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Articles 1 - 10 of 10
Full-Text Articles in Medicine and Health Sciences
Proliferation Of Acid-Secretory Cells In The Kidney During Adaptive Remodelling Of The Collecting Duct, Desa Welsh-Bacic, Marta Nowik, Brigitte Kaissling, Carsten A. Wagner
Proliferation Of Acid-Secretory Cells In The Kidney During Adaptive Remodelling Of The Collecting Duct, Desa Welsh-Bacic, Marta Nowik, Brigitte Kaissling, Carsten A. Wagner
Desa Welsh
The renal collecting duct adapts to changes in acid-base metabolism by remodelling and altering the relative number of acid or alkali secreting cells, a phenomenon termed plasticity. Acid secretory A intercalated cells (A-IC) express apical H+-ATPases and basolateral bicarbonate exchanger AE1 whereas bicarbonate secretory B intercalated cells (B-IC) express basolateral (and apical) H+-ATPases and the apical bicarbonate exchanger pendrin. Intercalated cells were thought to be terminally differentiated and unable to proliferate. However, a recent report in mouse kidney suggested that intercalated cells may proliferate and that this process is in part dependent on GDF-15. Here we extend these observations to …
Alcohol And Hepatitis C Virus--Interactions In Immune Dysfunctions And Liver Damage, Gyongyi Szabo, Jack Wands, Ahment Eken, Natalia Osna, Steven Weinman, Keigo Machida, Joe Wang
Alcohol And Hepatitis C Virus--Interactions In Immune Dysfunctions And Liver Damage, Gyongyi Szabo, Jack Wands, Ahment Eken, Natalia Osna, Steven Weinman, Keigo Machida, Joe Wang
Gyongyi Szabo
Hepatitis C virus infection affects 170 million people worldwide, and the majority of individuals exposed to HCV develop chronic hepatitis leading to progressive liver damage, cirrhosis, and hepatocellular cancer. The natural history of HCV infection is influenced by genetic and environmental factors of which chronic alcohol use is an independent risk factor for cirrhosis in HCV-infected individuals. Both the hepatitis C virus and alcohol damage the liver and result in immune alterations contributing to both decreased viral clearance and liver injury. This review will capture the major components of the interactions between alcohol and HCV infection to provide better understanding …
Factors That Determine The Development And Progression Of Gastroesophageal Varices In Patients With Chronic Hepatitis C, Robert Fontana, Arun Sanyal, Marc Ghany, William Lee, Andrea Reid, Deepa Naishadham, Gregory Everson, Jeffrey Kahn, Adrian Di Bisceglie, Gyongyi Szabo, Timothy Morgan, James Everhart
Factors That Determine The Development And Progression Of Gastroesophageal Varices In Patients With Chronic Hepatitis C, Robert Fontana, Arun Sanyal, Marc Ghany, William Lee, Andrea Reid, Deepa Naishadham, Gregory Everson, Jeffrey Kahn, Adrian Di Bisceglie, Gyongyi Szabo, Timothy Morgan, James Everhart
Gyongyi Szabo
BACKGROUND and AIMS: We aimed to identify the incidence and predictors of de novo gastroesophageal variceal formation and progression in a large cohort of patients with chronic hepatitis C and advanced fibrosis. METHODS: All participants in the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis Trial were offered an endoscopy before treatment and again after 4 years. Patients with varices at baseline also had an endoscopy at 2 years. Baseline laboratory and clinical parameters were analyzed as predictors of de novo variceal formation and variceal progression. RESULTS: De novo varices developed in 157 of the 598 (26.2%) patients. Most of the …
Type I Interferons Protect From Toll-Like Receptor 9-Associated Liver Injury And Regulate Il-1 Receptor Antagonist In Mice, Jan Petrasek, Angela Dolganiuc, Timea Csak, Evelyn Kurt-Jones, Gyongyi Szabo
Type I Interferons Protect From Toll-Like Receptor 9-Associated Liver Injury And Regulate Il-1 Receptor Antagonist In Mice, Jan Petrasek, Angela Dolganiuc, Timea Csak, Evelyn Kurt-Jones, Gyongyi Szabo
Gyongyi Szabo
BACKGROUND and AIMS: Liver inflammation and injury are mediated by the innate immune response, which is regulated by Toll-like receptors (TLR). Activation of TLR9 induces type I interferons (IFNs) via the interferon regulatory factor (IRF)-7. We investigated the roles of type I IFNs in TLR9-associated liver injury. METHODS: Wild-type (WT), IRF7-deficient, and IFN-alpha/beta receptor 1 (IFNAR1)-deficient mice were stimulated with TLR9 or TLR2 ligands. Findings from mice were verified in cultured hepatocytes and liver mononuclear cells (LMNCs) as well as in vivo experiments using recombinant type I IFN and interleukin-1 receptor antagonist (IL-1ra). RESULTS: Type I IFNs were up-regulated during …
Deficiency In Myeloid Differentiation Factor-2 And Toll-Like Receptor 4 Expression Attenuates Non-Alcoholic Steatohepatitis And Fibrosis In Mice, Timea Csak, Arumugam Velayudham, Istvan Hritz, Jan Petrasek, Ivan Levin, Dora Lippai, Donna Catalano, Pranoti Mandrekar, Angela Dolganiuc, Evelyn Kurt-Jones, Gyongyi Szabo
Deficiency In Myeloid Differentiation Factor-2 And Toll-Like Receptor 4 Expression Attenuates Non-Alcoholic Steatohepatitis And Fibrosis In Mice, Timea Csak, Arumugam Velayudham, Istvan Hritz, Jan Petrasek, Ivan Levin, Dora Lippai, Donna Catalano, Pranoti Mandrekar, Angela Dolganiuc, Evelyn Kurt-Jones, Gyongyi Szabo
Gyongyi Szabo
Toll-like receptor 4 (TLR4), and its co-receptor, Myeloid Differentiation Factor 2 (MD-2), are key in recognition of lipopolysaccharide (LPS) and activation of pro-inflammatory pathways. Here we tested the hypothesis that TLR4 and its co-receptor MD-2 play a central role in non-alcoholic steatohepatitis (NASH) and liver fibrosis in non-alcoholic fatty liver disease. Mice of control genotypes and those deficient in MD-2 or TLR4 (knock-out, KO) received methionine-choline-deficient (MCD) or methionine-choline-supplemented (MCS) diet. In mice of control genotypes MCD diet resulted in non-alcoholic steatohepatitis, liver triglycerides accumulation and increased Thiobarbituric Acid Reactive Substances (TBARS), a marker of lipid peroxidation, compared to MCS …
Interferon Regulatory Factor 3 And Type I Interferons Are Protective In Alcoholic Liver Injury In Mice By Way Of Crosstalk Of Parenchymal And Myeloid Cells, Jan Petrasek, Angela Dolganiuc, Timea Csak, Bharath Nath, Istvan Hritz, Karen Kodys, Donna Catalano, Evelyn Kurt-Jones, Pranoti Mandrekar, Gyongyi Szabo
Interferon Regulatory Factor 3 And Type I Interferons Are Protective In Alcoholic Liver Injury In Mice By Way Of Crosstalk Of Parenchymal And Myeloid Cells, Jan Petrasek, Angela Dolganiuc, Timea Csak, Bharath Nath, Istvan Hritz, Karen Kodys, Donna Catalano, Evelyn Kurt-Jones, Pranoti Mandrekar, Gyongyi Szabo
Gyongyi Szabo
Alcoholic liver disease (ALD) features increased hepatic exposure to bacterial lipopolysaccharide (LPS). Toll-like receptor-4 (TLR4) recognizes LPS and activates signaling pathways depending on MyD88 or TRIF adaptors. We previously showed that MyD88 is dispensable in ALD. TLR4 induces Type I interferons (IFNs) in an MyD88-independent manner that involves interferon regulatory factor-3 (IRF3). We fed alcohol or control diets to wild-type (WT) and IRF3 knock-out (KO) mice, and to mice with selective IRF3 deficiency in liver parenchymal and bone marrow-derived cells. Whole-body IRF3-KO mice were protected from alcohol-induced liver injury, steatosis, and inflammation. In contrast to WT or bone marrow-specific IRF3-KO …
The 40th Anniversary Of The National Institute On Alcoholism And Alcohol Abuse: The Impact On Liver Disease, Gyongyi Szabo
The 40th Anniversary Of The National Institute On Alcoholism And Alcohol Abuse: The Impact On Liver Disease, Gyongyi Szabo
Gyongyi Szabo
No abstract provided.
Innate Immunity And Alcoholic Liver Disease, Bin Gao, Ekihiro Seki, Jessica Cohen, Laura Nagy, Gyongyi Szabo, Samir Zakhari
Innate Immunity And Alcoholic Liver Disease, Bin Gao, Ekihiro Seki, Jessica Cohen, Laura Nagy, Gyongyi Szabo, Samir Zakhari
Gyongyi Szabo
Excessive alcohol consumption is a leading cause of chronic liver disease in the Western world. Alcohol-induced hepatotoxicity and oxidative stress are important mechanisms contributing to the pathogenesis of alcoholic liver disease. However, emerging evidence suggests that activation of innate immunity involving TLR4 and complement also plays an important role in initiating alcoholic steatohepatitis and fibrosis, but the role of adaptive immunity in the pathogenesis of alcoholic liver disease remains obscure. Activation of a TLR4-mediated MyD88-independent (TRIF/IRF-3) signaling pathway in Kupffer cells contributes to alcoholic steatohepatitis, while activation of TLR4 signaling in hepatic stellate cells promotes liver fibrosis. Alcohol consumption activates …
Alcohol Exposure As A Risk Factor For Adverse Outcomes In Elective Surgery, Bharath Nath, Youfu Li, James Carroll, Gyongyi Szabo, Jennifer Tseng, Shimul Shah
Alcohol Exposure As A Risk Factor For Adverse Outcomes In Elective Surgery, Bharath Nath, Youfu Li, James Carroll, Gyongyi Szabo, Jennifer Tseng, Shimul Shah
Gyongyi Szabo
BACKGROUND AND AIMS: Alcohol consumption is a well-documented determinant of adverse perioperative outcome. We sought to determine the effect of active alcohol consumption following elective surgery. METHODS: We queried discharge records from the American College of Surgeons' National Surgical Quality Improvement Program (NSQIP, 2005-2007) for all elective adult admissions. The 7,631 (2.5%) patients with documented alcohol use (active alcohol use of at least two drinks per day within 2 weeks of surgery; ETOH use) underwent elective surgery; 301,994 (97.5%) patients denied ETOH use. Multivariate analysis was performed with adjustments for demographic and comorbid factors. Primary outcome measures included length of …
Up-Regulation Of Microrna-155 In Macrophages Contributes To Increased Tumor Necrosis Factor {Alpha} (Tnf{Alpha}) Production Via Increased Mrna Half-Life In Alcoholic Liver Disease, Shashi Bala, Miguel Marcos, Karen Kodys, Timea Csak, Donna Catalano, Pranoti Mandrekar, Gyongyi Szabo
Up-Regulation Of Microrna-155 In Macrophages Contributes To Increased Tumor Necrosis Factor {Alpha} (Tnf{Alpha}) Production Via Increased Mrna Half-Life In Alcoholic Liver Disease, Shashi Bala, Miguel Marcos, Karen Kodys, Timea Csak, Donna Catalano, Pranoti Mandrekar, Gyongyi Szabo
Gyongyi Szabo
Activation of Kupffer cells (KCs) by gut-derived lipopolysaccharide (LPS) and Toll-Like Receptors 4 (TLR4)-LPS-mediated increase in TNFalpha production has a central role in the pathogenesis of alcoholic liver disease. Micro-RNA (miR)-125b, miR-146a, and miR-155 can regulate inflammatory responses to LPS. Here we evaluated the involvement of miRs in alcohol-induced macrophage activation. Chronic alcohol treatment in vitro resulted in a time-dependent increase in miR-155 but not miR-125b or miR-146a levels in RAW 264.7 macrophages. Furthermore, alcohol pretreatment augmented LPS-induced miR-155 expression in macrophages. We found a linear correlation between alcohol-induced increase in miR-155 and TNFalpha induction. In a mouse model of …