Philippe Mavier, Jean Rosenbaum, Anne‐Marie Preaux, Ariane Mallat, Daniel Dhumeaux – 1 December 1990 – We have recently demonstrated that polymorphonuclear neutrophils were toxic to hepatocytes through a protease‐mediated mechanism. Since synthesis of antiproteases is markedly increased during acute inflammatory reaction, the aim of this work was to investigate the toxicity of neutrophils against normal vs. inflammatory rat hepatocytes. Acute inflammatory reaction was induced by subcutaneous injection of turpentine 24 hr before the experiments.

De Feng Wu, Liviu Clejan, Barry Potter, Arthur I. Cederbaum – 1 December 1990 – Studies were conducted to evaluate the possible induction or the maintenance of cytochrome P‐450IIE1 in primary hepatocyte cultures by the inducing agent 4‐methylpyrazole. Hepatocytes were isolated from control (noninduced) rats and from rats treated in vivo with either pyrazole or 4‐methylpyrazole to induce P‐450IIE1. The content of P‐450IIE1 was determined by Western blots with antipyrazole P‐450 IgG, and catalytic activity was assessed by assays of dimethyl‐nitrosamine demethylase activity.

Toni Andreani, Reneé E. Poupon, Beverley J. Balkau, Jean‐Claude Trinchet, Jean‐Didier Grange, Nicolas Peigney, Michel Beaugrand, Raoul Poupon – 1 December 1990 – Propranolol and endoscopic sclerosis of esophageal varices are the two approaches currently used in prophylaxis of the first gastrointestinal hemorrhage in the cirrhotic patient. One hundred twenty‐six cirrhotic patients with esophageal varices and no histories of bleeding were included in the trial regardless of the gravity of the cirrhosis or the size of the esophageal varices.

Peter A. Ward – 1 December 1990

1 November 1990

Kai O. Lindros, Yuan Cai, Kai E. Penttilä – 1 November 1990 – The ethanol‐inducible form of cytochrome P‐450 (IIE1) is expressed and induced by ethanol, predominantly in the centrilobular region. Because this isoenzyme has a particularly high capacity to convert carbon tetrachloride and several other hepatotoxins into reactive intermediates, its role in producing damage was studied by comparing the effect of carbon tetrachloride exposure on hepatocytes isolated from either the periportal or the perivenous region by digitonin‐collagenase perfusion.

Linda J. Scully, David Brown, Chris Lloyd, Ruvan Shein, Howard C. Thomas – 1 November 1990 – Lymphoblastoid interferon is effective therapy in some but not all patients with chronic hepatitis B virus infection. To assess whether immunological parameters were predictive of response to interferon therapy, we determined the human leukocyte antigen type, CD4/CD8 ratio, natural killer cell activity, IgM anti‐HBc antibody levels and concanavalin A—induced lymphocyte proliferative response in 30 patients before treatment.

Yao Zhiqiang, Yang Weisong, Zhang Wenbin, Chen Yong, Yang Fengyi – 1 November 1990 – Current support or replacement therapies for fulminant acute hepatic failure are frequently very disappointing. In this study, human hepatic stimulator substance—a liver‐specific growth factor—was partially purified from human fetal liver cells and characterized by its biological effects. Almost 70‐fold protein content was purified with an approximately 80‐fold increase in specific growth stimulator activity.

Jiřina Martínková, Josef Bulas, Vladimír Krejčí, Miroslav Hartman, Ivan Tilšer, Petr Hůlek – 1 November 1990 – We have studied the action of a series of vasoactive and antispasmodic agents on the intrahepatic vasoconstriction induced by adrenaline in the isolated perfused liver of rabbits. The arterial and portal venous resistance, oxygen consumption, liver weight and bile flow were investigated.

Ieharu Hishinuma, Jun‐Ichi Nagakawa, Kazuo Hirota, Kaname Miyamoto, Kazuo Tsukidate, Takashi Yamanaka, Kou‐Ichi Katayama, Isao Yamatsu – 1 November 1990 – Intravenous injection of lipopolysaccharide and D‐galactosamine, at doses of 0.2 μg/kg and 800 mg/kg, respectively, elicited massive hepatic necrosis within 24 hr in C3H/HeN mice. The plasma L‐alanine aminotransferase (ALT, E.C. 2.6.1.2) or L‐aspartate aminotransferase (AST, E.C. 2.6.1.1) activities at this point reached more than 2,000 IU/L.