Juanjuan Chen, Neal C. Robinson, Steven Schenker, Teri A. Frosto, George I. Henderson – 30 December 2003 – This study addresses the role of the lipid peroxidation product, 4‐hydroxynonenal (HNE), in ethanol‐related damage of cytochrome c oxidase (COX) in vivo. It utilizes an animal model with acute ethanol exposure in which HNE levels in liver mitochondria are strikingly increased. Pregnant female Sprague‐Dawley rats were administered 5 doses of ethanol (4 gm/kg, po at 12‐hour intervals) beginning on day 17 of gestation and were sacrificed on day 19.

Massimino Carrella, Douglas Feldman, Susanna Cogoi, Annalisa Csillaghy, Paul A. Weinhold – 30 December 2003 – An increase of biliary lipid secretion is known to occur in the rat under sustained administration of statin‐type 3‐hydroxy‐3‐methylglutaryl (HMG) coenzyme A (CoA) reductase inhibitors. The present study has addressed critical mechanisms of hepatic lipid synthesis and phosphatidylcholine (PC) biliary transport in the rat fed with a 0.075% pravastatin diet for 3 weeks.

Mercedes Fernandez, Herbert L. Bonkovsky – 30 December 2003 – Heme oxygenase (HO) catalyzes the conversion of heme into biliverdin, iron, and carbon monoxide (CO). Two isoforms of HO have been identified: the inducible HO‐1 and the constitutive HO‐2. CO, like nitric oxide, is an endogenous vasodilator that could contribute to modulation of systemic and local vascular tone. The aim of the present study was to determine the expression of HO isoforms in liver cells and splanchnic organs from portal hypertensive (PH) and sham‐operated (SO) rats.

Miriam T. Levy, Geoffrey W. McCaughan, Catherine A. Abbott, John E. Park, Anne M. Cunningham, Erika Müller, Wolfgang J. Rettig, Mark D. Gorrell – 30 December 2003 – Fibroblast activation protein (FAP) is a cell surface–bound protease of the prolyl oligopeptidase gene family expressed at sites of tissue remodelling. This study aimed to delineate the expression of FAP in cirrhotic human liver and examine its biochemical activities. Seventeen cirrhotic and 8 normal liver samples were examined by immunohistochemistry and reverse‐transcriptase polymerase chain reaction (RT‐PCR).

Mikiji Mori, Makoto Suematsu, Takanori Kyokane, Tsuyoshi Sano, Hidekazu Suzuki, Tokio Yamaguchi, Yuzuru Ishimura, Hiromasa Ishii – 30 December 2003 – This study aimed to examine whether acetaminophen (AAP), an anti‐inflammatory agent producing hepatocellular damages with its overdose, evokes hepatocellular dysfunction through mechanisms involving carbon monoxide (CO) generated by heme oxygenase (HO). In perfused rat livers, CO and bilirubin were determined in venous perfusate and bile samples as indices of heme degradation.

Hiroyuki Yoshidome, Atsushi Kato, Michael J. Edwards, Alex B. Lentsch – 30 December 2003 – Ischemia/reperfusion injury of the liver requires the participation of proinflammatory cytokines, chemokines, and adhesion molecules, many of which are regulated by the transcription factor nuclear factor κB (NFκB). The anti‐inflammatory cytokine, interleukin‐10 (IL‐10) affects inflammatory reactions, at least in part, through inhibitory effects on the transcription factor, NFκB.

G. Aravinda Upadhya, Steven M. Strasberg – 30 December 2003 – Cold preservation induces the secretion of matrix metalloproteinases (MMPs) by hepatic sinusoidal endothelial cells (SECs). These enzymes are important mediators of cold preservation injury. The purpose of this study was to determine if low temperature caused actin disassembly in SECs and whether actin disassembly was required for secretion of MMPs under these conditions.

Markus Selzner, Carlos A. Camargo, Pierre‐Alain Clavien – 30 December 2003 – The effects of ischemia on the regenerative capacity of the liver after major tissue loss remain unclear. Interleukin‐6 (IL‐6) has been shown to confer protection in models of normothermic ischemia and reperfusion injury and to initiate hepatocyte proliferation after major hepatectomy.

B. Le Bail, J. Carles, J. Saric, C. Balabaud, P. Bioulac‐Sage – 30 December 2003

Christophe Hézode, Christophe Duvoux, Georgios Germanidis, Françoise Roudot‐Thoraval, Anne‐Laure Vincens, Philippe Gaulard, Daniel Cherqui, Jean‐Michel Pawlotsky, Daniel Dhumeaux – 30 December 2003 – It has been suggested that hepatitis C virus (HCV) infection could be associated with B‐cell clonal expansion. The aim of this study was to analyze the relationship between lymphoproliferative disorders and HCV infection in liver transplant recipients. We studied 157 patients receiving a liver transplant between January 1989 and May 1997 with a follow‐up longer than 3 months.