T Kimura, K Suzuki, S Inada, A Hayashi, M Isobe, Y Matsuzaki, N Tanaka, T Osuga, M Fujiwara – 1 October 1996 – Interaction between intercellular adhesion molecule 1 (ICAM‐1) and lymphocyte function‐associated antigen 1 (LFA‐1) might be involved in the pathogenesis of liver diseases. We investigated whether monoclonal antibodies (mAbs) against these two adhesion molecules could inhibit the formation of primary biliary cirrhosis (PBC)‐like lesions in an animal model using graft‐versus‐host reaction (GVHR) with major histocompatibility complex class II disparity.

I P Hällström, D Liao, Y Assefaw‐Redda, L C Ohlson, L Sahlin, P Eneroth, L Eriksson, J Gustafsson, A Blanck – 1 October 1996 – Synthetic estrogens act as tumor promoters in rat liver. Because estrogen treatment markedly increases the secretion of pituitary prolactin, also shown to be a tumor promoter in rat liver, the possibility of a pituitary influence in estrogen promotion was investigated in Wistar rats.

J Napoli, G A Bishop, P H McGuinness, D M Painter, G W McCaughan – 1 October 1996 – An imbalance between T helper cell (Th)1 and Th2‐like cytokines has been described in several chronic infectious diseases. We therefore analyzed the intrahepatic messenger RNA (mRNA) expression of Th1‐like (interleukin [IL]‐2, interferon [IFN]‐gamma) and Th2‐like (IL‐4, IL‐10) cytokines in chronic hepatitis C patients (n = 17) and controls (n = 6) and correlated the results with liver histology and intrahepatic viral load.

Andrew L. Mason, Robert P. Perrillo – 1 September 1996

R Ling, D Mutimer, M Ahmed, E H Boxall, E Elias, G M Dusheiko, T J Harrison – 1 September 1996 – We describe mutations in the hepatitis B virus (HBV) polymerase gene in viruses which reactivated in two patients during therapy with ‐2′‐deoxy‐ 3′‐thiacytidine, or lamivudine (3TC), and following orthotopic liver transplantation for chronic hepatitis B.

O Fonia, R Weizman, R Coleman, E Kaganovskaya, M Gavish – 1 September 1996 – There is evidence to suggest that peripheral‐type benzodiazepine receptors (PBR) are involved in porphyrin transport during erythroid differentiation, and it is possible that these receptors have an important role in heme biosynthesis. We examined the biochemical and ultrastructural alterations in rat liver following experimentally induced acute hepatic porphyria, as well as the effects of the administration of a selective PBR ligand, PK 11195.

E Hatano, A Tanaka, S Iwata, S Satoh, T Kitai, S Tsunekawa, T Inomoto, H Shinohara, B Chance, Y Yamaoka – 1 September 1996 – The liver plays an important role in maintaining homeostasis during endotoxin‐triggered systemic inflammatory response. To study the effects of phosphocreatine on hepatic energy metabolism after endotoxin administration, we used transgenic mice whose livers express creatine kinase (CK). CK catalyzes a phosphocreatine/creatine reaction, that is, an adenosine triphosphate (ATP) reservoir system.

C N Van Der Veere, B Schoemaker, C Bakker, R Van Der Meer, P L Jansen, R P Elferink – 1 September 1996 – The aim of this study was to test a possible form of therapy that could be used in the management of unconjugated hyperbilirubinemia. We hypothesized that unconjugated bilirubin (UCB) can permeate the intestinal wall and can thus be secreted with the feces. We have previously observed that UCB binds to amorphous calcium phosphate in vitro.

N Nakayama, H Kashiwazaki, N Kobayashi, J Hamada, Y Ogiso, Y Itakura, K Matsumoto, T Nakamura, T Koike, N Kuzumaki, N Takeichi – 1 September 1996 – The Long‐Evans Cinnamon (LEC) rat is characterized by the spontaneous onset of acute and chronic hepatitis, followed by occurrence of liver cancer, and is thus able to provide a unique experimental model for human genetical liver disease, Wilson's disease. Hepatocyte growth factor (HGF) is a potent hepatotrophic factor in liver regeneration, and its expression is up‐regulated in response to liver injuries.

R Huang, C Chen, Y Huang, D Hsieh, C Hu, C Chen, C Chang – 1 September 1996 – During screening of Chinese herbal medicines for the activities against hepatitis B virus (HBV), a known pure compound, osthole, was found to inhibit the secretion of HBV surface antigens in vitro. The secretion of hepatitis B surface antigen (HBsAg) in culture medium of MS‐G2 and HuH‐7 cells transfected with HBV DNA decreased by 60% to 70% after osthole treatment, without any detectable cytotoxic effects.