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13 results match your criteria: "West Haven Veterans Medical Center[Affiliation]"
J Hepatol
January 2025
Section of Digestive Diseases, Yale School of Medicine and Department of Gastroenterology, West Haven Veterans Medical Center, USA. Electronic address:
J Hepatol
November 2024
Division of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria; Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria; Center for Molecular Medicine (CeMM) of the Austrian Academy of Science, Vienna, Austria.
J Hepatol
April 2024
Section of Digestive Diseases, Yale School of Medicine and Department of Gastroenterology, West Haven Veterans Medical Center, United States. Electronic address:
World J Gastroenterol
March 2023
Section of Digestive Diseases, Yale School of Medicine, New Haven, CT 06510, United States.
Repurposing of the widely available and relatively cheap generic cardiac gly-coside digoxin for non-cardiac indications could have a wide-ranging impact on the global burden of several diseases. Over the past several years, there have been significant advances in the study of digoxin pharmacology and its potential non-cardiac clinical applications, including anti-inflammatory, antineoplastic, metabolic, and antimicrobial use. Digoxin holds promise in the treatment of gastrointestinal disease, including nonalcoholic steatohepatitis and alcohol-associated steatohepatitis as well as in obesity, cancer, and treatment of viral infections, among other conditions.
View Article and Find Full Text PDFHepatology
November 2023
Department of Internal Medicine, Section of Digestive Diseases, Yale School of Medicine, New Haven, Connecticut, USA.
Background And Aims: TGF-β induces multiple structural and functional changes in quiescent HSCs, including an increase in proliferation, mitochondrial mass, and matrix deposition. HSC transdifferentiation requires significant bioenergetic capacity, and it is not known how TGF-β-mediated transcriptional upregulation is coordinated with the bioenergetic capacity of HSCs.
Approach And Results: Mitochondria are key bioenergetic organelles, and here, we report that TGF-β induces release of mitochondrial DNA (mtDNA) from healthy HSCs through voltage-dependent anion channels (VDACs), with the formation of an mtDNA-CAP on the external mitochondrial membrane.
Trends Pharmacol Sci
April 2023
Section of Digestive Diseases, Yale School of Medicine, PO Box 208019, New Haven, CT 06520, USA. Electronic address:
The cardiac glycoside (CG) digoxin is a generic drug approved for the treatment of heart failure and supraventricular arrhythmias. Over the past few decades, substantial strides have been made toward repurposing digoxin to treat various noncardiac diseases. Here, we evaluate recent insights into basic and clinical work related to noncardiac use of digoxin.
View Article and Find Full Text PDFHepatology
August 2019
NAFLD Research Center, Division of Gastroenterology, University of California at San Diego, La Jolla, CA.
J Hepatol
September 2018
Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT 06520, USA; USA West Haven Veterans Medical Center, West Haven, CT 06516, USA. Electronic address:
Background & Aims: Sterile inflammation resulting in alcoholic hepatitis (AH) occurs unpredictably after many years of excess alcohol intake. The factors responsible for the development of AH are not known but mitochondrial damage with loss of mitochondrial function are common features. Hcar2 is a G-protein coupled receptor which is activated by β-hydroxybutyrate (BHB).
View Article and Find Full Text PDFCell Metab
February 2018
Section of Digestive Diseases, Yale University, New Haven, CT 06520, USA; West Haven Veterans Medical Center, West Haven, CT 06516, USA. Electronic address:
Sterile inflammation after tissue damage is a ubiquitous response, yet it has the highest amplitude in the liver. This has major clinical consequences, for alcoholic and non-alcoholic steatohepatitis (ASH and NASH) account for the majority of liver disease in industrialized countries and both lack therapy. Requirements for sustained sterile inflammation include increased oxidative stress and activation of the HIF-1α signaling pathway.
View Article and Find Full Text PDFSemin Liver Dis
February 2016
Department of Pediatrics, University of California San Diego (UCSD), and Rady Children's Hospital, San Diego, California.
Nonalcoholic fatty liver disease represents a wide spectrum of conditions and is currently the most common form of chronic liver disease affecting both adults and children in the United States and many other parts of the world. Great effort has been focused on the development of novel therapies for those patients with the more advanced forms of the disease, in particular those with nonalcoholic steatohepatitis (NASH) and liver fibrosis that can be associated with significant morbidity and mortality. In this review, the authors focus on the role of cell death and sterile inflammatory pathways as well as the self-perpetuating deleterious cycle they may trigger as novel therapeutic targets for the treatment of fibrotic NASH.
View Article and Find Full Text PDFBiochim Biophys Acta
July 2013
Section of Digestive Diseases, Yale University, New Haven, CT, USA; West Haven Veterans Medical Center, New Haven, CT, USA.
Pathogens and sterile insults both result in an inflammatory response. A significant part of this response is mediated by cytosolic machinery termed as the inflammasome which results in the activation and secretion of the cytokines interleukin-1β (IL-1β) and IL-18. Both of these are known to result in the activation of an acute inflammatory response, resulting in the production of downstream inflammatory cytokines such as tumor necrosis factor (TNF-α), interferon-gamma (IFN-γ), chemotaxis of immune cells, and induction of tissue injury.
View Article and Find Full Text PDFJ Hepatol
May 2013
Section of Digestive Diseases, Yale University, and West Haven Veterans Medical Center, New Haven, CT, United States.
Tissue stress and cell death result in inflammation even in the absence of pathogens. Such sterile inflammation is dependent on a cytosolic complex of proteins inside immune cells termed the inflammasome. This complex converts two groups of extracellular signals into an inflammatory response via activation of caspase-1 and secretion of IL-1β and IL-18.
View Article and Find Full Text PDFGastroenterology
November 2012
Section of Digestive Diseases, Yale University, and West Haven Veterans Medical Center, New Haven, Connecticut. Electronic address:
Inflammation In the absence of pathogens occurs in all tissues in response to a wide range of stimuli that cause tissue stress and injury. Such sterile inflammation (SI) is a key process in drug-induced liver injury, nonalcoholic steatohepatitis, and alcoholic steatohepatitis and is a major determinant of fibrosis and carcinogenesis. In SI, endogenous damage-associated molecular patterns (DAMPS), which are usually hidden from the extracellular environment, are released on tissue injury and activate receptors on immune cells.
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