Michael W. Fried, Teerha Piratvisuth, George K. K. Lau, Patrick Marcellin, Wan‐Cheng Chow, Graham Cooksley, Kang‐Xian Luo, Seung Woon Paik, Yun‐Fan Liaw, Peter Button, Matei Popescu – 26 January 2008 – The aims of this study were to evaluate the usefulness of quantitative hepatitis B e antigen (HBeAg) values for predicting HBeAg seroconversion in patients treated with peginterferon alfa‐2a and to assess the dynamic changes in quantitative HBeAg during therapy, compared with conventional measures of serum hepatitis B virus DNA.

Norberto C. Chávez‐Tapia, Felix I. Tellez‐Avila, Misael Uribe – 26 January 2008

Luca Fabris, Massimiliano Cadamuro, Louis Libbrecht, Peggy Raynaud, Carlo Spirlì, Romina Fiorotto, Lajos Okolicsanyi, Frederic Lemaigre, Mario Strazzabosco, Tania Roskams – 26 January 2008 – Intrahepatic bile ducts maintain a close anatomical relationship with hepatic arteries. During liver ontogenesis, the development of the hepatic artery appears to be modulated by unknown signals originating from the bile duct.

Bo Shen, Jun Yu, Shiyan Wang, Eagle S.H. Chu, V.W.S. Wong, Xin Zhou, Ge Lin, Joseph J.Y. Sung, Henry L.Y. Chan – 26 January 2008 – Hepatic oxidative stress plays a critical role in metabolic forms of steatohepatitis. Phyllanthus urinaria, an herbal medicine, has been reported to have potential antioxidant properties. We tested the effects of P. urinaria on nutritional steatohepatitis both in vitro and in vivo. Immortalized normal hepatocytes (AML‐12) or primary hepatocytes were exposed to control, the methionine‐and‐choline‐deficient (MCD) culture medium, in the presence or absence of P.

Mladen I. Yovchev, Petar N. Grozdanov, Hongchao Zhou, Harini Racherla, Chandan Guha, Mariana D. Dabeva – 26 January 2008 – Oval cells appear and expand in the liver when hepatocyte proliferation is compromised. Many different markers have been attributed to these cells, but their nature still remains obscure. This study is a detailed gene expression analysis aimed at revealing their identity and repopulating in vivo capacity. Oval cells were activated in 2‐acetylaminofluorene–treated rats subjected to partial hepatectomy or in D‐galactosamine–treated rats.

Michael Charlton, Paul Angulo, Naga Chalasani, Ralph Merriman, Kimberly Viker, Phunchai Charatcharoenwitthaya, Schuyler Sanderson, Samer Gawrieh, Anuradha Krishnan, Keith Lindor – 26 January 2008 – The biological basis of variability in histological progression of nonalcoholic fatty liver disease (NAFLD) is unknown. Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone and has been shown to influence sensitivity to oxidative stress, insulin sensitivity, and expression of peroxisome proliferator‐activated receptor alpha and procollagen messenger RNA.

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.

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.

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.

Ian Homer Y. Cua, Jacob George – 26 January 2008