Recurrence of autoimmune disease, primary sclerosing cholangitis, primary biliary cirrhosis, and autoimmune hepatitis after liver transplantation
Jean‐Charles Duclos‐Vallee, Mylène Sebagh – 29 October 2009 – Key Points
Jean‐Charles Duclos‐Vallee, Mylène Sebagh – 29 October 2009 – Key Points
Sandra Ciesek, Eike Steinmann, Heiner Wedemeyer, Michael P. Manns, Johann Neyts, Norbert Tautz, Vanesa Madan, Ralf Bartenschlager, Thomas von Hahn, Thomas Pietschmann – 29 October 2009 – Numerous anti‐hepatitis C virus (HCV) drugs targeting either the viral nonstructural 3 (NS3) protease or NS5B polymerase are currently in clinical testing. However, rapid resistance development is a major problem and optimal therapy will clearly require a combination of multiple mechanisms of action.
Puneet Puri, Arun J. Sanyal – 29 October 2009
Neal D. Freedman, James E. Everhart, Karen L. Lindsay, Marc G. Ghany, Teresa M. Curto, Mitchell L. Shiffman, William M. Lee, Anna S. Lok, Adrian M. Di Bisceglie, Herbert L. Bonkovsky, John C. Hoefs, Jules L. Dienstag, Chihiro Morishima, Christian C. Abnet, Rashmi Sinha, HALT‐C Trial Group – 29 October 2009 – Higher coffee consumption has been associated inversely with the incidence of chronic liver disease in population studies. We examined the relationship of coffee consumption with liver disease progression in individuals with advanced hepatitis C–related liver disease.
Rachel Kassel, Michael W. Cruise, Julia C. Iezzoni, Nicholas A. Taylor, Timothy L. Pruett, Young S. Hahn – 29 October 2009 – Hepatitis B virus, hepatitis C virus, autoimmune hepatitis, and nonalcoholic fatty liver disease can induce chronic liver disease. The Programmed Death‐1 (PD‐1) inhibitory pathway assists in T cell response regulation during acute and chronic inflammation and participates in the progression of inflammatory liver disease.
Sven Schüngel, Laura Elisa Buitrago‐Molina, Padmavathi devi Nalapareddy, Margitta Lebofsky, Michael P. Manns, Hartmut Jaeschke, Atan Gross, Arndt Vogel – 29 October 2009 – The BH3‐interacting domain death agonist Bid has been shown to be critical for Fas‐induced hepatocellular apoptosis. Furthermore, some studies have suggested that phosphorylation of Bid may determine its apoptotic function and may act as a switch to nonapoptotic functions. The aim of this study was to evaluate the role of Bid and phosphorylated Bid for Fas ligand (FasL)‐induced apoptosis in murine livers.
Emily M. Fredericks – 29 October 2009 – Key Points
John Bucuvalas – 29 October 2009 – Key Points
Niloofar Ale‐Agha, Stefanie Galban, Christiane Sobieroy, Kotb Abdelmohsen, Myriam Gorospe, Helmut Sies, Lars‐Oliver Klotz – 29 October 2009 – Gap junctional intercellular communication (GJIC) plays a critical role in the regulation of tissue homeostasis and carcinogenesis and is modulated by the levels, subcellular localization, and posttranslational modification of gap junction proteins, the connexins (Cx). Here, using oval cell‐like rat liver epithelial cells, we demonstrate that the RNA‐binding protein HuR promotes GJIC through two mechanisms.