Tom Luedde, Maria E. Rodriguez, Frank Tacke, Yue Xiong, David A. Brenner, Christian Trautwein – 30 December 2003 – p18(INK4c) belongs to the family of cyclin‐dependent kinase inhibitory proteins that target the cyclin‐dependent kinases and inhibit their catalytic activity. The role of p18(INK4c) for cell cycle progression in vivo is characterized poorly. Therefore, we studied the expression and physiologic relevance of p18 in quiescent and proliferating hepatocytes during liver regeneration.

Amir Shlomai, Yosef Shaul – 30 December 2003 – RNA interference (RNAi) is the process of sequence‐specific gene silencing, initiated by double‐stranded RNA (dsRNA) that is homologous in sequence to the target gene. Because it has been shown that RNAi can be accomplished in cultured mammalian cells by introducing small interfering RNAs (siRNAs), much effort has been invested in exploiting this phenomenon for experimental and therapeutic means.

Giulio Marchesini, Elisabetta Bugianesi, Gabriele Forlani, Fernanda Cerrelli, Marco Lenzi, Rita Manini, Stefania Natale, Ester Vanni, Nicola Villanova, Nazario Melchionda, Mario Rizzetto – 30 December 2003 – Nonalcoholic fatty liver disease (NAFLD) has been associated with the insulin‐resistance syndrome, at present defined as the metabolic syndrome, whose limits were recently set. We assessed the prevalence of the metabolic syndrome in 304 consecutive NAFLD patients without overt diabetes, on the basis of 3 or more criteria out of 5 defined by the U.S.

Shinji Tanaka, Keishi Sugimachi, Toshifumi Kameyama, Shin‐ichiro Maehara, Ken Shirabe, Mitsuo Shimada, Jack R. Wands, Yoshihiko Maehara – 30 December 2003 – Family members of the connective tissue growth factor, cysteine‐rich 61, nephroblastoma over‐expressed gene (CCN) encode cysteine‐rich secreted proteins with roles in human fibrotic disorders and tumor progression. In this study, we identified a CCN family member, WISP1v, as over‐expressed in human cholangiocarcinomas. Genetic analysis of WISP1v was performed on surgically resected specimens of cholangiocarcinoma.

David E. Johnston – 30 December 2003

Catherine Sgro, François Clinard, Kader Ouazir, Henry Chanay, Christian Allard, Christian Guilleminet, Claude Lenoir, Alain Lemoine, Patrick Hillon – 30 December 2003 – The incidence of hepatic adverse drug reactions (ADRs) remains unknown in the general population. The goal of this population‐based study was to assess the incidence and seriousness of hepatic ADRs.

Yun Ma, Giorgina Mieli‐Vergani, Diego Vergani – 30 December 2003

Gautam P. Yagnik, Yoshihito Takahashi, George Tsoulfas, Kaye Reid, Noriko Murase, David A. Geller – 30 December 2003 – Organ graft preservation injury is a major problem complicating liver transplantation. The L‐arginine/nitric oxide pathway has protective effects in several models of liver injury. The purpose of this study was to evaluate the role of the L‐arginine/NO synthase (NOS) pathway on liver preservation injury and to characterize endogenous inducible NOS (iNOS) expression.

Lars E. Schmidt, Kim Dalhoff – 30 December 2003 – Hypophosphatemia is frequently observed in acetaminophen‐induced hepatotoxicity and may be involved in the pathogenesis of hepatic failure. The aim of the study was to evaluate the prognostic value of serial measurements of serum phosphate in patients with severe acetaminophen poisoning. Prospectively, serial measurements of serum phosphate were performed in 125 patients with severe acetaminophen poisoning. The optimum threshold value of serum phosphate to discriminate nonsurvivors was identified.

Steven P. Anderson, Lawrence Yoon, Erika B. Richard, Corrie S. Dunn, Russell C. Cattley, J. Christopher Corton – 30 December 2003 – Peroxisome proliferator chemicals, acting via the peroxisome proliferator‐activated receptor‐α (Pparα), are potent hepatic mitogens and carcinogens in mice and rats. To test whether Pparα is required for hepatic growth in response to other stimuli, we studied liver regeneration and hepatic gene expression following partial hepatectomy (PH) of wild‐type and Pparα‐null mice.