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Article: Analysis of the Combined Effect of rs699 and rs5051 on Angiotensinogen Expression and Hypertension.

Powell, Nicholas R / Shugg, Tyler / Leighty, Jacob / Martin, Matthew / Kreutz, Rolf P / Eadon, Michael T / Lai, Dongbing / Lu, Tao / Skaar, Todd C

bioRxiv : the preprint server for biology

2023

Abstract: Hypertension (HTN) involves genetic variability in the renin-angiotensin system and characterizing this variability will help advance precision antihypertensive treatments. We previously reported that angiotensinogen ( ...

Abstract	Hypertension (HTN) involves genetic variability in the renin-angiotensin system and characterizing this variability will help advance precision antihypertensive treatments. We previously reported that angiotensinogen (
Language	English
Publishing date	2023-04-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.07.536073
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Article: Experimental models for the autoimmune and inflammatory blistering disease, Bullous pemphigoid.

Leighty, Lisa / Li, Ning / Diaz, Luis A / Liu, Zhi

Archives of dermatological research

2007 Volume 299, Issue 9, Page(s) 417–422

Abstract: Bullous pemphigoid (BP) is a subepidermal skin blistering disease characterized immunohistologically by dermal-epidermal junction (DEJ) separation, an inflammatory cell infiltrate in the upper dermis, and autoantibodies targeted toward the hemidesmosomal ...

Abstract	Bullous pemphigoid (BP) is a subepidermal skin blistering disease characterized immunohistologically by dermal-epidermal junction (DEJ) separation, an inflammatory cell infiltrate in the upper dermis, and autoantibodies targeted toward the hemidesmosomal proteins BP230 and BP180. Development of an IgG passive transfer mouse model of BP that reproduces these key features of human BP has demonstrated that subepidermal blistering is initiated by anti-BP180 antibodies and mediated by complement activation, mast cell degranulation, neutrophil infiltration, and proteinase secretion. This model is not compatible with study of human pathogenic antibodies, as the human and murine antigenic epitopes are not cross-reactive. The development of two novel humanized mouse models for the first time has enabled study of disease mechanisms caused by BP autoantibodies, and presents an ideal in vivo system to test novel therapeutic strategies for disease management.
MeSH term(s)	Animals ; Autoantibodies/blood ; Autoantigens/genetics ; Autoantigens/immunology ; Cricetinae ; Disease Models, Animal ; Epitope Mapping ; Genotype ; Humans ; Immunoglobulin G/blood ; Mice ; Mice, Transgenic ; Non-Fibrillar Collagens/genetics ; Non-Fibrillar Collagens/immunology ; Pemphigoid, Bullous/genetics ; Pemphigoid, Bullous/immunology ; Pemphigoid, Bullous/pathology ; Phenotype ; Rabbits ; Collagen Type XVII
Chemical Substances	Autoantibodies ; Autoantigens ; Immunoglobulin G ; Non-Fibrillar Collagens
Language	English
Publishing date	2007-09-19
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	130131-7
ISSN	1432-069X ; 0340-3696
ISSN (online)	1432-069X
ISSN	0340-3696
DOI	10.1007/s00403-007-0790-5
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Article ; Online: Small Molecule Targeting of Specific BAF (mSWI/SNF) Complexes for HIV Latency Reversal.

Marian, Christine A / Stoszko, Mateusz / Wang, Lili / Leighty, Matthew W / de Crignis, Elisa / Maschinot, Chad A / Gatchalian, Jovylyn / Carter, Benjamin C / Chowdhury, Basudev / Hargreaves, Diana C / Duvall, Jeremy R / Crabtree, Gerald R / Mahmoudi, Tokameh / Dykhuizen, Emily C

Cell chemical biology

2018 Volume 25, Issue 12, Page(s) 1443–1455.e14

Abstract: The persistence of a pool of latently HIV-1-infected cells despite combination anti-retroviral therapy treatment is the major roadblock for a cure. The BAF (mammalian SWI/SNF) chromatin remodeling complex is involved in establishing and maintaining viral ...

Abstract	The persistence of a pool of latently HIV-1-infected cells despite combination anti-retroviral therapy treatment is the major roadblock for a cure. The BAF (mammalian SWI/SNF) chromatin remodeling complex is involved in establishing and maintaining viral latency, making it an attractive drug target for HIV-1 latency reversal. Here we report a high-throughput screen for inhibitors of BAF-mediated transcription in cells and the subsequent identification of a 12-membered macrolactam. This compound binds ARID1A-specific BAF complexes, prevents nucleosomal positioning, and relieves transcriptional repression of HIV-1. Through this mechanism, these compounds are able to reverse HIV-1 latency in an in vitro T cell line, an ex vivo primary cell model of HIV-1 latency, and in patient CD4+ T cells without toxicity or T cell activation. These macrolactams represent a class of latency reversal agents with unique mechanism of action, and can be combined with other latency reversal agents to improve reservoir targeting.
MeSH term(s)	Animals ; Cell Line ; Chromosomal Proteins, Non-Histone/antagonists & inhibitors ; Chromosomal Proteins, Non-Histone/metabolism ; HIV-1/drug effects ; HIV-1/growth & development ; High-Throughput Screening Assays ; Mice ; Small Molecule Libraries/chemistry ; Small Molecule Libraries/pharmacology ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Virus Latency/drug effects ; Virus Latency/genetics
Chemical Substances	Chromosomal Proteins, Non-Histone ; SWI-SNF-B chromatin-remodeling complex ; Small Molecule Libraries ; Transcription Factors
Language	English
Publishing date	2018-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2451-9448
ISSN (online)	2451-9448
DOI	10.1016/j.chembiol.2018.08.004
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Article ; Online: Molecular and organismal changes in offspring of male mice treated with chemical stressors.

Shiao, Yih-Horng / Leighty, Robert M / Wang, Cuiju / Ge, Xin / Crawford, Erik B / Spurrier, Joshua M / McCann, Sean D / Fields, Janet R / Fornwald, Laura / Riffle, Lisa / Driver, Craig / Kasprzak, Kazimierz S / Quiñones, Octavio A / Wilson, Ralph E / Travlos, Gregory S / Alvord, W Gregory / Anderson, Lucy M

Environmental and molecular mutagenesis

2012 Volume 53, Issue 5, Page(s) 392–407

Abstract: Both gene methylation changes and genetic instability have been noted in offspring of male rodents exposed to radiation or chemicals, but few specific gene targets have been established. Previously, we identified the gene for ribosomal RNA, rDNA, as ... ...

Abstract	Both gene methylation changes and genetic instability have been noted in offspring of male rodents exposed to radiation or chemicals, but few specific gene targets have been established. Previously, we identified the gene for ribosomal RNA, rDNA, as showing methylation change in sperm of mice treated with the preconceptional carcinogen, chromium(III) chloride. rDNA is a critical cell growth regulator. Here, we investigated the effects of paternal treatments on rDNA in offspring tissue. A total of 93 litters and 758 offspring were obtained, permitting rigorous mixed-effects models statistical analysis of the results. We show that the offspring of male mice treated with Cr(III) presented increased methylation in a promoter sequence of the rDNA gene, specifically in lung. Furthermore polymorphic variants of the multi-copy rDNA genes displayed altered frequencies indicative of structural changes, as a function of both tissue type and paternal treatments. Organismal effects also occurred: some groups of offspring of male mice treated with either Cr(III) or its vehicle, acidic saline, compared with those of untreated mice, had altered average body and liver weights and levels of serum glucose and leptin. Males treated directly with Cr(III) or acidic saline presented serum hormone changes consistent with a stress response. These results establish for the first time epigenetic and genetic instability effects in a gene of central physiological importance, in offspring of male mice exposed preconceptionally to chemicals, possibly related to a stress response in these males.
MeSH term(s)	Animals ; DNA Methylation ; DNA, Ribosomal/genetics ; Genotype ; Insulin-Like Growth Factor I/genetics ; Male ; Mice ; Regulatory Sequences, Nucleic Acid ; Stress, Physiological/drug effects
Chemical Substances	DNA, Ribosomal ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2012-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.21701
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Article ; Online: Interleukin-1 and interferon-γ orchestrate β-glucan-activated human dendritic cell programming via IκB-ζ modulation.

Cardone, Marco / Dzutsev, Amiran K / Li, Hongchuan / Riteau, Nicolas / Gerosa, Franca / Shenderov, Kevin / Winkler-Pickett, Robin / Provezza, Lisa / Riboldi, Elena / Leighty, Robert M / Orr, Selinda J / Steinhagen, Folkert / Wewers, Mark D / Sher, Alan / Anderson, Stephen K / Goldszmid, Romina / McVicar, Daniel W / Lyakh, Lyudmila / Trinchieri, Giorgio

PloS one

2014 Volume 9, Issue 12, Page(s) e114516

Abstract: Recognition of microbial components via innate receptors including the C-type lectin receptor Dectin-1, together with the inflammatory environment, programs dendritic cells (DCs) to orchestrate the magnitude and type of adaptive immune responses. The ... ...

Abstract	Recognition of microbial components via innate receptors including the C-type lectin receptor Dectin-1, together with the inflammatory environment, programs dendritic cells (DCs) to orchestrate the magnitude and type of adaptive immune responses. The exposure to β-glucan, a known Dectin-1 agonist and component of fungi, yeasts, and certain immune support supplements, activates DCs to induce T helper (Th)17 cells that are essential against fungal pathogens and extracellular bacteria but may trigger inflammatory pathology or autoimmune diseases. However, the exact mechanisms of DC programming by β-glucan have not yet been fully elucidated. Using a gene expression/perturbation approach, we demonstrate that in human DCs β-glucan transcriptionally activates via an interleukin (IL)-1- and inflammasome-mediated positive feedback late-induced genes that bridge innate and adaptive immunity. We report that in addition to its known ability to directly prime T cells toward the Th17 lineage, IL-1 by promoting the transcriptional cofactor inhibitor of κB-ζ (IκB-ζ) also programs β-glucan-exposed DCs to express cell adhesion and migration mediators, antimicrobial molecules, and Th17-polarizing factors. Interferon (IFN)-γ interferes with the IL-1/IκB-ζ axis in β-glucan-activated DCs and promotes T cell-mediated immune responses with increased release of IFN-γ and IL-22, and diminished production of IL-17. Thus, our results identify IL-1 and IFN-γ as regulators of DC programming by β-glucan. These molecular networks provide new insights into the regulation of the Th17 response as well as new targets for the modulation of immune responses to β-glucan-containing microorganisms.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Cells, Cultured ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Humans ; I-kappa B Proteins/metabolism ; Interferon-gamma/physiology ; Interleukin 1 Receptor Antagonist Protein/physiology ; Interleukin-1/physiology ; Interleukin-23 Subunit p19/genetics ; Interleukin-23 Subunit p19/metabolism ; Lipopolysaccharides/pharmacology ; Nuclear Proteins/metabolism ; Promoter Regions, Genetic ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/metabolism ; Transcription, Genetic ; Transcriptional Activation ; Transcriptome ; beta-Glucans/pharmacology
Chemical Substances	Adaptor Proteins, Signal Transducing ; I-kappa B Proteins ; IL23A protein, human ; Interleukin 1 Receptor Antagonist Protein ; Interleukin-1 ; Interleukin-23 Subunit p19 ; Lipopolysaccharides ; NFKBIZ protein, human ; Nuclear Proteins ; beta-Glucans ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2014-12-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0114516
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Article ; Online: Ontogeny-driven rDNA rearrangement, methylation, and transcription, and paternal influence.

Shiao, Yih-Horng / Leighty, Robert M / Wang, Cuiju / Ge, Xin / Crawford, Erik B / Spurrier, Joshua M / McCann, Sean D / Fields, Janet R / Fornwald, Laura / Riffle, Lisa / Driver, Craig / Quiñones, Octavio A / Wilson, Ralph E / Kasprzak, Kazimierz S / Travlos, Gregory S / Alvord, W Gregory / Anderson, Lucy M

PloS one

2011 Volume 6, Issue 7, Page(s) e22266

Abstract: Gene rearrangement occurs during development in some cell types and this genome dynamics is modulated by intrinsic and extrinsic factors, including growth stimulants and nutrients. This raises a possibility that such structural change in the genome and ... ...

Abstract	Gene rearrangement occurs during development in some cell types and this genome dynamics is modulated by intrinsic and extrinsic factors, including growth stimulants and nutrients. This raises a possibility that such structural change in the genome and its subsequent epigenetic modifications may also take place during mammalian ontogeny, a process undergoing finely orchestrated cell division and differentiation. We tested this hypothesis by comparing single nucleotide polymorphism-defined haplotype frequencies and DNA methylation of the rDNA multicopy gene between two mouse ontogenic stages and among three adult tissues of individual mice. Possible influences to the genetic and epigenetic dynamics by paternal exposures were also examined for Cr(III) and acid saline extrinsic factors. Variables derived from litters, individuals, and duplicate assays in large mouse populations were examined using linear mixed-effects model. We report here that active rDNA rearrangement, represented by changes of haplotype frequencies, arises during ontogenic progression from day 8 embryos to 6-week adult mice as well as in different tissue lineages and is modifiable by paternal exposures. The rDNA methylation levels were also altered in concordance with this ontogenic progression and were associated with rDNA haplotypes. Sperm showed highest level of methylation, followed by lungs and livers, and preferentially selected haplotypes that are positively associated with methylation. Livers, maintaining lower levels of rDNA methylation compared with lungs, expressed more rRNA transcript. In vitro transcription demonstrated haplotype-dependent rRNA expression. Thus, the genome is also dynamic during mammalian ontogeny and its rearrangement may trigger epigenetic changes and subsequent transcriptional controls, that are further influenced by paternal exposures.
MeSH term(s)	Animals ; Base Sequence ; CpG Islands/genetics ; DNA Methylation/genetics ; DNA, Ribosomal/genetics ; Epigenesis, Genetic ; Gene Rearrangement/genetics ; Haplotypes/genetics ; Male ; Mice ; Models, Genetic ; Molecular Sequence Data ; Paternal Exposure ; Promoter Regions, Genetic/genetics ; Sequence Analysis, DNA ; Transcription, Genetic
Chemical Substances	DNA, Ribosomal
Language	English
Publishing date	2011-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0022266
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Article ; Online: Interleukin-1 and interferon-γ orchestrate β-glucan-activated human dendritic cell programming via IκB-ζ modulation.

Marco Cardone / Amiran K Dzutsev / Hongchuan Li / Nicolas Riteau / Franca Gerosa / Kevin Shenderov / Robin Winkler-Pickett / Lisa Provezza / Elena Riboldi / Robert M Leighty / Selinda J Orr / Folkert Steinhagen / Mark D Wewers / Alan Sher / Stephen K Anderson / Romina Goldszmid / Daniel W McVicar / Lyudmila Lyakh / Giorgio Trinchieri

PLoS ONE, Vol 9, Iss 12, p e

2014 Volume 114516

Abstract	Recognition of microbial components via innate receptors including the C-type lectin receptor Dectin-1, together with the inflammatory environment, programs dendritic cells (DCs) to orchestrate the magnitude and type of adaptive immune responses. The exposure to β-glucan, a known Dectin-1 agonist and component of fungi, yeasts, and certain immune support supplements, activates DCs to induce T helper (Th)17 cells that are essential against fungal pathogens and extracellular bacteria but may trigger inflammatory pathology or autoimmune diseases. However, the exact mechanisms of DC programming by β-glucan have not yet been fully elucidated. Using a gene expression/perturbation approach, we demonstrate that in human DCs β-glucan transcriptionally activates via an interleukin (IL)-1- and inflammasome-mediated positive feedback late-induced genes that bridge innate and adaptive immunity. We report that in addition to its known ability to directly prime T cells toward the Th17 lineage, IL-1 by promoting the transcriptional cofactor inhibitor of κB-ζ (IκB-ζ) also programs β-glucan-exposed DCs to express cell adhesion and migration mediators, antimicrobial molecules, and Th17-polarizing factors. Interferon (IFN)-γ interferes with the IL-1/IκB-ζ axis in β-glucan-activated DCs and promotes T cell-mediated immune responses with increased release of IFN-γ and IL-22, and diminished production of IL-17. Thus, our results identify IL-1 and IFN-γ as regulators of DC programming by β-glucan. These molecular networks provide new insights into the regulation of the Th17 response as well as new targets for the modulation of immune responses to β-glucan-containing microorganisms.
Keywords	Medicine ; R ; Science ; Q
Subject code	572
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Ontogeny-driven rDNA rearrangement, methylation, and transcription, and paternal influence.

Yih-Horng Shiao / Robert M Leighty / Cuiju Wang / Xin Ge / Erik B Crawford / Joshua M Spurrier / Sean D McCann / Janet R Fields / Laura Fornwald / Lisa Riffle / Craig Driver / Octavio A Quiñones / Ralph E Wilson / Kazimierz S Kasprzak / Gregory S Travlos / W Gregory Alvord / Lucy M Anderson

PLoS ONE, Vol 6, Iss 7, p e

2011 Volume 22266

Abstract	Gene rearrangement occurs during development in some cell types and this genome dynamics is modulated by intrinsic and extrinsic factors, including growth stimulants and nutrients. This raises a possibility that such structural change in the genome and its subsequent epigenetic modifications may also take place during mammalian ontogeny, a process undergoing finely orchestrated cell division and differentiation. We tested this hypothesis by comparing single nucleotide polymorphism-defined haplotype frequencies and DNA methylation of the rDNA multicopy gene between two mouse ontogenic stages and among three adult tissues of individual mice. Possible influences to the genetic and epigenetic dynamics by paternal exposures were also examined for Cr(III) and acid saline extrinsic factors. Variables derived from litters, individuals, and duplicate assays in large mouse populations were examined using linear mixed-effects model. We report here that active rDNA rearrangement, represented by changes of haplotype frequencies, arises during ontogenic progression from day 8 embryos to 6-week adult mice as well as in different tissue lineages and is modifiable by paternal exposures. The rDNA methylation levels were also altered in concordance with this ontogenic progression and were associated with rDNA haplotypes. Sperm showed highest level of methylation, followed by lungs and livers, and preferentially selected haplotypes that are positively associated with methylation. Livers, maintaining lower levels of rDNA methylation compared with lungs, expressed more rRNA transcript. In vitro transcription demonstrated haplotype-dependent rRNA expression. Thus, the genome is also dynamic during mammalian ontogeny and its rearrangement may trigger epigenetic changes and subsequent transcriptional controls, that are further influenced by paternal exposures.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Lack of increased hepatotoxicity in HIV-infected pregnant women receiving nevirapine compared with other antiretrovirals.

Ouyang, David W / Brogly, Susan B / Lu, Ming / Shapiro, David E / Hershow, Ronald C / French, Audrey L / Leighty, Robert M / Thompson, Bruce / Tuomala, Ruth E

AIDS (London, England)

2009 Volume 24, Issue 1, Page(s) 109–114

Abstract: Objective: To estimate whether HIV-infected pregnant women were at an increased risk of hepatotoxicity when taking nevirapine (NVP)-containing regimens compared with HIV-infected pregnant women taking antiretroviral therapy (ART) not containing NVP.: ... ...

Abstract	Objective: To estimate whether HIV-infected pregnant women were at an increased risk of hepatotoxicity when taking nevirapine (NVP)-containing regimens compared with HIV-infected pregnant women taking antiretroviral therapy (ART) not containing NVP. Methods: This analysis included HIV-infected pregnant women on ART from two multicenter, prospective cohorts: the Women and Infants Transmission Study and the International Maternal Pediatric Adolescent AIDS Clinical Trials protocol P1025. Multivariate Cox proportional hazards regression models were used to investigate the association between NVP use and hepatotoxicity. NVP use was dichotomized as use or no use and further categorized according to ART exposure history. We investigated two outcomes: any liver enzyme elevation (LEE) (grade 1-4) and severe LEE (grade 3-4). Results: A total of 1229 women with ART use during pregnancy were studied, 218 (17.7%) of whom received NVP. Among the women receiving NVP, 137 (62.8%) were NVP naive. Twenty-nine women (13.3%) who received NVP developed any LEE and one (0.5%) developed severe LEE. Of the 1011 women on non-NVP regimens, 145 (14.3%) developed any LEE and 14 (1.4%) developed severe LEE. There were no maternal deaths. In univariate models, LEE was not significantly associated with CD4 cell count above 250 cells/mul or NVP use. In adjusted multivariate models, no significant increased risk of LEE (any or severe) in women taking NVP was detected as compared to those taking other ART regardless of prior exposure history. Conclusion: We did not observe an increased risk of hepatotoxicity among HIV-infected pregnant women on NVP versus other ART, including women who were ART naive.
MeSH term(s)	Anti-HIV Agents/adverse effects ; Antiretroviral Therapy, Highly Active ; CD4 Lymphocyte Count ; Chemical and Drug Induced Liver Injury/prevention & control ; Cohort Studies ; Female ; HIV Infections/complications ; HIV Infections/drug therapy ; HIV-1 ; Humans ; Nevirapine/adverse effects ; Pregnancy ; Pregnancy Complications, Infectious/drug therapy ; Regression Analysis
Chemical Substances	Anti-HIV Agents ; Nevirapine (99DK7FVK1H)
Language	English
Publishing date	2009-11-20
Publishing country	England
Document type	Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0b013e3283323941
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Article ; Online: Increased risk of hepatotoxicity in HIV-infected pregnant women receiving antiretroviral therapy independent of nevirapine exposure.

Ouyang, David W / Shapiro, David E / Lu, Ming / Brogly, Susan B / French, Audrey L / Leighty, Robert M / Thompson, Bruce / Tuomala, Ruth E / Hershow, Ronald C

AIDS (London, England)

2009 Volume 23, Issue 18, Page(s) 2425–2430

Abstract: Objective: To estimate whether the association between nevirapine (NVP) and hepatotoxicity differs according to pregnancy status in HIV-infected women.: Methods: The present analysis included HIV-infected pregnant women on antiretroviral therapy (ART) ...

Abstract	Objective: To estimate whether the association between nevirapine (NVP) and hepatotoxicity differs according to pregnancy status in HIV-infected women. Methods: The present analysis included HIV-infected pregnant women on antiretroviral therapy (ART) from two multicenter, prospective cohorts - the Women and Infants Transmission Study and the International Maternal Pediatric Adolescent AIDS Clinical Trials protocol P1025 - and HIV-infected nonpregnant women from one multicenter, prospective cohort - the Women's Interagency HIV Study. Using multivariate Cox proportional hazards regression, the interaction between NVP and pregnancy status in terms of hepatotoxicity was investigated. NVP use was dichotomized as use or no use and was further categorized according to ART exposure history. We investigated two outcomes: any liver enzyme elevation (LEE; grade 1-4) and severe LEE (grade 3-4). Results: Data on 2050 HIV-infected women taking ART were included: 1229 (60.0%) pregnant and 821 (40.0%) nonpregnant. Among the pregnant women, 174 (14.2%) developed any LEE and 15 (1.2%) developed severe LEE as compared with 75 (9.1%) and 5 (0.6%), respectively, of the nonpregnant women. In multivariate adjusted models, NVP was not significantly associated with risk of LEE, regardless of pregnancy status; however, pregnancy was associated with an increased risk of any LEE (relative risk 4.7, confidence interval = 3.4-6.5) and severe LEE (relative risk 3.8, confidence interval = 1.3-11.1). The association of pregnancy and LEE was seen, regardless of prior ART and NVP exposure history. Conclusion: No significant association between NVP and LEE was observed, regardless of pregnancy status, but pregnancy was significantly associated with increased hepatotoxocity in HIV-infected women.
MeSH term(s)	Anti-HIV Agents/adverse effects ; Anti-Retroviral Agents/adverse effects ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/prevention & control ; Female ; HIV Infections/complications ; HIV Infections/drug therapy ; HIV Infections/transmission ; Humans ; Infectious Disease Transmission, Vertical/prevention & control ; Nevirapine/adverse effects ; Pregnancy ; Pregnancy Complications, Infectious/drug therapy ; Prospective Studies ; Regression Analysis ; Treatment Outcome
Chemical Substances	Anti-HIV Agents ; Anti-Retroviral Agents ; Nevirapine (99DK7FVK1H)
Language	English
Publishing date	2009-07-17
Publishing country	England
Document type	Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0b013e32832e34b1
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