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 284
IP  - 1
DP  - 2003 Jan
TI  - Redox-regulated mechanisms of IL-4-induced MCP-1 expression in human
      vascular endothelial cells.
PG  - H185-92
AB  - The present study focused on the molecular signaling pathways of monocyte
      chemoattractant protein-1 (MCP-1) induction by interleukin-4 (IL-4) in
      human umbilical vein endothelial cells (HUVEC). RT-PCR showed that MCP-1
      mRNA accumulation was markedly increased in IL-4-treated HUVEC in a time-
      and dose-dependent manner. Antioxidants, such as pyrrolidine
      dithiocarbamate (PDTC) and N-acetylcysteine (NAC), significantly
      inhibited IL-4-induced MCP-1 mRNA expression. These effects correlated
      well with the PDTC-mediated inhibition of MCP-1 promoter transcriptional
      activity observed in IL-4-treated HUVEC. IL-4-induced MCP-1 gene
      expression was paralleled by a concomitant production of MCP-1 protein.
      In agreement with MCP-1 gene expression, PDTC attenuated IL-4-mediated
      induction of MCP-1 protein expression. In addition, IL-4 dramatically
      increased the transcription factor signal transducers and activators of
      transcription 1 (STAT1) DNA binding activity, an effect that was
      attenuated by PDTC. The role of STAT1 in the regulation of the
      IL-4-induced MCP-1 gene expression was further confirmed in HUVEC
      transfected with a reporter construct of the MCP-1 promoter with a
      mutated STAT1 binding site. These results demonstrate that IL-4-dependent
      MCP-1 induction in HUVEC is mediated by redox-regulated STAT1 activation.
FAU - Lee, Yong Woo
AU  - Lee YW
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington
      40536, USA.
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20020926
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (STAT1 protein, human)
RN  - 0 (Thiocarbamates)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - 135467-92-4 (prolinedithiocarbamate)
RN  - 207137-56-2 (Interleukin-4)
RN  - 9007-49-2 (DNA)
RN  - 9DLQ4CIU6V (Proline)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - DNA/antagonists & inhibitors/metabolism
MH  - DNA-Binding Proteins/metabolism/physiology
MH  - Endothelium, Vascular/*metabolism
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Interleukin-4/*pharmacology
MH  - Oxidation-Reduction
MH  - Proline/*analogs & derivatives/pharmacology
MH  - STAT1 Transcription Factor
MH  - Thiocarbamates/pharmacology
MH  - Trans-Activators/metabolism/physiology
MH  - Transcription Factors/physiology
EDAT- 2002/10/22 04:00
MHDA- 2003/01/18 04:00
CRDT- 2002/10/22 04:00
PHST- 2002/10/22 04:00 [pubmed]
PHST- 2003/01/18 04:00 [medline]
PHST- 2002/10/22 04:00 [entrez]
AID - 10.1152/ajpheart.00524.2002 [doi]
AID - 00524.2002 [pii]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2003 Jan;284(1):H185-92. doi:
      10.1152/ajpheart.00524.2002. Epub 2002 Sep 26.

PMID- 12485413
OWN - NLM
STAT- MEDLINE
DCOM- 20030123
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 84
IP  - 1
DP  - 2003 Jan
TI  - HIV-Tat protein induces oxidative and inflammatory pathways in brain
      endothelium.
PG  - 169-79
AB  - Impaired function of the brain vasculature might contribute to the
      development of HIV-associated dementia. For example, injury or
      dysfunction of brain microvascular endothelial cells (BMEC) can lead to
      the breakdown of the blood-brain barrier (BBB) and thus allow accelerated
      entry of the HIV-1 virus into the CNS. Mechanisms of injury to BMEC
      during HIV-1 infection are not fully understood, but the viral gene
      product Tat may be, at least in part, responsible for this effect. Tat
      can be released from infected perivascular macrophages in the CNS of
      patients with AIDS, and thus BMEC can be directly exposed to high
      concentrations of this protein. To study oxidative and inflammatory
      mechanisms associated with Tat-induced toxicity, BMEC were exposed to
      increasing doses of Tat1-72, and markers of oxidative stress, as well as
      redox-responsive transcription factors such as nuclear factor-kappaB (NF-
      kappaB) and activator protein-1 (AP-1), were measured. Tat1-72 treatment
      markedly increased cellular oxidative stress, decreased levels of
      intracellular glutathione and activated DNA binding activity and
      transactivation of NF-kappaB and AP-1. To determine if Tat1-72 can
      stimulate inflammatory responses in brain endothelium in vivo, expression
      of monocyte chemoattractant protein-1 (MCP-1), an NF-kappaB and
      AP-1-dependent chemokine, was studied in brain tissue in mice injected
      with Tat1-72 into the right hippocampus. Tat1-72 markedly elevated the
      MCP-1 mRNA levels in brain tissue. In addition, a double
      immunohistochemistry study revealed that MCP-1 protein was markedly
      overexpressed on brain vascular endothelium. These data indicate that
      Tat1-72 can induce redox-related inflammatory responses both in in vitro
      and in vivo environments. These changes can directly lead to disruption
      of the BBB. Thus, Tat can play an important role in the development of
      detrimental vascular changes in the brains of HIV-infected patients.
FAU - Toborek, Michal
AU  - Toborek M
AD  - Department of Surgery, Animal Sciences and Neurology, University of
      Kentucky Medical Center, Lexington, Kentucky 40536, USA.
      mjtobo00@pop.uky.edu
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Pu, Hong
AU  - Pu H
FAU - Malecki, Andrzej
AU  - Malecki A
FAU - Flora, Govinder
AU  - Flora G
FAU - Garrido, Rosario
AU  - Garrido R
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Bauer, Hans-Christian
AU  - Bauer HC
FAU - Nath, Avindra
AU  - Nath A
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AA013843/AA/NIAAA NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Gene Products, tat)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 0 (tat peptide (1-72), Human immunodeficiency virus 1)
SB  - IM
MH  - Animals
MH  - *Cerebrovascular Circulation/*drug effects
MH  - Chemokine CCL2/genetics
MH  - Clone Cells
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Gene Products, tat/*pharmacology
MH  - Microcirculation/drug effects
MH  - NF-kappa B/physiology
MH  - *Oxidative Stress
MH  - RNA, Messenger/metabolism
MH  - Swine
MH  - Transcription Factor AP-1/physiology
MH  - Transcriptional Activation/drug effects
MH  - Vasculitis/*chemically induced/metabolism
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2002/12/18 04:00
MHDA- 2003/01/24 04:00
CRDT- 2002/12/18 04:00
PHST- 2002/12/18 04:00 [pubmed]
PHST- 2003/01/24 04:00 [medline]
PHST- 2002/12/18 04:00 [entrez]
AID - 1543 [pii]
AID - 10.1046/j.1471-4159.2003.01543.x [doi]
PST - ppublish
SO  - J Neurochem. 2003 Jan;84(1):169-79. doi:
      10.1046/j.1471-4159.2003.01543.x.

PMID- 12504868
OWN - NLM
STAT- MEDLINE
DCOM- 20030130
LR  - 20190722
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 179
IP  - 1
DP  - 2003 Jan
TI  - Methamphetamine potentiates HIV-1 Tat protein-mediated activation of
      redox-sensitive pathways in discrete regions of the brain.
PG  - 60-70
AB  - Tat is a major regulatory protein encoded by human immunodeficiency viral
      genome, which has been implicated in the pathogenesis of HIV infection,
      including neurologic complications associated with this disease. In
      addition, drug abuse has been identified as a major risk factor of HIV
      infection. We hypothesize that abusive drugs, such as methamphetamine
      (METH), can directly influence specific molecular processes that can
      further contribute to toxic effects of Tat. To elucidate the molecular
      signaling pathways of Tat- and/or METH-induced toxicity, we investigated
      the effects of a single injection of Tat (25 microg/microl into the right
      hippocampus) and/or METH (10 mg/kg, intraperitoneally) on the generation
      of cellular oxidative stress, DNA-binding activity of specific redox-
      responsive transcription factors, and expression of inflammatory genes.
      Administration of Tat or METH resulted in stimulation of cellular
      oxidative stress and activation of redox-regulated transcription factors
      in the cortical, striatal, and hippocampal regions of the mouse brain. In
      addition, DNA-binding activities of NF-kappaB, AP-1, and CREB in the
      frontal cortex and hippocampus were more pronounced in mice injected with
      Tat plus METH compared to the effects of Tat or METH alone. Intercellular
      adhesion molecule-1 gene expression also was upregulated in a synergistic
      manner in cortical, striatal, and hippocampal regions in mice which
      received injections of Tat combined with METH compared to the effects of
      these agents alone. Moreover, synergistic effects of Tat plus METH on the
      tumor necrosis factor-alpha and interleukin-1beta mRNA levels were
      observed in the striatal region. These results indicate that Tat and METH
      can cross-amplify their cellular effects, leading to alterations of
      redox-regulated inflammatory pathways in the brain. Such synergistic
      proinflammatory stimulation may have significant implications in HIV-
      infected patients who abuse drugs.
FAU - Flora, Govinder
AU  - Flora G
AD  - Department of Surgery, University of Kentucky Medical Center, 800 Rose
      Street, Lexington, KY 40536, USA.
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Nath, Avindra
AU  - Nath A
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Maragos, William
AU  - Maragos W
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - MH 63022/MH/NIMH NIH HHS/United States
GR  - NS 39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Gene Products, tat)
RN  - 0 (Interleukin-1)
RN  - 0 (Peptide Fragments)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 44RAL3456C (Methamphetamine)
SB  - IM
MH  - Animals
MH  - Brain/cytology/*drug effects/metabolism
MH  - Cerebellum/cytology/drug effects/metabolism
MH  - Corpus Striatum/cytology/drug effects/metabolism
MH  - Drug Administration Routes
MH  - Drug Synergism
MH  - Frontal Lobe/cytology/drug effects/metabolism
MH  - Gene Expression/drug effects
MH  - Gene Products, tat/genetics/*pharmacology
MH  - *HIV-1
MH  - Hippocampus/drug effects
MH  - Intercellular Adhesion Molecule-1/biosynthesis/genetics
MH  - Interleukin-1/biosynthesis/genetics
MH  - Male
MH  - Methamphetamine/*pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mutagenesis, Site-Directed
MH  - Oxidation-Reduction/drug effects
MH  - Oxidative Stress/drug effects
MH  - Peptide Fragments/genetics/*pharmacology
MH  - Sequence Deletion
MH  - Signal Transduction/drug effects
MH  - Transcription Factors/metabolism
MH  - Tumor Necrosis Factor-alpha/biosynthesis/genetics
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2002/12/31 04:00
MHDA- 2003/01/31 04:00
CRDT- 2002/12/31 04:00
PHST- 2002/12/31 04:00 [pubmed]
PHST- 2003/01/31 04:00 [medline]
PHST- 2002/12/31 04:00 [entrez]
AID - S0014488602980489 [pii]
AID - 10.1006/exnr.2002.8048 [doi]
PST - ppublish
SO  - Exp Neurol. 2003 Jan;179(1):60-70. doi: 10.1006/exnr.2002.8048.

PMID- 12237866
OWN - NLM
STAT- MEDLINE
DCOM- 20021122
LR  - 20161019
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 70
IP  - 1
DP  - 2002 Oct 1
TI  - Methamphetamine activates DNA binding of specific redox-responsive
      transcription factors in mouse brain.
PG  - 82-9
AB  - Cellular oxidative stress and alterations in redox status can be
      implicated in methamphetamine (METH)-induced neurotoxicity. To elucidate
      the molecular signaling pathways of METH-induced neurotoxicity, we
      investigated the effects of a single intraperitoneal injection of METH
      (1.0, 10, or 20 mg/kg) on DNA-binding activity of specific redox-
      sensitive transcription factors in mouse brain. Transcription factors
      studied included activator protein-1 (AP-1), nuclear factor-kappaB (NF-
      kappaB), cAMP-responsive element-binding protein (CREB), SP-1, and signal
      transducers and activators of transcription (STAT1 and STAT3).
      Significant and dose-dependent inductions of AP-1 and CREB DNA-binding
      activities were observed in four different regions (striatum, frontal
      cortex, hippocampus, and cerebellum) isolated from the brains of mice
      injected with METH. However, injections with METH did not affect DNA
      binding activities of NF-kappaB, SP-1, STAT1, and STAT3. These results
      suggest that METH-induced oxidative stress may trigger the molecular
      signaling pathways via specific and selective activation of AP-1 and
      CREB.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Lee, Yong Woo
AU  - Lee YW
AD  - Division of Neurosurgery, Department of Surgery, University of Kentucky
      Medical Center, Lexington, Kentucky 40536, USA.
FAU - Son, Kwang Won
AU  - Son KW
FAU - Flora, Govinder
AU  - Flora G
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Nath, Avindra
AU  - Nath A
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Activating Transcription Factor 1)
RN  - 0 (Atf1 protein, mouse)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Dopamine Uptake Inhibitors)
RN  - 0 (NF-kappa B)
RN  - 0 (Phosphorus Isotopes)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Stat1 protein, mouse)
RN  - 0 (Stat3 protein, mouse)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 44RAL3456C (Methamphetamine)
RN  - 6QYI7Y8OBO (mitopodozide)
RN  - 9000-55-9 (Podophyllin)
RN  - L36H50F353 (Podophyllotoxin)
SB  - IM
MH  - Activating Transcription Factor 1
MH  - Analysis of Variance
MH  - Animals
MH  - Brain/anatomy & histology/*drug effects/metabolism
MH  - Cell Nucleus/drug effects/metabolism
MH  - Cerebellum/drug effects/metabolism/physiology
MH  - Cerebral Cortex/drug effects/metabolism/physiology
MH  - Corpus Striatum/drug effects/metabolism/physiology
MH  - DNA-Binding Proteins/*drug effects/metabolism/physiology
MH  - Dopamine Uptake Inhibitors/*pharmacology
MH  - Electrophoretic Mobility Shift Assay
MH  - Hippocampus/drug effects/metabolism/physiology
MH  - Male
MH  - Methamphetamine/*pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/drug effects/metabolism
MH  - Oxidation-Reduction/drug effects
MH  - Phosphorus Isotopes
MH  - Podophyllin/*analogs & derivatives/metabolism
MH  - Podophyllotoxin/analogs & derivatives
MH  - Proto-Oncogene Proteins c-fos/metabolism
MH  - Proto-Oncogene Proteins c-jun/metabolism
MH  - STAT1 Transcription Factor
MH  - STAT3 Transcription Factor
MH  - Trans-Activators/drug effects/physiology
MH  - Transcription Factor AP-1/drug effects/metabolism
MH  - Transcription Factors/*drug effects/metabolism
EDAT- 2002/09/19 10:00
MHDA- 2002/11/26 04:00
CRDT- 2002/09/19 10:00
PHST- 2002/09/19 10:00 [pubmed]
PHST- 2002/11/26 04:00 [medline]
PHST- 2002/09/19 10:00 [entrez]
AID - 10.1002/jnr.10370 [doi]
PST - ppublish
SO  - J Neurosci Res. 2002 Oct 1;70(1):82-9. doi: 10.1002/jnr.10370.

PMID- 12079426
OWN - NLM
STAT- MEDLINE
DCOM- 20020724
LR  - 20190727
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 181
IP  - 3
DP  - 2002 Jun 15
TI  - Proinflammatory properties of coplanar PCBs: in vitro and in vivo
      evidence.
PG  - 174-83
AB  - So-called coplanar polychlorinated biphenyls (PCBs), as well as other
      environmental contaminants that are aryl hydrocarbon receptor (AhR)
      agonists, may compromise the normal functions of vascular endothelial
      cells by activating oxidative stress-sensitive signaling pathways and
      subsequent proinflammatory events critical in the pathology of
      atherosclerosis and cardiovascular disease. To test this hypothesis,
      porcine endothelial cells were exposed to PCB 153 and to three coplanar
      PCBs (PCB 77, PCB 126, or PCB 169). In contrast to PCB 153, which is not
      a ligand for the Ah receptor (AhR), all coplanar PCBs disrupted
      endothelial barrier function. All coplanar PCBs increased expression of
      the CYP1A1 gene, oxidative stress (DCF fluorescence), and the DNA-binding
      activity of nuclear factor kappaB (NF-kappaB). PCB-induced oxidative
      stress was concentration-dependent, with PCB 126 exhibiting a maximal
      response at the lowest concentration (0.5 microM) tested. The increase in
      NF-kappaB-dependent transcriptional activity was confirmed in endothelial
      cells by a luciferase reporter gene assay. In contrast to PCB 153,
      coplanar PCBs that are AhR ligands increased endothelial production of
      interleukin-6. At 3.4 microM, expression of the adhesion molecule VCAM-1
      was most sensitive to PCB 77 and 169. We also provide in vivo evidence,
      suggesting that binding to the AhR is critical for the proinflammatory
      properties of PCBs. Twenty hours after a single administration of PCB 77,
      VCAM-1 expression was increased only in wild-type mice, while mice
      lacking the AhR gene showed no increased staining for VCAM-1. These data
      provide evidence that coplanar PCBs, agonists for the AhR, and inducers
      of cytochrome P450 1A1, produce oxidative stress and an inflammatory
      response in vascular endothelial cells. An intact AhR may be necessary
      for the observed PCB-induced responses. These findings suggest that
      activation of the AhR can be an underlying mechanism of atherosclerosis
      mediated by certain environmental contaminants.
CI  - (c) 2002 Elsevier Science (USA).
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Cell Nutrition Group, Department of Animal Sciences, University of
      Kentucky, Lexington 40506-0054, USA. bhennig@uky.edu
FAU - Meerarani, Purushothaman
AU  - Meerarani P
FAU - Slim, Rabih
AU  - Slim R
FAU - Toborek, Michal
AU  - Toborek M
FAU - Daugherty, Alan
AU  - Daugherty A
FAU - Silverstone, Allen E
AU  - Silverstone AE
FAU - Robertson, Larry W
AU  - Robertson LW
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - ES 07216/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Environmental Pollutants)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.13.12.- (Luciferases)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/chemically induced/pathology
MH  - Blood-Air Barrier/drug effects
MH  - Cell Nucleus/chemistry
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/metabolism
MH  - Electrophoresis
MH  - Endothelium, Vascular/chemistry/drug effects
MH  - Environmental Pollutants/*toxicity
MH  - Immunohistochemistry
MH  - In Vitro Techniques
MH  - Inflammation/*chemically induced/pathology
MH  - Interleukin-6/biosynthesis
MH  - Luciferases/genetics
MH  - Mice
MH  - Mice, Knockout
MH  - NF-kappa B/drug effects
MH  - Oxidative Stress/drug effects
MH  - Polychlorinated Biphenyls/chemistry/*toxicity
MH  - Receptors, Aryl Hydrocarbon/agonists/deficiency
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Structure-Activity Relationship
MH  - Swine
EDAT- 2002/06/25 10:00
MHDA- 2002/07/26 10:01
CRDT- 2002/06/25 10:00
PHST- 2002/06/25 10:00 [pubmed]
PHST- 2002/07/26 10:01 [medline]
PHST- 2002/06/25 10:00 [entrez]
AID - S0041008X02994081 [pii]
AID - 10.1006/taap.2002.9408 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2002 Jun 15;181(3):174-83. doi:
      10.1006/taap.2002.9408.

PMID- 12018021
OWN - NLM
STAT- MEDLINE
DCOM- 20021105
LR  - 20161019
IS  - 1438-4639 (Print)
IS  - 1438-4639 (Linking)
VI  - 205
IP  - 1-2
DP  - 2002 Mar
TI  - PCB-induced oxidative stress in endothelial cells: modulation by
      nutrients.
PG  - 95-102
AB  - There is an increasing body of evidence suggesting that exposure to
      Superfund chemicals may have adverse consequences on many organ systems,
      as well as carcinogenic and atherogenic effects. This is particularly
      true for polyhalogenated aromatic hydrocarbons such as the
      polychlorinated biphenyls (PCBs). The vascular endothelium, which is
      constantly exposed to blood components including environmental
      contaminants, is extremely vulnerable to chemical insult as well as
      necrotic and apoptotic injury. Our recent studies suggest that certain
      PCBs, especially coplanar PCBs, can compromise normal functions of
      vascular endothelial cells by activating oxidative stress-sensitive
      signaling pathways and subsequent proinflammatory events critical in the
      pathology of atherosclerosis and cardiovascular disease. Our findings
      suggest that an increase in the level of cellular oxidative stress is a
      significant event in PCB-mediated endothelial cell dysfunction and that
      nutrients can modulate PCB-induced oxidative stress and endothelial
      toxicity. We have demonstrated that the dietary fat linoleic acid, the
      parent unsaturated fatty acid of the omega-6 family, can increase
      endothelial dysfunction induced by selected PCBs, probably by
      contributing to oxidative stress and as the result of the production of
      toxic metabolites called leukotoxins. The subsequent imbalance in the
      overall cellular oxidant/antioxidant status can activate oxidative
      stress- or redoxsensitive transcription factors, which in turn promote
      gene expression for inflammatory cytokines and adhesion molecules,
      intensifying the inflammatory response and endothelial cell dysfunction.
      Our data also suggest that antioxidant nutrients such as vitamin E can
      protect against endothelial cell damage mediated by PCBs or
      polyunsaturated dietary fats by interfering with oxidative stress-
      sensitive and proinflammatory signaling pathways. The concept that
      nutrition can modify or ameliorate the toxicity of Superfund chemicals is
      provocative and warrants further study as the implications for human
      health are significant. The information from such studies could be used
      to develop dietary recommendations and nutritional interventions for
      populations at high risk for exposure to PCBs, including communities
      living near Superfund sites and those exposed via occupation or diet.
FAU - Hennig, Bernhard
AU  - Hennig B
AD  - Cell Nutrition Group, Department of Animal Sciences, University of
      Kentucky, Lexington, KY 40546, USA. bhennig@uky.edu
FAU - Hammock, Bruce D
AU  - Hammock BD
FAU - Slim, Rabih
AU  - Slim R
FAU - Toborek, Michal
AU  - Toborek M
FAU - Saraswathi, Viswanathan
AU  - Saraswathi V
FAU - Robertson, Larry W
AU  - Robertson LW
LA  - eng
GR  - 04699/PHS HHS/United States
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P30 ES05707/ES/NIEHS NIH HHS/United States
GR  - P42 ES 07380/ES/NIEHS NIH HHS/United States
GR  - R01 ES02710/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Germany
TA  - Int J Hyg Environ Health
JT  - International journal of hygiene and environmental health
JID - 100898843
RN  - 0 (Dietary Fats)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Fatty Acids, Omega-6)
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 1406-18-4 (Vitamin E)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Diet
MH  - Dietary Fats
MH  - Drug Interactions
MH  - Endothelium/*cytology/drug effects/pathology
MH  - Environmental Pollutants/*adverse effects
MH  - Fatty Acids, Omega-6
MH  - Fatty Acids, Unsaturated/*pharmacology
MH  - Guidelines as Topic
MH  - Humans
MH  - Linoleic Acid/pharmacology
MH  - *Oxidative Stress
MH  - Polychlorinated Biphenyls/*adverse effects
MH  - Public Health
MH  - Risk Assessment
MH  - Vitamin E/*pharmacology
EDAT- 2002/05/23 10:00
MHDA- 2002/11/26 04:00
CRDT- 2002/05/23 10:00
PHST- 2002/05/23 10:00 [pubmed]
PHST- 2002/11/26 04:00 [medline]
PHST- 2002/05/23 10:00 [entrez]
AID - S1438-4639(04)70132-7 [pii]
AID - 10.1078/1438-4639-00134 [doi]
PST - ppublish
SO  - Int J Hyg Environ Health. 2002 Mar;205(1-2):95-102. doi:
      10.1078/1438-4639-00134.

PMID- 11756069
OWN - NLM
STAT- MEDLINE
DCOM- 20020115
LR  - 20201216
IS  - 0002-9165 (Print)
IS  - 0002-9165 (Linking)
VI  - 75
IP  - 1
DP  - 2002 Jan
TI  - Unsaturated fatty acids selectively induce an inflammatory environment in
      human endothelial cells.
PG  - 119-25
AB  - BACKGROUND: Activation of the vascular endothelium by dietary fatty acids
      may be among the most critical early events in the development of
      atherosclerosis. However, the specific effects of fatty acids on
      inflammatory responses in endothelial cells are not fully understood.
      OBJECTIVE: The present study focused on the induction of inflammatory
      genes in human endothelial cells exposed to individual dietary fatty
      acids. Because of the significance of nuclear factor kappaB (NF-kappaB)
      and activator protein 1 (AP-1) in the regulation of inflammatory gene
      expression, we also determined the effects of fatty acids on NF-kappaB
      and AP-1 transcriptional activation. DESIGN: Human umbilical vein
      endothelial cells were exposed to dietary mono- and polyunsaturated
      18-carbon fatty acids. Transcriptional activation of NF-kappaB and AP-1
      was determined in human umbilical vein endothelial cells transfected with
      reporter constructs regulated by these transcription factors. Induction
      of the inflammatory genes was studied by use of reverse transcriptase-
      polymerase chain reaction. RESULTS: Of the fatty acids studied, linoleic
      acid stimulated NF-kappaB and AP-1 transcriptional activation the most.
      In addition, treatment with this fatty acid markedly enhanced messenger
      RNA levels of tumor necrosis factor alpha, monocyte chemoattractant
      protein 1, vascular cell adhesion molecule 1, and intercellular adhesion
      molecule 1. Treatment with linolenic acid stimulated only a moderate
      induction of the genes encoding for these inflammatory mediators, and
      exposure to oleic acid either had no effect or resulted in decreased
      inflammatory gene messenger RNA. In addition, exposure to both linoleic
      and linolenic acids strongly stimulated induction of the phospholipid
      hydroperoxide glutathione peroxidase gene. CONCLUSION: Specific
      unsaturated dietary fatty acids, particularly linoleic acid, can
      selectively stimulate the development of a proinflammatory environment
      within the vascular endothelium.
FAU - Toborek, Michal
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington
      40536, USA. mjtobo00@pop.uky.edu
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Garrido, Rosario
AU  - Garrido R
FAU - Kaiser, Simone
AU  - Kaiser S
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factors)
SB  - AIM
SB  - IM
CIN - Am J Clin Nutr. 2002 Jan;75(1):4. PMID: 11756052
MH  - Arteriosclerosis/etiology
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Fatty Acids, Unsaturated/*pharmacology
MH  - Genes, Reporter/drug effects
MH  - Humans
MH  - NF-kappa B/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transcription Factors/*genetics
MH  - Umbilical Veins
EDAT- 2002/01/05 10:00
MHDA- 2002/01/16 10:01
CRDT- 2002/01/05 10:00
PHST- 2002/01/05 10:00 [pubmed]
PHST- 2002/01/16 10:01 [medline]
PHST- 2002/01/05 10:00 [entrez]
AID - 10.1093/ajcn/75.1.119 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 2002 Jan;75(1):119-25. doi: 10.1093/ajcn/75.1.119.

PMID- 12125348
OWN - NLM
STAT- MEDLINE
DCOM- 20020812
LR  - 20190712
IS  - 0076-6879 (Print)
IS  - 0076-6879 (Linking)
VI  - 352
DP  - 2002
TI  - Measurement of inflammatory properties of fatty acids in human
      endothelial cells.
PG  - 198-219
FAU - Toborek, Michal
AU  - Toborek M
AD  - Department of Surgery, Division of Neurosurgery, University of Kentucky
      Medical Center, Lexington, Kentucky 40536, USA.
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Kaiser, Simone
AU  - Kaiser S
FAU - Hennig, Bernhard
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Methods Enzymol
JT  - Methods in enzymology
JID - 0212271
RN  - 0 (Fatty Acids)
RN  - EC 1.13.12.- (Luciferases)
RN  - GAN16C9B8O (Glutathione)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Cell Nucleus/metabolism
MH  - Endothelium, Vascular/*metabolism
MH  - Fatty Acids/*metabolism
MH  - Flow Cytometry
MH  - Glutathione/metabolism
MH  - Humans
MH  - Luciferases/metabolism
MH  - Microscopy, Confocal/*methods
MH  - Oxidative Stress
MH  - Oxygen/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transfection
MH  - Umbilical Veins/cytology
EDAT- 2002/07/20 10:00
MHDA- 2002/08/13 10:01
CRDT- 2002/07/20 10:00
PHST- 2002/07/20 10:00 [pubmed]
PHST- 2002/08/13 10:01 [medline]
PHST- 2002/07/20 10:00 [entrez]
AID - 10.1016/s0076-6879(02)52020-6 [doi]
PST - ppublish
SO  - Methods Enzymol. 2002;352:198-219. doi: 10.1016/s0076-6879(02)52020-6.

PMID- 12230306
OWN - NLM
STAT- MEDLINE
DCOM- 20030206
LR  - 20181113
IS  - 1535-1084 (Print)
IS  - 1535-1084 (Linking)
VI  - 2
IP  - 1
DP  - 2002
TI  - Methamphetamine-induced TNF-alpha gene expression and activation of AP-1
      in discrete regions of mouse brain: potential role of reactive oxygen
      intermediates and lipid peroxidation.
PG  - 71-85
AB  - Cellular and molecular mechanisms of methamphetamine (METH)-induced
      neurotoxicity may involve alterations of cellular redox status and
      induction of inflammatory genes. To study this hypothesis, molecular
      signaling pathways of METH-induced inflammatory responses via activation
      of redox-sensitive transcription factors were investigated in discrete
      regions (corpus striatum, frontal cortex, and hippocampus) of mouse
      brain. Intraperitoneal injection of METH at a dose of 10 mg/kg body
      weight resulted in a significant increase in oxidative stress, as
      measured by 2,7-dichlorofluorescein (DCF) fluorescence assay,
      thiobarbituric acid-reactive substances (TBARS), and total glutathione
      levels. Glutathione peroxidase activity was also significantly increased
      after METH exposure. In addition, DNA binding activity of activator
      protein-1 (AP-1), a redox-responsive transcription factor, was increased
      in all studied brain regions in response to METH treatment. Because AP-1
      is known to regulate expression of inflammatory genes, levels of TNF-
      alpha mRNA were also studied. Expression of the tumor necrosis factor-
      alpha (TNF-alpha) gene was induced 3 h after METH injection and remained
      elevated for up to 6 h of METH exposure. In addition, stimulation of the
      TNF-alpha gene was associated with increased TNF-a protein production in
      the frontal cortex. These results suggest that METH-induced disturbances
      in cellular redox status and that activation of AP-1 can play a critical
      role in signaling pathways leading to upregulation of inflammatory genes
      in vivo. Furthermore, these data provide evidence for the role of
      oxidative stress in the neurotoxic effects of METH.
FAU - Flora, Govinder
AU  - Flora G
AD  - Departments of Surgery, University of Kentucky, Lexington 40536, USA.
FAU - Lee, Yong Woo
AU  - Lee YW
FAU - Nath, Avindra
AU  - Nath A
FAU - Maragos, William
AU  - Maragos W
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - MH63022/MH/NIMH NIH HHS/United States
GR  - NS39254/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Neuromolecular Med
JT  - Neuromolecular medicine
JID - 101135365
RN  - 0 (Central Nervous System Stimulants)
RN  - 0 (Dopamine Agents)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 44RAL3456C (Methamphetamine)
RN  - 9007-49-2 (DNA)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Brain Chemistry/*drug effects
MH  - Central Nervous System Stimulants/administration &
      dosage/*pharmacology/toxicity
MH  - Corpus Striatum/drug effects/metabolism
MH  - DNA/genetics/metabolism
MH  - Dopamine Agents/administration & dosage/*pharmacology/toxicity
MH  - Frontal Lobe/drug effects/metabolism
MH  - Glutathione/analysis
MH  - Glutathione Peroxidase/metabolism
MH  - Hippocampus/drug effects/metabolism
MH  - Inflammation/genetics
MH  - Injections, Intraperitoneal
MH  - Lipid Peroxidation/drug effects
MH  - Male
MH  - Methamphetamine/administration & dosage/*pharmacology/toxicity
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nerve Tissue Proteins/genetics/*metabolism
MH  - Oxidative Stress
MH  - Signal Transduction/drug effects
MH  - Thiobarbituric Acid Reactive Substances/analysis
MH  - Transcription Factor AP-1/*metabolism
MH  - Transcription, Genetic/drug effects
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/genetics
EDAT- 2002/09/17 10:00
MHDA- 2003/02/07 04:00
CRDT- 2002/09/17 10:00
PHST- 2002/09/17 10:00 [pubmed]
PHST- 2003/02/07 04:00 [medline]
PHST- 2002/09/17 10:00 [entrez]
AID - NMM:2:1:71 [pii]
AID - 10.1385/NMM:2:1:71 [doi]
PST - ppublish
SO  - Neuromolecular Med. 2002;2(1):71-85. doi: 10.1385/NMM:2:1:71.

PMID- 11716818
OWN - NLM
STAT- MEDLINE
DCOM- 20020207
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 920
IP  - 1-2
DP  - 2001 Nov 30
TI  - Cocaine activates redox-regulated transcription factors and induces TNF-
      alpha expression in human brain endothelial cells.
PG  - 125-33
AB  - Cocaine abuse is frequently associated with cerebrovascular pathology.
      Although the cellular and molecular mechanisms of these alterations are
      not fully understood, they may involve oxidative injury or dysfunction of
      brain microvascular endothelial cells. To test this hypothesis, total
      glutathione levels, activation of nuclear factor-kappaB (NF-kappaB) and
      activator protein-1 (AP-1), as well as induction of the TNF-alpha gene
      expression were determined in human brain microvascular endothelial cells
      (HBMEC) exposed to cocaine. Exposure of HBMEC to cocaine resulted in a
      dose-dependent depletion of total glutathione levels. In addition,
      cocaine markedly activated redox-regulated transcription factors, NF-
      kappaB and AP-1. Activation of these transcription factors was
      accompanied by induction of AP-1- or NF-kappaB-dependent transcription,
      as measured by dual luciferase assay in HBMEC transfected with the AP-1-
      or NF-kappaB-responsive reporter constructs. Furthermore, HBMEC treatment
      with cocaine induced a dose-dependent expression of the tumor necrosis
      factor-alpha (TNF-alpha) gene. These results indicate that exposure to
      cocaine can trigger inflammatory pathways via activation of redox-
      sensitive transcription factors and induction of expression of the
      inflammatory genes in HBMEC. These events may contribute to the
      cerebrovascular insults observed in cocaine-abused patients.
FAU - Lee, Y W
AU  - Lee YW
AD  - Department of Surgery, Division of Neurosurgery, University of Kentucky
      Medical Center, 800 Rose Street, Lexington, KY 40536, USA.
FAU - Hennig, B
AU  - Hennig B
FAU - Fiala, M
AU  - Fiala M
FAU - Kim, K S
AU  - Kim KS
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - MH63022-01A1/MH/NIMH NIH HHS/United States
GR  - NS39254-01A1/NS/NINDS NIH HHS/United States
GR  - NS39254-01A1S1/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Dopamine Uptake Inhibitors)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.13.12.- (Luciferases)
RN  - GAN16C9B8O (Glutathione)
RN  - I5Y540LHVR (Cocaine)
SB  - IM
MH  - Brain Chemistry/*drug effects
MH  - Capillaries/cytology/drug effects/metabolism
MH  - Cells, Cultured
MH  - Cocaine/*pharmacology
MH  - Dopamine Uptake Inhibitors/*pharmacology
MH  - Electrophoresis
MH  - Endothelium, Vascular/cytology/drug effects/*metabolism
MH  - Glutathione/metabolism
MH  - Humans
MH  - Luciferases/metabolism
MH  - NF-kappa B/drug effects/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/drug effects
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/drug effects
MH  - Transcription Factor AP-1/drug effects/metabolism
MH  - Transcription Factors/*drug effects
MH  - Transfection
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 2001/11/22 10:00
MHDA- 2002/02/08 10:01
CRDT- 2001/11/22 10:00
PHST- 2001/11/22 10:00 [pubmed]
PHST- 2002/02/08 10:01 [medline]
PHST- 2001/11/22 10:00 [entrez]
AID - S0006-8993(01)03047-5 [pii]
AID - 10.1016/s0006-8993(01)03047-5 [doi]
PST - ppublish
SO  - Brain Res. 2001 Nov 30;920(1-2):125-33. doi:
      10.1016/s0006-8993(01)03047-5.

PMID- 11746378
OWN - NLM
STAT- MEDLINE
DCOM- 20020124
LR  - 20161019
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 66
IP  - 4
DP  - 2001 Nov 15
TI  - Methamphetamine induces AP-1 and NF-kappaB binding and transactivation in
      human brain endothelial cells.
PG  - 583-91
AB  - Cellular and molecular mechanisms of methamphetamine (METH)-induced
      neurotoxicity may involve alterations of cellular redox status and
      induction of inflammatory genes in endothelial cells. To study these
      hypotheses, molecular signaling pathways of METH-induced inflammatory
      responses via activation of redox-sensitive transcription factors were
      investigated in human brain microvascular endothelial cells (HBMEC). A
      dose-dependent depletion of total glutathione levels was detected in
      HBMEC exposed to METH. In addition, electrophoretic mobility shift assay
      (EMSA) showed significant increases in DNA binding activities of redox-
      responsive transcription factors, AP-1 and NF-kappaB, in HBMEC treated
      with METH. METH-mediated AP-1 or NF-kappaB activation was accompanied by
      induction of transactivation of AP-1 or NF-kappaB, as measured by dual
      luciferase assay using specific reporter plasmids. Because NF-kappaB and
      AP-1 are known to regulate expression of inflammatory genes, expression
      of the gene encoding for tumor necrosis factor-alpha (TNF-alpha) was also
      studied in METH-treated HBMEC. A dose-dependent overexpression of the
      TNF-alpha gene was observed in HBMEC treated with METH. The importance of
      AP-1 and NF-kappaB in METH-induced TNF-alpha gene was confirmed in
      functional promoter studies using constructs of the TNF-alpha promoter
      with mutated AP-1 or NF-kappaB sites. These results indicate that METH-
      induced disturbances in cellular redox status and activation of AP-1 and
      NF-kappaB can play critical roles in the signaling pathways leading to
      upregulation of inflammatory genes in human brain endothelial cells.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Lee, Y W
AU  - Lee YW
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      Kentucky 40536, USA.
FAU - Hennig, B
AU  - Hennig B
FAU - Yao, J
AU  - Yao J
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - NS39254-01A1/NS/NINDS NIH HHS/United States
GR  - NS39254-01A1S1/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 44RAL3456C (Methamphetamine)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Amphetamine-Related Disorders/genetics/metabolism/physiopathology
MH  - Binding Sites/drug effects/physiology
MH  - Blood-Brain Barrier/drug effects/physiology
MH  - Brain/*drug effects/metabolism/physiopathology
MH  - Cells, Cultured/drug effects/metabolism
MH  - Encephalitis/chemically induced/*genetics/metabolism
MH  - Endothelium, Vascular/*drug effects/metabolism/physiopathology
MH  - Gene Expression Regulation/drug effects/physiology
MH  - Genes, Reporter/drug effects/physiology
MH  - Glutathione/drug effects/metabolism
MH  - Humans
MH  - Methamphetamine/*toxicity
MH  - Microcirculation/drug effects/metabolism/physiopathology
MH  - NF-kappa B/*drug effects/genetics/metabolism
MH  - Oxidation-Reduction/drug effects
MH  - Oxidative Stress/*drug effects/genetics
MH  - RNA, Messenger/drug effects/metabolism
MH  - Signal Transduction/drug effects/genetics
MH  - Transcription Factor AP-1/*drug effects/genetics/metabolism
MH  - Transcription, Genetic/drug effects/physiology
MH  - Transfection
MH  - Tumor Necrosis Factor-alpha/drug effects/genetics/metabolism
EDAT- 2001/12/18 10:00
MHDA- 2002/01/25 10:01
CRDT- 2001/12/18 10:00
PHST- 2001/12/18 10:00 [pubmed]
PHST- 2002/01/25 10:01 [medline]
PHST- 2001/12/18 10:00 [entrez]
AID - 10.1002/jnr.1248 [pii]
AID - 10.1002/jnr.1248 [doi]
PST - ppublish
SO  - J Neurosci Res. 2001 Nov 15;66(4):583-91. doi: 10.1002/jnr.1248.

PMID- 12031258
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 12
IP  - 11
DP  - 2001 Nov
TI  - Linoleic acid induces MCP-1 gene expression in human microvascular
      endothelial cells through an oxidative mechanism.
PG  - 648-654
AB  - Linoleic acid is a dietary fatty acid that appears to play an important
      role in activation of the vascular endothelium under a variety of
      pathological conditions, including development of atherosclerosis or
      cancer metastasis. Evidence indicates that inflammatory responses may be
      an underlying cause of endothelial cell pathology induced by linoleic
      acid. However, the profile of inflammatory mediators and the potential
      mechanisms involved in inflammatory reactions stimulated by the exposure
      to linoleic acid are not fully understood. The present study focused on
      the mechanisms of linoleic acid-induced expression of monocyte
      chemoattractant protein-1 (MCP-1) gene in human microvascular endothelial
      cells (HMEC-1). Treatment of HMEC-1 with increasing doses of linoleic
      acid markedly activated an oxidative stress-responsive transcription
      factor, nuclear factor-kappaB (NF-kappaB). In addition, exposure to
      linoleic acid induced a time- and concentration-dependent overexpression
      of the MCP-1 gene. Increased MCP-1 mRNA levels were observed in HMEC-1
      treated with linoleic acid at doses as low as 10 &mgr;M. Linoleic acid-
      induced overexpression of the MCP-1 gene was associated with a
      significant elevation of MCP-1 protein levels. Most importantly,
      preexposure of HMEC-1 to antioxidants, such as pyrrolidine
      dithiocarbamate (PDTC) or N-acetylcysteine (NAC), attenuated linoleic
      acid-induced MCP-1 mRNA expression. The obtained results indicate that
      linoleic acid triggers MCP-1 gene expression in human microvascular
      endothelial cells through oxidative stress/redox-related mechanisms.
FAU - Woo Lee, Yong
AU  - Woo Lee Y
AD  - Department of Surgery, Division of Neurosurgery, University of Kentucky
      Medical Center, 800 Rose Street, 40536, Lexington, KY, USA
FAU - Joo Park, Hyen
AU  - Joo Park H
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
EDAT- 2002/05/29 10:00
MHDA- 2002/05/29 10:01
CRDT- 2002/05/29 10:00
PHST- 2002/05/29 10:00 [pubmed]
PHST- 2002/05/29 10:01 [medline]
PHST- 2002/05/29 10:00 [entrez]
AID - S0955-2863(01)00186-3 [pii]
AID - 10.1016/s0955-2863(01)00186-3 [doi]
PST - ppublish
SO  - J Nutr Biochem. 2001 Nov;12(11):648-654. doi:
      10.1016/s0955-2863(01)00186-3.

PMID- 11448612
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1873-4847 (Electronic)
IS  - 0955-2863 (Linking)
VI  - 12
IP  - 7
DP  - 2001 Jul
TI  - Letter from the editor.
PG  - 380
FAU - Hennig, B
AU  - Hennig B
AD  - College of Agriculture, Cell Nutrition Group, University of Kentucky,
      Lexington, Department of Animal Science, 204 Funkhouser Building,
      40506-0054, Lexington, KY, USA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - J Nutr Biochem
JT  - The Journal of nutritional biochemistry
JID - 9010081
EDAT- 2001/07/13 10:00
MHDA- 2001/07/13 10:01
CRDT- 2001/07/13 10:00
PHST- 2001/07/13 10:00 [pubmed]
PHST- 2001/07/13 10:01 [medline]
PHST- 2001/07/13 10:00 [entrez]
AID - S095528630100170X [pii]
AID - 10.1016/s0955-2863(01)00170-x [doi]
PST - ppublish
SO  - J Nutr Biochem. 2001 Jul;12(7):380. doi: 10.1016/s0955-2863(01)00170-x.

PMID- 11352986
OWN - NLM
STAT- MEDLINE
DCOM- 20010830
LR  - 20210217
IS  - 0022-2275 (Print)
IS  - 0022-2275 (Linking)
VI  - 42
IP  - 5
DP  - 2001 May
TI  - Interleukin 4 induces transcription of the 15-lipoxygenase I gene in
      human endothelial cells.
PG  - 783-91
AB  - The reticulocyte-type 15-lipoxygenase (15-LO-I) has been implicated in
      atherogenesis because of its capability of oxidizing low density
      lipoprotein. Therefore, we investigated the expression of the 15-LO-I
      gene in human umbilical vein endothelial cells (HUVEC). Nonactivated
      HUVEC did not exhibit detectable 15-LO-I mRNA. However, exposure of the
      cells to interleukin 4 (IL-4) induced the transcription of the 15-LO-I
      gene in a time- and concentration-dependent manner. Interestingly, this
      induction was not paralleled by a concomitant production of the
      functional 15-LO-I enzyme, as indicated by activity assays and
      immunoblotting. To gain more information about the mechanism of the
      induction process, we investigated IL-4-dependent activation of nuclear
      transcription factors for which binding sites were previously identified
      in the 5'-flanking region of the human 15-LO-I gene. Electrophoretic
      mobility shift assays revealed that IL-4 can activate signal transducer
      and activator of transcription 6, activator protein 2, GATA motif-binding
      transcription factor 1, nuclear factor 1, and SP-1 in HUVEC in a time-
      and concentration-dependent manner. Activation of these transcription
      factors was observed as early as 30 min after cytokine exposure. These
      data indicate that IL-4 upregulates the transcription of the 15-LO-I gene
      in human vascular endothelial cells, and this process may involve the
      activation of several nuclear transcription factors. The lack of active
      15-LO-I protein in the presence of functional 15-LO-I mRNA suggests
      additional regulatory elements of 15-LO expression at posttranscriptional
      levels.
FAU - Lee, Y W
AU  - Lee YW
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      KY 40536, USA.
FAU - Kuhn, H
AU  - Kuhn H
FAU - Kaiser, S
AU  - Kaiser S
FAU - Hennig, B
AU  - Hennig B
FAU - Daugherty, A
AU  - Daugherty A
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Lipid Res
JT  - Journal of lipid research
JID - 0376606
RN  - 0 (CCAAT-Enhancer-Binding Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Erythroid-Specific DNA-Binding Factors)
RN  - 0 (NFI Transcription Factors)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (STAT6 Transcription Factor)
RN  - 0 (STAT6 protein, human)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factor AP-2)
RN  - 0 (Transcription Factors)
RN  - 0 (Y-Box-Binding Protein 1)
RN  - 0 (YBX1 protein, human)
RN  - 207137-56-2 (Interleukin-4)
RN  - 98600C0908 (Cycloheximide)
RN  - EC 1.13.11.33 (Arachidonate 15-Lipoxygenase)
SB  - IM
MH  - Arachidonate 15-Lipoxygenase/*genetics/metabolism
MH  - Arteriosclerosis/physiopathology
MH  - CCAAT-Enhancer-Binding Proteins/genetics/metabolism
MH  - Cells, Cultured
MH  - Chromatography, High Pressure Liquid
MH  - Cycloheximide/pharmacology
MH  - DNA-Binding Proteins/genetics/metabolism
MH  - Endothelium, Vascular/cytology/drug effects/*enzymology
MH  - Erythroid-Specific DNA-Binding Factors
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Immunoblotting
MH  - Interleukin-4/*pharmacology
MH  - NFI Transcription Factors
MH  - Nuclear Proteins
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - STAT6 Transcription Factor
MH  - Trans-Activators/genetics/metabolism
MH  - Transcription Factor AP-2
MH  - Transcription Factors/genetics/metabolism
MH  - *Transcription, Genetic
MH  - Y-Box-Binding Protein 1
EDAT- 2001/05/16 10:00
MHDA- 2001/08/31 10:01
CRDT- 2001/05/16 10:00
PHST- 2001/05/16 10:00 [pubmed]
PHST- 2001/08/31 10:01 [medline]
PHST- 2001/05/16 10:00 [entrez]
AID - S0022-2275(20)31641-2 [pii]
PST - ppublish
SO  - J Lipid Res. 2001 May;42(5):783-91.

PMID- 11349944
OWN - NLM
STAT- MEDLINE
DCOM- 20011101
LR  - 20201216
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 20
IP  - 2 Suppl
DP  - 2001 Apr
TI  - High-energy diets, fatty acids and endothelial cell function:
      implications for atherosclerosis.
PG  - 97-105
AB  - Diets high in fat and/or calories can lead to hypertriglyceridemia and
      postprandial lipemia and thus are considered a risk factor for the
      development of atherosclerosis. Plasma chylomicron levels are elevated in
      humans after consuming a high-fat meal, and hepatic synthesis of VLDL is
      increased when caloric intake is in excess of body needs. High
      lipoprotein lipase activity and subsequent hydrolysis of triglyceride-
      rich lipoproteins may be an important source of elevated concentrations
      of fatty acid anions in the proximity to the endothelium and hence a
      major risk factor for atherosclerosis. We have shown that selected fatty
      acids, as well as lipoprotein lipase-derived remnants of lipoproteins
      isolated from hypertriglyceridemic subjects, can activate vascular
      endothelial cells and disrupt endothelial integrity. Our studies suggest
      that omega-6 fatty acids, and especially linoleic acid, cause endothelial
      cell dysfunction most markedly as well as can potentiate TNF-mediated
      endothelial cell injury. We propose that high-energy diets, and
      especially diets rich in linoleic acid, are atherogenic by contributing
      to an imbalance in cellular oxidative stress/antioxidant status of the
      endothelium, which can lead to activation of oxidative stress-responsive
      transcription factors, inflammatory cytokine production and the
      expression of adhesion molecules. Our data also suggest that nutrients,
      which have antioxidant and/or membrane stabilizing properties, can
      protect endothelial cells. These findings contribute to the understanding
      of the interactive role of high fat/calorie diets and subsequent
      hypertriglyceridemia with inflammatory components and nutrients that
      exhibit antiatherogenic properties in the development of atherosclerosis.
      Moreover, results from our research further support the concept that
      high-fat/calorie diets and associated postprandial hypertriglyceridemia
      are significant risk factors for atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Animal Sciences, and Graduate Center for Nutritional
      Sciences, University of Kentucky, Lexington 40506-0054, USA.
      bhennig@pop.uky.edu
FAU - Toborek, M
AU  - Toborek M
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Antioxidants)
RN  - 0 (Dietary Fats)
RN  - 0 (Fatty Acids, Omega-6)
RN  - 0 (Fatty Acids, Unsaturated)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Arteriosclerosis/blood/*etiology
MH  - Diabetes Mellitus, Type 2/complications
MH  - Dietary Fats/*administration & dosage/metabolism
MH  - Endothelium, Vascular/cytology/drug effects/*physiology
MH  - *Energy Intake
MH  - Fatty Acids, Omega-6
MH  - Fatty Acids, Unsaturated/adverse effects
MH  - Humans
MH  - Hyperlipidemias/*complications/metabolism
MH  - Hypertriglyceridemia/complications/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress
MH  - Postprandial Period
MH  - Risk Factors
RF  - 112
EDAT- 2001/05/15 10:00
MHDA- 2001/11/03 10:01
CRDT- 2001/05/15 10:00
PHST- 2001/05/15 10:00 [pubmed]
PHST- 2001/11/03 10:01 [medline]
PHST- 2001/05/15 10:00 [entrez]
AID - 10.1080/07315724.2001.10719021 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 2001 Apr;20(2 Suppl):97-105. doi:
      10.1080/07315724.2001.10719021.

PMID- 11243918
OWN - NLM
STAT- MEDLINE
DCOM- 20010419
LR  - 20161124
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 171
IP  - 3
DP  - 2001 Mar 15
TI  - The role of methyl-linoleic acid epoxide and diol metabolites in the
      amplified toxicity of linoleic acid and polychlorinated biphenyls to
      vascular endothelial cells.
PG  - 184-93
AB  - Selected dietary lipids may increase the atherogenic effects of
      environmental chemicals, such as polychlorinated biphenyls (PCBs), by
      cross-amplifying mechanisms leading to dysfunction of the vascular
      endothelium. We have shown previously that the omega-6 parent fatty acid,
      linoleic acid, or 3,3',4,4'-tetrachlorobiphenyl (PCB 77), an aryl
      hydrocarbon (Ah) receptor agonist, independently can cause disruption of
      endothelial barrier function. Furthermore, cellular enrichment with
      linoleic acid can amplify PCB-induced endothelial cell dysfunction. We
      hypothesize that the amplified toxicity of linoleic acid and PCBs to
      endothelial cells could be mediated in part by cytotoxic epoxide
      metabolites of linoleic acid called leukotoxins (LTX) or their diol
      derivatives (LTXD). Exposure to LTXD resulted in a dose-dependent
      increase in albumin transfer across endothelial cell monolayers, whereas
      this disruption of endothelial barrier function was observed only at a
      high concentration of LTX. Pretreatment with the cytosolic epoxide
      hydrolase inhibitor 1-cyclohexyl-3-dodecyl urea partially protected
      against the observed LTX-induced endothelial dysfunction. Endothelial
      cell activation mediated by LTX and/or LTXD also enhanced nuclear
      translocation of the transcription factor NF-kappa B and gene expression
      of the inflammatory cytokine IL-6. Inhibiting cytosolic epoxide hydrolase
      decreased the LTX-mediated induction of both NF-kappa B and the IL-6
      gene, whereas the antioxidant vitamin E did not block LTX-induced
      endothelial cell activation. Most importantly, inhibition of cytosolic
      epoxide hydrolase blocked both linoleic acid-induced cytotoxicity, as
      well as the additive toxicity of linoleic acid plus PCB 77 to endothelial
      cells. Interestingly, cellular uptake and accumulation of linoleic acid
      was markedly enhanced in the presence of PCB 77. These data suggest that
      cytotoxic epoxide metabolites of linoleic acid play a critical role in
      linoleic acid-induced endothelial cell dysfunction. Furthermore, the
      severe toxicity of PCBs in the presence of linoleic acid may be due in
      part to the generation of epoxide and diol metabolites. These findings
      have implications in understanding interactive mechanisms of how dietary
      fats can modulate dysfunction of the vascular endothelium mediated by
      certain environmental contaminants.
CI  - Copyright 2001 Academic Press.
FAU - Slim, R
AU  - Slim R
AD  - Graduate Center for Toxicology, University of Kentucky, Lexington,
      Kentucky 40506-0054, USA.
FAU - Hammock, B D
AU  - Hammock BD
FAU - Toborek, M
AU  - Toborek M
FAU - Robertson, L W
AU  - Robertson LW
FAU - Newman, J W
AU  - Newman JW
FAU - Morisseau, C H
AU  - Morisseau CH
FAU - Watkins, B A
AU  - Watkins BA
FAU - Saraswathi, V
AU  - Saraswathi V
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - P30 ES 05707/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES 04699/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES 07380/ES/NIEHS NIH HHS/United States
GR  - R01 ES02710/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Alcohols)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Epoxy Compounds)
RN  - 0 (Fatty Acids)
RN  - 0 (Interleukin-6)
RN  - 0 (Linoleic Acids)
RN  - 0 (NF-kappa B)
RN  - 24N6726DE5 (methyl linoleate)
RN  - 9035-51-2 (Cytochrome P-450 Enzyme System)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.- (Steroid Hydroxylases)
RN  - EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases)
RN  - EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase)
RN  - EC 3.3.2.- (Epoxide Hydrolases)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Alcohols/metabolism
MH  - Animals
MH  - *Aryl Hydrocarbon Hydroxylases
MH  - Cell Nucleus/metabolism
MH  - Cells, Cultured
MH  - Cytochrome P-450 Enzyme System/metabolism
MH  - Electrophoresis
MH  - Endothelium, Vascular/cytology/*drug effects/enzymology
MH  - Enzyme Inhibitors/pharmacology
MH  - Epoxide Hydrolases/antagonists & inhibitors
MH  - Epoxy Compounds/metabolism
MH  - Fatty Acids/metabolism
MH  - Interleukin-6/biosynthesis/genetics
MH  - Linoleic Acid/metabolism/*toxicity
MH  - Linoleic Acids/*metabolism
MH  - NF-kappa B/metabolism
MH  - Polychlorinated Biphenyls/metabolism/*toxicity
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - *Steroid 16-alpha-Hydroxylase
MH  - Steroid Hydroxylases/metabolism
MH  - Swine
EDAT- 2001/03/13 10:00
MHDA- 2001/04/21 10:01
CRDT- 2001/03/13 10:00
PHST- 2001/03/13 10:00 [pubmed]
PHST- 2001/04/21 10:01 [medline]
PHST- 2001/03/13 10:00 [entrez]
AID - 10.1006/taap.2001.9131 [doi]
AID - S0041-008X(01)99131-8 [pii]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2001 Mar 15;171(3):184-93. doi:
      10.1006/taap.2001.9131.

PMID- 11238724
OWN - NLM
STAT- MEDLINE
DCOM- 20010405
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 76
IP  - 5
DP  - 2001 Mar
TI  - Nicotine protects against arachidonic-acid-induced caspase activation,
      cytochrome c release and apoptosis of cultured spinal cord neurons.
PG  - 1395-403
AB  - Hydrolysis of membrane phospholipids of spinal cord neurons is one of the
      first events initiated in spinal cord trauma. In this process, free fatty
      acids, and in particular arachidonic acid, are released. Exposure of
      spinal cord neurons to free arachidonic acid can compromise cell survival
      and initiate apoptotic cell death. In order to determine potential
      mechanisms of apoptosis induced by arachidonic acid, activation of
      caspases -3, -8, and -9, as well as the release of cytochrome c into the
      cytoplasm were measured in cultured spinal cord neurons exposed to 10
      microM of this fatty acid. In addition, because nicotine can exert a
      variety of neuroprotective effects, we hypothesized that it can prevent
      arachidonic acid induced apoptosis of spinal cord neurons. To study this
      hypothesis, spinal cord neurons were pretreated with nicotine (10 microM
      for 2 h) before arachidonic acid exposure and caspase activation as well
      as markers of apoptotic cell death were studied. Treatment of spinal cord
      neurons with arachidonic acid for up to 24 h significantly increased
      cytoplasmic levels of cytochrome c, induced caspase activation and
      induced DNA laddering, a hallmark of apoptotic cell death. Nicotine
      pretreatment markedly attenuated all these effects. In addition,
      antagonist studies suggest that the alpha7 nicotinic receptor is
      primarily responsible for these anti-apoptotic effects of nicotine. These
      results indicate that nicotine can exert potent neuroprotective effects
      by inhibiting arachidonic acid induced apoptotic cascades of spinal cord
      neurons.
FAU - Garrido, R
AU  - Garrido R
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      Kentucky, USA.
FAU - Mattson, M P
AU  - Mattson MP
FAU - Hennig, B
AU  - Hennig B
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Cytochrome c Group)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 6M3C89ZY6R (Nicotine)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/*physiology
MH  - Arachidonic Acid/*pharmacology
MH  - Caspases/*metabolism
MH  - Cells, Cultured
MH  - Cytochrome c Group/*metabolism
MH  - DNA Fragmentation
MH  - Embryo, Mammalian
MH  - Kinetics
MH  - Mice
MH  - Mitochondria/drug effects/*metabolism
MH  - Neurons/cytology/*drug effects/physiology
MH  - Nicotine/*pharmacology
MH  - Proto-Oncogene Proteins c-bcl-2/genetics/metabolism
MH  - Spinal Cord/*cytology
MH  - Time Factors
EDAT- 2001/03/10 10:00
MHDA- 2001/04/06 10:01
CRDT- 2001/03/10 10:00
PHST- 2001/03/10 10:00 [pubmed]
PHST- 2001/04/06 10:01 [medline]
PHST- 2001/03/10 10:00 [entrez]
AID - 10.1046/j.1471-4159.2001.00135.x [doi]
PST - ppublish
SO  - J Neurochem. 2001 Mar;76(5):1395-403. doi:
      10.1046/j.1471-4159.2001.00135.x.

PMID- 11133225
OWN - NLM
STAT- MEDLINE
DCOM- 20010329
LR  - 20161025
IS  - 0022-2828 (Print)
IS  - 0022-2828 (Linking)
VI  - 33
IP  - 1
DP  - 2001 Jan
TI  - IL-4-induced oxidative stress upregulates VCAM-1 gene expression in human
      endothelial cells.
PG  - 83-94
AB  - Vascular cell adhesion molecule-1 (VCAM-1) is expressed in early stages
      of atherosclerosis; however, the mechanisms of its upregulation are not
      fully understood. In the present study, we examined the effects of
      interleukin-4 (IL-4) on VCAM-1 gene expression and its transcriptional
      regulatory mechanism in human umbilical vein endothelial cells (HUVEC).
      Reverse transcription-polymerase chain reaction showed that VCAM-1 mRNA
      was induced in IL-4-treated HUVEC in a time- and dose-dependent manner.
      Among known transcription factors that have binding sites in the promoter
      region of the VCAM-1 gene, IL-4 activated only SP-1. In contrast, nuclear
      factor- kappa B (NF- kappa B), activator protein-1 (AP-1) and interferon
      regulatory factor-1 (IRF-1), which also have consensus binding sequences
      in the 5'-flanking region of the human VCAM-1 gene, were not activated.
      The role of SP-1 in IL-4-induced VCAM-1 expression was confirmed in HUVEC
      transfected with a reporter construct of the VCAM-1 promoter with mutated
      SP-1 binding site. As IL-4 treatment of HUVEC enhanced the intracellular
      oxidizing potential, as indicated by an increase in
      2',7'-dichlorofluorescein (DCF) fluorescence, we studied the effect of
      antioxidants on IL-4-induced VCAM-1 expression. Pretreatment of HUVEC
      with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC)
      completely prevented IL-4-induced VCAM-1 expression. In addition, PDTC
      inhibited IL-4-related activation of SP-1. These results suggest that
      IL-4-induced oxidative stress upregulates the expression of VCAM-1 gene
      in HUVEC at transcriptional levels via activation of SP-1 transcription
      factor. In contrast, NF- kappa B, AP-1 or IRF-1 do not appear to be
      involved in the signal transduction cascade.
FAU - Lee, Y W
AU  - Lee YW
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      KY 40536, USA.
FAU - Kuhn, H
AU  - Kuhn H
FAU - Hennig, B
AU  - Hennig B
FAU - Neish, A S
AU  - Neish AS
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - 0 (Pyrrolidines)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Thiocarbamates)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 207137-56-2 (Interleukin-4)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Arteriosclerosis/etiology
MH  - Cells, Cultured/drug effects/metabolism
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Genes, Reporter
MH  - Humans
MH  - Inflammation/metabolism
MH  - Interleukin-4/antagonists & inhibitors/*pharmacology
MH  - Oxidative Stress/drug effects/*genetics
MH  - Promoter Regions, Genetic
MH  - Pyrrolidines/pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sp1 Transcription Factor/*physiology
MH  - Thiocarbamates/pharmacology
MH  - Transcription Factors/physiology
MH  - Transcription, Genetic/drug effects
MH  - Transfection
MH  - Umbilical Veins
MH  - Up-Regulation/*drug effects
MH  - Vascular Cell Adhesion Molecule-1/*biosynthesis/genetics
EDAT- 2001/01/03 11:00
MHDA- 2001/04/03 10:01
CRDT- 2001/01/03 11:00
PHST- 2001/01/03 11:00 [pubmed]
PHST- 2001/04/03 10:01 [medline]
PHST- 2001/01/03 11:00 [entrez]
AID - 10.1006/jmcc.2000.1278 [doi]
AID - S0022-2828(00)91278-1 [pii]
PST - ppublish
SO  - J Mol Cell Cardiol. 2001 Jan;33(1):83-94. doi: 10.1006/jmcc.2000.1278.

PMID- 12094615
OWN - NLM
STAT- MEDLINE
DCOM- 20021213
LR  - 20161025
IS  - 0163-5581 (Print)
IS  - 0163-5581 (Linking)
VI  - 41
IP  - 1-2
DP  - 2001
TI  - Linoleic acid-induced VCAM-1 expression in human microvascular
      endothelial cells is mediated by the NF-kappa B-dependent pathway.
PG  - 126-34
AB  - Vascular cell adhesion molecule-1 (VCAM-1) has been reported to play an
      important role in cancer metastasis via the adhesive interaction between
      tumor cells and endothelial cells. In this study, we examined the effects
      of linoleic acid on VCAM-1 expression and its transcriptional regulatory
      mechanism in human microvascular endothelial cells (HMEC-1). Time- and
      dose-dependent increases of VCAM-1 mRNA levels were observed in linoleic
      acid-treated HMEC-1 as detected by reverse transcriptase-polymerase chain
      reaction. Flow cytometry analysis showed a significant and dose-dependent
      upregulation of VCAM-1 expression in HMEC-1 stimulated with linoleic acid
      compared with controls. To clarify the transcriptional regulatory
      pathway, we investigated the role of nuclear factor-kappa B (NF-kappa B)
      in the expression of VCAM-1 by linoleic acid in HMEC-1. Nuclear extracts
      from HMEC-1 stimulated with linoleic acid showed a dose-dependent
      increase in binding activity to the NF-kappa B consensus sequences. These
      effects were preventable by cotreatment with inhibitors of NF-kappa B
      activity, such as sodium salicylate, aspirin, or pyrrolidine
      dithiocarbamate. In addition, pretreatment with NF-kappa B inhibitors
      markedly suppressed the ability of linoleic acid to induce VCAM-1 gene
      expression. The role of NF-kappa B in linoleic acid-induced VCAM-1
      expression was confirmed by functional promoter studies in HMEC-1
      transfected with reporter constructs of the VCAM-1 promoter with or
      without mutated NF-kappa B binding site. These results indicate that
      linoleic acid upregulates VCAM-1 expression in HMEC-1 through the NF-
      kappa B-dependent pathway.
FAU - Park, H J
AU  - Park HJ
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      KY 40536, USA.
FAU - Lee, Y W
AU  - Lee YW
FAU - Hennig, B
AU  - Hennig B
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Nutr Cancer
JT  - Nutrition and cancer
JID - 7905040
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 9007-49-2 (DNA)
RN  - 9KJL21T0QJ (Linoleic Acid)
SB  - IM
MH  - Binding Sites
MH  - Cells, Cultured
MH  - DNA/metabolism
MH  - Endothelium, Vascular/*metabolism
MH  - Flow Cytometry
MH  - Gene Expression/*drug effects
MH  - Humans
MH  - Linoleic Acid/*pharmacology
MH  - Microcirculation/*metabolism
MH  - Mutation
MH  - NF-kappa B/*physiology
MH  - Promoter Regions, Genetic
MH  - RNA, Messenger/analysis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transfection
MH  - Vascular Cell Adhesion Molecule-1/analysis/*genetics
EDAT- 2002/07/04 10:00
MHDA- 2002/12/17 04:00
CRDT- 2002/07/04 10:00
PHST- 2002/07/04 10:00 [pubmed]
PHST- 2002/12/17 04:00 [medline]
PHST- 2002/07/04 10:00 [entrez]
AID - 10.1080/01635581.2001.9680623 [doi]
PST - ppublish
SO  - Nutr Cancer. 2001;41(1-2):126-34. doi: 10.1080/01635581.2001.9680623.

PMID- 11094153
OWN - NLM
STAT- MEDLINE
DCOM- 20001228
LR  - 20190621
IS  - 0014-5793 (Print)
IS  - 0014-5793 (Linking)
VI  - 485
IP  - 2-3
DP  - 2000 Nov 24
TI  - IL-4 induces apoptosis of endothelial cells through the
      caspase-3-dependent pathway.
PG  - 122-6
AB  - The present study was designed to investigate the hypothesis that
      interleukin-4 (IL-4) can induce apoptosis of human endothelial cells and
      to study regulatory pathways of this process. Indeed, DNA ladder assay
      and flow cytometry study showed that IL-4 can induce apoptosis of
      endothelial cells in a time- and dose-dependent manner. In addition, IL-4
      markedly increased activity of caspase-3, and inhibition of this enzyme
      suppressed IL-4-induced apoptosis in a dose-dependent manner. These
      results provide the first evidence that IL-4 can induce apoptosis of
      human endothelial cells. In addition, the data indicate that the
      caspase-3-dependent pathway is critically involved in this process.
FAU - Lee, Y W
AU  - Lee YW
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington,
      40536, USA.
FAU - Kuhn, H
AU  - Kuhn H
FAU - Hennig, B
AU  - Hennig B
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - FEBS Lett
JT  - FEBS letters
JID - 0155157
RN  - 207137-56-2 (Interleukin-4)
RN  - EC 3.4.22.- (CASP3 protein, human)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - *Apoptosis
MH  - Caspase 3
MH  - Caspases/*metabolism
MH  - Cells, Cultured
MH  - DNA Fragmentation
MH  - Endothelium, Vascular/*cytology
MH  - Flow Cytometry
MH  - Humans
MH  - Interleukin-4/*pharmacology
MH  - Umbilical Veins
EDAT- 2000/11/30 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/11/30 11:00
PHST- 2000/11/30 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/11/30 11:00 [entrez]
AID - S0014-5793(00)02208-0 [pii]
AID - 10.1016/s0014-5793(00)02208-0 [doi]
PST - ppublish
SO  - FEBS Lett. 2000 Nov 24;485(2-3):122-6. doi:
      10.1016/s0014-5793(00)02208-0.

PMID- 10954018
OWN - NLM
STAT- MEDLINE
DCOM- 20000830
LR  - 20201216
IS  - 0026-0495 (Print)
IS  - 0026-0495 (Linking)
VI  - 49
IP  - 8
DP  - 2000 Aug
TI  - Fatty acid-mediated activation of vascular endothelial cells.
PG  - 1006-13
AB  - Vascular endothelial cell activation and dysfunction are critical early
      events in atherosclerosis. Selected dietary lipids (eg, fatty acids) may
      be atherogenic by activating endothelial cells and by potentiating an
      inflammatory response. Due to their prooxidant property, unsaturated
      fatty acids may play a critical role in endothelial cell activation and
      injury. To test this hypothesis, porcine endothelial cells were exposed
      to 18-carbon fatty acids differing in the degree of unsaturation, ie, 90
      micromol/L stearic (18:0), oleic (18:1n-9), linoleic (18:2n-6), or
      linolenic acid (18:3n-3) for 6 to 24 hours and/or tumor necrosis factor
      alpha ([TNF-alpha] 500 U/L) for up to 3 hours. Compared with control
      cultures, treatment with 18:0 and 18:2 decreased glutathione levels,
      suggesting an increase in cellular oxidative stress. Both 18:2 and 18:0
      activated the transcription factor nuclear factor kappaB (NF-kappaB) the
      most and 18:1 the least. This NF-kappaB-dependent transcription was
      confirmed in endothelial cells by luciferase reporter gene assay. The
      fatty acid-mediated activation of NF-kappaB was blocked by preenrichment
      of the cultures with 25 micromol/L vitamin E. All fatty acids except 18:1
      and 18:3 increased transendothelial albumin transfer, and 18:2 caused the
      most marked disruption of endothelial integrity. Preenrichment of
      endothelial cells with 18:2 followed by exposure to TNF-alpha resulted in
      a 100% increase in interleukin-6 (IL-6) production compared with TNF-
      alpha exposure alone. In contrast, cellular preenrichment with 18:0,
      18:1, or 18:3 had no effect on TNF-alpha-mediated production of IL-6.
      Cellular release of radiolabeled arachidonic acid (20:4) was markedly
      increased only by cell exposure to 18:2 and 18:3, and the release of 20:4
      appeared to be mainly from the phosphatidylethanolamine fraction. These
      data suggest that oleic acid does not activate endothelial cells.
      Furthermore, linoleic acid and other omega-6 fatty acids appear to be the
      most proinflammatory and possibly atherogenic fatty acids.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Meerarani, P
AU  - Meerarani P
FAU - Ramadass, P
AU  - Ramadass P
FAU - Watkins, B A
AU  - Watkins BA
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Stearic Acids)
RN  - 0RBV727H71 (alpha-Linolenic Acid)
RN  - 2UMI9U37CP (Oleic Acid)
RN  - 4ELV7Z65AP (stearic acid)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*drug effects/metabolism/*physiology
MH  - Fatty Acids, Unsaturated/*pharmacology
MH  - Gene Expression Regulation/drug effects
MH  - Glutathione/metabolism
MH  - Interleukin-6/biosynthesis
MH  - Linoleic Acid/pharmacology
MH  - NF-kappa B/physiology
MH  - Oleic Acid/pharmacology
MH  - Oxidation-Reduction
MH  - Oxidative Stress/physiology
MH  - Pulmonary Artery/cytology/drug effects/physiology
MH  - Stearic Acids/pharmacology
MH  - Structure-Activity Relationship
MH  - Swine
MH  - alpha-Linolenic Acid/pharmacology
EDAT- 2000/08/23 11:00
MHDA- 2000/09/02 11:01
CRDT- 2000/08/23 11:00
PHST- 2000/08/23 11:00 [pubmed]
PHST- 2000/09/02 11:01 [medline]
PHST- 2000/08/23 11:00 [entrez]
AID - S0026-0495(00)97008-2 [pii]
AID - 10.1053/meta.2000.7736 [doi]
PST - ppublish
SO  - Metabolism. 2000 Aug;49(8):1006-13. doi: 10.1053/meta.2000.7736.

PMID- 10873716
OWN - NLM
STAT- MEDLINE
DCOM- 20000815
LR  - 20161124
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 166
IP  - 1
DP  - 2000 Jul 1
TI  - Cellular glutathione status modulates polychlorinated biphenyl-induced
      stress response and apoptosis in vascular endothelial cells.
PG  - 36-42
AB  - Exposure to environmental contaminants, such as polychlorinated biphenyls
      (PCBs), may severely compromise normal function of vascular endothelial
      cells (EC). We have previously shown that PCB 77
      (3,3',4,4'-tetrachlorobiphenyl), an arylhydrocarbon receptor (AhR)
      agonist, can induce oxidative stress in cultured EC. We now show that PCB
      77 can activate EC and induce a cellular stress response that is
      reflected by the activation of c-Jun N-terminal/stress-activated protein
      kinases (JNK/SAPK). Our data also suggest that this PCB 77-mediated
      stress response can be modulated by the intracellular glutathione
      content. EC treated with buthionine-sulphoximine (BSO), an inhibitor of
      glutathione synthesis, further enhanced PCB-induced JNK/SAPK activity.
      This stress response was sustained only in the presence of BSO plus PCB
      77. Media supplementation with the glutathione precursor N-acetyl-
      cysteine (NAC) reduced PCB 77-induced JNK/SAPK. Intracellular glutathione
      also may be implicated in PCB-induced EC apoptosis. Individual treatment
      with PCB, BSO, or linoleic acid induced activation of caspase 3. Compared
      to PCB 77 alone, annexin V activity was further amplified during combined
      treatment with BSO and PCB 77. DNA fragmentation was mostly observed when
      cells were treated with both BSO and PCB 77. The caspase 3-specific
      inhibitor DEVD-CHO protected cells against PCB 77/BSO-mediated apoptosis
      and inhibited the caspase activity without affecting JNK/SAPK activation
      or cellular glutathione levels. These results suggest that AhR ligands,
      such as PCB 77, cause vascular EC dysfunction by modulating intracellular
      glutathione, which subsequently leads to activation of stress-specific
      kinases. Furthermore, inhibition of glutathione synthesis by BSO can
      further potentiate the PCB 77-induced stress response and ultimately lead
      to apoptotic cell death.
CI  - Copyright 2000 Academic Press.
FAU - Slim, R
AU  - Slim R
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Robertson, L W
AU  - Robertson LW
FAU - Lehmler, H J
AU  - Lehmler HJ
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Environmental Pollutants)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
RN  - GAN16C9B8O (Glutathione)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Caspase 3
MH  - Caspases/metabolism
MH  - Endothelium, Vascular/*drug effects/enzymology/metabolism/pathology
MH  - Environmental Pollutants/pharmacology
MH  - Enzyme Activation
MH  - Glutathione/*metabolism
MH  - JNK Mitogen-Activated Protein Kinases
MH  - Mitogen-Activated Protein Kinase 8
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Polychlorinated Biphenyls/*pharmacology
MH  - Swine
EDAT- 2000/06/30 11:00
MHDA- 2000/08/19 11:00
CRDT- 2000/06/30 11:00
PHST- 2000/06/30 11:00 [pubmed]
PHST- 2000/08/19 11:00 [medline]
PHST- 2000/06/30 11:00 [entrez]
AID - 10.1006/taap.2000.8944 [doi]
AID - S0041-008X(00)98944-0 [pii]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2000 Jul 1;166(1):36-42. doi:
      10.1006/taap.2000.8944.

PMID- 10943440
OWN - NLM
STAT- MEDLINE
DCOM- 20001228
LR  - 20161025
IS  - 1210-7778 (Print)
IS  - 1210-7778 (Linking)
VI  - 8 Suppl
DP  - 2000 Jul
TI  - Effects of lipids and antioxidants on PCB-mediated dysfunction of
      vascular endothelial cells (EC).
PG  - 18-9
AB  - Our findings suggest that exposure to specific environmental contaminants
      can trigger diseases of the vasculature, e.g., cardiovascular disease. In
      addition, high-fat diets may potentiate and diets high in antioxidant
      nutrients may protect against PCB-mediated endothelial cell dysfunction.
      Our data give an insight into the potential use of vitamin E and related
      antioxidants to limit PCB-mediated cell injury. These studies are
      significant for providing new insights into potential nutrition
      interventions in diseases that can be induced by the toxicity of PCBs and
      other halogenated compounds.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506 0054, USA. bhennig@pop.uky.edu
FAU - Slim, R
AU  - Slim R
FAU - Toborek, M
AU  - Toborek M
FAU - Malecki, A
AU  - Malecki A
FAU - Robertson, L W
AU  - Robertson LW
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Czech Republic
TA  - Cent Eur J Public Health
JT  - Central European journal of public health
JID - 9417324
RN  - 0 (Antioxidants)
RN  - 0 (Fatty Acids)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Endothelium, Vascular/cytology/*drug effects
MH  - Fatty Acids/*pharmacology
MH  - Polychlorinated Biphenyls/antagonists & inhibitors/*toxicity
MH  - Swine
EDAT- 2000/08/16 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/08/16 11:00
PHST- 2000/08/16 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/08/16 11:00 [entrez]
PST - ppublish
SO  - Cent Eur J Public Health. 2000 Jul;8 Suppl:18-9.

PMID- 10820187
OWN - NLM
STAT- MEDLINE
DCOM- 20000602
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 74
IP  - 6
DP  - 2000 Jun
TI  - 4-Hydroxynonenal induces oxidative stress and death of cultured spinal
      cord neurons.
PG  - 2278-87
AB  - Primary spinal cord trauma can trigger a cascade of secondary processes
      leading to delayed and amplified injury to spinal cord neurons. Release
      of fatty acids, in particular arachidonic acid, from cell membranes is
      believed to contribute significantly to these events. Mechanisms of fatty
      acid-induced injury to spinal cord neurons may include lipid
      peroxidation. One of the major biologically active products of
      arachidonic acid peroxidation is 4-hydroxynonenal (HNE). The levels of
      HNE-protein conjugates in cultured spinal cord neurons increased in a
      dose-dependent manner after a 24-h exposure to arachidonic acid. To study
      cellular effects of HNE, spinal cord neurons were treated with different
      doses of HNE, and cellular oxidative stress, intracellular calcium, and
      cell viability were determined. A 3-h exposure to 10 microM HNE caused
      approximately 80% increase in oxidative stress and 30% elevation of
      intracellular calcium. Exposure of spinal cord neurons to HNE caused a
      dramatic loss of cellular viability, indicated by a dose-dependent
      decrease in MTS [3-(4,
      5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-s ulfophenyl)-
      2H-tetrazolium, inner salt] conversion. The cytotoxic effect of HNE was
      diminished by pretreating neurons with ebselen or N-acetylcysteine. These
      data support the hypothesis that formation of HNE may be responsible, at
      least in part, for the cytotoxic effects of membrane-released arachidonic
      acid to spinal cord neurons.
FAU - Malecki, A
AU  - Malecki A
AD  - Department of Surgery, University of Kentucky, Lexington 40536, USA.
FAU - Garrido, R
AU  - Garrido R
FAU - Mattson, M P
AU  - Mattson MP
FAU - Hennig, B
AU  - Hennig B
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Aldehydes)
RN  - 0 (Antioxidants)
RN  - 0 (Azoles)
RN  - 0 (Cysteine Proteinase Inhibitors)
RN  - 0 (Organoselenium Compounds)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 40X2P7DPGH (ebselen)
RN  - K1CVM13F96 (4-hydroxy-2-nonenal)
RN  - SY7Q814VUP (Calcium)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Aldehydes/*pharmacology
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Apoptosis/*drug effects
MH  - Arachidonic Acid/pharmacology
MH  - Azoles/pharmacology
MH  - Calcium/metabolism
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cysteine Proteinase Inhibitors/*pharmacology
MH  - DNA Fragmentation
MH  - Fetus/cytology
MH  - Lipid Peroxidation/drug effects
MH  - Mice
MH  - Neurons/*cytology/drug effects/enzymology
MH  - Organoselenium Compounds/pharmacology
MH  - Oxidative Stress/*drug effects
MH  - Spinal Cord/*cytology
EDAT- 2000/05/23 09:00
MHDA- 2000/06/10 09:00
CRDT- 2000/05/23 09:00
PHST- 2000/05/23 09:00 [pubmed]
PHST- 2000/06/10 09:00 [medline]
PHST- 2000/05/23 09:00 [entrez]
AID - 10.1046/j.1471-4159.2000.0742278.x [doi]
PST - ppublish
SO  - J Neurochem. 2000 Jun;74(6):2278-87. doi:
      10.1046/j.1471-4159.2000.0742278.x.

PMID- 10751565
OWN - NLM
STAT- MEDLINE
DCOM- 20000606
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 861
IP  - 1
DP  - 2000 Apr 7
TI  - Nicotine attenuates arachidonic acid-induced neurotoxicity in cultured
      spinal cord neurons.
PG  - 59-68
AB  - Arachidonic acid release from cellular membranes due to spinal cord
      trauma may be one of the principal destructive events that can lead to
      progressive injury to spinal cord tissue. Exposure to arachidonic acid
      can compromise neuronal survival and viability. Because nicotine is known
      to be a neuroprotective agent, we propose that it can prevent arachidonic
      acid-induced neurotoxicity. To study this hypothesis, effects of nicotine
      on mitochondrial function, cellular energy content and apoptotic cell
      death were measured in cultured spinal cord neurons treated with
      arachidonic acid. Nicotine attenuated arachidonic acid-induced
      compromised cell viability and cellular ATP levels in spinal cord
      neurons. Nicotine exerted these protective effects when used at the
      concentration of 10 microM and only after a 2-h pre-treatment before a
      co-exposure to arachidonic acid. Antagonists of nicotinic receptors, such
      as alpha-bungarotoxin or mecamylamine, only partially reversed these
      neuroprotective effects of nicotine. In addition, nicotine prevented
      arachidonic acid-induced activation of caspase-3 activity and apoptotic
      cell death. These results indicate that nicotine pre-treatment can exert
      a protective effect against arachidonic acid-induced injury to spinal
      cord neurons.
FAU - Garrido, R
AU  - Garrido R
AD  - Department of Surgery, Division of Neurosurgery, University of Kentucky
      Medical Center, Lexington, KY 40536, USA.
FAU - Malecki, A
AU  - Malecki A
FAU - Hennig, B
AU  - Hennig B
FAU - Toborek, M
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Ganglionic Stimulants)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 6M3C89ZY6R (Nicotine)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Apoptosis/*drug effects/physiology
MH  - Arachidonic Acid/*antagonists & inhibitors
MH  - Caspase 3
MH  - Caspases/drug effects/metabolism
MH  - Cells, Cultured
MH  - Embryo, Mammalian
MH  - Embryo, Nonmammalian
MH  - Ganglionic Stimulants/*pharmacology
MH  - L-Lactate Dehydrogenase/drug effects/metabolism
MH  - Neurons/*drug effects/metabolism
MH  - Nicotine/*pharmacology
MH  - Spinal Cord/cytology/*drug effects/metabolism
EDAT- 2000/04/07 09:00
MHDA- 2000/06/10 09:00
CRDT- 2000/04/07 09:00
PHST- 2000/04/07 09:00 [pubmed]
PHST- 2000/06/10 09:00 [medline]
PHST- 2000/04/07 09:00 [entrez]
AID - S0006-8993(00)01977-6 [pii]
AID - 10.1016/s0006-8993(00)01977-6 [doi]
PST - ppublish
SO  - Brain Res. 2000 Apr 7;861(1):59-68. doi: 10.1016/s0006-8993(00)01977-6.

PMID- 10686080
OWN - NLM
STAT- MEDLINE
DCOM- 20000329
LR  - 20161025
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 161
IP  - 2
DP  - 2000 Feb
TI  - Nicotine attenuates arachidonic acid-induced overexpression of nitric
      oxide synthase in cultured spinal cord neurons.
PG  - 609-20
AB  - Primary spinal cord trauma can initiate a cascade of pathophysiologic
      events which markedly contribute to the expansion and amplification of
      the primary insult. The detailed mechanisms of these secondary
      neurochemical reactions are largely unknown; however, they involve
      membrane lipid derangements with the release of free fatty acids, in
      particular, arachidonic acid (AA). AA can induce several injury effects
      on spinal cord neurons. We hypothesize that upregulation of nitric oxide
      synthase (NOS) is among the most important mechanisms of arachidonic-
      acid-induced neuronal dysfunction and that nicotine can attenuate this
      effect. To study these hypotheses, spinal cord neurons were exposed to AA
      and/or nicotine, and several markers of neuronal nitric oxide synthase
      (nNOS) metabolism were measured. In addition, cotreatments with either
      inhibitors of nicotinic receptors or inhibitors of specific NOS isoforms
      were employed. Treatment with AA markedly increased activity of nNOS, as
      well as mRNA and protein levels of this enzyme. Changes in nNOS
      expression were accompanied by an increase in cellular cGMP and medium
      nitrite levels. Pretreatment with nicotine decreased AA-induced
      overexpression of nNOS and elevation of nitrite levels. In addition, it
      appeared that these nicotine effects could be partially modulated both by
      the alpha7 nicotinic receptors or by nonreceptor mechanisms.
      Alternatively, the observed changes could also be mediated by an
      alternate nicotinic receptor mechanism which is not blocked by alpha-
      bungarotoxin or mecamylamine. Results of the present study indicate that
      exposure to AA can lead to induction of nNOS in cultured spinal cord
      neurons. In addition, nicotine can exert a neuroprotective effect by
      attenuation of AA-induced upregulation of nNOS metabolism. These data may
      have therapeutic implications for the treatment of acute spinal cord
      trauma.
CI  - Copyright 2000 Academic Press.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky, Lexington, Kentucky,
      40536, USA. mjtobo00@pop.uky.edu
FAU - Garrido, R
AU  - Garrido R
FAU - Malecki, A
AU  - Malecki A
FAU - Kaiser, S
AU  - Kaiser S
FAU - Mattson, M P
AU  - Mattson MP
FAU - Hennig, B
AU  - Hennig B
FAU - Young, B
AU  - Young B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Nitrites)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 6M3C89ZY6R (Nicotine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 1.14.13.39 (Nos1 protein, mouse)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Animals
MH  - Arachidonic Acid/antagonists & inhibitors/*pharmacology
MH  - Cells, Cultured
MH  - Cyclic GMP/metabolism
MH  - Fetus
MH  - Gene Expression Regulation, Enzymologic/*drug effects
MH  - Kinetics
MH  - Mice
MH  - Neurons/cytology/*enzymology
MH  - Nicotine/*pharmacology
MH  - Nitric Oxide Synthase/*genetics/metabolism
MH  - Nitric Oxide Synthase Type I
MH  - Nitrites/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Spinal Cord/cytology/*enzymology
EDAT- 2000/02/25 09:00
MHDA- 2000/04/01 09:00
CRDT- 2000/02/25 09:00
PHST- 2000/02/25 09:00 [pubmed]
PHST- 2000/04/01 09:00 [medline]
PHST- 2000/02/25 09:00 [entrez]
AID - 10.1006/exnr.1999.7308 [doi]
AID - S0014-4886(99)97308-9 [pii]
PST - ppublish
SO  - Exp Neurol. 2000 Feb;161(2):609-20. doi: 10.1006/exnr.1999.7308.

PMID- 10617950
OWN - NLM
STAT- MEDLINE
DCOM- 20000127
LR  - 20180330
IS  - 0002-9165 (Print)
IS  - 0002-9165 (Linking)
VI  - 71
IP  - 1
DP  - 2000 Jan
TI  - Zinc protects against apoptosis of endothelial cells induced by linoleic
      acid and tumor necrosis factor alpha.
PG  - 81-7
AB  - BACKGROUND: Zinc requirements of the vascular endothelium may be
      increased in inflammatory conditions, ie, atherosclerosis, in which
      apoptotic cell death is prevalent. OBJECTIVE: We hypothesized that zinc
      deficiency may potentiate disruption of endothelial cell integrity
      mediated by fatty acids and inflammatory cytokines by enhancing pathways
      that lead to apoptosis and up-regulation of caspase genes. DESIGN:
      Endothelial cells were maintained in low-serum medium or grown in culture
      media containing selected chelators, ie, diethylenetriaminepentaacetate
      or N,N,N', N'-tetrakis(2-pyridylmethyl)-ethylenediamine (TPEN), with or
      without zinc supplementation. Subsequently, cells were treated with
      linoleic acid, tumor necrosis factor alpha (TNF-alpha), or both. We
      studied the effect of zinc deficiency and supplementation on the
      induction of apoptosis by measuring caspase-3 activity, cell binding of
      annexin V, and DNA fragmentation. RESULTS: Our results indicated that
      linoleic acid and TNF-alpha independently, but more markedly in concert,
      up-regulated caspase-3 activity and induced annexin V binding and DNA
      fragmentation. Zinc deficiency, especially when induced by TPEN,
      dramatically increased apoptotic cell death induced by cytokines and
      lipids compared with control cultures. Supplementation of low-serum- or
      chelator-treated endothelial cells with physiologic amounts of zinc
      caused a marked attenuation of apoptosis induced by linoleic acid and
      TNF-alpha. Morphologic changes of cells observed during zinc deficiency
      were prevented by zinc supplementation. Media supplementation with other
      divalent cations (eg, calcium and magnesium) did not mimic the protective
      role of zinc against apoptosis. CONCLUSIONS: Our data indicate that zinc
      is vital to vascular endothelial cell integrity, possibly by regulating
      signaling events to inhibit apoptotic cell death.
FAU - Meerarani, P
AU  - Meerarani P
AD  - Departments of Nutrition and Food Science and Surgery, University of
      Kentucky, Lexington, and the Molecular Biology Institute, Austrian
      Academy of Sciences, Salzburg.
FAU - Ramadass, P
AU  - Ramadass P
FAU - Toborek, M
AU  - Toborek M
FAU - Bauer, H C
AU  - Bauer HC
FAU - Bauer, H
AU  - Bauer H
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
RN  - 0 (Annexin A5)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
RN  - J41CSQ7QDS (Zinc)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Annexin A5/metabolism
MH  - Apoptosis/*drug effects
MH  - Caspase 3
MH  - Caspases/*metabolism
MH  - Cell Death/drug effects
MH  - Cells, Cultured
MH  - DNA Fragmentation/drug effects
MH  - Endothelium, Vascular/*drug effects/enzymology/metabolism
MH  - Flow Cytometry
MH  - Linoleic Acid/*adverse effects/antagonists & inhibitors
MH  - Pulmonary Artery
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/*adverse effects/antagonists & inhibitors
MH  - Zinc/*deficiency/*pharmacology
EDAT- 2000/01/05 00:00
MHDA- 2000/01/05 00:01
CRDT- 2000/01/05 00:00
PHST- 2000/01/05 00:00 [pubmed]
PHST- 2000/01/05 00:01 [medline]
PHST- 2000/01/05 00:00 [entrez]
AID - 10.1093/ajcn/71.1.81 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 2000 Jan;71(1):81-7. doi: 10.1093/ajcn/71.1.81.

PMID- 10630576
OWN - NLM
STAT- MEDLINE
DCOM- 20000210
LR  - 20190513
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 52
IP  - 2
DP  - 1999 Dec
TI  - Antioxidant protection against PCB-mediated endothelial cell activation.
PG  - 232-9
AB  - Certain environmental contaminants such as polyhalogenated aromatic
      hydrocarbons may be implicated in diseases of the vasculature by
      compromising normal functions of vascular endothelial cells. We have
      shown previously that 3,3',4,4'-tetrachlorobiphenyl (PCB 77), an aryl
      hydrocarbon (Ah) receptor agonist, can cause disruption of endothelial
      barrier function. This was supported by an increase in oxidative stress
      as measured by enhanced 2',7'-dichlorofluorescein (DCF) fluorescence and
      activation of the oxidative stress-sensitive transcription factor NF-
      kappaB. We have now tested the protective effects of antioxidants vitamin
      E (alpha-tocopherol) and pyrrolidine dithiocarbamate (PDTC) on
      endothelial cell activation induced by PCB 77. Only vitamin E completely
      blocked PCB 77-mediated endothelial barrier dysfunction. This protective
      effect by vitamin E was associated with a decrease in both oxidative
      stress, as measured by DCF fluorescence, as well as in NF-kappaB
      activation. Furthermore, vitamin E decreased PCB 77-mediated production
      of the inflammatory cytokine IL-6. Although pretreatment of endothelial
      cells with PDTC prevented the induction of NF-kappaB by PCB 77, this
      inhibition was not associated with a decrease in DCF levels or protection
      against endothelial barrier dysfunction. Pretreatment with alpha-
      naphthoflavone (alpha-NF), an Ah receptor partial antagonist and specific
      inhibitor of cytochrome P450 1A, partially protected against PCB
      77-induced endothelial barrier dysfunction. This observation was
      paralleled by the fact that alpha-NF did not fully antagonize the PCB-
      induced increase in DCF in endothelial cells. Furthermore, PCB-mediated
      induction of NF-kappaB and production of IL-6 were only partially blocked
      by alpha-NF. Of all the tested compounds (vitamin E, PDTC and alpha-NF),
      vitamin E was most potent in blocking PCB 77-mediated endothelial cell
      activation. These data give an insight into the potential use of vitamin
      E and related antioxidants to limit PCB-mediated cell injury and into the
      use of alpha-NF to explore mechanisms underlying the injurious potential
      of Ah receptor agonists.
FAU - Slim, R
AU  - Slim R
AD  - Department of Nutrition and Food Science, Graduate Center for Toxicology,
      University of Kentucky, Lexington 40506-0054, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Robertson, L W
AU  - Robertson LW
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (Albumins)
RN  - 0 (Antioxidants)
RN  - 0 (Benzoflavones)
RN  - 0 (Carcinogens)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Pyrrolidines)
RN  - 0 (Thiocarbamates)
RN  - 1406-18-4 (Vitamin E)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - 604-59-1 (alpha-naphthoflavone)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Albumins/metabolism
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Benzoflavones/pharmacology
MH  - Carcinogens/*antagonists & inhibitors/chemical synthesis/*toxicity
MH  - Cell Nucleus/drug effects/metabolism
MH  - Cytosol/drug effects/metabolism
MH  - Electrophoresis
MH  - Endothelium, Vascular/*cytology
MH  - Interleukin-6/biosynthesis
MH  - NF-kappa B/antagonists & inhibitors/metabolism
MH  - Oxidative Stress/drug effects
MH  - Polychlorinated Biphenyls/*antagonists & inhibitors/chemical
      synthesis/*toxicity
MH  - Pyrrolidines/pharmacology
MH  - Swine
MH  - Thiocarbamates/pharmacology
MH  - Vitamin E/pharmacology
EDAT- 2000/01/12 00:00
MHDA- 2000/01/12 00:01
CRDT- 2000/01/12 00:00
PHST- 2000/01/12 00:00 [pubmed]
PHST- 2000/01/12 00:01 [medline]
PHST- 2000/01/12 00:00 [entrez]
AID - 10.1093/toxsci/52.2.232 [doi]
PST - ppublish
SO  - Toxicol Sci. 1999 Dec;52(2):232-9. doi: 10.1093/toxsci/52.2.232.

PMID- 10497308
OWN - NLM
STAT- MEDLINE
DCOM- 19991101
LR  - 20161124
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 181
IP  - 2
DP  - 1999 Nov
TI  - 4-Hydroxynonenal induces dysfunction and apoptosis of cultured
      endothelial cells.
PG  - 295-303
AB  - Lipolytic products of triglyceride-rich lipoproteins, i.e., free fatty
      acids, may cause activation and dysfunction of the vascular endothelium.
      Mechanisms of these effects may include lipid peroxidation. One of the
      major and biologically active products of peroxidation of n-6 fatty
      acids, such as linoleic acid or arachidonic acid, is the aldehyde
      4-hydroxynonenal (HNE). To study the hypothesis that HNE may be a
      critical factor in endothelial cell dysfunction caused by free fatty
      acids, human umbilical endothelial cells (HUVEC) were treated with up
      to160 microM of linoleic or arachidonic acid. HNE formation was detected
      by immunocytochemistry in cells treated for 24 h with either fatty acid,
      but more markedly with arachidonic acid. To study the cellulareffects of
      HNE, HUVEC were treated with different concentrations of this aldehyde,
      and several markers of endothelial cell dysfunction were determined.
      Exposure to HNE for 6 and 9 h resulted in increased cellular oxidative
      stress. However, short time treatment with HNE did not cause activation
      of nuclear factor-kappaB (NF-kappaB). In addition, HUVEC exposure to HNE
      caused a dose-dependent decrease in production of both interleukin-8
      (IL-8) and intercellular adhesion molecule-1 (ICAM-1). On the other hand,
      HNE exerted prominent cytotoxic effects in cultured HUVEC, manifested by
      morphological changes, diminished cellular viability, and impaired
      endothelial barrier function. Furthermore, HNE treatment induced
      apoptosis of HUVEC. These data provide evidence that HNE does not
      contribute to NF-kappaB-related mechanisms of the inflammatory response
      in HUVEC, but rather to endothelial dysfunction, cytotoxicity, and
      apoptotic cell death.
CI  - Copyright 1999 Wiley-Liss, Inc.
FAU - Herbst, U
AU  - Herbst U
AD  - Department of Nutrition, University of Kentucky, Lexington, Kentucky,
      USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Kaiser, S
AU  - Kaiser S
FAU - Mattson, M P
AU  - Mattson MP
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Aldehydes)
RN  - 0 (Interleukin-8)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - K1CVM13F96 (4-hydroxy-2-nonenal)
SB  - IM
MH  - Aldehydes/*pharmacology
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Endothelium, Vascular/cytology/*drug effects/physiology
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Immunohistochemistry
MH  - Intercellular Adhesion Molecule-1/genetics
MH  - Interleukin-8/genetics
MH  - Kinetics
MH  - Pulmonary Artery
MH  - Swine
MH  - Time Factors
MH  - Umbilical Veins
EDAT- 1999/09/25 00:00
MHDA- 1999/09/25 00:01
CRDT- 1999/09/25 00:00
PHST- 1999/09/25 00:00 [pubmed]
PHST- 1999/09/25 00:01 [medline]
PHST- 1999/09/25 00:00 [entrez]
AID - 10.1002/(SICI)1097-4652(199911)181:2<295::AID-JCP11>3.0.CO;2-I [pii]
AID - 10.1002/(SICI)1097-4652(199911)181:2<295::AID-JCP11>3.0.CO;2-I [doi]
PST - ppublish
SO  - J Cell Physiol. 1999 Nov;181(2):295-303. doi:
      10.1002/(SICI)1097-4652(199911)181:2<295::AID-JCP11>3.0.CO;2-I.

PMID- 10501286
OWN - NLM
STAT- MEDLINE
DCOM- 19991029
LR  - 20190915
IS  - 0899-9007 (Print)
IS  - 0899-9007 (Linking)
VI  - 15
IP  - 10
DP  - 1999 Oct
TI  - Zinc nutrition and apoptosis of vascular endothelial cells: implications
      in atherosclerosis.
PG  - 744-8
AB  - Little is known about the requirements and function of zinc in
      maintaining endothelial cell integrity, especially during stressful
      conditions, such as the inflammatory response in cardiovascular disease.
      There is evidence that zinc requirements of the vascular endothelium are
      increased during inflammatory conditions such as atherosclerosis, where
      apoptotic cell death is also prevalent. Apoptosis is a morphologically
      distinct mechanism of programmed cell death which involves the activation
      of a cell-intrinsic suicide program, and there is evidence that factors
      such as inflammatory cytokines (e.g., tumor necrosis factor [TNF]) and
      pure or oxidized lipids are necessary to induce the cell death pathway.
      Because of its constant exposure to blood components, including
      prooxidants, diet-derived fats, and their derivatives, the endothelium is
      very susceptible to oxidative stress and to apoptotic injury mediated by
      blood lipid components, prooxidants, and cytokines. Thus, it is likely
      that the cellular lipid environment, primarily polyunsaturated fatty
      acids, can potentiate the overall endothelial cell injury by increasing
      cellular oxidative stress and cytokine release in proximity to the
      endothelium, which then could further induce apoptosis and disrupt
      endothelial barrier function. Our data suggest that zinc deficiency
      exacerbates the detrimental effects of specific fatty acids (e.g.,
      linoleic acid) and inflammatory cytokines, such as TNF, on vascular
      endothelial functions. We propose that a major mechanism of zinc
      protection against disruption of endothelial cell integrity during
      inflammatory conditions, is by the ability of zinc to inhibit the
      pathways of signal transduction leading to apoptosis and especially
      mechanisms that lead to upregulation of caspase genes.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition, University of Kentucky, Lexington 40506-0054,
      USA.
FAU - Meerarani, P
AU  - Meerarani P
FAU - Ramadass, P
AU  - Ramadass P
FAU - Toborek, M
AU  - Toborek M
FAU - Malecki, A
AU  - Malecki A
FAU - Slim, R
AU  - Slim R
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Nutrition
JT  - Nutrition (Burbank, Los Angeles County, Calif.)
JID - 8802712
RN  - 0 (Antioxidants)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Antioxidants/metabolism
MH  - *Apoptosis
MH  - Arteriosclerosis/*pathology
MH  - Endothelium, Vascular/*pathology
MH  - Humans
MH  - *Nutritional Status
MH  - Oxidative Stress
MH  - Tumor Necrosis Factor-alpha/physiology
MH  - Zinc/*physiology
RF  - 69
EDAT- 1999/09/29 00:00
MHDA- 1999/09/29 00:01
CRDT- 1999/09/29 00:00
PHST- 1999/09/29 00:00 [pubmed]
PHST- 1999/09/29 00:01 [medline]
PHST- 1999/09/29 00:00 [entrez]
AID - S0899900799001483 [pii]
AID - 10.1016/s0899-9007(99)00148-3 [doi]
PST - ppublish
SO  - Nutrition. 1999 Oct;15(10):744-8. doi: 10.1016/s0899-9007(99)00148-3.

PMID- 10428065
OWN - NLM
STAT- MEDLINE
DCOM- 19990813
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 73
IP  - 2
DP  - 1999 Aug
TI  - Arachidonic acid-induced oxidative injury to cultured spinal cord
      neurons.
PG  - 684-92
AB  - Spinal cord trauma can cause a marked release of free fatty acids, in
      particular, arachidonic acid (AA), from cell membranes. Free fatty acids,
      and AA by itself, may lead to secondary damage to spinal cord neurons. To
      study this hypothesis, cultured spinal cord neurons were exposed to
      increasing concentrations of AA (0.01-10 microM). AA-induced injury to
      spinal cord neurons was assessed by measurements of cellular oxidative
      stress, intracellular calcium levels, activation of nuclear factor-KB
      (NF-kappaB), and cell viability. AA treatment increased intracellular
      calcium concentrations and decreased cell viability. Oxidative stress
      increased significantly in neurons exposed to 1 and 10 microM AA. In
      addition, AA treatment activated NF-kappaB and decreased levels of the
      inhibitory subunit, IKB. It is interesting that manganese superoxide
      dismutase protein levels and levels of intracellular total glutathione
      increased in neurons exposed to this fatty acid for 24 h, consistent with
      a compensatory response to increased oxidative stress. These results
      strongly support the hypothesis that free fatty acids contribute to the
      tissue injury observed following spinal cord trauma.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky, Lexington, USA.
FAU - Malecki, A
AU  - Malecki A
FAU - Garrido, R
AU  - Garrido R
FAU - Mattson, M P
AU  - Mattson MP
FAU - Hennig, B
AU  - Hennig B
FAU - Young, B
AU  - Young B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (NF-kappa B)
RN  - 0 (Phosphatidylcholines)
RN  - 0 (Phosphatidylethanolamines)
RN  - 0 (Phosphatidylinositols)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Arachidonic Acid/*toxicity
MH  - Calcium/metabolism
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Enhancer Elements, Genetic/physiology
MH  - Fatty Acids, Nonesterified/metabolism
MH  - Female
MH  - Fetus/cytology
MH  - Mice
MH  - NF-kappa B/genetics/metabolism
MH  - Neurons/*cytology/*enzymology
MH  - Oxidative Stress/*physiology
MH  - Phosphatidylcholines/metabolism
MH  - Phosphatidylethanolamines/metabolism
MH  - Phosphatidylinositols/metabolism
MH  - Pregnancy
MH  - Spinal Cord/*cytology
MH  - Spinal Cord Injuries/metabolism
MH  - Superoxide Dismutase/metabolism
EDAT- 1999/07/31 00:00
MHDA- 1999/07/31 00:01
CRDT- 1999/07/31 00:00
PHST- 1999/07/31 00:00 [pubmed]
PHST- 1999/07/31 00:01 [medline]
PHST- 1999/07/31 00:00 [entrez]
AID - 10.1046/j.1471-4159.1999.0730684.x [doi]
PST - ppublish
SO  - J Neurochem. 1999 Aug;73(2):684-92. doi:
      10.1046/j.1471-4159.1999.0730684.x.

PMID- 10204831
OWN - NLM
STAT- MEDLINE
DCOM- 19990527
LR  - 20190909
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 18
IP  - 2
DP  - 1999 Apr
TI  - Antioxidant-like properties of zinc in activated endothelial cells.
PG  - 152-8
AB  - OBJECTIVE: The objective of this study was to test the hypothesis that
      zinc deficiency in endothelial cells may potentiate the inflammatory
      response mediated by certain lipids and cytokines, possibly via
      mechanisms associated with increased cellular oxidative stress. Our
      experimental approach was to compare conditions of cellular zinc
      deficiency and zinc supplementation with oxidative stress-mediated
      molecular and biochemical changes in vascular endothelial cells. METHODS:
      To investigate our hypothesis, porcine pulmonary artery-derived
      endothelial cells were depleted of zinc by culture in media containing 1%
      fetal bovine serum for eight days. Subsequently, endothelial cells were
      exposed to media enriched with or without zinc (10 microM) for two days,
      followed by exposure to either tumor necrosis factor-alpha (TNF, 500
      U/mL) or linoleic acid (90 microM), before measurement of oxidative
      stress (DCF fluorescence), activation of nuclear factor kappaB (NF-
      kappaB) or activator protein-1 (AP-1) and production of the inflammatory
      cytokine interleukin 6 (IL-6). RESULTS: Oxidative stress was increased
      markedly in zinc-deficient endothelial cells following treatment with
      fatty acid or TNF. This increase in oxidative stress was partially
      blocked by prior zinc supplementation. The oxidative stress-sensitive
      transcription factor NF-kappaB was up-regulated by zinc deficiency and
      fatty acid treatment. The up-regulation mediated by fatty acids was
      markedly reduced by zinc supplementation. Similar results were obtained
      with AP-1. Furthermore, endothelial cell production of IL-6 was increased
      in zinc-deficient endothelial cells following treatment with fatty acids
      or TNF. This increase in production of inflammatory cytokines was
      partially blocked by zinc supplementation. DISCUSSION: Our previous data
      clearly show that zinc is a protective and critical nutrient for
      maintenance of endothelial integrity. The present data suggest that zinc
      may in part be antiatherogenic by inhibiting oxidative stress-responsive
      events in endothelial cell dysfunction. This may have implications in
      understanding mechanisms of atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Meerarani, P
AU  - Meerarani P
FAU - Toborek, M
AU  - Toborek M
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Antioxidants)
RN  - 0 (Culture Media)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Cells, Cultured
MH  - Culture Media
MH  - Endothelium, Vascular/*metabolism
MH  - Interleukin-6/biosynthesis
MH  - Linoleic Acid/pharmacology
MH  - NF-kappa B/metabolism
MH  - Oxidative Stress
MH  - Pulmonary Artery
MH  - Swine
MH  - Transcription Factor AP-1/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Zinc/*administration & dosage/*pharmacology
EDAT- 1999/04/16 00:00
MHDA- 1999/04/16 00:01
CRDT- 1999/04/16 00:00
PHST- 1999/04/16 00:00 [pubmed]
PHST- 1999/04/16 00:01 [medline]
PHST- 1999/04/16 00:00 [entrez]
AID - 10.1080/07315724.1999.10718843 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1999 Apr;18(2):152-8. doi:
      10.1080/07315724.1999.10718843.

PMID- 9890193
OWN - NLM
STAT- MEDLINE
DCOM- 19990310
LR  - 20191102
IS  - 1095-6670 (Print)
IS  - 1095-6670 (Linking)
VI  - 13
IP  - 2
DP  - 1999
TI  - Linoleic acid amplifies polychlorinated biphenyl-mediated dysfunction of
      endothelial cells.
PG  - 83-91
AB  - Selected dietary lipids may increase the atherogenicity of environmental
      chemicals, such as polychlorinated biphenyls (PCBs), by cross-amplifying
      mechanisms leading to dysfunction of the vascular endothelium. To
      investigate this hypothesis, cultured endothelial cells were treated with
      90 microM linoleic acid (18:2n-6), followed by either one of two PCBs,
      3,3',4,4'-tetrachlorobiphenyl (PCB 77) or
      2,2'4,4',5,5'-hexachlorobiphenyl (PCB 153). These PCBs were selected for
      their varying binding activities with the aryl hydrocarbon (Ah) receptor
      and differences in their induction of cytochrome P450. PCB 77 disrupted
      endothelial barrier function by allowing an increase in albumin transfer
      across endothelial monolayers. Prior cellular enrichment with 18:2 before
      PCB treatment further diminished endothelial barrier function, as
      compared to cells treated only with the PCB. This phenomenon appears to
      be mediated by increased oxidative stress, which is supported by enhanced
      2,7-dichlorofluorescein fluorescence, activation data of the oxidative
      stress-sensitive nuclear transcription factor-kappaB (NF-kappaB), as well
      as an observed decrease in vitamin E content in the culture media.
      Similar to the endothelial permeability data, pre-enrichment of cells
      with 18:2 further increased the PCB-mediated induction of cytochrome P450
      1A. In contrast to PCB 77, PCB 153 (or 18:2 plus PCB 153) had little or
      no effect on endothelial barrier function. Our results suggest that
      certain unsaturated fatty acids can potentiate PCB-mediated endothelial
      cell dysfunction and that oxidative stress and activation of the
      cytochrome P450 1A subfamily may be, in part, responsible for these
      metabolic events. These findings have implications for understanding the
      involvement of certain environmental contaminants in diseases that
      involve dysfunction of the vascular endothelium.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, Graduate Center for Toxicology,
      University of Kentucky, Lexington 40506-0054, USA.
FAU - Slim, R
AU  - Slim R
FAU - Toborek, M
AU  - Toborek M
FAU - Robertson, L W
AU  - Robertson LW
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 P42 ES 07380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biochem Mol Toxicol
JT  - Journal of biochemical and molecular toxicology
JID - 9717231
RN  - 0 (DNA Primers)
RN  - 0 (NF-kappa B)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/metabolism
MH  - DNA Primers
MH  - Endothelium, Vascular/*drug effects/enzymology/metabolism
MH  - Linoleic Acid/*pharmacology
MH  - NF-kappa B/metabolism
MH  - Polychlorinated Biphenyls/*pharmacology
MH  - Swine
EDAT- 1999/01/16 03:13
MHDA- 2000/08/12 11:00
CRDT- 1999/01/16 03:13
PHST- 1999/01/16 03:13 [pubmed]
PHST- 2000/08/12 11:00 [medline]
PHST- 1999/01/16 03:13 [entrez]
AID - 10.1002/(SICI)1099-0461(1999)13:2<83::AID-JBT4>3.0.CO;2-7 [pii]
AID - 10.1002/(sici)1099-0461(1999)13:2<83::aid-jbt4>3.0.co;2-7 [doi]
PST - ppublish
SO  - J Biochem Mol Toxicol. 1999;13(2):83-91. doi:
      10.1002/(sici)1099-0461(1999)13:2<83::aid-jbt4>3.0.co;2-7.

PMID- 9591748
OWN - NLM
STAT- MEDLINE
DCOM- 19980528
LR  - 20190725
IS  - 0026-0495 (Print)
IS  - 0026-0495 (Linking)
VI  - 47
IP  - 5
DP  - 1998 May
TI  - Effect of linoleic acid on endothelial cell inflammatory mediators.
PG  - 566-72
AB  - Selected lipids may influence the inflammatory cascade within the
      vascular endothelium. To test this hypothesis, endothelial cells were
      treated with linoleic acid (18:2, n - 6) for 12 hours and/or tumor
      necrosis factor-alpha (TNF) for 4 hours. For a combined exposure to 18:2
      and TNF (18:2 + TNF), cells were first preenriched with 18:2 for 8 hours
      before exposure to TNF for an additional 4 hours. Exposure to 18:2
      increased cellular oxidative stress, activated nuclear factor-kappaB (NF-
      kappaB), increased interleukin-8 (IL-8) production, and elevated
      intercellular adhesion molecule-1 (ICAM-1) levels. A combined exposure to
      18:2+ TNF resulted in decreased NF-kappaB activation compared with TNF
      treatment alone. In addition, preexposure to 18:2 altered TNF-mediated
      IkappaB-alpha signaling. Within the first 15 minutes of a 90-minute
      period, cytoplasmic levels of IkappaB-alpha decreased more rapidly in
      cells treated with 18:2 + TNF compared with TNF, suggesting translocation
      and activation of NF-kappaB in cultures that were pretreated with 18:2
      before TNF exposure. A combined exposure to 18:2+TNF had various effects
      on IL-8 production and ICAM-1 levels depending on the time of exposure.
      For example, 18:2 + TNF treatment increased ICAM-1 levels at 12 hours but
      decreased ICAM-1 levels at 24 hours compared with treatment with TNF
      alone. These data suggest that selected fatty acids such as 18:2 can
      exert proinflammatory effects and, in addition, may markedly alter TNF-
      mediated inflammatory events.
FAU - Young, V M
AU  - Young VM
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Yang, F
AU  - Yang F
FAU - McClain, C J
AU  - McClain CJ
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Fatty Acids)
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-8)
RN  - 0 (Linoleic Acids)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Cells, Cultured
MH  - DNA-Binding Proteins/drug effects/metabolism
MH  - Endothelium, Vascular/chemistry/*cytology/drug effects
MH  - Fatty Acids/administration & dosage/pharmacology
MH  - Fatty Acids, Unsaturated/administration & dosage/pharmacology
MH  - Gene Expression/genetics
MH  - Humans
MH  - Inflammation Mediators/*metabolism
MH  - Intercellular Adhesion Molecule-1/drug effects/genetics
MH  - Interleukin-8/metabolism
MH  - Linoleic Acids/administration & dosage/*pharmacology
MH  - NF-kappa B/drug effects/metabolism
MH  - Oxidative Stress/drug effects
MH  - Tumor Necrosis Factor-alpha/administration & dosage/pharmacology
MH  - Umbilical Veins/chemistry/cytology/drug effects
EDAT- 1998/05/20 00:00
MHDA- 1998/05/20 00:01
CRDT- 1998/05/20 00:00
PHST- 1998/05/20 00:00 [pubmed]
PHST- 1998/05/20 00:01 [medline]
PHST- 1998/05/20 00:00 [entrez]
AID - S0026-0495(98)90241-4 [pii]
AID - 10.1016/s0026-0495(98)90241-4 [doi]
PST - ppublish
SO  - Metabolism. 1998 May;47(5):566-72. doi: 10.1016/s0026-0495(98)90241-4.

PMID- 9932524
OWN - NLM
STAT- MEDLINE
DCOM- 19990303
LR  - 20201216
IS  - 0306-0225 (Print)
IS  - 0306-0225 (Linking)
VI  - 30
DP  - 1998
TI  - The role of linoleic acid in endothelial cell gene expression.
      Relationship to atherosclerosis.
PG  - 415-36
AB  - There is evidence that linoleic acid plays a critical role in gene
      expression and vascular function as it relates to the pathogenesis of
      atherosclerosis. The lipid environment, particularly linoleic acid and
      its derivatives, of the vascular endothelium may profoundly influence the
      inflammatory response mediated by cytokines. Modulations in the level of
      activity of a select set of endothelial transcription factors appear to
      provide a mechanism for linking lipid/cytokine-mediated vessel wall
      dysfunction, including endothelial cell activation, altered proteoglycan
      metabolism, and endothelial barrier dysfunction, with the onset of
      atherosclerotic lesion formation. The activity of endothelial
      transcription factors is in part regulated by the balance of cellular
      oxidative stress and antioxidant status. Our data suggest that linoleic
      acid can activate the vascular endothelium and may thus be an atherogenic
      fatty acid. Furthermore, nutrients/chemicals with antioxidant properties
      can protect endothelial cells against lipid-mediated cell injury,
      suggesting that oxidative stress is a critical component in linoleic
      acid-mediated gene expression. Our discoveries that linoleic acid can
      influence significantly the cytokine-mediated inflammatory response may
      open new fields in dietary intervention of atherosclerosis.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington
      40536, USA.
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Subcell Biochem
JT  - Sub-cellular biochemistry
JID - 0316571
RN  - 0 (Cytokines)
RN  - 0 (Fatty Acids)
RN  - 0 (NF-kappa B)
RN  - 0 (Proteoglycans)
RN  - 9KJL21T0QJ (Linoleic Acid)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/*etiology/genetics/metabolism
MH  - Cytokines/metabolism
MH  - Endothelium, Vascular/cytology/immunology/*metabolism
MH  - Fatty Acids/chemistry/metabolism
MH  - Gene Expression
MH  - Humans
MH  - Linoleic Acid/*metabolism
MH  - NF-kappa B/metabolism
MH  - Oxidation-Reduction
MH  - Proteoglycans/metabolism
MH  - Signal Transduction
RF  - 93
EDAT- 1999/02/05 00:00
MHDA- 1999/02/05 00:01
CRDT- 1999/02/05 00:00
PHST- 1999/02/05 00:00 [pubmed]
PHST- 1999/02/05 00:01 [medline]
PHST- 1999/02/05 00:00 [entrez]
AID - 10.1007/978-1-4899-1789-8_17 [doi]
PST - ppublish
SO  - Subcell Biochem. 1998;30:415-36. doi: 10.1007/978-1-4899-1789-8_17.

PMID- 9322188
OWN - NLM
STAT- MEDLINE
DCOM- 19971030
LR  - 20190909
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 16
IP  - 5
DP  - 1997 Oct
TI  - Zinc attenuates tumor necrosis factor-mediated activation of
      transcription factors in endothelial cells.
PG  - 411-7
AB  - OBJECTIVE: The objective of the study was to test the hypothesis that
      zinc can protect against endothelial dysfunction by interfering with
      oxidative stress-mediated cellular signaling and subsequent inhibition of
      an endothelial cell inflammatory response. Our approach was to compare
      alterations on molecular and biochemical levels with changes in
      endothelial barrier function that occur in zinc deficient conditions.
      METHODS: To investigate our hypothesis, endothelial cells were exposed to
      zinc deficient media for 2 to 10 days to deplete cellular zinc stores.
      Following this, half of the groups received zinc supplementation (9.2
      microM) for 48 hours. The other half served as zinc deficient controls.
      These cells were then challenged with tumor necrosis factor-alpha (TNF)
      for varying time periods. Nuclear extracts were prepared from cells and
      analyzed for nuclear factor kappa B (NF-kappa B) and activator protein-1
      (AP-1) binding. Media from cells were analyzed for interleukin 8 (IL-8)
      production, and cellular proteins were determined. RESULTS: Zinc
      supplementation resulted in a 74% increase in cellular zinc content. It
      was also shown that a 1.5 hour exposure to TNF (100 U/mL medium)
      significantly increased NF-kappa B and AP-1 binding, which was lowered
      considerably when cells were supplemented with physiological levels of
      zinc. Zinc supplementation also caused a marked attenuation in IL-8
      expression by endothelial cells in response to TNF-mediated cell
      activation. DISCUSSION: Our previous data clearly show that zinc is a
      protective and critical nutrient for maintenance of endothelial
      integrity. The present data suggest that zinc may protect against
      cytokine-mediated activation of oxidative stress sensitive transcription
      factors, upregulation of inflammatory cytokines and endothelial cell
      dysfunction. This may have implications in understanding mechanisms of
      atherosclerosis.
FAU - Connell, P
AU  - Connell P
AD  - Multidisciplinary Doctoral Program in Nutritional Sciences, University of
      Kentucky, Lexington 40506-0054, USA.
FAU - Young, V M
AU  - Young VM
FAU - Toborek, M
AU  - Toborek M
FAU - Cohen, D A
AU  - Cohen DA
FAU - Barve, S
AU  - Barve S
FAU - McClain, C J
AU  - McClain CJ
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Culture Media)
RN  - 0 (Interleukin-8)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
CIN - J Am Coll Nutr. 1997 Oct;16(5):395-6. PMID: 9322185
MH  - Animals
MH  - Cell Nucleus/chemistry/metabolism
MH  - Cells, Cultured
MH  - Culture Media
MH  - Endothelium, Vascular/*metabolism
MH  - Humans
MH  - Interleukin-8/biosynthesis
MH  - NF-kappa B/*metabolism
MH  - Swine
MH  - Transcription Factor AP-1/*metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Zinc/administration & dosage/metabolism/*pharmacology
EDAT- 1997/10/10 00:00
MHDA- 1997/10/10 00:01
CRDT- 1997/10/10 00:00
PHST- 1997/10/10 00:00 [pubmed]
PHST- 1997/10/10 00:01 [medline]
PHST- 1997/10/10 00:00 [entrez]
AID - 10.1080/07315724.1997.10718706 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1997 Oct;16(5):411-7. doi:
      10.1080/07315724.1997.10718706.

PMID- 9109512
OWN - NLM
STAT- MEDLINE
DCOM- 19970515
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 68
IP  - 5
DP  - 1997 May
TI  - Amyloid beta-peptide induces cell monolayer albumin permeability, impairs
      glucose transport, and induces apoptosis in vascular endothelial cells.
PG  - 1870-81
AB  - Amyloid beta-peptide (A beta) is deposited as insoluble fibrils in the
      brain parenchyma and cerebral blood vessels in Alzheimer's disease (AD).
      In addition to neuronal degeneration, cerebral vascular alterations
      indicative of damage to vascular endothelial cells and disruption of the
      blood-brain barrier occur in AD. Here we report that A beta25-35 can
      impair regulatory functions of endothelial cells (ECs) from porcine
      pulmonary artery and induce their death. Subtoxic exposures to A
      beta25-35 induced albumin transfer across EC monolayers and impaired
      glucose transport into ECs. Cell death induced by A beta25-35 was of an
      apoptotic form, characterized by DNA condensation and fragmentation, and
      prevented by inhibitors of macromolecular synthesis and endonucleases.
      The effects of A beta25-35 were specific because A beta1-40 also induced
      apoptosis in ECs with the apoptotic cells localized to the
      microenvironment of A beta1-40 aggregates and because astrocytes did not
      undergo similar changes after exposure to A beta25-35. Damage and death
      of ECs induced by A beta25-35 were attenuated by antioxidants, a calcium
      channel blocker, and a chelator of intracellular calcium, indicating the
      involvement of free radicals and dysregulation of calcium homeostasis.
      The data show that A beta induces increased permeability of EC monolayers
      to macromolecules, impairs glucose transport, and induces apoptosis. If
      similar mechanisms are operative in vivo, then A beta and other
      amyloidogenic peptides may be directly involved in vascular EC damage
      documented in AD and other disorders that involve vascular amyloid
      accumulation.
FAU - Blanc, E M
AU  - Blanc EM
AD  - Sanders Brown Research Center on Aging, University of Kentucky, Lexington
      40536-0230, U.S.A.
FAU - Toborek, M
AU  - Toborek M
FAU - Mark, R J
AU  - Mark RJ
FAU - Hennig, B
AU  - Hennig B
FAU - Mattson, M P
AU  - Mattson MP
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AG10836/AG/NIA NIH HHS/United States
GR  - NS30583/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Free Radicals)
RN  - 0 (Peptide Fragments)
RN  - 0 (Serum Albumin)
RN  - 0 (amyloid beta-protein (25-35))
RN  - IY9XDZ35W2 (Glucose)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Amyloid beta-Peptides/*pharmacology
MH  - Animals
MH  - *Apoptosis
MH  - Biological Transport/drug effects
MH  - Calcium/metabolism
MH  - Cell Death
MH  - Endothelium, Vascular/cytology/*drug effects/*metabolism
MH  - Free Radicals
MH  - Glucose/*metabolism
MH  - Intracellular Membranes/metabolism
MH  - Osmolar Concentration
MH  - Peptide Fragments/pharmacology
MH  - Permeability
MH  - Serum Albumin/*pharmacokinetics
MH  - Swine
EDAT- 1997/05/01 00:00
MHDA- 1997/05/01 00:01
CRDT- 1997/05/01 00:00
PHST- 1997/05/01 00:00 [pubmed]
PHST- 1997/05/01 00:01 [medline]
PHST- 1997/05/01 00:00 [entrez]
AID - 10.1046/j.1471-4159.1997.68051870.x [doi]
PST - ppublish
SO  - J Neurochem. 1997 May;68(5):1870-81. doi:
      10.1046/j.1471-4159.1997.68051870.x.

PMID- 9251245
OWN - NLM
STAT- MEDLINE
DCOM- 19970929
LR  - 20190920
IS  - 1357-2725 (Print)
IS  - 1357-2725 (Linking)
VI  - 29
IP  - 5
DP  - 1997 May
TI  - Oxidative stress mediates monocrotaline-induced alterations in tenascin
      expression in pulmonary artery endothelial cells.
PG  - 775-87
AB  - Oxidative stress may be involved in monocrotaline (MCT)-induced
      endothelial cell injury and upregulation of extracellular matrix proteins
      in the pulmonary vasculature. To test this hypothesis, cytotoxicity,
      expression and distribution of tenascin (TN) as well as cellular
      oxidation were determined in porcine pulmonary artery endothelial cells
      (PAECs) exposed to MCT and/or to an oxygen radical scavenger,
      dimethylthiourea (DMTU). Relative to controls, treatment with 2.5 mM MCT
      for 24 hr produced cytotoxicity as evidenced by changes in cellular
      morphology, cell detachment, hypertrophy, reduction in cellular
      proliferation and severe cytoplasmic vacuolization. Parallel studies
      showed that MCT markedly altered the expression and distribution of TN in
      PAEC as determined by immunocytochemistry. Western analysis showed that
      MCT increased cellular TN content and promoted the appearance of an
      additional, smaller TN isoform. Northern analysis demonstrated an
      increase in the steady-state level of TN-specific mRNA in response to MCT
      treatment. Exposure to MCT also increased the synthesis of cell-
      associated and media-associated TN as determined by immunoprecipitation.
      In addition, MCT increased the intensity of cellular oxidative stress as
      measured by 2,7-dichlorofluorescein fluorescence. Co-treatment with DMTU
      prevented MCT-induced cytotoxicity, alterations in TN distribution and
      content, and reduced the increase in DCF fluorescence. These results
      suggest that MCT-induced cytotoxicity and upregulation of TN are
      mediated, at least in part, by induction of cellular oxidative stress.
FAU - Aziz, S M
AU  - Aziz SM
AD  - Division of Pharmacology and Experimental Therapeutics, University of
      Kentucky, Lexington 40536, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Hennig, B
AU  - Hennig B
FAU - Mattson, M P
AU  - Mattson MP
FAU - Guo, H
AU  - Guo H
FAU - Lipke, D W
AU  - Lipke DW
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0 (Carcinogens)
RN  - 0 (Free Radical Scavengers)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tenascin)
RN  - 73077K8HYV (Monocrotaline)
RN  - 8P30PMD17W (1,3-dimethylthiourea)
RN  - GYV9AM2QAG (Thiourea)
SB  - IM
MH  - Animals
MH  - Carcinogens/*pharmacology
MH  - DNA Fragmentation/drug effects
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Free Radical Scavengers/pharmacology
MH  - Immunoenzyme Techniques
MH  - Monocrotaline/*pharmacology
MH  - *Oxidative Stress
MH  - Pulmonary Artery/cytology/metabolism
MH  - Pulmonary Circulation
MH  - RNA, Messenger/metabolism
MH  - Swine
MH  - Tenascin/genetics/*metabolism
MH  - Thiourea/analogs & derivatives/pharmacology
EDAT- 1997/05/01 00:00
MHDA- 1997/05/01 00:01
CRDT- 1997/05/01 00:00
PHST- 1997/05/01 00:00 [pubmed]
PHST- 1997/05/01 00:01 [medline]
PHST- 1997/05/01 00:00 [entrez]
AID - S1357-2725(97)00010-1 [pii]
AID - 10.1016/s1357-2725(97)00010-1 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 1997 May;29(5):775-87. doi:
      10.1016/s1357-2725(97)00010-1.

PMID- 9013431
OWN - NLM
STAT- MEDLINE
DCOM- 19970502
LR  - 20190909
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 16
IP  - 1
DP  - 1997 Feb
TI  - Aortic antioxidant defense and lipid peroxidation in rabbits fed diets
      supplemented with different animal and plant fats.
PG  - 32-8
AB  - OBJECTIVE: To test the hypothesis that dietary fats, depending on the fat
      source, may modulate aortic lipid peroxidation and antioxidant
      protection. METHODS: Rabbits were fed a low fat (LF, 2 g/100 g corn oil)
      diet or LF enriched with 16 g/100 g (w/w) of corn oil (CO), corn oil plus
      cholesterol (23.5 mg/100 g diet, CO + C), bovine milk fat (MF), chicken
      fat (CF), beef tallow (BT) or lard (L). After a 30-day feeding period,
      aortic lipid peroxidation, as well as antioxidant enzymes and vitamin E
      were measured. RESULTS: In rabbits fed CO or L, aortic TBARS (a marker of
      lipid peroxidation) and total glutathione concentrations were greater but
      vitamin E levels were lower compared with the LF treatment. Moreover, in
      rabbits fed CO, elevated activities of glutathione peroxidase and
      glutathione reductase but lowered activity of superoxide dismutase were
      observed. In rabbits fed the remaining high fat diets, including the CO +
      C diet, aortic lipid peroxidation and antioxidant activities/levels did
      not differ from those fed LF. Feeding rabbits high-fat diets for 30 days
      did not induce aortic lipid deposition. CONCLUSIONS: The present results
      indicate CO, and possibly L, as the fat sources which significantly
      increase aortic oxidative stress. Because long-term disturbances in redox
      status may be implicated in atherogenesis, excessive dietary intake of CO
      or L may significantly contribute to the injury of the vessel wall.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington
      40536, USA.
FAU - Feldman, D L
AU  - Feldman DL
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Cholesterol, Dietary)
RN  - 0 (Dietary Fats)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 1406-18-4 (Vitamin E)
RN  - 8001-30-7 (Corn Oil)
SB  - IM
MH  - Animal Nutritional Physiological Phenomena
MH  - Animals
MH  - Arteriosclerosis/etiology
MH  - Cattle
MH  - Chickens
MH  - Cholesterol, Dietary/administration & dosage/toxicity
MH  - Corn Oil/administration & dosage/toxicity
MH  - Dietary Fats/administration & dosage/analysis/*toxicity
MH  - Lipid Peroxidation/*physiology
MH  - Male
MH  - Oxidative Stress
MH  - Rabbits
MH  - Random Allocation
MH  - Swine
MH  - Thiobarbituric Acid Reactive Substances/*analysis
MH  - Vitamin E/*blood
EDAT- 1997/02/01 00:00
MHDA- 1997/02/01 00:01
CRDT- 1997/02/01 00:00
PHST- 1997/02/01 00:00 [pubmed]
PHST- 1997/02/01 00:01 [medline]
PHST- 1997/02/01 00:00 [entrez]
AID - 10.1080/07315724.1997.10718646 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1997 Feb;16(1):32-8. doi: 10.1080/07315724.1997.10718646.

PMID- 8951801
OWN - NLM
STAT- MEDLINE
DCOM- 19970307
LR  - 20190822
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 47
IP  - 5
DP  - 1996 Nov
TI  - Is endothelial cell autocrine production of tumor necrosis factor a
      mediator of lipid-induced endothelial dysfunction?
PG  - 377-82
AB  - Injury or dysfunction of the vascular endothelium is one of the first
      events in the development of atherosclerosis. Individual lipids, e.g.
      fatty acids or lipoproteins, are among the most critical factors which
      may induce injury to the endothelium. Selected fatty acids, such as
      linoleic acid, can disrupt endothelial barrier function and increase the
      inflammatory response of the vascular endothelium. The mechanisms of
      these processes are not fully understood. It is hypothesized that
      selected fatty acids can mediate the autocrine production of tumor
      necrosis factor-alpha in endothelial cells. This will activate a variety
      of intracellular signaling pathways and further potentiate endothelial
      injury initially induced by fatty acids.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington
      40536, USA.
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Lipoproteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/etiology/*physiopathology
MH  - Cell Adhesion Molecules/physiology
MH  - Endothelium, Vascular/injuries/*physiology/*physiopathology
MH  - Fatty Acids, Nonesterified/metabolism
MH  - Humans
MH  - Lipoproteins/metabolism
MH  - Models, Cardiovascular
MH  - NF-kappa B/metabolism
MH  - Signal Transduction
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - S0306-9877(96)90217-0 [pii]
AID - 10.1016/s0306-9877(96)90217-0 [doi]
PST - ppublish
SO  - Med Hypotheses. 1996 Nov;47(5):377-82. doi:
      10.1016/s0306-9877(96)90217-0.

PMID- 8936496
OWN - NLM
STAT- MEDLINE
DCOM- 19970314
LR  - 20190914
IS  - 0899-9007 (Print)
IS  - 0899-9007 (Linking)
VI  - 12
IP  - 10
DP  - 1996 Oct
TI  - Antiatherogenic properties of zinc: implications in endothelial cell
      metabolism.
PG  - 711-7
AB  - Zinc is an essential component of biomembranes and is necessary for
      maintenance of membrane structure and function. There is evidence that
      zinc can provide antiatherogenic properties by preventing metabolic
      physiologic derangements of the vascular endothelium. Because of its
      antioxidant and membrane-stabilizing properties, zinc appears to be
      crucial for the protection against cell-destabilizing agents such as
      polyunsaturated lipids and inflammatory cytokines. Zinc also may be
      antiatherogenic by interfering with signaling pathways involved in
      apoptosis. Most importantly, we have evidence that zinc can protect
      against inflammatory cytokine-mediated activation of oxidative stress-
      responsive transcription factors, such as nuclear factor kappa B and
      AP-1. It is very likely that certain lipids and zinc deficiency may
      potentiate the cytokine-mediated inflammatory response and endothelial
      cell dysfunction in atherosclerosis. Thus, the antiatherogenic role of
      zinc appears to be in its ability to inhibit oxidative stress-responsive
      factors involved in disruption of endothelial integrity and
      atherosclerosis. We discuss antiatherogenic properties of zinc with a
      focus on endothelial cell metabolism.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Mcclain, C J
AU  - Mcclain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
GR  - MO1 RR02602-08/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Nutrition
JT  - Nutrition (Burbank, Los Angeles County, Calif.)
JID - 8802712
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Arteriosclerosis/*etiology/prevention & control
MH  - Cytokines/*physiology
MH  - Endothelium, Vascular/*cytology/metabolism/pathology
MH  - Humans
MH  - NF-kappa B/*antagonists & inhibitors
MH  - Zinc/*physiology
RF  - 90
EDAT- 1996/10/01 00:00
MHDA- 1996/10/01 00:01
CRDT- 1996/10/01 00:00
PHST- 1996/10/01 00:00 [pubmed]
PHST- 1996/10/01 00:01 [medline]
PHST- 1996/10/01 00:00 [entrez]
AID - S0899900796001256 [pii]
AID - 10.1016/s0899-9007(96)00125-6 [doi]
PST - ppublish
SO  - Nutrition. 1996 Oct;12(10):711-7. doi: 10.1016/s0899-9007(96)00125-6.

PMID- 8829090
OWN - NLM
STAT- MEDLINE
DCOM- 19961219
LR  - 20190909
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 15
IP  - 4
DP  - 1996 Aug
TI  - Nutritional implications in vascular endothelial cell metabolism.
PG  - 345-58
AB  - Endothelial cells interact with blood components and the abluminal
      tissues, thus playing an active role in many aspects of vascular
      function. Numerous physiologic and pathophysiologic stimuli are often
      mediated by nutrients that can contribute to the overall functions of
      endothelial cells in the regulation of vascular tone, coagulation,
      cellular growth, immune and inflammatory responses. Therefore, nutrient-
      mediated functional changes of the endothelium and the underlying tissues
      may be significantly involved in disease processes such as
      atherosclerosis. There is evidence that individual nutrients or nutrient
      derivatives may either provoke or prevent metabolic and physiologic
      perturbations of the vascular endothelium. Diets high in fat and/or
      calories are considered a risk factor for the development of
      atherosclerosis. Our research has shown that certain diet-derived lipids
      and their derivatives can disrupt normal endothelial integrity, thus
      reducing the ability of the endothelium to act as a selectively permeable
      barrier to blood components. Mechanisms underlying fatty acid-mediated
      endothelial cell dysfunction may be related to changes in fatty acid
      composition as well as to an increase in cellular oxidative stress.
      Selective lipid accumulation and fatty acid changes in endothelial cells
      can modulate membrane fluidity, proteoglycan metabolism and signal
      transduction mechanisms. Most importantly, dietary fats rich in certain
      unsaturated fatty acids, may be atherogenic by enhancing the formation of
      reactive oxygen intermediates. A subsequent imbalance in cellular
      oxidative stress/antioxidant status can activate oxidative stress-
      responsive transcription factors, which in turn may promote cytokine
      production, expression of adhesion molecules on the surface of
      endothelial cells, and thus intensify an inflammatory response in
      atherosclerosis. Our data also suggest that certain nutrients, which have
      antioxidant and/or membrane stabilizing properties, can protect
      endothelial cells by interfering with lipid/cytokine-mediated endothelial
      cell dysfunction. These findings contribute to the understanding of the
      interactive role of dietary fats with inflammatory components, as well as
      with nutrients that exhibit antiatherogenic properties, in the
      development of atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition, University of Kentucky 40506-0054, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - McClain, C J
AU  - McClain CJ
FAU - Diana, J N
AU  - Diana JN
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL 36552/HL/NHLBI NIH HHS/United States
GR  - MO1 RR02602-08/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Antioxidants)
RN  - 0 (Cytokines)
RN  - 0 (Dietary Fats)
RN  - 0 (Proteoglycans)
RN  - 1406-18-4 (Vitamin E)
RN  - GAN16C9B8O (Glutathione)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Antioxidants/*metabolism
MH  - Arteriosclerosis/etiology/immunology
MH  - Cytokines/metabolism
MH  - Dietary Fats/*adverse effects
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Extracellular Matrix/metabolism
MH  - Glutathione/metabolism
MH  - Humans
MH  - Oxidation-Reduction
MH  - *Oxidative Stress
MH  - Proteoglycans/metabolism
MH  - Vitamin E/physiology
MH  - Zinc/physiology
RF  - 138
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - 10.1080/07315724.1996.10718609 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1996 Aug;15(4):345-58. doi:
      10.1080/07315724.1996.10718609.

PMID- 8935445
OWN - NLM
STAT- MEDLINE
DCOM- 19961231
LR  - 20190909
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 15
IP  - 3
DP  - 1996 Jun
TI  - Susceptibility to hepatic oxidative stress in rabbits fed different
      animal and plant fats.
PG  - 289-94
AB  - OBJECTIVE: This study was designed to determine the effect of diets
      enriched with plant and animal fats on oxidative stress and glutathione
      metabolism in rabbit liver tissues. This study was conducted to
      investigate whether the type of dietary fat will impact fatty acid
      composition and oxidant/antioxidant status in tissues. METHODS: Rabbits
      were fed diets containing 2 g corn oil/100 g diet (low fat diet, LF) and
      LF supplemented with 16 g/100 g diet of either corn oil (CO), CO with
      added cholesterol (CO + C), milk fat (MF), chicken fat (CF), beef tallow
      (BT), or lard (L) for 30 days. After the feeding period, livers were
      analyzed for total fatty acid composition, thiobarbituric acid reactive
      substances (TBARS), conjugated dienes, and reduced glutathione (GSH), as
      well as for activities of glutathione peroxidase (GP) and glutathione
      reductase (GR). Moreover, to fully determine the oxidative stability and
      free radical trapping capacity, TBARS levels were measured after
      additional exposure of liver homogenates to 10 mM 2,2(1)-azo-bis-
      amidinopropane- hydrochloride (AAPH) for up to 21 hours. RESULTS: CO and
      CF, but not saturated fats such as MF, increased liver conjugated diene
      and TBARS levels and decreased liver GSH levels and GP activity. In
      tissues additionally exposed to AAPH, the maximum oxidation, measured as
      TBARS, was reached between 6 and 7 hours of treatment, independent of
      dietary fat. In addition, there was a marked effect of AAPH on the
      maximum rate of TBARS formation with the following descending order: CO >
      CF > CO + C > L > MF > BT > LF. This high susceptibility to oxidative
      stress in liver tissues of rabbits fed the CO diet may be explained in
      part by the significant elevation in linoleic acid (18:2n-6). DISCUSSION:
      There appears to be an inverse correlation between dietary fat-mediated
      oxidative stress and antioxidant enzyme activities. The present data
      suggest that high levels of dietary unsaturated fat should be avoided if
      oxidative stress is a critical issue in nutrition-related diseases. In
      addition, these data support our hypothesis that diets rich in MF provide
      a lipid environment with low susceptibility to oxidative stress.
FAU - Slim, R M
AU  - Slim RM
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Watkins, B A
AU  - Watkins BA
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL36552/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Amidines)
RN  - 0 (Antioxidants)
RN  - 0 (Cholesterol, Dietary)
RN  - 0 (Dietary Fats)
RN  - 0 (Fats)
RN  - 0 (Fatty Acids)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 7381JDR72F (2,2'-azobis(2-amidinopropane))
RN  - 8001-30-7 (Corn Oil)
RN  - 98HPY76U4W (tallow)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.8.1.7 (Glutathione Reductase)
RN  - GAN16C9B8O (Glutathione)
RN  - SI6O3IW77Z (lard)
SB  - IM
MH  - Amidines/pharmacology
MH  - Animals
MH  - Antioxidants/analysis
MH  - Cattle
MH  - Chickens
MH  - Cholesterol, Dietary
MH  - Corn Oil/metabolism
MH  - Dietary Fats/*metabolism
MH  - Fats
MH  - Fatty Acids/analysis
MH  - Glutathione/analysis/*metabolism
MH  - Glutathione Peroxidase/analysis/metabolism
MH  - Glutathione Reductase/analysis/metabolism
MH  - Lipid Peroxidation
MH  - Liver/chemistry/drug effects/enzymology/*metabolism
MH  - Male
MH  - Oxidative Stress/*physiology
MH  - Rabbits
MH  - Thiobarbituric Acid Reactive Substances/analysis
EDAT- 1996/06/01 00:00
MHDA- 1996/06/01 00:01
CRDT- 1996/06/01 00:00
PHST- 1996/06/01 00:00 [pubmed]
PHST- 1996/06/01 00:01 [medline]
PHST- 1996/06/01 00:00 [entrez]
AID - 10.1080/07315724.1996.10718600 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1996 Jun;15(3):289-94. doi:
      10.1080/07315724.1996.10718600.

PMID- 8862533
OWN - NLM
STAT- MEDLINE
DCOM- 19961213
LR  - 20190914
IS  - 0899-9007 (Print)
IS  - 0899-9007 (Linking)
VI  - 12
IP  - 4
DP  - 1996 Apr
TI  - Growth requirements of endothelial cells in culture: variations in serum
      and amino acid concentrations.
PG  - 266-70
AB  - Endothelial cell growth in vitro is limited to the availability of
      nutrients from commercially available media and added serum. Nutrients,
      such as amino acids, are chiefly derived from the cell culture medium,
      rather than from added serum, and optimal endothelial cell growth may be
      dependent on amino acid levels in the culture media. To test this
      hypothesis, porcine pulmonary artery-derived endothelial cells were
      exposed to culture medium 199 (M199), amino acid-deficient M199 (dM199),
      as well as dM199 supplemented with amino acids. Cell protein was similar
      in cells cultured for 3 d in M199 supplemented with 1, 3, 5 or 10% bovine
      calf serum, respectively. Addition of amino acid solutions (L-amino acids
      [Laa], DL-amino acids [DLaa], 2Laa, or Laa+glutamine) to dM199
      demonstrated a cell dependence for optimal growth on the type of amino
      acids as well as on the total available nitrogen in the media. Compared
      with M199, dM199 supplemented with Laa only partially supported long-term
      growth of endothelial cells in culture. On the other hand, dM199
      supplemented with either 2Laa, DLaa, or Laa+ glutamine was superior over
      M199 with regard to endothelial cell growth. The addition of
      Laa+glutamine to dM199 was most growth-supporting, with an increase of
      over 2.6-fold in total cell protein compared with cells cultured with
      M199. These results suggest that, in addition to the presence of
      essential amino acids, total available nitrogen in culture media may be a
      critical factor for optimal endothelial cell growth.
FAU - Gorman, L
AU  - Gorman L
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington, Kentucky 40506, USA.
FAU - Mercer, L P
AU  - Mercer LP
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Nutrition
JT  - Nutrition (Burbank, Los Angeles County, Calif.)
JID - 8802712
RN  - 0 (Amino Acids)
RN  - 0 (Culture Media)
RN  - 0 (Proteins)
SB  - IM
MH  - Amino Acids/analysis/metabolism
MH  - Animals
MH  - Cattle
MH  - Cell Division
MH  - Cells, Cultured
MH  - Culture Media/*chemistry
MH  - Endothelium, Vascular/*cytology/metabolism
MH  - Evaluation Studies as Topic
MH  - Proteins/metabolism
MH  - Swine
EDAT- 1996/04/01 00:00
MHDA- 1996/04/01 00:01
CRDT- 1996/04/01 00:00
PHST- 1996/04/01 00:00 [pubmed]
PHST- 1996/04/01 00:01 [medline]
PHST- 1996/04/01 00:00 [entrez]
AID - S0899-9007(96)90854-0 [pii]
AID - 10.1016/s0899-9007(96)90854-0 [doi]
PST - ppublish
SO  - Nutrition. 1996 Apr;12(4):266-70. doi: 10.1016/s0899-9007(96)90854-0.

PMID- 8602587
OWN - NLM
STAT- MEDLINE
DCOM- 19960503
LR  - 20180330
IS  - 0002-9165 (Print)
IS  - 0002-9165 (Linking)
VI  - 63
IP  - 3
DP  - 1996 Mar
TI  - Linoleic acid activates nuclear transcription factor-kappa B (NF-kappa B)
      and induces NF-kappa B-dependent transcription in cultured endothelial
      cells.
PG  - 322-8
AB  - High dietary intakes of unsaturated fats may be atherogenic by disrupting
      normal functions of the vascular endothelium, due in part to the ability
      of linoleic acid (18:2n-6) to contribute to an increase in cellular
      oxidative stress and related injurious events. Exposing endothelial cells
      to 90 micromol linoleic acid/L for 6 h resulted in a significant increase
      in lipid hydroperoxides that coincided wih an increase in intracellular
      calcium concentrations. Treatment with this fatty acid caused an initial
      decrease in glutathione concentrations, which was followed by an increase
      at later time points. Most importantly, a significant activation of the
      oxidative stress-sensitive nuclear transcription factor-kappa B (NF-kappa
      B) was achieved after a 6-h exposure to 18:2n-6, which is the time point
      at which maximal depletion of cellular glutathione was observed. The
      fatty acid-mediated NF-kappa B activation was accompanied by induction of
      NF-kappa B-dependent transcription, as measured by chloramphenicol
      acetyltransferase (CAT) assay of an NF-kappa B-responsive promoter
      construct. Pretreatment of endothelial cells with vitamin E and N-acetyl
      cysteine inhibited the fatty acid-induced activation of NF-kappa B and
      formation of lipid hydroperoxides. These data suggest that oxidative
      stress-induced cellular changes are critical early events in fatty acid-
      mediated endothelial cell dysfunction.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Joshi-Barve, S
AU  - Joshi-Barve S
FAU - Barger, S W
AU  - Barger SW
FAU - Barve, S
AU  - Barve S
FAU - Mattson, M P
AU  - Mattson MP
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1P01 HL36552/HL/NHLBI NIH HHS/United States
GR  - M01 RR02602-08/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
RN  - 0 (Linoleic Acids)
RN  - 0 (NF-kappa B)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - GAN16C9B8O (Glutathione)
RN  - SY7Q814VUP (Calcium)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Calcium/metabolism
MH  - Cells, Cultured
MH  - Endothelium, Vascular/drug effects/*metabolism
MH  - Glutathione/metabolism
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Lipid Peroxidation/drug effects
MH  - Molecular Sequence Data
MH  - NF-kappa B/*physiology
MH  - Pulmonary Artery
MH  - Swine
MH  - Transcription, Genetic/*drug effects
EDAT- 1996/03/01 00:00
MHDA- 1996/03/01 00:01
CRDT- 1996/03/01 00:00
PHST- 1996/03/01 00:00 [pubmed]
PHST- 1996/03/01 00:01 [medline]
PHST- 1996/03/01 00:00 [entrez]
AID - 10.1093/ajcn/63.3.322 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 1996 Mar;63(3):322-8. doi: 10.1093/ajcn/63.3.322.

PMID- 8645361
OWN - NLM
STAT- MEDLINE
DCOM- 19960718
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 120
IP  - 1-2
DP  - 1996 Feb
TI  - Oxidized lipid-mediated alterations in proteoglycan metabolism in
      cultured pulmonary endothelial cells.
PG  - 199-208
AB  - Compared to cholesterol or linoleic acid (18:2), oxidized lipids such as
      cholestan-3 beta, 5 alpha, 6 beta-triol (triol) and hydroperoxy linoleic
      acid (HPODE) markedly impair endothelial barrier function in culture
      [Hennig and Boissonneault, 1987; Hennig et al. 1986]. Because
      proteoglycans contribute to vascular permeability properties, the effects
      of cholesterol and 18:2 and their oxidation products, triol and HPODE, on
      endothelial proteoglycan metabolism were determined. While cholesterol
      was without effect, a concentration-dependent decrease in cellular
      proteoglycans (measured by 35S incorporation) was observed after exposure
      to triol. Compared to control cultures, cholesterol reduced mRNA levels
      for the proteoglycans, perlecan and biglycan. Triol had a similar effect
      on biglycan but not an perlecan mRNA levels. Compared to 18:2, 1,3 and 5
      microM HPODE depressed cellular proteoglycans. Perlecan mRNA levels were
      reduced more by HPODE when compared to 18:2. Biglycan mRNA levels were
      reduced by 3 microM, but not by 5 microM HPODE. These data demonstrate
      that oxidized lipids such as triol and HPODE can decrease cellular
      proteoglycan metabolism in endothelial monolayers and alter mRNA levels
      of major specific proteoglycans in a concentration-dependent manner. This
      may have implications in lipid-mediated disruption of endothelial barrier
      function and atherosclerosis.
FAU - Ramasamy, S
AU  - Ramasamy S
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506, USA.
FAU - Lipke, D W
AU  - Lipke DW
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Guo, H
AU  - Guo H
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Biglycan)
RN  - 0 (Cholestanols)
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (Heparan Sulfate Proteoglycans)
RN  - 0 (Linoleic Acids)
RN  - 0 (Proteoglycans)
RN  - 0 (RNA, Messenger)
RN  - 115510-05-9 (cholestane-3,5,6-triol)
RN  - 143343-95-7 (8-hydroperoxylinoleic acid)
RN  - 143972-95-6 (perlecan)
RN  - 9050-30-0 (Heparitin Sulfate)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - 9KJL21T0QJ (Linoleic Acid)
SB  - IM
MH  - Animals
MH  - Biglycan
MH  - Capillary Permeability/drug effects
MH  - Cells, Cultured
MH  - Cholestanols/*pharmacology
MH  - Cholesterol/*pharmacology
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Extracellular Matrix Proteins
MH  - Gene Expression Regulation/drug effects
MH  - *Heparan Sulfate Proteoglycans
MH  - Heparitin Sulfate/biosynthesis/genetics
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Lipid Peroxidation/drug effects
MH  - Oxidation-Reduction
MH  - Oxidative Stress
MH  - Proteoglycans/biosynthesis/genetics/*metabolism
MH  - Pulmonary Artery/*cytology
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Swine
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - 0021-9150(95)05702-1 [pii]
AID - 10.1016/0021-9150(95)05702-1 [doi]
PST - ppublish
SO  - Atherosclerosis. 1996 Feb;120(1-2):199-208. doi:
      10.1016/0021-9150(95)05702-1.

PMID- 8820108
OWN - NLM
STAT- MEDLINE
DCOM- 19961206
LR  - 20210217
IS  - 0022-2275 (Print)
IS  - 0022-2275 (Linking)
VI  - 37
IP  - 1
DP  - 1996 Jan
TI  - Linoleic acid and TNF-alpha cross-amplify oxidative injury and
      dysfunction of endothelial cells.
PG  - 123-35
AB  - Factors implicated in the development of atherosclerosis include
      metabolic alterations of the endothelium induced by certain lipids and
      inflammatory cytokines. To study the hypothesis that the combined
      presence of unsaturated fatty acids and inflammatory cytokines may cross-
      amplify their individual injurious effects, cultured endothelial cells
      were treated with 90 mu M of linoleic acid (18:2 n-6) and/or 20 ng/ml
      (100 U/ml) of tumor necrosis factor-alpha (TNF) for up to 24 h.
      Disturbances in endothelial cell metabolism were determined by measuring
      cellular oxidative stress, oxidative stress-inducible nuclear factor-
      kappa B (NF-kappa B) and NF-kappa B-related transcription, intracellular
      calcium levels, and endothelial barrier function reflected by
      transendothelial albumin movement. Both 18:2 and TNF increased cellular
      oxidation, intracellular calcium, and endothelial barrier permeability.
      These changes were cross-amplified in cells treated both with 18:2 and
      TNF, compared with 18:2 or TNF alone. In contrast, a combined exposure to
      18:2 and TNF did not potentiate effects mediated by 18:2 or TNF alone on
      NF-kappa B activation or NF-kappa B-related transcription. Pretreatment
      with 25 mu M vitamin E attenuated 18:2 and/or TNF-mediated endothelial
      cell dysfunction. These results suggest that certain unsaturated fatty
      acids can potentiate TNF-mediated endothelial cell dysfunction and that
      oxidative stress may be partially responsible for these metabolic events.
      These findings have implications for understanding lipid-mediated
      inflammatory responses in atherosclerosis.
FAU - Toborek, M
AU  - Toborek M
AD  - Departments of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Barger, S W
AU  - Barger SW
FAU - Mattson, M P
AU  - Mattson MP
FAU - Barve, S
AU  - Barve S
FAU - McClain, C J
AU  - McClain CJ
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Lipid Res
JT  - Journal of lipid research
JID - 0376606
RN  - 0 (Linoleic Acids)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1406-18-4 (Vitamin E)
RN  - 9KJL21T0QJ (Linoleic Acid)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/etiology
MH  - Dose-Response Relationship, Drug
MH  - Drug Interactions
MH  - Endothelium, Vascular/cytology/*drug effects
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Oxidative Stress/*drug effects
MH  - Pulmonary Artery/cytology
MH  - Swine
MH  - Transcription, Genetic
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Vitamin E/pharmacology
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - S0022-2275(20)37641-0 [pii]
PST - ppublish
SO  - J Lipid Res. 1996 Jan;37(1):123-35.

PMID- 8596769
OWN - NLM
STAT- MEDLINE
DCOM- 19960418
LR  - 20190914
IS  - 0952-3278 (Print)
IS  - 0952-3278 (Linking)
VI  - 53
IP  - 5
DP  - 1995 Nov
TI  - Role of fatty acids and eicosanoids in modulating proteoglycan metabolism
      in endothelial cells.
PG  - 315-24
AB  - Endothelial cell dysfunction is considered to be a critical event in the
      etiology of atherosclerosis. Thus, the preservation of endothelial
      structure and function are a prerequisite for normal control of vascular
      permeability properties, mediation of both inflammatory and immunologic
      responses and the general 'communication' between blood-borne cells and
      abluminal tissues. Many of these properties can be influenced by
      proteoglycans present in vascular tissues. There is evidence that
      selected lipids can be atherogenic by altering endothelial proteoglycan
      metabolism. Little is known about the role of fatty acids in modulating
      proteoglycan composition in endothelial cells. Data suggest, however,
      that linoleic acid in particular can adversely alter proteoglycan
      metabolism, which may be related to an imbalance in eicosanoid synthesis
      patterns. These events could be sufficient to disrupt normal endothelial
      barrier function, initiate smooth muscle migration and proliferation, and
      result in other metabolic dysfunctions associated with the etiology of
      vascular diseases such as atherosclerosis. Thus, the focus of this review
      is on fatty acids and eicosanoids as they may alter proteoglycan
      metabolism of vascular tissues and in particular of the endothelium.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nurition, College of Pharmacy, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Lipke, D W
AU  - Lipke DW
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Ramasamy, S
AU  - Ramasamy S
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - Scotland
TA  - Prostaglandins Leukot Essent Fatty Acids
JT  - Prostaglandins, leukotrienes, and essential fatty acids
JID - 8802730
RN  - 0 (Cytokines)
RN  - 0 (Eicosanoids)
RN  - 0 (Fatty Acids)
RN  - 0 (Proteoglycans)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/etiology
MH  - Cytokines/physiology
MH  - Eicosanoids/*physiology
MH  - Endothelium, Vascular/*metabolism
MH  - Fatty Acids/*physiology
MH  - Humans
MH  - Proteoglycans/*physiology
RF  - 114
EDAT- 1995/11/01 00:00
MHDA- 1995/11/01 00:01
CRDT- 1995/11/01 00:00
PHST- 1995/11/01 00:00 [pubmed]
PHST- 1995/11/01 00:01 [medline]
PHST- 1995/11/01 00:00 [entrez]
AID - 10.1016/0952-3278(95)90050-0 [doi]
PST - ppublish
SO  - Prostaglandins Leukot Essent Fatty Acids. 1995 Nov;53(5):315-24. doi:
      10.1016/0952-3278(95)90050-0.

PMID- 8801863
OWN - NLM
STAT- MEDLINE
DCOM- 19960930
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 117
IP  - 2
DP  - 1995 Oct
TI  - Role of glutathione redox cycle in TNF-alpha-mediated endothelial cell
      dysfunction.
PG  - 179-88
AB  - Modulation of the glutathione redox cycle may influence tumor necrosis
      factor-alpha (TNF)-mediated disturbances of endothelial integrity. To
      test this hypothesis, normal endothelial cells or cells with either
      increased or decreased glutathione levels were exposed to 100 ng (500 U)
      TNF/ml. Increased glutathione levels were achieved by exposure to 0.2 mM
      N-acetyl-L-cysteine (NAC) and decreased glutathione levels by exposure to
      25 microM buthionine sulfoximine (BSO). Several components of the
      glutathione redox cycle as well as markers of endothelial integrity, such
      as cytoplasmic free calcium and transendothelial albumin transfer, were
      measured in the treated cells. Exposure to TNF for 3 and 6 h decreased
      total glutathione levels, which was followed by an increase at later time
      points. Moreover, treatment with TNF resulted in an increase in the ratio
      of oxidized to reduced glutathione, intracellular free calcium, albumin
      transfer across endothelial monolayers and lipid hydroperoxides. However,
      an increase in lipid hydroperoxides was seen only when endothelial cell
      cultures were supplemented with iron. BSO treatment increased
      susceptibility of endothelial cells to TNF-mediated metabolic
      disturbances. On the other hand, NAC partially protected against TNF-
      induced injury to endothelial monolayers. Our results demonstrate the
      important role of the glutathione redox cycle in TNF-mediated
      disturbances of the vascular endothelium and indicate that modulation of
      glutathione levels may potentiate the injurious effects of this
      inflammatory cytokine.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Barger, S W
AU  - Barger SW
FAU - Mattson, M P
AU  - Mattson MP
FAU - McClain, C J
AU  - McClain CJ
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Lipid Peroxides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1982-67-8 (Methionine Sulfoximine)
RN  - 5072-26-4 (Buthionine Sulfoximine)
RN  - GAN16C9B8O (Glutathione)
RN  - SY7Q814VUP (Calcium)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Animals
MH  - Buthionine Sulfoximine
MH  - Calcium/metabolism
MH  - Cell Membrane Permeability
MH  - Endothelium, Vascular/*metabolism/physiology
MH  - Glutathione/*metabolism
MH  - Lipid Peroxides/metabolism
MH  - Methionine Sulfoximine/analogs & derivatives/pharmacology
MH  - Oxidation-Reduction
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/pharmacology/*physiology
EDAT- 1995/10/01 00:00
MHDA- 1995/10/01 00:01
CRDT- 1995/10/01 00:00
PHST- 1995/10/01 00:00 [pubmed]
PHST- 1995/10/01 00:01 [medline]
PHST- 1995/10/01 00:00 [entrez]
AID - 0021-9150(95)05568-H [pii]
AID - 10.1016/0021-9150(95)05568-h [doi]
PST - ppublish
SO  - Atherosclerosis. 1995 Oct;117(2):179-88. doi:
      10.1016/0021-9150(95)05568-h.

PMID- 7643238
OWN - NLM
STAT- MEDLINE
DCOM- 19950915
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 125
IP  - 8
DP  - 1995 Aug
TI  - Animal and plant fats selectively modulate oxidizability of rabbit LDL
      and LDL-mediated disruption of endothelial barrier function.
PG  - 2045-54
AB  - Enrichment of lipoproteins with fatty acids derived from animal and/or
      plant fats may modify the oxidizability of lipoproteins and their effects
      on endothelial barrier function. To test this hypothesis, rabbits were
      fed for 30 days diets containing 2 g corn oil/100 g diet (low fat diet)
      or low fat supplemented with 16 g/100 g diet of corn oil, corn oil with
      added cholesterol, milk fat, chicken fat, beef tallow or lard. Compared
      with those fed the low fat, serum and LDL cholesterol concentrations were
      significantly lower in rabbits fed corn oil and greater in animals fed
      corn oil with added cholesterol or chicken fat. In contrast to the
      cholesterol data, lipid hydroperoxide levels were highest in oxidized LDL
      derived from rabbits fed corn oil or lard. LDL vitamin E levels were
      highest in rabbits fed corn oil with added cholesterol. The significant
      elevations in linoleic acid [18:2(n-6)] in serum and LDL may partially
      explain the high oxidizability of LDL in rabbits fed corn oil. LDL
      isolated from animals fed corn oil, lard or milk fat had significantly
      greater albumin transfer across cultured endothelial monolayers compared
      with those of the low fat diet group. Their oxidative modification
      further contributed to endothelial barrier dysfunction. Dietary
      cholesterol supplementation to the corn oil diet decreased oxidizability
      of LDL and partially protected the oxidized LDL-mediated endothelial cell
      dysfunction as compared with the corn oil diet group. These data suggest
      that beef tallow and chicken fat are the least atherogenic fats if
      oxidative modification of LDL is a critical issue in atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506, USA.
FAU - Toborek, M
AU  - Toborek M
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Shantha, N C
AU  - Shantha NC
FAU - Decker, E A
AU  - Decker EA
FAU - Oeltgen, P R
AU  - Oeltgen PR
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1P01 HL36552/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Dietary Fats)
RN  - 0 (Fatty Acids)
RN  - 0 (Lipoproteins, LDL)
RN  - 1406-18-4 (Vitamin E)
RN  - 8001-30-7 (Corn Oil)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - SI6O3IW77Z (lard)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cholesterol/metabolism/*pharmacology
MH  - Corn Oil/administration & dosage/pharmacology
MH  - Dietary Fats/administration & dosage/*pharmacology
MH  - Endothelium/drug effects/physiology
MH  - Fatty Acids/blood
MH  - Lipoproteins, LDL/drug effects/*metabolism/physiology
MH  - Male
MH  - Oxidation-Reduction/drug effects
MH  - Rabbits
MH  - Swine
MH  - Vitamin E/blood
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - 10.1093/jn/125.8.2045 [doi]
PST - ppublish
SO  - J Nutr. 1995 Aug;125(8):2045-54. doi: 10.1093/jn/125.8.2045.

PMID- 7645031
OWN - NLM
STAT- MEDLINE
DCOM- 19950921
LR  - 20161123
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 133
IP  - 2
DP  - 1995 Aug
TI  - Fumonisin B1 alters sphingolipid metabolism and disrupts the barrier
      function of endothelial cells in culture.
PG  - 343-8
AB  - Fumonisins are responsible for at least two diseases of veterinary
      importance (equine leukoencephalomalacia and porcine pulmonary edema) and
      are carcinogenic for experimental animals and, perhaps, humans. They have
      been found to disrupt sphingolipid metabolism in many types of cells,
      including hepatocytes, neurons, and renal cells. In this study,
      endothelial cells form porcine pulmonary arteries were cultured on
      micropore filters as a model for the endothelial barrier, and barrier
      function was quantitated as the movement of albumin across the
      endothelial monolayers. Fumonisin B1 increased the amount of free
      sphinganine by 20- to 30-fold within 3 hr, as expected for inhibition of
      sphinganine (sphingosine) N-acyltransferase by this mycotoxin. At 30 to
      50 microM, fumonisin B1 doubled the rate of albumin transfer across
      endothelial monolayers; however, there was no loss of cell viability
      based on morphology or trypan blue exclusion. When 15 microM D-erythro-
      sphinganine was added to the cells, the rate of albumin transfer also
      doubled (after 24 hr incubation) without a loss of viability; however,
      this treatment increased the cellular level of sphinganine by > 100-fold.
      Addition of 25 microM sphinganine caused even greater albumin transfer,
      but also resulted in significant cell death. These results establish that
      fumonisin B1 and D-erythro-sphinganine allow accelerated passage of
      macromolecules across the endothelium. Fumonisin B1 alters sphingolipid
      biosynthesis with an elevation of sphinganine in the cells which may, at
      least in part, explain the observed disruption of endothelial barrier
      function.
FAU - Ramasamy, S
AU  - Ramasamy S
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington, USA.
FAU - Wang, E
AU  - Wang E
FAU - Hennig, B
AU  - Hennig B
FAU - Merrill, A H Jr
AU  - Merrill AH Jr
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - GM46368/GM/NIGMS NIH HHS/United States
GR  - HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Albumins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Fumonisins)
RN  - 0 (Mycotoxins)
RN  - 3ZZM97XZ32 (fumonisin B1)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - I2ZWO3LS3M (Trypan Blue)
RN  - NGZ37HRE42 (Sphingosine)
RN  - OWA98U788S (safingol)
SB  - IM
MH  - Albumins/metabolism
MH  - Analysis of Variance
MH  - Animals
MH  - Cell Communication/drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Enzyme Inhibitors/analysis/*metabolism
MH  - *Fumonisins
MH  - Mycotoxins/*toxicity
MH  - Protein Kinase C/antagonists & inhibitors
MH  - Pulmonary Artery
MH  - Signal Transduction/drug effects
MH  - Sphingosine/*analogs & derivatives/analysis/*metabolism
MH  - Swine
MH  - Trypan Blue/metabolism
EDAT- 1995/08/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - S0041-008X(85)71159-3 [pii]
AID - 10.1006/taap.1995.1159 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 1995 Aug;133(2):343-8. doi:
      10.1006/taap.1995.1159.

PMID- 8568836
OWN - NLM
STAT- MEDLINE
DCOM- 19960304
LR  - 20191101
IS  - 0887-2082 (Print)
IS  - 0887-2082 (Linking)
VI  - 10
IP  - 4
DP  - 1995 Aug
TI  - Exposure to polychlorinated biphenyls causes endothelial cell
      dysfunction.
PG  - 219-26
AB  - Environmental chemicals, such as polychlorinated biphenyls (PCBs), may be
      atherogenic by disrupting normal functions of the vascular endothelium.
      To investigate this hypothesis, porcine pulmonary artery-derived
      endothelial cells were exposed to 3,3',4,4'-tetrachlorobiphenyl (PCB 77),
      2,3,4,4',5-pentachlorobiphenyl (PCB 114), or
      2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) for up to 24 hours. These
      PCBs were selected for their varying binding avidities with the aryl
      hydrocarbon (Ah) receptor and differences in their induction of
      cytochrome P450. PCB 77 and PCB 114 significantly disrupted, in a dose-
      dependent manner, endothelial barrier function by allowing an increase in
      albumin transfer across endothelial monolayers. These PCBs also
      contributed markedly to cellular oxidative stress, as measured by
      2,7-dichlorofluorescin (DCF) fluorescence and lipid hydroperoxides, and
      caused a significant increase in intracellular calcium ([Ca2+]i) levels.
      Enhanced oxidative stress and [Ca2+]i in PCB 77- and PCB 114-treated
      cells were accompanied by increased activity and content of cytochrome
      P450 1A and by a decrease in the vitamin E content in the culture medium.
      In contrast to the effects of PCB 77 and PCB 114, cell exposure to PCB
      153 had no effect on cellular oxidation, [Ca2+]i, or endothelial barrier
      function. These results suggest that certain PCBs may play a role in the
      development of atherosclerosis by causing endothelial cell dysfunction
      and a decrease in the barrier function of the vascular endothelium. It is
      possible that interaction of PCBs with the Ah receptor and activation of
      the cytochrome P450 1A subfamily are involved in this pathology.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054, USA.
FAU - Barger, S W
AU  - Barger SW
FAU - Mattson, M P
AU  - Mattson MP
FAU - Espandiari, P
AU  - Espandiari P
FAU - Robertson, L W
AU  - Robertson LW
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - CA57423/CA/NCI NIH HHS/United States
GR  - HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biochem Toxicol
JT  - Journal of biochemical toxicology
JID - 8700114
RN  - 1406-18-4 (Vitamin E)
RN  - 9035-51-2 (Cytochrome P-450 Enzyme System)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/metabolism
MH  - Cells, Cultured
MH  - Cytochrome P-450 Enzyme System/biosynthesis
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Enzyme Induction
MH  - Oxidative Stress/drug effects
MH  - Permeability
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Structure-Activity Relationship
MH  - Swine
MH  - Vitamin E/analysis
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - 10.1002/jbt.2570100406 [doi]
PST - ppublish
SO  - J Biochem Toxicol. 1995 Aug;10(4):219-26. doi: 10.1002/jbt.2570100406.

PMID- 7648422
OWN - NLM
STAT- MEDLINE
DCOM- 19950928
LR  - 20190920
IS  - 1357-2725 (Print)
IS  - 1357-2725 (Linking)
VI  - 27
IP  - 7
DP  - 1995 Jul
TI  - Electron spin resonance studies of fatty acid-induced alterations in
      membrane fluidity in cultured endothelial cells.
PG  - 665-73
AB  - Endothelial cell dysfunction has been implicated in the development of
      atherosclerosis. Of vital importance to the maintenance of endothelial
      cell integrity is the preservation of membrane functional and structural
      properties, such as membrane fluidity. The aim of this study was to
      develop a model for studying the relationship between endothelial cell
      integrity and membrane fluidity alterations in a well-defined cell
      culture setting. Alterations in membrane fluidity were assessed using
      electron spin resonance after labeling endothelial cells with the lipid-
      specific spin labels, CAT-16 and 12-nitroxide stearic acid. Endothelial
      cells were exposed to various 18-carbon fatty acids, i.e. stearic (18:0),
      oleic (18:1), linoleic (18:2), or linolenic (18:3), in addition to
      lipolyzed HDL (L-HDL) and benzyl alcohol. Membrane phospholipid fatty
      acid composition of endothelial cells supplemented with these fatty acids
      was analyzed using gas chromatography. All fatty acids, except 18:0,
      decreased membrane fluidity. A relationship between membrane fluidity and
      fatty acid compositional alterations in cellular phospholipids was
      observed. In particular, the arachidonic acid content decreased following
      exposure to 18:1, 18:2, or 18:3. Exposure of endothelial cells to L-HDL,
      lipoprotein particles which contain high levels of 18:1 and 18:2, also
      decreased membrane fluidity. The stabilization of cytoskeletal actin
      filaments by phalloidin partially prevented 18:2-induced increases in
      albumin transfer, thus implicating a cytoskeletal involvement in the
      18:2-induced membrane fluidity changes involved in endothelial cell
      dysfunction. The present study shows that the exposure of endothelial
      cells to various lipids causes membrane fluidity alterations which may
      contribute to endothelial cell dysfunction and atherosclerosis.
FAU - Cader, A A
AU  - Cader AA
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington, USA.
FAU - Butterfield, D A
AU  - Butterfield DA
FAU - Watkins, B A
AU  - Watkins BA
FAU - CHung, B H
AU  - CHung BH
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AG 10836/AG/NIA NIH HHS/United States
GR  - HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0 (Benzyl Alcohols)
RN  - 0 (Fatty Acids)
RN  - 0 (Lipoproteins, HDL)
RN  - 0 (Phospholipids)
RN  - 0 (Spin Labels)
RN  - 1406-18-4 (Vitamin E)
RN  - 17466-45-4 (Phalloidine)
RN  - LKG8494WBH (Benzyl Alcohol)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/etiology
MH  - Benzyl Alcohol
MH  - Benzyl Alcohols/pharmacology
MH  - Cell Membrane/chemistry
MH  - Cells, Cultured
MH  - Electron Spin Resonance Spectroscopy
MH  - Endothelium, Vascular/*cytology
MH  - Fatty Acids/analysis/*pharmacology
MH  - Lipoproteins, HDL/pharmacology
MH  - Membrane Fluidity/*drug effects
MH  - Molecular Structure
MH  - Phalloidine/pharmacology
MH  - Phospholipids/pharmacology
MH  - Pulmonary Artery
MH  - Spin Labels
MH  - Swine
MH  - Vitamin E/pharmacology
EDAT- 1995/07/01 00:00
MHDA- 1995/07/01 00:01
CRDT- 1995/07/01 00:00
PHST- 1995/07/01 00:00 [pubmed]
PHST- 1995/07/01 00:01 [medline]
PHST- 1995/07/01 00:00 [entrez]
AID - 135727259500036O [pii]
AID - 10.1016/1357-2725(95)00036-o [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 1995 Jul;27(7):665-73. doi:
      10.1016/1357-2725(95)00036-o.

PMID- 7749257
OWN - NLM
STAT- MEDLINE
DCOM- 19950622
LR  - 20161019
IS  - 0899-9007 (Print)
IS  - 0899-9007 (Linking)
VI  - 11
IP  - 1 Suppl
DP  - 1995 Jan-Feb
TI  - Zinc and endothelial function.
PG  - 117-20
AB  - Zinc (Zn), an essential trace element, has antioxidant functions,
      stabilizes membranes, and plays a role in the activity of a host of Zn
      metalloenzymes. Zn deficiency has been shown to increase erythrocyte
      fragility, decrease the Zn content of the erythrocyte membrane, and alter
      erythrocyte membrane fluidity. Recent studies have shown that Zn
      deficiency induced by various mechanisms disrupts endothelial barrier
      cell function in vitro, and this was corrected with Zn supplementation.
      Moreover, physiological amounts of Zn attenuated the barrier dysfunction
      produced by the inflammatory cytokine tumor necrosis factor. These data
      have important implications for acute vascular processes, e.g., adult
      respiratory distress syndrome, and chronic vascular processes, e.g.,
      atherosclerosis. The mechanisms by which Zn may affect endothelial cell
      function and attenuate cytokine-induced endothelial cell dysfunction are
      important areas of continuing investigation.
FAU - McClain, C
AU  - McClain C
AD  - Department of Medicine, University of Kentucky, Lexington, USA.
FAU - Morris, P
AU  - Morris P
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1P01NS31220-01A1/NS/NINDS NIH HHS/United States
GR  - 3M01-2602-07S1/PHS HHS/United States
GR  - M01-RR-02602-07/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Nutrition
JT  - Nutrition (Burbank, Los Angeles County, Calif.)
JID - 8802712
RN  - 0 (Cytokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Arteriosclerosis
MH  - Cytokines/physiology
MH  - Endothelium, Vascular/*physiology
MH  - Erythrocytes/physiology
MH  - Humans
MH  - Tumor Necrosis Factor-alpha
MH  - Zinc/administration & dosage/deficiency/*physiology
RF  - 35
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PST - ppublish
SO  - Nutrition. 1995 Jan-Feb;11(1 Suppl):117-20.

PMID- 7814444
OWN - NLM
STAT- MEDLINE
DCOM- 19950203
LR  - 20161019
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 162
IP  - 1
DP  - 1995 Jan
TI  - Tumor necrosis factor reduces proteoglycan synthesis in cultured
      endothelial cells.
PG  - 119-26
AB  - Tumor necrosis factor (TNF)-induced disruption of vascular endothelial
      barrier function may be due in part to alterations in proteoglycan
      metabolism. To test this hypothesis, confluent endothelial cell
      monolayers were exposed for 24 h to 500 or 1,000 U of TNF per milliliter
      of culture medium together with 20 microCi Na2 35SO4. HPLC anion-exchange
      separation of proteoglycans secreted into media of control as well as
      TNF-treated cultures revealed one major peak (representing 95% of total
      radioactivity) and one minor peak (representing 5% of total
      radioactivity), which eluted at 0.6 and 0.9 M NaCl, respectively. One
      single peak was obtained from control as well as TNF-treated endothelial
      cell monolayers and eluted at 1.2 M NaCl. TNF treatment did not change
      the total quantity of radioactive proteoglycans secreted into the media
      but significantly decreased the amount of proteoglycans in endothelial
      cell monolayers. However, TNF treatment did not alter the size or
      glycosaminoglycan (GAG) composition of the proteoglycans either in the
      media or in the cell monolayers. In addition, mRNA levels of specific
      proteoglycans, perlecan and biglycan, were measured upon TNF treatment,
      using Northern analysis. TNF treatment caused a dose-dependent decrease
      in mRNA levels for the core proteins of perlecan, a major heparan sulfate
      proteoglycan (HSPG), and biglycan in endothelial cultures. These results
      suggest that TNF decreases production of proteoglycans and alters normal
      endothelial cell proteoglycan metabolism which may be sufficient to
      impair endothelial barrier function.
FAU - Ramasamy, S
AU  - Ramasamy S
AD  - Departments of Nutrition, College of Pharmacy, University of Kentucky,
      Lexington 40506.
FAU - Lipke, D W
AU  - Lipke DW
FAU - McClain, C J
AU  - McClain CJ
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1P01HL36552/HL/NHLBI NIH HHS/United States
GR  - MO1 RR02602-08/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Glycosaminoglycans)
RN  - 0 (Proteoglycans)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/*cytology/*metabolism
MH  - Glycosaminoglycans/analysis/metabolism
MH  - Proteoglycans/analysis/genetics/*metabolism
MH  - RNA, Messenger/analysis/genetics
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
AID - 10.1002/jcp.1041620114 [doi]
PST - ppublish
SO  - J Cell Physiol. 1995 Jan;162(1):119-26. doi: 10.1002/jcp.1041620114.

PMID- 8077569
OWN - NLM
STAT- MEDLINE
DCOM- 19940930
LR  - 20190909
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 13
IP  - 3
DP  - 1994 Jun
TI  - Influence of nutrients and cytokines on endothelial cell metabolism.
PG  - 224-31
AB  - The vascular endothelium plays an active role in physiological processes
      such as hemostasis, regulation of vessel tone and vascular permeability.
      Cell injury, or any event which disrupts endothelial integrity and thus
      endothelial permeability properties, may be involved in the early events
      leading to atherosclerotic lesion formation. Because of its constant
      exposure to blood components, including prooxidants, diet-derived fats
      and their derivatives, the endothelium is susceptible to oxidative stress
      and to injury mediated by blood lipid components. It is likely that these
      events potentiate the overall inflammatory response to injury by
      increasing cytokine release in proximity to the endothelium, which then
      could further disrupt endothelial barrier function. Even though
      mechanisms associated with lipid/cytokine-mediated endothelial cell
      dysfunction are unclear, our data suggest that they may be both oxidative
      and non-oxidative in nature. We suggest that dietary fats, rich in
      certain unsaturated fatty acids are atherogenic by enhancing the
      formation of reactive oxygen intermediates. These intermediates can
      activate oxidative stress-responsive transcription factors, such as NF-
      kappa B, which in turn may promote cytokine production, adhesion molecule
      expression and ultimately endothelial barrier dysfunction. The resulting
      disturbances in endothelial integrity possibly allow increased
      penetration of cholesterol-rich lipoprotein remnants into the arterial
      wall, a critical event in the etiology of atherosclerosis. Data suggest
      that certain nutrients, which have antioxidant and/or membrane
      stabilizing properties, protect endothelial cells by interfering with the
      above proposed mechanisms of endothelial cell dysfunction.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Diana, J N
AU  - Diana JN
FAU - Toborek, M
AU  - Toborek M
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
GR  - MO1 RR02602-08/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
SB  - IM
MH  - Arteriosclerosis/metabolism
MH  - Cell Adhesion Molecules/physiology
MH  - Cytokines/*physiology
MH  - Endothelium, Vascular/*metabolism
MH  - Humans
MH  - Lipid Metabolism
MH  - NF-kappa B/metabolism
MH  - Nutritional Physiological Phenomena/*physiology
MH  - Oxidation-Reduction
RF  - 73
EDAT- 1994/06/01 00:00
MHDA- 1994/06/01 00:01
CRDT- 1994/06/01 00:00
PHST- 1994/06/01 00:00 [pubmed]
PHST- 1994/06/01 00:01 [medline]
PHST- 1994/06/01 00:00 [entrez]
AID - 10.1080/07315724.1994.10718401 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1994 Jun;13(3):224-31. doi:
      10.1080/07315724.1994.10718401.

PMID- 8013743
OWN - NLM
STAT- MEDLINE
DCOM- 19940725
LR  - 20190830
IS  - 0020-711X (Print)
IS  - 0020-711X (Linking)
VI  - 26
IP  - 4
DP  - 1994 Apr
TI  - Disruption of endothelial barrier function: relationship to fluidity of
      membrane extracellular lamella.
PG  - 575-81
AB  - 1. Endothelial cells were cultured in tissue culture flasks or on
      microcarrier beads and labeled with a lipid specific spin-label. 2.
      Exposure of endothelial cells to benzyl alcohol caused a dose- and time-
      dependent increase in membrane fluidity using electron spin resonance
      (ESR). Maximum fluidity was reached after a 5-min exposure to 100 mM
      benzyl alcohol. 3. Albumin permeability across endothelial cells cultured
      on micropore filters was used as an indication of endothelial monolayer
      integrity. 4. A significant increase in permeability occurred with 50 mM
      benzyl alcohol. Maximal albumin permeability was reached after a 5-min
      exposure to 100 mM benzyl alcohol.
FAU - Alvarado, A
AU  - Alvarado A
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Butterfield, D A
AU  - Butterfield DA
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - AG10836/AG/NIA NIH HHS/United States
GR  - HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Int J Biochem
JT  - The International journal of biochemistry
JID - 0250365
RN  - 0 (Albumins)
RN  - 0 (Benzyl Alcohols)
RN  - 0 (Spin Labels)
RN  - LKG8494WBH (Benzyl Alcohol)
SB  - IM
MH  - Albumins/pharmacokinetics
MH  - Animals
MH  - Benzyl Alcohol
MH  - Benzyl Alcohols/pharmacology
MH  - Cell Membrane Permeability/drug effects
MH  - Cells, Cultured
MH  - Electron Spin Resonance Spectroscopy
MH  - Endothelium, Vascular/drug effects/*physiology
MH  - *Membrane Fluidity/drug effects
MH  - Spin Labels
MH  - Swine
EDAT- 1994/04/01 00:00
MHDA- 1994/04/01 00:01
CRDT- 1994/04/01 00:00
PHST- 1994/04/01 00:00 [pubmed]
PHST- 1994/04/01 00:01 [medline]
PHST- 1994/04/01 00:00 [entrez]
AID - 10.1016/0020-711x(94)90016-7 [doi]
PST - ppublish
SO  - Int J Biochem. 1994 Apr;26(4):575-81. doi: 10.1016/0020-711x(94)90016-7.

PMID- 8068200
OWN - NLM
STAT- MEDLINE
DCOM- 19940926
LR  - 20190116
IS  - 1040-8398 (Print)
IS  - 1040-8398 (Linking)
VI  - 34
IP  - 3
DP  - 1994
TI  - Nutrition, endothelial cell metabolism, and atherosclerosis.
PG  - 253-82
AB  - The vascular endothelium that forms an interface between the blood and
      the surrounding tissues is continuously exposed to both physiologic and
      pathophysiologic stimuli. These stimuli are often mediated by nutrients
      that can contribute to the overall function of the endothelial cell in
      the regulation of vascular tone, coagulation and fibrinolysis, cellular
      growth and differentiation, and immune and inflammatory responses.
      Therefore, nutrient-mediated functional changes of the endothelium and
      the underlying tissues may be significantly involved in the
      atherosclerotic disease process. There is evidence that individual
      nutrients or nutrient derivatives may either provoke or prevent metabolic
      and physiologic perturbations of the vascular endothelium. Preservation
      of nutrients that exhibit antiatherogenic properties may, therefore, be a
      critical issue in the preparation and processing of foods. This review
      focuses on selected nutrients as they affect endothelial cell metabolism
      and their possible implications in atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Toborek, M
AU  - Toborek M
FAU - Cader, A A
AU  - Cader AA
FAU - Decker, E A
AU  - Decker EA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Crit Rev Food Sci Nutr
JT  - Critical reviews in food science and nutrition
JID - 8914818
RN  - 0 (Amino Acids)
RN  - 0 (Fatty Acids)
RN  - 0 (Minerals)
RN  - 0 (Vitamins)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Amino Acids/metabolism/pharmacology
MH  - Animals
MH  - Arteriosclerosis/*metabolism/*prevention & control
MH  - Cholesterol/blood/metabolism
MH  - Endothelium, Vascular/*cytology/drug effects/*metabolism
MH  - Fatty Acids/metabolism/pharmacology
MH  - Glucose/metabolism/pharmacology
MH  - Humans
MH  - Minerals/metabolism/pharmacology
MH  - *Nutritional Physiological Phenomena
MH  - Vitamins/metabolism/pharmacology
RF  - 317
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.1080/10408399409527663 [doi]
PST - ppublish
SO  - Crit Rev Food Sci Nutr. 1994;34(3):253-82. doi:
      10.1080/10408399409527663.

PMID- 8279404
OWN - NLM
STAT- MEDLINE
DCOM- 19940207
LR  - 20180330
IS  - 0002-9165 (Print)
IS  - 0002-9165 (Linking)
VI  - 59
IP  - 1
DP  - 1994 Jan
TI  - Fatty acid-mediated effects on the glutathione redox cycle in cultured
      endothelial cells.
PG  - 60-5
AB  - Endothelial barrier dysfunction after exposure to fatty acids may be
      mediated by disturbances in antioxidant protection. To evaluate this
      hypothesis, components of the glutathione redox cycle such as total,
      reduced, and oxidized glutathione and glutathione reductase and
      peroxidase were measured in cultured porcine endothelial cells exposed to
      90 mumol/L of stearic acid (18:0), oleic acid (18:1 omega-9), linoleic
      acid (18:2 omega-6), linolenic acid (18:3 omega-3), and/or buthionine
      sulfoximine (BSO). Treatment with fatty acids caused an initial decrease
      in glutathione concentrations, which was followed by an increase at later
      time points. The most marked changes in glutathione redox cycle
      components were induced by 18:2. BSO increased susceptibility of fatty
      acid-mediated injury to endothelial monolayers. The results indicate a
      fundamental role of the glutathione redox cycle in protection against
      fatty acid-mediated injury to the vascular endothelium.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL-36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
RN  - 0 (Fatty Acids)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.8.1.7 (Glutathione Reductase)
RN  - GAN16C9B8O (Glutathione)
SB  - AIM
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Fatty Acids/*pharmacology
MH  - Glutathione/*metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Glutathione Reductase/metabolism
MH  - Oxidation-Reduction/drug effects
MH  - Swine
MH  - Time Factors
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.1093/ajcn/59.1.60 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 1994 Jan;59(1):60-5. doi: 10.1093/ajcn/59.1.60.

PMID- 8292102
OWN - NLM
STAT- MEDLINE
DCOM- 19940223
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 103
IP  - 2
DP  - 1993 Nov
TI  - Proteoglycans and endothelial barrier function: effect of linoleic acid
      exposure to porcine pulmonary artery endothelial cells.
PG  - 279-90
AB  - Certain fatty acids induce changes in endothelial barrier function which
      may be mediated by alterations in normal proteoglycan
      synthesis/metabolism. To test this hypothesis, pulmonary artery derived
      endothelial cells were treated with media supplemented with linoleic acid
      (18:2), and/or a known proteoglycan synthesis inhibitor, beta-D-xyloside.
      Independent exposure to 1 mM beta-D-xyloside or 90 microM 18:2 increased
      albumin transfer, i.e., decreased barrier function, when compared with
      control cultures. 18:2 and beta-D-xyloside increased albumin transfer
      additively, suggesting that the mechanisms by which 18:2 and beta-D-
      xyloside alter the proteoglycan metabolism are different. Compared with
      the control group, treatment with 18:2 inhibited proteoglycan synthesis,
      decreased anionic properties of heparan sulfate proteoglycans in the cell
      monolayers and caused the release of a unique chondroitin sulfate
      proteoglycan into the culture media. Treatment with beta-D-xyloside
      caused an increased incorporation of radioactive sulfate into
      glycosaminoglycans but inhibited proteoglycan synthesis. These results
      suggest that the fatty acid- and beta-D-xyloside-induced impairment in
      endothelial barrier function may involve changes in the synthesis,
      release and physicochemical properties of proteoglycans.
FAU - Ramasamy, S
AU  - Ramasamy S
AD  - Department of Nutrition, College of Pharmacy, University of Kentucky,
      Lexington 40506.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Lipke, D W
AU  - Lipke DW
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Albumins)
RN  - 0 (Glycosides)
RN  - 0 (Linoleic Acids)
RN  - 0 (Proteoglycans)
RN  - 0 (xylosides)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - YOW8V9698H (Dimethyl Sulfoxide)
SB  - IM
MH  - Albumins/metabolism
MH  - Animals
MH  - Biological Transport
MH  - Cells, Cultured
MH  - Chromatography, Ion Exchange
MH  - Dimethyl Sulfoxide/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/*metabolism
MH  - Glycosides/pharmacology
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Proteoglycans/*metabolism
MH  - Pulmonary Artery/*metabolism
MH  - Swine
EDAT- 1993/11/01 00:00
MHDA- 1993/11/01 00:01
CRDT- 1993/11/01 00:00
PHST- 1993/11/01 00:00 [pubmed]
PHST- 1993/11/01 00:01 [medline]
PHST- 1993/11/01 00:00 [entrez]
AID - 0021-9150(93)90270-5 [pii]
AID - 10.1016/0021-9150(93)90270-5 [doi]
PST - ppublish
SO  - Atherosclerosis. 1993 Nov;103(2):279-90. doi:
      10.1016/0021-9150(93)90270-5.

PMID- 8320562
OWN - NLM
STAT- MEDLINE
DCOM- 19930803
LR  - 20191210
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 123
IP  - 7
DP  - 1993 Jul
TI  - Selective disruption of endothelial barrier function in culture by pure
      fatty acids and fatty acids derived from animal and plant fats.
PG  - 1208-16
AB  - Endothelial cell integrity has been suggested to play a role in the
      development of atherosclerosis. The effects of fatty acids on endothelial
      barrier function were tested by measuring albumin transport across
      endothelial monolayers cultured on polycarbonate filters. Compared with
      control cultures, a 24-h exposure to 90 mumol/L lauric (12:0) and
      linoleic acid (18:2) but not to butyric (4:0), hexanoic (6:0), octanoic
      (8:0), decanoic (10:0), myristic (14:0), palmitic (16:0) or stearic acid
      (18:0) caused an increase in albumin transfer across endothelial
      monolayers. Selective enrichment of a "physiological" serum fatty acid
      mixture (FA-Mix; 90 mumol/L) with 90 mumol/L of 12:0 or 18:2
      significantly increased albumin transfer, whereas enrichment with 90
      mumol/L of 4:0, 16:0 or 18:0 significantly decreased albumin transfer
      relative to 180 mumol/L FA-Mix. Only 12:0- or 18:2-treated cultures
      showed increased Ca(++)-ATPase activity and the presence of lipid
      droplets. Fatty acids (60 mumol/L) extracted from butter fat and beef
      tallow had no effect on albumin transfer, whereas fatty acids extracted
      from chicken fat and corn oil consistently disrupted endothelial barrier
      function. This fat-induced disruption of endothelial barrier function
      seems to be related to the amount of 18:2 present in each fat source.
      These data indicate that unsaturated fats cause cellular perturbations
      that result in a decrease in endothelial barrier function in this model
      system, and that high dietary levels of unsaturated fats may be
      detrimental to cell integrity.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Ramasamy, S
AU  - Ramasamy S
FAU - Alvarado, A
AU  - Alvarado A
FAU - Shantha, N C
AU  - Shantha NC
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Decker, E A
AU  - Decker EA
FAU - Watkins, B A
AU  - Watkins BA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Albumins)
RN  - 0 (Fatty Acids)
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (Plant Extracts)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
SB  - IM
MH  - Albumins/metabolism
MH  - Animals
MH  - Calcium-Transporting ATPases/metabolism
MH  - Cattle
MH  - Cell Membrane/drug effects/metabolism
MH  - Cells, Cultured
MH  - Chickens
MH  - Endothelium, Vascular/*drug effects/enzymology/metabolism
MH  - Fatty Acids/*pharmacology
MH  - Fatty Acids, Unsaturated/*pharmacology
MH  - Plant Extracts/*pharmacology
MH  - Swine
EDAT- 1993/07/01 00:00
MHDA- 1993/07/01 00:01
CRDT- 1993/07/01 00:00
PHST- 1993/07/01 00:00 [pubmed]
PHST- 1993/07/01 00:01 [medline]
PHST- 1993/07/01 00:00 [entrez]
AID - 10.1093/jn/123.7.1208 [doi]
PST - ppublish
SO  - J Nutr. 1993 Jul;123(7):1208-16. doi: 10.1093/jn/123.7.1208.

PMID- 8403435
OWN - NLM
STAT- MEDLINE
DCOM- 19931028
LR  - 20190706
IS  - 0009-8981 (Print)
IS  - 0009-8981 (Linking)
VI  - 215
IP  - 2
DP  - 1993 Jun 16
TI  - Vitamin E attenuates induction of elastase-like activity by tumor
      necrosis factor-alpha, cholestan-3 beta,5 alpha,6 beta-triol and linoleic
      acid in cultured endothelial cells.
PG  - 201-11
AB  - Disturbances in arterial wall elastin metabolism appear to be important
      factors in atherosclerosis development. To evaluate this hypothesis,
      elastase-like activity was determined in cultured endothelial cells and
      their surrounding media after exposure to tumor necrosis factor-alpha
      (TNF), cholestan-3 beta,5 alpha,6 beta-triol (Triol) and linoleic acid
      (18:2). Significant increases in elastase-like activity both in the cells
      and in the media were observed when subconfluent endothelial cells were
      treated with 12 microM Triol, 500 U TNF/ml, or 90 microM 18:2, for 72 h
      in the presence of 5% calf serum. Even higher activities were measured
      when endothelial cells were seeded directly into media enriched with
      18:2, TNF or Triol and treated for 72 h. Vitamin E supplementation (25
      microM) attenuated elastase-like activity in cells and media, independent
      of treatment. These results suggest that elastase-like enzyme induction
      in endothelial cells may be involved in cellular perturbations induced by
      certain lipids and cytokines. Vitamin E may provide a protective function
      by preventing the induction of elastolytic enzymes. This may have
      implications in elastin metabolism and atherosclerosis.
FAU - Toborek, M
AU  - Toborek M
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL-36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Clin Chim Acta
JT  - Clinica chimica acta; international journal of clinical chemistry
JID - 1302422
RN  - 0 (Cholestanols)
RN  - 0 (Culture Media)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Linoleic Acids)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 115510-05-9 (cholestane-3,5,6-triol)
RN  - 1406-18-4 (Vitamin E)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 3.4.21.36 (Pancreatic Elastase)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cholestanols/*pharmacology
MH  - Culture Media
MH  - Endothelium, Vascular/drug effects/*enzymology
MH  - Enzyme Induction/drug effects
MH  - Hypolipidemic Agents/pharmacology
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Pancreatic Elastase/*biosynthesis
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Vitamin E/*pharmacology
EDAT- 1993/06/16 00:00
MHDA- 1993/06/16 00:01
CRDT- 1993/06/16 00:00
PHST- 1993/06/16 00:00 [pubmed]
PHST- 1993/06/16 00:01 [medline]
PHST- 1993/06/16 00:00 [entrez]
AID - 0009-8981(93)90126-O [pii]
AID - 10.1016/0009-8981(93)90126-o [doi]
PST - ppublish
SO  - Clin Chim Acta. 1993 Jun 16;215(2):201-11. doi:
      10.1016/0009-8981(93)90126-o.

PMID- 8389399
OWN - NLM
STAT- MEDLINE
DCOM- 19930706
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 123
IP  - 6
DP  - 1993 Jun
TI  - Zinc protects against tumor necrosis factor-induced disruption of porcine
      endothelial cell monolayer integrity.
PG  - 1003-9
AB  - Some nutrients influence the metabolic response of cytokines such as
      tumor necrosis factor. Inadequate levels of the essential trace element
      zinc may play a role in tumor necrosis factor-induced disruption of the
      vascular endothelial barrier function. To test this hypothesis,
      endothelial cells cultured on polycarbonate filters or culture plates
      were exposed to six different treatments for 3 d: medium 199 enriched
      with 5% fetal bovine serum (control), control+two levels of supplemental
      zinc (7.7 and 12.3 mumol/L medium), tumor necrosis factor (5 x 10(5) U/L)
      and tumor necrosis factor+the two levels of Zn as noted previously.
      Endothelial barrier function, expressed as albumin transfer across
      cultured endothelial monolayers, was not affected by Zn enrichment alone.
      Tumor necrosis factor treatment significantly increased albumin transfer
      compared with control cultures. The lower concentration of Zn partially
      and the higher concentration totally prevented the tumor necrosis factor-
      induced increase in albumin transfer. The increase in cytosolic release
      of [3H]adenine (marker of cell injury) induced by tumor necrosis factor
      was prevented by added Zn. Tumor necrosis factor treatment significantly
      decreased angiotensin-converting enzyme activity, and tumor necrosis
      factor also decreased activities of two other membrane-bound enzymes,
      total ATPase and Ca(2+)-ATPase. These activities all were restored by Zn
      enrichment. Tumor necrosis factor treatment caused a decrease in cellular
      Zn concentration, which was prevented when the culture media were
      enriched with Zn. These data suggest that an important relationship
      exists between Zn status and tumor necrosis factor-induced endothelial
      cell dysfunction.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington.
FAU - Wang, Y
AU  - Wang Y
FAU - Ramasamy, S
AU  - Ramasamy S
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
GR  - MO1 RR 02602-08/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Albumins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - EC 3.6.1.- (Adenosine Triphosphatases)
RN  - J41CSQ7QDS (Zinc)
RN  - JAC85A2161 (Adenine)
SB  - IM
MH  - Adenine/metabolism
MH  - Adenosine Triphosphatases/drug effects/metabolism
MH  - Albumins/metabolism
MH  - Animals
MH  - Cell Membrane Permeability/*drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Membrane Potentials/*drug effects
MH  - Peptidyl-Dipeptidase A/drug effects/metabolism
MH  - Pulmonary Artery/cytology
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Zinc/metabolism/*pharmacology
EDAT- 1993/06/01 00:00
MHDA- 1993/06/01 00:01
CRDT- 1993/06/01 00:00
PHST- 1993/06/01 00:00 [pubmed]
PHST- 1993/06/01 00:01 [medline]
PHST- 1993/06/01 00:00 [entrez]
AID - 10.1093/jn/123.6.1003 [doi]
PST - ppublish
SO  - J Nutr. 1993 Jun;123(6):1003-9. doi: 10.1093/jn/123.6.1003.

PMID- 8512265
OWN - NLM
STAT- MEDLINE
DCOM- 19930715
LR  - 20190616
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 686
DP  - 1993 May 28
TI  - Function of vitamin E and zinc in maintaining endothelial integrity.
      Implications in atherosclerosis.
PG  - 99-109; discussion 109-11
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington.
FAU - McClain, C J
AU  - McClain CJ
FAU - Diana, J N
AU  - Diana JN
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Antioxidants)
RN  - 0 (Cytokines)
RN  - 1406-18-4 (Vitamin E)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Arteriosclerosis/*etiology
MH  - Cytokines/physiology
MH  - Diet
MH  - Endothelium, Vascular/*drug effects
MH  - Humans
MH  - Myocardial Ischemia/etiology
MH  - Smoking/adverse effects
MH  - Vitamin E/*pharmacology
MH  - Zinc/*pharmacology
RF  - 73
EDAT- 1993/05/28 00:00
MHDA- 1993/05/28 00:01
CRDT- 1993/05/28 00:00
PHST- 1993/05/28 00:00 [pubmed]
PHST- 1993/05/28 00:01 [medline]
PHST- 1993/05/28 00:00 [entrez]
AID - 10.1111/j.1749-6632.1993.tb39161.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 1993 May 28;686:99-109; discussion 109-11. doi:
      10.1111/j.1749-6632.1993.tb39161.x.

PMID- 8372227
OWN - NLM
STAT- MEDLINE
DCOM- 19931008
LR  - 20161025
IS  - 0306-0632 (Print)
IS  - 0306-0632 (Linking)
VI  - 17
IP  - 2
DP  - 1993 Apr-Jun
TI  - Nutrition and endothelial cell integrity: implications in
      atherosclerosis.
PG  - 119-57
AB  - Loss of functional integrity of the vascular endothelium may be one of
      the initiating events in the etiology of atherosclerosis. Endothelial
      cells interact with blood components and the abluminal tissues, thus
      playing an active role in many aspects of vascular functions, such as
      permeability and vessel tone regulation. Endothelial cells constantly are
      exposed to nutrients which can modulate enzymes, receptors, transport
      molecules and various vasoactive mediators, resulting in significant
      functional changes of the endothelium and the underlying tissues.
      Nutrition may play an important role in the atherosclerotic disease
      process. There is evidence that certain vitamins and minerals prevent
      some metabolic and physiological perturbations of the vascular
      endothelium. This review focuses on selected lipids which cause
      endothelial cell injury or dysfunction and on nutrients which may exhibit
      antiatherogenic properties by being able to function as antioxidants or
      membrane stabilizers.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Alvarado, A
AU  - Alvarado A
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - England
TA  - Prog Food Nutr Sci
JT  - Progress in food & nutrition science
JID - 7508713
RN  - 0 (Dietary Fats)
RN  - 0 (Minerals)
RN  - 0 (Vitamins)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/*etiology
MH  - Blood Coagulation
MH  - Dietary Fats/pharmacology
MH  - Endothelium, Vascular/pathology/*physiopathology
MH  - Humans
MH  - Minerals/therapeutic use
MH  - *Nutritional Physiological Phenomena
MH  - Vitamins/therapeutic use
RF  - 250
EDAT- 1993/04/01 00:00
MHDA- 1993/04/01 00:01
CRDT- 1993/04/01 00:00
PHST- 1993/04/01 00:00 [pubmed]
PHST- 1993/04/01 00:01 [medline]
PHST- 1993/04/01 00:00 [entrez]
PST - ppublish
SO  - Prog Food Nutr Sci. 1993 Apr-Jun;17(2):119-57.

PMID- 8159964
OWN - NLM
STAT- MEDLINE
DCOM- 19940519
LR  - 20161025
IS  - 0355-3140 (Print)
IS  - 0355-3140 (Linking)
VI  - 19 Suppl 1
DP  - 1993
TI  - Zinc and the stress response.
PG  - 132-3
FAU - McClain, C J
AU  - McClain CJ
AD  - Department of Medicine, University of Kentucky Medical Center, Lexington
      40536-0084.
FAU - McClain, M L
AU  - McClain ML
FAU - Boosalis, M G
AU  - Boosalis MG
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Clinical Trial
PT  - Journal Article
PT  - Randomized Controlled Trial
PL  - Finland
TA  - Scand J Work Environ Health
JT  - Scandinavian journal of work, environment & health
JID - 7511540
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Burns/metabolism
MH  - Craniocerebral Trauma/*drug therapy/metabolism
MH  - Female
MH  - Inflammation/metabolism
MH  - Rats
MH  - Stress, Physiological/*metabolism
MH  - Zinc/*metabolism/therapeutic use
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
AID - 1540 [pii]
PST - ppublish
SO  - Scand J Work Environ Health. 1993;19 Suppl 1:132-3.

PMID- 1333499
OWN - NLM
STAT- MEDLINE
DCOM- 19930107
LR  - 20190907
IS  - 0731-5724 (Print)
IS  - 0731-5724 (Linking)
VI  - 11
IP  - 5
DP  - 1992 Oct
TI  - Oxysterol-induced endothelial cell dysfunction in culture.
PG  - 532-8
AB  - Cholesterol oxidation products (oxysterols), such as cholestan-3 beta,5
      alpha,6 beta-triol (Triol), may be atherogenic by altering the barrier
      function of the vascular endothelium. We have shown that incubation of
      endothelial cell monolayers with Triol increased transendothelial albumin
      transfer (i.e., decreased barrier function) in a concentration- and time-
      dependent manner. Such dysfunction of endothelium could result from
      alterations in membrane characteristics, including changes in membrane-
      associated enzyme activities. To test this hypothesis, endothelial
      monolayers were treated with 20 microM Triol and the activities of
      selected membrane enzymes were measured at 0, 2, 4, 6, 12 and 24 hours.
      Calcium-adenosine triphosphatase (Ca(++)-ATPase) and sodium, potassium,
      magnesium-adenosine triphosphatase (Na+, K+, Mg(++)-ATPase) activities
      were significantly increased after 4 or 2 hours incubation with 20 microM
      Triol, respectively. 5'-nucleotidase activity was significantly elevated
      only after a 24-hour exposure to Triol, whereas there was no change in
      angiotensin-converting enzyme (ACE) activity in response to 20 microM
      Triol treatment at any time studied. Compared with all concentrations
      tested 40 microM Triol increased Ca(++)-ATPase activity most markedly,
      with a significant increase already after a 2-hour exposure. No major
      morphological changes were noted until 12 hours of exposure to 20 microM
      Triol; obvious cellular damage was observed by 24 hours. Cultures treated
      with Triol for 24 hours showed significant signs of toxicity, measured by
      an elevated [3H]adenine release, compared with control cultures. These
      data demonstrate that Triol alters the activity of certain membrane-bound
      enzymes, particularly Na+, K+, Mg(++)-ATPase and Ca(++)-ATPase.(ABSTRACT
      TRUNCATED AT 250 WORDS)
FAU - Ramasamy, S
AU  - Ramasamy S
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Am Coll Nutr
JT  - Journal of the American College of Nutrition
JID - 8215879
RN  - 0 (Albumins)
RN  - 0 (Cholestanols)
RN  - 10028-17-8 (Tritium)
RN  - 115510-05-9 (cholestane-3,5,6-triol)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - JAC85A2161 (Adenine)
SB  - IM
MH  - Adenine/analysis
MH  - Albumins/metabolism
MH  - Animals
MH  - Cells, Cultured
MH  - Cholestanols/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/*drug effects/enzymology/pathology
MH  - Peptidyl-Dipeptidase A/analysis
MH  - Pulmonary Artery/cytology
MH  - Swine
MH  - Tritium
EDAT- 1992/10/01 00:00
MHDA- 1992/10/01 00:01
CRDT- 1992/10/01 00:00
PHST- 1992/10/01 00:00 [pubmed]
PHST- 1992/10/01 00:01 [medline]
PHST- 1992/10/01 00:00 [entrez]
AID - 10.1080/07315724.1992.10718258 [doi]
PST - ppublish
SO  - J Am Coll Nutr. 1992 Oct;11(5):532-8. doi:
      10.1080/07315724.1992.10718258.

PMID- 1418097
OWN - NLM
STAT- MEDLINE
DCOM- 19921104
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 95
IP  - 2-3
DP  - 1992 Aug
TI  - Disruption of endothelial barrier function by lipolytic remnants of
      triglyceride-rich lipoproteins.
PG  - 235-47
AB  - Remnants, resulting from the lipolysis of triglyceride-rich lipoproteins,
      injured cultured endothelial cells and resulted in decreased barrier
      function of the vascular endothelium. Endothelial cells were cultured on
      micropore filters. Albumin transfer across endothelial cell monolayers
      was measured after a 24-h exposure to media enriched with control or in
      vitro-lipolyzed samples of various hypertriglyceridemic (HTG) sera and
      its isolated lipoprotein (VLDL, LDL and HDL) and serum free protein (d
      greater than 1.21 g/ml) fractions. Compared with control cultures,
      neither control HTG serum nor its isolated lipoprotein and serum-free
      protein fractions had any effect on albumin transfer. In contrast,
      lipolyzed HTG (L-HTG) serum and all of its isolated lipoprotein fractions
      (L-VLDL, L-IDL, L-LDL and L-HDL) caused a marked decrease in endothelial
      barrier function, evidenced by a significant increase in albumin transfer
      across endothelial monolayers. The L-IDL and L-HDL fractions were more
      effective in increasing albumin transfer than the L-VLDL and L-LDL
      fractions. The extent of the L-IDL and L-HDL mediated increases in
      albumin transfer was concentration dependent. An exposure of 12 h was
      required for L-HDL to increase albumin transfer. The L-HDL mediated
      increase in albumin transfer was reversible only after a 12-h exposure at
      low concentrations. The free protein fraction from L-HTG serum had no
      significant effect on the barrier function of endothelial cells. The
      presence of normolipidemic HDL in culture medium prevented disruption of
      the endothelial barrier induced by L-IDL but not by L-HDL. The decrease
      in endothelial barrier function induced by lipolyzed samples of HTG serum
      or lipoproteins appeared to be correlated with the level of free fatty
      acids contained in lipolytic remnants. Enrichment of LDL, and in
      particular HDL, with fatty acid significantly increased albumin transfer.
      Compared with lipolyzed samples, sera/lipoproteins oxidized in vitro by
      Cu2+ ions had little effect on endothelial barrier function, which did
      not correlate with their respective thiobarbituric acid-reacting
      substance (TBARS) values. TBARS remained within normal range after L-HDL
      incubation with endothelial cells for up to 48 h. At most concentrations
      tested, exposure to lipolyzed but not oxidized lipoproteins resulted in
      morphological perturbations of cell monolayers. These data suggest that
      lipolytic remnants of triglyceride-rich lipoproteins may play an
      important role in the development of atherosclerosis by decreasing the
      barrier function of the vascular endothelium. The remnant-induced injury
      of the arterial wall may permit the entry of cholesterol-rich lipolytic
      remnants as well as LDL into the arterial wall.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Chung, B H
AU  - Chung BH
FAU - Watkins, B A
AU  - Watkins BA
FAU - Alvarado, A
AU  - Alvarado A
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL-36552/HL/NHLBI NIH HHS/United States
GR  - HL-37833/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Culture Media)
RN  - 0 (Lipoproteins)
RN  - 0 (Lipoproteins, IDL)
RN  - 0 (Serum Albumin)
RN  - 0 (Triglycerides)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Culture Media
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Hypertriglyceridemia/blood
MH  - *Lipolysis
MH  - Lipoproteins/metabolism/pharmacology/*physiology
MH  - Lipoproteins, IDL
MH  - Serum Albumin/pharmacokinetics
MH  - Swine
MH  - Time Factors
MH  - Triglycerides/metabolism/*physiology
EDAT- 1992/08/01 00:00
MHDA- 1992/08/01 00:01
CRDT- 1992/08/01 00:00
PHST- 1992/08/01 00:00 [pubmed]
PHST- 1992/08/01 00:01 [medline]
PHST- 1992/08/01 00:00 [entrez]
AID - 0021-9150(92)90027-E [pii]
AID - 10.1016/0021-9150(92)90027-e [doi]
PST - ppublish
SO  - Atherosclerosis. 1992 Aug;95(2-3):235-47. doi:
      10.1016/0021-9150(92)90027-e.

PMID- 1316957
OWN - NLM
STAT- MEDLINE
DCOM- 19920625
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 122
IP  - 6
DP  - 1992 Jun
TI  - Zinc deficiency alters barrier function of cultured porcine endothelial
      cells.
PG  - 1242-7
AB  - Zinc is necessary for normal membrane function and stability. We
      postulated that Zn deficiency may disrupt the integrity of the vascular
      endothelium by decreasing its barrier function. To test this hypothesis,
      endothelial cells were cultured on polycarbonate filters and exposed to
      media enriched with either 1% fetal bovine serum (FBS) (low FBS; total
      Zn, 1.07 mumols/L medium) or 5% FBS (control; total Zn, 2.29 mumols/L) or
      low FBS plus two supplemental levels of Zn, 3.36 and 5.66 mumols total
      zinc/L. Endothelial cell barrier function, expressed as albumin transfer
      across cultured endothelial monolayers, was significantly lower in
      cultures exposed to low FBS compared with control medium. Supplementation
      with 5.66 mumols total Zn/L completely restored endothelial barrier
      function. A divalent cation chelator, 1,10-orthophenanthroline, was used
      to induce Zn deficiency in vitro. Compared with control cultures, the
      presence of 1,10-orthophenanthroline in the culture medium resulted in
      markedly lower endothelial barrier function that was increased by the
      addition of Zn but not calcium or magnesium. Activity of the membrane-
      bound zinc-dependent angiotensin-converting enzyme (ACE) was depressed by
      low zinc medium, whereas membrane-bound Ca(2+)-ATPase and total ATPase
      were not depressed. Furthermore, cells cultivated in low zinc medium did
      not have greater cytosolic release of adenine, indicating no increase in
      cell injury or death. These data suggest that Zn is vital to endothelial
      cell integrity and that Zn may play an important role in vascular
      endothelial barrier function.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington.
FAU - Wang, Y
AU  - Wang Y
FAU - Ramasamy, S
AU  - Ramasamy S
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 R01 NS22712-01A1/NS/NINDS NIH HHS/United States
GR  - HL-36552/HL/NHLBI NIH HHS/United States
GR  - MO1RRO26O2-O7/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Albumins)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - EC 3.6.1.- (Adenosine Triphosphatases)
RN  - J41CSQ7QDS (Zinc)
RN  - JAC85A2161 (Adenine)
SB  - IM
MH  - Adenine/metabolism
MH  - Adenosine Triphosphatases/metabolism
MH  - Albumins/metabolism
MH  - Animals
MH  - Cattle
MH  - Cell Membrane/*physiology
MH  - Cell Membrane Permeability/physiology
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*physiology
MH  - Fetal Blood
MH  - Peptidyl-Dipeptidase A/metabolism
MH  - Swine
MH  - Zinc/*deficiency/physiology
EDAT- 1992/06/01 00:00
MHDA- 1992/06/01 00:01
CRDT- 1992/06/01 00:00
PHST- 1992/06/01 00:00 [pubmed]
PHST- 1992/06/01 00:01 [medline]
PHST- 1992/06/01 00:00 [entrez]
AID - 10.1093/jn/122.6.1242 [doi]
PST - ppublish
SO  - J Nutr. 1992 Jun;122(6):1242-7. doi: 10.1093/jn/122.6.1242.

PMID- 1831858
OWN - NLM
STAT- MEDLINE
DCOM- 19910927
LR  - 20191210
IS  - 0887-2082 (Print)
IS  - 0887-2082 (Linking)
VI  - 6
IP  - 1
DP  - 1991 Spring
TI  - Linoleic acid-induced endothelial cell injury: role of membrane-bound
      enzyme activities and lipid oxidation.
PG  - 29-35
AB  - High plasma levels of linoleic acid (18:2) may injure endothelial cells,
      resulting in decreased barrier function of the vascular endothelium. The
      effects of linoleic acid on endothelial barrier function
      (transendothelial movement of albumin), membrane-bound enzyme activities,
      and possible autooxidation of linoleic acid under experimental conditions
      were studied. The exposure of endothelial monolayers to 18:2 for 24 hr at
      60, 90, and 120 microM fatty acid concentrations caused a significant
      increase in transendothelial movement of albumin, with maximum albumin
      transfer at 90 microM. Fatty acid treatment resulted in the increased
      appearance of cytosolic lipid droplets. Activities of the membrane-bound
      enzymes, angiotensin-converting enzyme (ACE), and Ca(2+)-ATPase increased
      steadily with increasing time of cell exposure to 90 microM 18:2,
      reaching significance at 24 hr. Treatment of endothelial cultures with up
      to 120 microM 18:2 did not cause cytotoxicity, as evidenced by a
      nonsignificant change in cellular release of [3H]-adenine. Incubation of
      18:2-supplemented serum-containing culture media with 1000 microM 18:2 at
      37 degrees C for up to 48 hr did not result in formation of autooxidation
      products. These results suggest that 18:2 itself, and not its oxidation
      products, plays a major role in disrupting endothelial barrier function.
FAU - Ramasamy, S
AU  - Ramasamy S
AD  - Department of Nutrition, University of Kentucky, Lexington 40506.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Decker, E A
AU  - Decker EA
FAU - Hennig, B
AU  - Hennig B
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
GR  - 1RO1 CA43719/CA/NCI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biochem Toxicol
JT  - Journal of biochemical toxicology
JID - 8700114
RN  - 0 (Linoleic Acids)
RN  - 0 (Peroxides)
RN  - 0 (Thiobarbiturates)
RN  - 27432CM55Q (Serum Albumin, Bovine)
RN  - 533-67-5 (Deoxyribose)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
SB  - IM
MH  - Animals
MH  - Calcium-Transporting ATPases/metabolism
MH  - Cell Membrane Permeability/drug effects
MH  - Cells, Cultured
MH  - Deoxyribose/metabolism
MH  - Endothelium, Vascular/*drug effects/metabolism/physiology
MH  - Linoleic Acid
MH  - Linoleic Acids/*toxicity
MH  - Lipid Metabolism
MH  - Oxidation-Reduction
MH  - Peroxides/metabolism
MH  - Serum Albumin, Bovine/metabolism
MH  - Swine
MH  - Thiobarbiturates/metabolism
MH  - Time Factors
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - 10.1002/jbt.2570060105 [doi]
PST - ppublish
SO  - J Biochem Toxicol. 1991 Spring;6(1):29-35. doi: 10.1002/jbt.2570060105.

PMID- 1998010
OWN - NLM
STAT- MEDLINE
DCOM- 19910402
LR  - 20200930
IS  - 0037-9727 (Print)
IS  - 0037-9727 (Linking)
VI  - 196
IP  - 3
DP  - 1991 Mar
TI  - Oxysterols, cholesterol biosynthesis, and vascular endothelial cell
      monolayer barrier function.
PG  - 338-43
AB  - A spectrum of cholesterol oxidation derivatives (oxysterols) is generated
      in food products exposed to heat or radiation in the presence of oxygen.
      One of these derivatives (cholestan-3 beta,5 alpha,6 beta-triol) was
      shown to compromise the selective barrier function of cultured vascular
      endothelial cell monolayers, an action that may initiate atherosclerotic
      lesion formation. This study sought to investigate the relationship of
      cholesterol synthesis inhibition by several naturally occurring
      oxysterols to depression of vascular endothelial cell monolayer barrier
      function, determined as an increase in albumin transfer across cultured
      endothelial monolayers. All oxysterols tested caused a variable time- and
      dose-dependent elevation in trans-endothelial albumin transfer, and they
      were also able to inhibit cholesterol biosynthesis to varying degrees.
      Pure cholesterol was without effect on both counts. The correlation
      between the increase in albumin transfer related to oxysterol exposure
      and the ability of oxysterols to suppress cholesterol biosynthesis was,
      however, poor. Moreover, mevinolin, a water-soluble competitive inhibitor
      of cholesterol synthesis, reduced the rate of cholesterol synthesis to
      0.9% of control but did not significantly increase albumin transfer.
      Cholestan-3 beta,5 alpha,6 beta-triol caused a 660% elevation in albumin
      transfer while cholesterol synthesis remained at 11% of control. We
      conclude that changes in endothelial barrier function caused by exposure
      to the oxysterols examined, but not pure cholesterol, are probably
      related to factors other than the well-known action of cholesterol
      biosynthesis inhibition. These findings may have implications in the
      development of atherosclerosis.
FAU - Boissonneault, G A
AU  - Boissonneault GA
AD  - Department of Clinical Sciences, University of Kentucky, Lexington 40536.
FAU - Hennig, B
AU  - Hennig B
FAU - Ouyang, C M
AU  - Ouyang CM
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Proc Soc Exp Biol Med
JT  - Proceedings of the Society for Experimental Biology and Medicine. Society
      for Experimental Biology and Medicine (New York, N.Y.)
JID - 7505892
RN  - 0 (Cholestanes)
RN  - 0 (Cholestanols)
RN  - 0 (Dehydrocholesterols)
RN  - 0 (Hydroxycholesterols)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Ketocholesterols)
RN  - 0 (Serum Albumin)
RN  - 115510-05-9 (cholestane-3,5,6-triol)
RN  - 1250-95-9 (cholesterol alpha-oxide)
RN  - 767JTD2N31 (25-hydroxycholesterol)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - 9LHU78OQFD (Lovastatin)
RN  - BK1IU07GKF (7-dehydrocholesterol)
RN  - O7676FE78M (7-ketocholesterol)
SB  - IM
MH  - Animals
MH  - Biological Transport
MH  - Cell Membrane Permeability/drug effects
MH  - Cholestanes/*pharmacology
MH  - Cholestanols/pharmacology
MH  - Cholesterol/analogs & derivatives/*biosynthesis/pharmacology
MH  - Dehydrocholesterols/pharmacology
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Endothelium/*physiology
MH  - Hydroxycholesterols/pharmacology
MH  - Hypolipidemic Agents/pharmacology
MH  - In Vitro Techniques
MH  - Ketocholesterols/pharmacology
MH  - Lovastatin/pharmacology
MH  - Serum Albumin/pharmacokinetics
MH  - Swine
MH  - Time Factors
EDAT- 1991/03/01 00:00
MHDA- 1991/03/01 00:01
CRDT- 1991/03/01 00:00
PHST- 1991/03/01 00:00 [pubmed]
PHST- 1991/03/01 00:01 [medline]
PHST- 1991/03/01 00:00 [entrez]
AID - 10.3181/00379727-196-43198 [doi]
PST - ppublish
SO  - Proc Soc Exp Biol Med. 1991 Mar;196(3):338-43. doi:
      10.3181/00379727-196-43198.

PMID- 1897903
OWN - NLM
STAT- MEDLINE
DCOM- 19911023
LR  - 20180215
IS  - 0250-6807 (Print)
IS  - 0250-6807 (Linking)
VI  - 35
IP  - 4
DP  - 1991
TI  - Effect of oxysterol-enriched low-density lipoprotein on endothelial
      barrier function in culture. Low-density lipoproteins.
PG  - 226-32
AB  - High levels of plasma low-density lipoproteins (LDL) are known to be a
      risk factor for developing coronary artery disease although the specific
      mechanism involved is unknown. It may be related to effects of oxidized
      lipid components of LDL on vascular endothelial barrier function (EBF).
      This study addressed the hypothesis that LDL-associated products of
      cholesterol oxidation, oxysterols, decrease EBF resulting in increased
      penetration of blood components such as LDL into the arterial wall. LDL
      from human volunteers and rabbits was enriched with cholesterol or
      cholestan-3 beta,5 alpha,6 beta triol (Triol) by in vitro incubation.
      Exposure of cultured vascular endothelial cell monolayers to LDL enriched
      with Triol reduced EBF, measured as an increase in transendothelial
      albumin transfer, whereas cholesterol enrichment, like un-enriched LDL,
      had no effect on EBF. In a second experimental series, rabbits were
      gavaged with 100 mg of cholesterol or Triol/kg body weight, and LDL was
      isolated from serum 24 h after gavage. As was seen with the in vitro
      experiments, Triol-enriched LDL markedly decreased EBF. Similarly, LDL
      from cholesterol-gavaged rabbits reduced EBF, while LDL from vehicle
      treated rabbits had no effect. These results suggest that LDL-associated
      oxysterols are detrimental to normal barrier function of the vascular
      endothelium. Disruption of this barrier function may serve as an
      initiating factor in atherosclerotic lesion formation.
FAU - Boissonneault, G A
AU  - Boissonneault GA
AD  - Department of Clinical Sciences, University of Kentucky, Lexington.
FAU - Hennig, B
AU  - Hennig B
FAU - Wang, Y
AU  - Wang Y
FAU - Ouyang, C M
AU  - Ouyang CM
FAU - Krahulik, K
AU  - Krahulik K
FAU - Cunnup, L
AU  - Cunnup L
FAU - Oeltgen, P R
AU  - Oeltgen PR
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 PO1 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Ann Nutr Metab
JT  - Annals of nutrition & metabolism
JID - 8105511
RN  - 0 (Albumins)
RN  - 0 (Lipoproteins, LDL)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Albumins/metabolism
MH  - Animals
MH  - Cells, Cultured
MH  - Cholesterol/analogs & derivatives/*metabolism
MH  - Endothelium, Vascular/*drug effects/physiology
MH  - Lipoproteins, LDL/*pharmacology
MH  - Swine
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - 10.1159/000177650 [doi]
PST - ppublish
SO  - Ann Nutr Metab. 1991;35(4):226-32. doi: 10.1159/000177650.

PMID- 2259250
OWN - NLM
STAT- MEDLINE
DCOM- 19910131
LR  - 20190828
IS  - 0047-6374 (Print)
IS  - 0047-6374 (Linking)
VI  - 56
IP  - 1
DP  - 1990 Oct
TI  - Aging and endothelial barrier function in culture: effects of chronic
      exposure to fatty acid hydroperoxides and vitamin E.
PG  - 1-9
AB  - As the endothelium ages it may become more susceptible to damage by
      atherogenic plasma components such as toxic lipid oxidation products.
      Vitamin E (vit E) might prove to be anti-atherogenic by reducing
      oxidative injury. This study investigated the effects of age and chronic
      exposure to fatty acid hydroperoxides (OFA) and/or vit E on endothelial
      barrier function (EBF) and cell growth characteristics. Chronic exposure
      to 5 microM OFA for 40 passages resulted in an age-related decrease in
      EBF, while supplementation of OFA-treated cultures with 25 microM vit E
      protected against the OFA-mediated decrease in EBF, independent of cell
      age. Vit E treatment alone had no significant effect on EBF relative to
      control cultures. No changes in growth characteristics, i.e., total DNA
      or protein per culture, were noted, regardless of treatment, although
      total DNA per culture decreased with increasing culture passage. These
      results suggest that chronic oxidative stress decreases EBF, predisposing
      the artery to infiltration by blood components and subsequent
      atherogenesis and that vit E delays cumulative changes in EBF related to
      chronic OFA exposure.
FAU - Boissonneault, G A
AU  - Boissonneault GA
AD  - Department of Clinical Sciences, University of Kentucky, Lexington 40536.
FAU - Hennig, B
AU  - Hennig B
FAU - Wang, Y
AU  - Wang Y
FAU - Wood, C L
AU  - Wood CL
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 P01 HL36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Mech Ageing Dev
JT  - Mechanisms of ageing and development
JID - 0347227
RN  - 0 (Lipid Peroxides)
RN  - 0 (Proteins)
RN  - 1406-18-4 (Vitamin E)
RN  - 27432CM55Q (Serum Albumin, Bovine)
SB  - IM
MH  - Aging/pathology/*physiology
MH  - Animals
MH  - Arteriosclerosis/etiology/prevention & control
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Endothelium, Vascular/cytology/*drug effects/physiology
MH  - Lipid Peroxides/*toxicity
MH  - Permeability
MH  - Proteins/metabolism
MH  - Serum Albumin, Bovine/pharmacokinetics
MH  - Vitamin E/*pharmacology
EDAT- 1990/10/01 00:00
MHDA- 1990/10/01 00:01
CRDT- 1990/10/01 00:00
PHST- 1990/10/01 00:00 [pubmed]
PHST- 1990/10/01 00:01 [medline]
PHST- 1990/10/01 00:00 [entrez]
AID - 0047-6374(90)90110-2 [pii]
AID - 10.1016/0047-6374(90)90110-2 [doi]
PST - ppublish
SO  - Mech Ageing Dev. 1990 Oct;56(1):1-9. doi: 10.1016/0047-6374(90)90110-2.

PMID- 2283660
OWN - NLM
STAT- MEDLINE
DCOM- 19910318
LR  - 20191029
IS  - 0887-2082 (Print)
IS  - 0887-2082 (Linking)
VI  - 5
IP  - 2
DP  - 1990 Summer
TI  - Induction of peroxisomal enzymes in cultured porcine endothelial cells by
      the hypolipidemic drug ciprofibrate.
PG  - 115-8
AB  - The purpose of this study was to determine if the hypolipidemic
      peroxisome proliferator ciprofibrate, which induces peroxisomes in the
      liver, can induce peroxisomes in cultured porcine pulmonary endothelial
      cells. Ciprofibrate was added at three concentrations to cell cultures
      for a 6-day period. The induction of peroxisomes in the cells was
      detected by determining total peroxisomal beta-oxidation and peroxisomal
      catalase activity. The addition of ciprofibrate was found to increase
      peroxisomal enzyme activities in a dose-dependent manner, with the
      highest activity being reached at 1000 microM ciprofibrate. Ciprofibrate
      also caused an increased transfer of albumin across endothelial cells
      cultured on micropore filters. This study shows that peroxisomal enzyme
      activities can be induced by ciprofibrate in endothelial cells, which may
      have implications in diseases mediated by vascular injury.
FAU - Glauert, H P
AU  - Glauert HP
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Hennig, B
AU  - Hennig B
FAU - Chow, H S
AU  - Chow HS
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - CA-43719/CA/NCI NIH HHS/United States
GR  - HL-34423/HL/NHLBI NIH HHS/United States
GR  - HL-36552/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biochem Toxicol
JT  - Journal of biochemical toxicology
JID - 8700114
RN  - 0 (Fibric Acids)
RN  - 0 (Hypolipidemic Agents)
RN  - 53PF01Q249 (Clofibric Acid)
RN  - EC 1.11.1.6 (Catalase)
RN  - F8252JGO9S (ciprofibrate)
SB  - IM
MH  - Animals
MH  - Catalase/metabolism
MH  - Cells, Cultured
MH  - Clofibric Acid/*analogs & derivatives/pharmacology
MH  - Endothelium/cytology/enzymology/metabolism
MH  - Enzyme Induction
MH  - Fibric Acids
MH  - Hypolipidemic Agents/*pharmacology
MH  - Lung/cytology/metabolism
MH  - Microbodies/*enzymology
MH  - Oxidation-Reduction
MH  - Swine
EDAT- 1990/01/01 00:00
MHDA- 1990/01/01 00:01
CRDT- 1990/01/01 00:00
PHST- 1990/01/01 00:00 [pubmed]
PHST- 1990/01/01 00:01 [medline]
PHST- 1990/01/01 00:00 [entrez]
AID - 10.1002/jbt.2570050206 [doi]
PST - ppublish
SO  - J Biochem Toxicol. 1990 Summer;5(2):115-8. doi: 10.1002/jbt.2570050206.

PMID- 2329387
OWN - NLM
STAT- MEDLINE
DCOM- 19900531
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 120
IP  - 4
DP  - 1990 Apr
TI  - Effect of vitamin E on linoleic acid-mediated induction of peroxisomal
      enzymes in cultured porcine endothelial cells.
PG  - 331-7
AB  - Linoleic acid decreases endothelial barrier function in culture. We
      hypothesize that the mechanism may involve induction of peroxisomes, with
      subsequent generation of hydrogen peroxide, and that vitamin E may
      protect against barrier function loss by preventing the induction of
      peroxisomal enzymes. To investigate this hypothesis, we exposed cultured
      endothelial cells to 0 or 90 mumols/L linoleic acid [18:2(n-6)], with or
      without 25 mumols/L supplemental vitamin E, for 5 d. The induction of
      peroxisomes by linoleic acid exposure was determined by measuring
      cellular peroxisomal beta-oxidation and catalase activity. Vitamin E
      alone had no effect on beta-oxidation or catalase activity, whereas
      linoleic acid exposure significantly increased both compared with control
      values. Vitamin E supplementation prevented induction of peroxisomal
      beta-oxidation and catalase activity by 18:2. In contrast, cell
      enrichment with vitamin E had no effect on 18:2-induced accumulation of
      cytoplasmic lipid-like droplets. These results confirm our hypothesis
      that the protective effects of vitamin E against fatty acid-mediated
      endothelial cell injury may be due in part to the ability of vitamin E to
      prevent the induction of peroxisomal beta-oxidation enzymes and thus the
      formation of excess hydrogen peroxide.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Chow, C K
AU  - Chow CK
FAU - Wang, Y
AU  - Wang Y
FAU - Matulionis, D H
AU  - Matulionis DH
FAU - Glauert, H P
AU  - Glauert HP
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL36552/HL/NHLBI NIH HHS/United States
GR  - 1RO1 CA43719/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Linoleic Acids)
RN  - 1406-18-4 (Vitamin E)
RN  - 9KJL21T0QJ (Linoleic Acid)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.11.1.6 (Catalase)
SB  - IM
MH  - Animals
MH  - Catalase/*metabolism
MH  - Cells, Cultured
MH  - Drug Synergism
MH  - Endothelium, Vascular/*drug effects/enzymology/ultrastructure
MH  - Enzyme Induction/drug effects
MH  - Hydrogen Peroxide/metabolism
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Microbodies/drug effects
MH  - Swine
MH  - Vitamin E/*pharmacology
EDAT- 1990/04/01 00:00
MHDA- 1990/04/01 00:01
CRDT- 1990/04/01 00:00
PHST- 1990/04/01 00:00 [pubmed]
PHST- 1990/04/01 00:01 [medline]
PHST- 1990/04/01 00:00 [entrez]
AID - 10.1093/jn/120.4.331 [doi]
PST - ppublish
SO  - J Nutr. 1990 Apr;120(4):331-7. doi: 10.1093/jn/120.4.331.

PMID- 2924805
OWN - NLM
STAT- MEDLINE
DCOM- 19890505
LR  - 20190707
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 181
IP  - 2
DP  - 1989 Apr
TI  - Effects of serum type on growth and permeability properties of cultured
      endothelial cells.
PG  - 589-96
AB  - Serum is frequently added to defined basal media as a source of certain
      nutrients and macromolecular growth factors essential for cell growth.
      The many different sera commercially available may not be equally
      suitable for all cell types. The effects of four sera, fetal bovine serum
      (FBS), calf bovine serum (CS), equine serum (ES-1), and plasma-derived
      equine serum (ES-2), on growth and permeability properties of cultured
      porcine endothelial cells were determined. The rate of DNA synthesis,
      measured as [3H]thymidine incorporation, reached a peak at around 24 h,
      regardless of serum type, and was most marked with ES-1- or ES-2-treated
      cells. However, when estimated by total DNA, FBS, CS, or ES-1 treatment
      resulted in greater cell proliferation than ES-2. Based on protein
      synthetic rate and total cell protein, both FBS and CS appeared to be
      most growth supporting. At 72 h after cell plating, albumin passage
      across cultured endothelial monolayers was elevated in ES-1- and
      ES-2-treated cells compared with FBS- or CS-treated cells. "Leaky" cell
      monolayers were most marked with ES-1-treated cells. Cells grown in ES-2-
      and particularly in ES-1-enriched media were larger and more spindle-
      shaped compared with the typical cobblestone appearance of cells cultured
      in media enriched with either FBS or CS. These data suggest that CS, but
      not ES-1 or ES-2, is an excellent substitute for FBS to support desirable
      growth properties of macrovascular endothelial cells in culture.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition, University of Kentucky, Lexington 40506.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Glauert, H P
AU  - Glauert HP
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL 34423/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Culture Media)
RN  - 27432CM55Q (Serum Albumin, Bovine)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Animals
MH  - Blood
MH  - Cattle/blood
MH  - Cell Division
MH  - Cells, Cultured
MH  - Culture Media
MH  - DNA/biosynthesis
MH  - Endothelium, Vascular/*cytology/physiology
MH  - Horses/blood
MH  - Permeability
MH  - Protein Biosynthesis
MH  - Serum Albumin, Bovine/metabolism
MH  - Swine
EDAT- 1989/04/01 00:00
MHDA- 1989/04/01 00:01
CRDT- 1989/04/01 00:00
PHST- 1989/04/01 00:00 [pubmed]
PHST- 1989/04/01 00:01 [medline]
PHST- 1989/04/01 00:00 [entrez]
AID - 10.1016/0014-4827(89)90116-x [doi]
PST - ppublish
SO  - Exp Cell Res. 1989 Apr;181(2):589-96. doi: 10.1016/0014-4827(89)90116-x.

PMID- 2494779
OWN - NLM
STAT- MEDLINE
DCOM- 19890502
LR  - 20190727
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 98
IP  - 1
DP  - 1989 Mar 15
TI  - Monokine-induced lung injury in rats: similarities to monocrotaline-
      induced pneumotoxicity.
PG  - 134-43
AB  - Previous studies have shown that abnormal alveolar macrophages and
      biological activity resembling the macrophage-derived mediator
      interleukin-1 (IL-1) can be detected in bronchoalveolar lavage fluid from
      rats with monocrotaline-induced lung injury and pulmonary hypertension.
      To determine if monokines might play a pathogenic role in this model, the
      present study evaluated the effects of a murine monokine preparation
      enriched in IL-1 bioactivity on selected events characterizing the early
      pneumotoxic response to monocrotaline, including pulmonary edema and
      protein extravasation, pulmonary vascular hyperreactivity, and enhanced
      lung tissue activity of the rate-limiting enzyme in polyamine
      biosynthesis, ornithine decarboxylase (ODC). Intravenous injection of the
      monokine preparation containing 200 units/kg IL-1 (quantified by
      lymphocyte activating factor assay) into intact rats produced pulmonary
      edema within 3 hr manifested by increases in the lung wet-to-dry weight
      ratio and in the extent of pulmonary albumin extravasation. The edema had
      resolved within 24 hr of monokine administration as indicated by a return
      to control levels of the wet-to-dry weight ratio and albumin
      extravasation index. The monokine preparation also increased the transfer
      of albumin across monolayers of cultured porcine pulmonary vascular
      endothelial cells. While salt solution-perfused rat lungs isolated from
      animals treated 3 hr previously with the monokine preparation were
      hyporesponsive to angiotensin II, preparations derived from animals
      treated 24 hr previously were markedly hyperresponsive to the
      vasoconstrictor actions of the peptide. Pressor responses to potassium
      chloride and prostaglandin F2a were unaffected by exposure to the
      monokine preparation. Lung ODC activity in monokine-exposed animals did
      not differ from control at 3, 6, or 24 hr after treatment. In contrast, a
      24-hr exposure of cultured pulmonary vascular endothelial cells to the
      monokine preparation increased ODC activity approximately 100-fold. These
      observations indicate that a monokine preparation containing IL-1
      bioactivity causes transient pulmonary edema and pulmonary vascular
      hyperreactivity and increases ODC activity in pulmonary vascular
      endothelial cells. Because the monokine preparation mimics certain
      aspects of monocrotaline-induced pneumotoxicity in the rat, it is
      reasonable to postulate that monokines could play a pathogenic role in
      this and similar animal models of lung injury and pulmonary hypertension.
FAU - Gillespie, M N
AU  - Gillespie MN
AD  - University of Kentucky College of Pharmacy, Division of Pharmacology and
      Toxicology, College of Medicine, Lexington.
FAU - Olson, J W
AU  - Olson JW
FAU - Hennig, B
AU  - Hennig B
FAU - Cohen, D A
AU  - Cohen DA
FAU - McClain, C J
AU  - McClain CJ
FAU - Goldblum, S E
AU  - Goldblum SE
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL-36404/HL/NHLBI NIH HHS/United States
GR  - HL-38495/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Biological Factors)
RN  - 0 (Monokines)
RN  - 0 (Pyrrolizidine Alkaloids)
RN  - 0 (Serum Albumin)
RN  - 73077K8HYV (Monocrotaline)
RN  - EC 4.1.1.17 (Ornithine Decarboxylase)
SB  - IM
MH  - Animals
MH  - Biological Factors/*toxicity
MH  - Cells, Cultured
MH  - Endothelium, Vascular/drug effects/enzymology
MH  - Hypertension, Pulmonary/chemically induced
MH  - Lung/blood supply/*drug effects/metabolism
MH  - Male
MH  - Monocrotaline
MH  - Monokines
MH  - Organ Size/drug effects
MH  - Ornithine Decarboxylase/metabolism
MH  - Perfusion
MH  - Pulmonary Edema/chemically induced
MH  - Pyrrolizidine Alkaloids/*toxicity
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Serum Albumin/metabolism
EDAT- 1989/03/15 00:00
MHDA- 1989/03/15 00:01
CRDT- 1989/03/15 00:00
PHST- 1989/03/15 00:00 [pubmed]
PHST- 1989/03/15 00:01 [medline]
PHST- 1989/03/15 00:00 [entrez]
AID - 10.1016/0041-008x(89)90141-5 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 1989 Mar 15;98(1):134-43. doi:
      10.1016/0041-008x(89)90141-5.

PMID- 2563626
OWN - NLM
STAT- MEDLINE
DCOM- 19890320
LR  - 20180330
IS  - 0002-9165 (Print)
IS  - 0002-9165 (Linking)
VI  - 49
IP  - 2
DP  - 1989 Feb
TI  - Linoleic acid and linolenic acid: effect on permeability properties of
      cultured endothelial cell monolayers.
PG  - 301-5
AB  - High circulating plasma levels of free fatty acids may injure endothelial
      cells, resulting in decreased barrier function of the vascular
      endothelium. The effect of media supplementation with varying
      concentrations of either linoleic (C18:2 omega 6) or linolenic acid
      (C18:3 omega 3) on albumin transfer across cultured endothelial
      monolayers was studied. A 24-h cell exposure to linoleic but not
      linolenic acid resulted in a concentration dependent and largely
      reversible increase in albumin transfer. Both fatty acids and in
      particular linolenic acid incorporated into cellular phospholipids. In
      contrast, only supplementation with linoleic but not linolenic acid
      resulted in an increased incorporation of this fatty acid into cell
      triglycerides. Similarly, only total cell triglyceride content increased
      after incubation with linoleic- but not with linolenic-enriched media.
      These results indicate that cellular enrichment with linoleic but not
      linolenic acid causes cellular perturbations that may be implicated in
      atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506-0054.
FAU - Watkins, B A
AU  - Watkins BA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL34423/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
RN  - 0 (Linoleic Acids)
RN  - 0 (Linolenic Acids)
RN  - 0RBV727H71 (alpha-Linolenic Acid)
RN  - 9KJL21T0QJ (Linoleic Acid)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Cell Membrane Permeability/*drug effects
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*cytology/drug effects
MH  - Linoleic Acid
MH  - Linoleic Acids/*pharmacology
MH  - Linolenic Acids/*pharmacology
MH  - Swine
MH  - alpha-Linolenic Acid
EDAT- 1989/02/01 00:00
MHDA- 1989/02/01 00:01
CRDT- 1989/02/01 00:00
PHST- 1989/02/01 00:00 [pubmed]
PHST- 1989/02/01 00:01 [medline]
PHST- 1989/02/01 00:00 [entrez]
AID - 10.1093/ajcn/49.2.301 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 1989 Feb;49(2):301-5. doi: 10.1093/ajcn/49.2.301.

PMID- 2599793
OWN - NLM
STAT- MEDLINE
DCOM- 19900202
LR  - 20161019
IS  - 0300-9831 (Print)
IS  - 0300-9831 (Linking)
VI  - 59
IP  - 3
DP  - 1989
TI  - Protective effects of vitamin E in age-related endothelial cell injury.
PG  - 273-9
AB  - Age is strongly correlated to the onset of atherosclerotic lesion
      formation in humans. This may be associated with an age-related increase
      in the susceptibility of the vascular endothelium to oxidative injury.
      Such injury may result in altered endothelial function as a barrier to
      plasma components, such as cholesterol-rich lipoprotein remnants. To
      investigate this hypothesis, the relationship between endothelial cell
      culture age, susceptibility to oxidative injury and protection against
      this injury by the nutrient/antioxidant vitamin E on endothelial barrier
      function (transfer of albumin across endothelial monolayers) was
      examined. An acute 24 h exposure to 30 microM linoleic acid hydroperoxide
      resulted in increased albumin transfer at all cell passages tested (up to
      passage 50). Pre-enrichment of cells with 25 microM vitamin E always
      protected endothelial cells against oxidized fatty acid-induced cell
      injury, independent of cell age. In comparison, patterns of total cell
      protein and DNA were not markedly influenced by experimental treatments,
      although age-related declines in total DNA were noted. These data suggest
      that the possible correlation between age and the onset of
      atherosclerosis may be in part related to a decrease in endothelial
      barrier function due to oxidative stress, permitting more blood
      components to enter the arterial wall. Furthermore, vitamin E may protect
      endothelial cells against oxidant-mediated vascular injury.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Wang, Y
AU  - Wang Y
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1PO1 HL 36552/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Int J Vitam Nutr Res
JT  - International journal for vitamin and nutrition research. Internationale
      Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international
      de vitaminologie et de nutrition
JID - 1273304
RN  - 0 (Linolenic Acids)
RN  - 0 (Lipid Peroxides)
RN  - 0 (Serum Albumin)
RN  - 1406-18-4 (Vitamin E)
RN  - 19356-22-0 (13-hydroperoxylinolenic acid)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - *Aging
MH  - Animals
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - DNA/analysis/drug effects
MH  - Endothelium/*drug effects/physiology
MH  - Linolenic Acids/pharmacology
MH  - Lipid Peroxides/pharmacology
MH  - Serum Albumin/metabolism
MH  - Swine
MH  - Vitamin E/*pharmacology
EDAT- 1989/01/01 00:00
MHDA- 1989/01/01 00:01
CRDT- 1989/01/01 00:00
PHST- 1989/01/01 00:00 [pubmed]
PHST- 1989/01/01 00:01 [medline]
PHST- 1989/01/01 00:00 [entrez]
PST - ppublish
SO  - Int J Vitam Nutr Res. 1989;59(3):273-9.

PMID- 3210085
OWN - NLM
STAT- MEDLINE
DCOM- 19890223
LR  - 20180330
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 118
IP  - 12
DP  - 1988 Dec
TI  - Tumor necrosis factor-mediated hypoalbuminemia in rabbits.
PG  - 1586-90
AB  - The serum albumin concentration is used clinically as an indicator of
      nutritional status and as a prognostic indicator. Critically ill
      patients, who display many aspects of the acute phase response,
      frequently have low serum albumin levels upon hospitalization. Cytokines,
      such as tumor necrosis factor (TNF), mediate many aspects of the acute
      phase response. One purpose of this study was to determine if TNF
      administration to healthy well-nourished rabbits could produce
      hypoalbuminemia. After intravenous administration of saline or TNF, the
      TNF-treated rabbits experienced significant hypoalbuminemia which was
      most prominent at 24 h and was partially corrected by 48 h. A second
      purpose was to evaluate the effects of TNF treatment on transendothelial
      movement of albumin using an in vitro porcine pulmonary artery-
      endothelial cell system. Exposure to TNF for 24 h resulted in a dose
      dependent increase in transendothelial passage of albumin. These data
      suggest that the mechanisms of hypoalbuminemia frequently observed in
      critically ill patients can be explained in part by cytokine
      (TNF)-induced endothelial cell injury, which results in enhanced
      endothelial permeability to albumin. The hypoalbuminemia observed in many
      critically ill patients thus may be unrelated to nutritional status, but
      rather may be related to the patient's underlying disease state.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40536-0084.
FAU - Honchel, R
AU  - Honchel R
FAU - Goldblum, S E
AU  - Goldblum SE
FAU - McClain, C J
AU  - McClain CJ
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL34423/HL/NHLBI NIH HHS/United States
GR  - NS22712/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Albumins)
RN  - 0 (Serum Albumin)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Albumins/deficiency/metabolism
MH  - Animals
MH  - Biological Transport/drug effects
MH  - Endothelium/metabolism
MH  - Energy Intake/drug effects
MH  - Nutritional Status
MH  - Pulmonary Artery/metabolism
MH  - Rabbits
MH  - Serum Albumin/*analysis
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1988/12/01 00:00
MHDA- 1988/12/01 00:01
CRDT- 1988/12/01 00:00
PHST- 1988/12/01 00:00 [pubmed]
PHST- 1988/12/01 00:01 [medline]
PHST- 1988/12/01 00:00 [entrez]
AID - 10.1093/jn/118.12.1586 [doi]
PST - ppublish
SO  - J Nutr. 1988 Dec;118(12):1586-90. doi: 10.1093/jn/118.12.1586.

PMID- 3261327
OWN - NLM
STAT- MEDLINE
DCOM- 19880922
LR  - 20161019
IS  - 0022-3085 (Print)
IS  - 0022-3085 (Linking)
VI  - 69
IP  - 3
DP  - 1988 Sep
TI  - Mechanisms and implications of hypoalbuminemia in head-injured patients.
PG  - 386-92
AB  - Severely head-injured patients are hypermetabolic/hypercatabolic and
      exhibit many aspects of the postinjury acute-phase response. These
      patients have hypoalbuminemia, hypozincemia, hypoferremia, hypercupria,
      fever, and increased synthesis of acute-phase proteins such as
      ceruloplasmin and higher C-reactive protein levels. It has been suggested
      that increased interleukin-1 (IL-1) in the ventricular fluid may be
      responsible, at least in part, for these metabolic abnormalities. In the
      present study, serum albumin levels were evaluated throughout an 18-day
      study period in 62 head-injured patients receiving aggressive nutritional
      support. Hypoalbuminemia (mean +/- standard error of the mean 3.10 +/-
      0.2 gm/dl; normal value 3.5 to 5 gm/dl) was observed upon hospital
      admission; these albumin levels continued to decrease until 2 weeks
      postinjury, despite aggressive nutritional support. This hypoalbuminemia
      may be mediated via altered endothelial permeability properties due to
      endothelial cell dysfunction caused by cytokines such as IL-1.
      Transendothelial movement of albumin was assayed using a pulmonary artery
      endothelial cell culture system. Both a crude macrophage supernatant
      derived from a murine P388D cell line having IL-1 activity (mIL-1) and
      human recombinant IL-1 (rIL-1) were tested. The amount of albumin
      transferred was time- and concentration-dependent, with maximal transfer
      at 24 hours and 20 U of mIL-1 per 0.5 ml of culture medium. Endothelial
      permeability changes observed after incubation with mIL-1 were confirmed
      using rIL-1. Compared to control cultures, 20 U of rIL-1 and 20 U of
      mIL-1 increased albumin transfer across endothelial monolayers 205% and
      459%, respectively. These findings suggest that the mechanism of
      hypoalbuminemia seen after severe head trauma can be explained in part by
      IL-1-induced endothelial cell injury, resulting in enhanced endothelial
      permeability to albumin.
FAU - McClain, C J
AU  - McClain CJ
AD  - Department of Medicine, University of Kentucky, Medical Center,
      Lexington.
FAU - Hennig, B
AU  - Hennig B
FAU - Ott, L G
AU  - Ott LG
FAU - Goldblum, S
AU  - Goldblum S
FAU - Young, A B
AU  - Young AB
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - 1 R01 NS22712-01A1/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosurg
JT  - Journal of neurosurgery
JID - 0253357
RN  - 0 (Interleukin-1)
RN  - 0 (Serum Albumin)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - J41CSQ7QDS (Zinc)
SB  - AIM
SB  - IM
MH  - Brain Injuries/blood/*physiopathology
MH  - C-Reactive Protein/analysis
MH  - Cell Membrane Permeability
MH  - Humans
MH  - Interleukin-1/physiology
MH  - Leukocyte Count
MH  - Serum Albumin/*metabolism
MH  - Zinc/blood
EDAT- 1988/09/01 00:00
MHDA- 1988/09/01 00:01
CRDT- 1988/09/01 00:00
PHST- 1988/09/01 00:00 [pubmed]
PHST- 1988/09/01 00:01 [medline]
PHST- 1988/09/01 00:00 [entrez]
AID - 10.3171/jns.1988.69.3.0386 [doi]
PST - ppublish
SO  - J Neurosurg. 1988 Sep;69(3):386-92. doi: 10.3171/jns.1988.69.3.0386.

PMID- 3342700
OWN - NLM
STAT- MEDLINE
DCOM- 19880407
LR  - 20190514
IS  - 0012-3692 (Print)
IS  - 0012-3692 (Linking)
VI  - 93
IP  - 3 Suppl
DP  - 1988 Mar
TI  - Growth factors and diacylglycerol stimulate pulmonary vascular
      endothelial ornithine decarboxylase activity.
PG  - 168S
FAU - Olson, J W
AU  - Olson JW
AD  - University of Kentucky A.B. Chandler Medical Center, College of Pharmacy,
      Lexington.
FAU - Hennig, B
AU  - Hennig B
FAU - Altiere, R J
AU  - Altiere RJ
FAU - Goldblum, S E
AU  - Goldblum SE
FAU - Gillespie, M N
AU  - Gillespie MN
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Chest
JT  - Chest
JID - 0231335
RN  - 0 (Diglycerides)
RN  - 0 (Glycerides)
RN  - 0 (Growth Substances)
RN  - EC 4.1.1.17 (Ornithine Decarboxylase)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Diglycerides/*pharmacology
MH  - Endothelium, Vascular/*drug effects/enzymology
MH  - Glycerides/*pharmacology
MH  - Growth Substances/*pharmacology
MH  - Ornithine Decarboxylase/*metabolism
MH  - Pulmonary Artery/drug effects/metabolism
MH  - Stimulation, Chemical
EDAT- 1988/03/01 00:00
MHDA- 1988/03/01 00:01
CRDT- 1988/03/01 00:00
PHST- 1988/03/01 00:00 [pubmed]
PHST- 1988/03/01 00:01 [medline]
PHST- 1988/03/01 00:00 [entrez]
AID - S0012-3692(16)40340-5 [pii]
AID - 10.1378/chest.93.3_supplement.168s [doi]
PST - ppublish
SO  - Chest. 1988 Mar;93(3 Suppl):168S. doi:
      10.1378/chest.93.3_supplement.168s.

PMID- 3278952
OWN - NLM
STAT- MEDLINE
DCOM- 19880415
LR  - 20190824
IS  - 0891-5849 (Print)
IS  - 0891-5849 (Linking)
VI  - 4
IP  - 2
DP  - 1988
TI  - Lipid peroxidation and endothelial cell injury: implications in
      atherosclerosis.
PG  - 99-106
AB  - Vascular endothelial cells, which play an active role in the
      physiological processes of vessel tone regulation and vascular
      permeability, form a border separating deeper layers of the blood vessel
      wall and cellular interstitial space from the blood and circulating
      cells. Damage or dysfunction of endothelial cells may reduce the
      effectiveness of the endothelium to act as a selectively permeable
      barrier to plasma components, including cholesterol-rich lipoprotein
      remnants. This may be involved in the etiology of atherosclerosis.
      Experimental evidence indicates that free radical-mediated lipid
      peroxidation can induce endothelial cell injury/dysfunction. Reactive
      oxygen species, including peroxidized lipids capable of initiating cell
      injury, may be generated within endothelial cells, be present in plasma
      components, or be derived from neutrophils or other blood-borne cells.
      Lipid peroxidation could initiate or promote the process of
      atherosclerotic lesion formation by directly damaging endothelial cells,
      and by enhancing the adhesion and activation of neutrophils and the
      susceptibility of platelets to aggregate. Endothelial cell injury by
      lipid hydroperoxides also could increase the uptake of LDL into the
      vessel wall. These events and other cellular dysfunctions may
      individually or collectively initiate and/or help to sustain the
      development of atherosclerosis.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Chow, C K
AU  - Chow CK
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Free Radic Biol Med
JT  - Free radical biology & medicine
JID - 8709159
RN  - 0 (Lipid Peroxides)
SB  - IM
MH  - Arteriosclerosis/*etiology
MH  - Endothelium/*cytology
MH  - Humans
MH  - Lipid Peroxides/*biosynthesis
MH  - Oxidation-Reduction
RF  - 77
EDAT- 1988/01/01 00:00
MHDA- 1988/01/01 00:01
CRDT- 1988/01/01 00:00
PHST- 1988/01/01 00:00 [pubmed]
PHST- 1988/01/01 00:01 [medline]
PHST- 1988/01/01 00:00 [entrez]
AID - 0891-5849(88)90070-6 [pii]
AID - 10.1016/0891-5849(88)90070-6 [doi]
PST - ppublish
SO  - Free Radic Biol Med. 1988;4(2):99-106. doi: 10.1016/0891-5849(88)90070-6.

PMID- 3384583
OWN - NLM
STAT- MEDLINE
DCOM- 19880809
LR  - 20161019
IS  - 0300-9831 (Print)
IS  - 0300-9831 (Linking)
VI  - 58
IP  - 1
DP  - 1988
TI  - Effect of vitamin E on oxysterol- and fatty acid hydroperoxide-induced
      changes of repair and permeability properties of cultured endothelial
      cell monolayers.
PG  - 41-7
AB  - Oxidation products of fatty acids (fatty acid hydroperoxides) or of
      cholesterol (oxysterols) may be atherogenic by being injurious to the
      vascular endothelium. Vitamin E may protect cells against such injury by
      acting as an antioxidant and by regulating cell growth and/or repair. As
      indices of proliferation and growth/repair, synthesis of DNA
      [3H]thymidine incorporation) and protein ([3H]leucine incorporation), as
      affected by exposure to linoleic acid hydroperoxide (18:2-OOH),
      cholestan-3 beta, 5 alpha, 6 beta-triol (Triol), and/or alpha-tocopherol,
      was determined in confluent vascular endothelial cell cultures. Cell
      injury was assessed by measuring the passage of albumin through a
      cultured endothelial monolayer. Exposure to either Triol or 18:2-OOH
      significantly increased the rate of albumin transfer across endothelial
      monolayers. Prior enrichment with vitamin E protected endothelial cells
      from injury by 18:2-OOH but not Triol. Cell exposure to 25 microM vitamin
      E increased DNA synthesis compared with control cultures. DNA synthesis
      was also elevated in 18:2-OOH exposed cells, whereas Triol had no effect
      on cell replication. Prior cell exposure to vitamin E prevented the
      marked increase in DNA synthesis seen with 18:2-OOH. Protein synthesis
      was increased by 18:2-OOH, but not by Triol or vitamin E treatment. These
      results show that 1) both Triol and 18:2-OOH are cytotoxic, 2) vitamin E
      stimulates cell proliferation, 3) vitamin E protects cells against
      18:2-OOH- but not Triol-induced cell injury (i.e., increased permeability
      to albumin), and 4) endothelial cell damage initiated by 18:2-OOH, but
      not Triol, stimulates synthesis of DNA and protein in an attempt to
      divide and repair the injury.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington.
FAU - Boissonneault, G A
AU  - Boissonneault GA
FAU - Fiscus, L J
AU  - Fiscus LJ
FAU - Marra, M E
AU  - Marra ME
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL34423/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Int J Vitam Nutr Res
JT  - International journal for vitamin and nutrition research. Internationale
      Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international
      de vitaminologie et de nutrition
JID - 1273304
RN  - 0 (Anticholesteremic Agents)
RN  - 0 (Fatty Acids)
RN  - 1406-18-4 (Vitamin E)
RN  - 7J48214Z9H (cholesterol hydroperoxide)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - GMW67QNF9C (Leucine)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Animals
MH  - Anticholesteremic Agents
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Cholesterol/*analogs & derivatives/toxicity
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Fatty Acids/*antagonists & inhibitors/toxicity
MH  - Leucine/metabolism
MH  - Oxidation-Reduction
MH  - Permeability
MH  - Thymidine/metabolism
MH  - Vitamin E/*pharmacology
EDAT- 1988/01/01 00:00
MHDA- 1988/01/01 00:01
CRDT- 1988/01/01 00:00
PHST- 1988/01/01 00:00 [pubmed]
PHST- 1988/01/01 00:01 [medline]
PHST- 1988/01/01 00:00 [entrez]
PST - ppublish
SO  - Int J Vitam Nutr Res. 1988;58(1):41-7.

PMID- 3426658
OWN - NLM
STAT- MEDLINE
DCOM- 19880212
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 68
IP  - 3
DP  - 1987 Dec
TI  - Cholestan-3 beta,5 alpha,6 beta-triol decreases barrier function of
      cultured endothelial cell monolayers.
PG  - 255-61
AB  - Cholesterol oxidation products (oxysterols) found in foods may be
      atherogenic, possibly by altering the barrier function of the vascular
      endothelium. To investigate this hypothesis, endothelial cells were
      cultured on micropore filters and the effect of cholesterol and the
      oxysterol cholestan-3 beta,5 alpha,6 beta-triol (Triol) on albumin
      transfer across cultured vascular endothelial monolayers (ECM) was
      studied. Exposure to Triol significantly increased albumin transfer
      across ECM. The effect of Triol on endothelial cell barrier function was
      time and concentration dependent, with maximum albumin transfer being
      reached at 20 microM Triol and after a 24-h exposure. Pure cholesterol,
      on the other hand, did not affect albumin transfer at concentrations as
      high as 130 microM. Although an increase in albumin transfer across ECM
      was observed after a 2-h incubation with Triol-enriched media, a 24-h
      incubation period was necessary to cause a significant release of
      cellular lactate dehydrogenase (LDH) into the culture media.
      Morphological perturbations of the cell monolayers were observed at
      approx. 14-18 h after cell exposure to Triol-enriched media. Enrichment
      with cholesterol or vitamin E did not prevent the Triol-induced increase
      in albumin transfer across ECM. These results suggest that exposure to
      oxidized cholesterol, but not cholesterol, itself, reduces the ability of
      the endothelium to act as a selectively permeable barrier to plasma
      components, and that these events may not be prevented by cholesterol or
      vitamin E.
FAU - Hennig, B
AU  - Hennig B
AD  - Department of Nutrition and Food Science, University of Kentucky,
      Lexington 40506.
FAU - Boissonneault, G A
AU  - Boissonneault GA
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
GR  - HL 34423/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Albumins)
RN  - 0 (Cholestanols)
RN  - 115510-05-9 (cholestane-3,5,6-triol)
RN  - 1406-18-4 (Vitamin E)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Albumins/metabolism
MH  - Animals
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cholestanols/*pharmacology
MH  - Cholesterol/pharmacology
MH  - Endothelium, Vascular/*drug effects
MH  - Permeability
MH  - Swine
MH  - Vitamin E/pharmacology
EDAT- 1987/12/01 00:00
MHDA- 1987/12/01 00:01
CRDT- 1987/12/01 00:00
PHST- 1987/12/01 00:00 [pubmed]
PHST- 1987/12/01 00:01 [medline]
PHST- 1987/12/01 00:00 [entrez]
AID - 0021-9150(87)90205-X [pii]
AID - 10.1016/0021-9150(87)90205-x [doi]
PST - ppublish
SO  - Atherosclerosis. 1987 Dec;68(3):255-61. doi:
      10.1016/0021-9150(87)90205-x.

TI  - The effect of silica-core gold-shell nanoparticles on the kinetics of biohydrogen production and hydrogenation application via organic acid photofermentation over enhanced near-infrared illumination
TA  - International journal of hydrogen energy

