Coffee intake is associated with lower rates of liver disease progression in chronic hepatitis C

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.

Chronically inflamed livers up‐regulate expression of inhibitory B7 family members

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.

The strength of the Fas ligand signal determines whether hepatocytes act as type 1 or type 2 cells in murine livers

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.

HuR regulates gap junctional intercellular communication by controlling β‐catenin levels and adherens junction integrity

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.

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