Hanns‐Ulrich Marschall, Udo C.I. Oppermann, Stefan Svensson, Erik Nordling, Bengt Persson, Jan‐Olov Höög, Hans Jörnvall – 30 December 2003 – 3β‐Hydroxy (iso) bile acids are formed during enterohepatic circulation from 3α‐hydroxy bile acids and constitute normal compounds in plasma but are virtually absent in bile. Isoursodeoxycholic acid (isoUDCA) is a major metabolite of UDCA. In a recent study it was found that after administration of isoUDCA, UDCA became the major acid in bile.

Pietro E. Majno, François P. Sarasin, Gilles Mentha, Antoine Hadengue – 30 December 2003 – Two treatments are accepted for patients with solitary hepatocellular carcinoma ≤5 cm in size and with preserved hepatic function: (1) liver resection, which can be performed without delay but has a high recurrence rate, and (2) liver transplantation, which has a better long‐term survival, but is not easily available because grafts are scarce.

Albert J. Czaja, Michawl P. Manns, Ian G. Mcfarlane, Jay H. Hoofnagle – 30 December 2003

Hiroshi Okabe, Iwao Ikai, Koichi Matsuo, Seiji Satoh, Hirohito Momoi, Tatsuhiko Kamikawa, Nagato Katsura, Ryuta Nishitai, Osamu Takeyama, Manabu Fukumoto, Yoshio Yamaoka – 30 December 2003 – To examine the role of the loss of heterozygosity (LOH) in hepatitis‐related carcinogenesis, we performed a genome‐wide scan of LOH in 44 tumors of hepatocellular carcinoma (HCC) using 216 microsatellite markers throughout all human chromosomes. A high frequency of LOH (>30% of informative cases) was observed at 33 loci on chromosome arms 4q, 6q, 8p, 8q, 9p, 9q, 13q, 16p, 16q, 17p, and 19p.

John G. Pastorino, Jan B. Hoek – 30 December 2003 – In the present study, tumor necrosis factor‐α (TNF‐α) cytotoxicity is shown to be potentiated by ethanol exposure in vitroin the human hepatoma cell line, HepG2, and in rat primary hepatocytes. Exposure of HepG2 cells and primary hepatocytes for 48 hours to concentrations of ethanol ranging between 50 and 100 mmol/L significantly increased TNF‐α cytotoxicity compared with cells treated with TNF‐α alone. The cell killing was associated with, and dependent on, the development of the mitochondrial permeability transition (MPT).

Marina Berenguer, F. Xavier López‐Labrador, Harry B. Greenberg, Teresa L. Wright – 30 December 2003

Paul Glue, Regine Rouzier‐Panis, Claude Raffanel, Ron Sabo, Samir K. Gupta, Margaret Salfi, Shiela Jacobs, Robert P. Clement – 30 December 2003 – The objectives of this study were to assess the safety, pharmacokinetics, and efficacy of pegylated interferon alfa‐2b (PEG‐Intron) plus ribavirin in patients with chronic hepatitis C. A total of 72 patients (35 men/37 women, age range 20‐68 years) with clinically compensated chronic hepatitis C virus (HCV) were enrolled into this open‐label, randomized, active controlled study.

Caroline Freathy, David G. Brown, Ruth A. Roberts, Kelvin Cain – 30 December 2003 – In mammalian cells, non receptor‐mediated apoptosis occurs via the cytochrome c–dependent assembly of a ∼700‐kd apoptotic protease‐activating factor 1 (Apaf‐1)/caspase‐9 containing apoptosome complex. This initiates the postmitochondrial‐mediated effector caspase cascade. We now show that receptor mediated transforming growth factor β1(TGF‐β1)–induced apoptosis in rat hepatoma cells is accompanied by processing and activation of caspases‐2, ‐3, ‐7, and ‐8.

Dominique Crenesse, Jean Gugenheim, Joelle Hornoy, Karine Tornieri, Marina Laurens, Beatrice Cambien, Gaelle Lenegrate, Rafaele Cursio, Georges De Souza, Patrick Auberger, Catherine Heurteaux, Bernard Rossi, Annie Schmid‐Alliana – 30 December 2003 – Ischemia‐reperfusion procedures induced severe hepatic damages owing to different processes related to hypoxia and reoxygenation (H/R) phases, including the consecutive oxygen free radical (OFR) release. Stress‐activated protein kinases (SAPKs) could be activated by extracellular stimuli.

Judy A. Lawson, Alan R. Burns, Anwar Farhood, Mary Lynn Bajt, Robert G. Collins, C. Wayne Smith, Hartmut Jaeschke – 30 December 2003 – Neutrophils can cause parenchymal cell injury in the liver during ischemia‐reperfusion and endotoxemia. Neutrophils relevant for the injury accumulate in sinusoids, transmigrate, and adhere to hepatocytes. To investigate the role of E‐ and L‐selectin in this process, C3Heb/FeJ mice were treated with 700 mg/kg galactosamine and 100 μg/kg endotoxin (Gal/ET).