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).

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.

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

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.

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.

John Tsiaoussis, Philip Noel Newsome, Leonard Joseph Nelson, Peter Clive Hayes, John Nicholas Plevris – 30 December 2003 – Liver failure, notwithstanding advances in medical management, remains a cause of considerable morbidity and mortality in the developed world. Although bioartificial liver (BAL) support systems offer the potential of significant therapeutic benefit for such patients, many issues relating to their use are still to be resolved.

Philippe Ichai, Emmanuel Huguet, Catherine Guettier, Daniel Azoulay, Maria Eugenia Gonzalez, Bernard Fromenty, Pascal Masnou, Faouzi Saliba, Bruno Roche, Fahed Zeitoun, Denis Castaing, Didier Samuel – 30 December 2003 – Fulminant liver failure is a rare complication of grand mal seizures with a high mortality, the prognosis being largely determined by the combination of the hepatic and neurologic insults. The mechanisms of acute liver failure secondary to grand mal epilepsy and the place of liver transplantation in this context are poorly defined and are the subject of this report.

Toshiyuki Maruyama, Hiroshi Mitsui, Kazuyuki Hanajiri, Yasuhiko Sugawara, Hiroshi Imamura, Masatoshi Makuuchi – 30 December 2003

Wolfgang Hempfling, Frank Grunhage, Karin Dilger, Christoph Reichel, Ulrich Beuers, Tilman Sauerbruch – 30 December 2003 – Budesonide has been discussed as a potential treatment option in primary biliary cirrhosis (PBC). Therefore, we studied the pharmacokinetics and pharmacodynamics of budesonide in patients with PBC stage I/II and stage IV. Twelve patients with early PBC stage I/II and 7 patients with PBC stage IV under continuous treatment with ursodeoxycholic acid (UDCA) were enrolled in an exploratory trial.

Yoko Yamagiwa, Carla Marienfeld, Laura Tadlock, Tushar Patel – 30 December 2003 – The p38 mitogen‐activated protein kinase (MAPK) signaling pathway is aberrantly expressed and maintains transformed cell growth in malignant human cholangiocytes. Because cell growth requires and is intimately related to protein synthesis, our aims were to assess the effect of p38 MAPK signaling on protein synthesis during growth of malignant human cholangiocytes. Inhibition of p38 MAPK activity during mitogenic stimulation decreased protein synthesis rates and tumor cell xenograft growth in nude mice.