Survival and recurrence of hepatitis C after liver transplantation in patients coinfected with human immunodeficiency virus and hepatitis C virus

Jean‐Charles Duclos‐Vallée, Cyrille Féray, Mylène Sebagh, Elina Teicher, Anne‐Marie Roque‐Afonso, Bruno Roche, Daniel Azoulay, René Adam, Henri Bismuth, Denis Castaing, Daniel Vittecoq, Didier Samuel, THEVIC Study Group – 26 January 2008 – Liver transplantation in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is a recent indication. In a single center, we have compared the survival and severity of recurrent HCV infection after liver transplantation in HIV‐HCV–coinfected and HCV‐monoinfected patients.

Coculture of human liver macrophages and cholangiocytes leads to CD40‐dependent apoptosis and cytokine secretion

Edward B. Alabraba, Vincent Lai, Louis Boon, Stephen J. Wigmore, David H. Adams, Simon C. Afford – 26 January 2008 – In the vanishing bile duct syndromes (VBDS), primary biliary cirrhosis and chronic allograft rejection, cholangiocyte apoptosis is associated with sustained macrophage infiltration of the liver, suggesting that these cells may mediate tissue damage and contribute to bile duct destruction. We have previously reported that activation of CD40 on cholangiocytes with either soluble CD154 or cross‐linking monoclonal antibody to CD40 induces apoptosis in vitro.

Hepatitis C virus receptor expression in normal and diseased liver tissue

Gary M. Reynolds, Helen J. Harris, Adam Jennings, Ke Hu, Joe Grove, Patricia F. Lalor, David H. Adams, Peter Balfe, Stefan G. Hübscher, Jane A. McKeating – 26 January 2008 – The principal site of hepatitis C virus (HCV) replication is the liver. HCV pseudoparticles infect human liver derived cell lines and this suggests that liver‐specific receptors contribute to defining HCV hepatotropism.

Systemic transmigration of allosensitizing donor dendritic cells to host secondary lymphoid organs after rat liver transplantation

Hisashi Ueta, Changde Shi, Nobutomo Miyanari, Xue‐Dong Xu, Shu Zhou, Masaki Yamashita, Taichi Ezaki, Kenjiro Matsuno – 25 January 2008 – Donor dendritic cell (DC) migration and allosensitization in host secondary lymphoid organs after liver transplantation are ill defined. We used rat models to investigate graft‐derived cells and intrahost allosensitization.

Caspase activation is associated with spontaneous recovery from acute liver failure

Xandra Volkmann, Matthias Anstaett, Johannes Hadem, Penelope Stiefel, Matthias J. Bahr, Frank Lehner, Michael P. Manns, Klaus Schulze‐Osthoff, Heike Bantel – 24 January 2008 – Acute liver failure (ALF) has various causes and is characterized by rapid hepatocyte dysfunction with development of encephalopathy in the absence of preexisting liver disease. Whereas most patients require liver transplantation to prevent the high mortality, some patients recover spontaneously and show complete liver regeneration.

Mesenchymal stem cell–derived molecules directly modulate hepatocellular death and regeneration in vitro and in vivo

Daan van Poll, Biju Parekkadan, Cheul H. Cho, François Berthiaume, Yaakov Nahmias, Arno W. Tilles, Martin L. Yarmush – 24 January 2008 – Orthotopic liver transplantation is the only proven effective treatment for fulminant hepatic failure (FHF), but its use is limited because of organ donor shortage, associated high costs, and the requirement for lifelong immunosuppression. FHF is usually accompanied by massive hepatocellular death with compensatory liver regeneration that fails to meet the cellular losses.

Mechanisms of hepatocyte growth factor–mediated and epidermal growth factor–mediated signaling in transdifferentiation of rat hepatocytes to biliary epithelium

Pallavi B. Limaye, William C. Bowen, Anne V. Orr, Jianhua Luo, George C. Tseng, George K. Michalopoulos – 21 January 2008 – Previous studies from our laboratory have demonstrated that hepatocytes can transdifferentiate into biliary epithelium (BE) both in vivo and in vitro; however, the mechanisms are unclear. The current study was designed to investigate the mechanisms of hepatocyte transdifferentiation in vitro.

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