Christian Pichoud, Béatrice Seignères, Zhirui Wang, Christian Trépo, Fabien Zoulim – 30 December 2003 – Prolonged therapy for chronic hepatitis B (HBV) with nucleoside analogs may result in the emergence of HBV mutants resistant to antivirals. Here, we describe the transient selection of an HBV polymerase gene mutant that was associated with viral persistence in an immune competent patient treated with famciclovir. Viral polymerase gene sequence was analyzed directly on polymerase chain reaction (PCR) products and also after cloning.

Anne‐Marie Bonnand, E. Jenny Heathcote, Keith D. Lindor, Renée Eugénie Poupon – 30 December 2003 – We determined whether the normalization of serum bilirubin level (SBL) induced by ursodeoxycholic acid (UDCA) therapy was associated with an improved clinical outcome in patients with primary biliary cirrhosis (PBC). We estimated the prognostic values of SBL measured after 6 months of UDCA treatment for survival free of orthotopic liver transplantation (OLT). We used a database of 548 patients with PBC followed in three trials of UDCA.

Josep M. Llovet, Javier Bustamante, Antoni Castells, Ramon Vilana, Maria Del Carmen Ayuso, Margarita Sala, Concepció Brú, Joan Rodés, Jordi Bruix – 30 December 2003 – This study analyzed the natural history and prognostic factors of patients with nonsurgical hepatocellular carcinoma (HCC). Twenty variables from 102 cirrhotic patients with HCC who were not treated within prospective randomized controlled trials (RCT) were investigated through uni‐ and multivariate analyses.

Frieder Berr, Marcus Wiedmann, Joachim Mössner, Andrea Tannapfel, Frank Schmidt – 30 December 2003

Cynthia R. Gross, Michael Malinchoc, W. Ray Kim, Roger W. Evans, Russell H. Wiesner, Janice L. Petz, Jeffrey S. Crippin, Goran B. Klintmalm, Marlon F. Levy, Paola Ricci, Terry M. Therneau, E. Rolland Dickson – 30 December 2003 – Liver transplantation (LT) is an established therapy for patients with end‐stage primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC). In this report, we describe the health status and quality of life (QOL) in patients with these cholestatic liver diseases before and after LT.

Itsuki Ajioka, Toshihiro Akaike, Yoshifumi Watanabe – 30 December 2003 – A complex vascular network forms an important component of the liver architecture. This network is essential for the supply of oxygen and nutrients to cells and delivery of molecules for metabolic exchange. In this study, we attempted to construct a vascular network in transplanted hepatic tissues and examined the effect of such network on tissue formation.

Andrew L. Mason, Johnson Y. Lau, Nicole Hoang, KePing Qian, Graeme J. Alexander, Lizhe Xu, Linsheng Guo, Sheraj Jacob, Fredric G. Regenstein, Robert Zimmerman, James E. Everhart, Clive Wasserfall, Noel K. Maclaren, Robert P. Perrillo – 30 December 2003 – While patients with liver disease are known to have a higher prevalence of glucose intolerance, preliminary studies suggest that hepatitis C virus (HCV) infection may be an additional risk factor for the development of diabetes mellitus.

Tsutomu Masaki, Masato Okada, Masaki Tokuda, Yasushi Shiratori, Osamu Hatase, Mutsunori Shirai, Mikio Nishioka, Masao Omata – 30 December 2003 – The proto‐oncogene product pp60c‐src is the cellular homologue of the Rous sarcoma transforming gene, and it is a non–receptor‐linked and membrane‐associated tyrosine kinase. There is a close correlation between elevated pp60c‐src activity and cell transformation. We have recently reported that pp60c‐src was activated in hepatocellular carcinoma (HCC) of human and Long‐Evans cinnamon (LEC) rats.

Michael Friedt, Patrick Gerner, Ekkehart Lausch, Hubert Trübel, Bernhard Zabel, Stefan Wirth – 30 December 2003 – The involvement of precore stop codon 1896‐A and base exchanges in the AT‐rich region at positions 1762 and 1764 of the hepatitis B core promotor has been controversely discussed in adults with fulminant hepatitis B. Because no data are currently available on children, we analyzed the basic core promotor (BCP) and precore region in children with chronic and fulminant hepatitis B. The BCP and precore region were sequenced directly and after cloning from mothers and infants.

Andrea Galli, Donna Price, David Crabb – 30 December 2003 – The mechanisms by which ethanol causes fatty liver are complex. Reducing equivalents generated during ethanol oxidation inhibit tricarboxylic acid cycle activity and fatty acid oxidation. In addition, ethanol inhibits lipoprotein export and increases fatty acid uptake and lipid peroxidation. To test the role that alcohol metabolism by alcohol dehydrogenase (ADH) has on cellular lipid metabolism, a cell line expressing rat ADH was generated by transducing HeLa cells with an ADH‐expressing retrovirus.