1 November 1993

Herbert Tilg, Wolfgang Vogel, Christian J. Wiedermann, Leland Shapiro, Manfred Herold, Gert Judmaier, Charles A. Dinarello – 1 November 1993 – The proinflammatory cytokines interleukin‐1 and tumor necrosis factor‐α are thought to play important roles in the pathophysiology of liver disease. Specific antagonists of these cytokines have been found in recent years. Interleukin‐1 receptor antagonist is a specific interleukin‐1 antagonist.

Dana Liang, Bruno Hagenbuch, Bruno Stieger, Peter J. Meier – 1 November 1993 – We investigated the molecular mechanism underlying the progressive loss of Na+ ‐dependent bile salt uptake in primary cultured rat hepatocytes. A specific cDNA probe was used to quantitate the levels of mRNA encoding the Na+ ‐taurocholate–cotransporting polypeptide at various culture times. Hepatocytes were cultured on collagen in the presence of insulin (10−7 mol/L), dexamethasone (10−7 mol/L) and 10% fetal calf serum for up to 72 hr.

Gilles Lesur, Philippe Levy, Jean‐François Flejou, Jacques Belghiti, François Fekete, Pierre Bernades – 1 November 1993 – In the course of alcoholic chronic pancreatitis, increased serum alkaline phosphatase level is usually caused by common bile duct stenosis but may also be due to alcoholic liver disease. The aims of this prospective study were to investigate whether clinical, biochemical and radiological factors could predict liver histopathological appearance.

Harushige Nakatsukasa, Jeffrey A. Silverman, Timothy W. Gant, Ritva P. Evarts, Snorri S. Thorgeirsson – 1 November 1993 – We analyzed expression of multidrug resistance (mdr) genes in rat liver during regeneration after partial hepatectomy or carbon tetrachloride–induced necrosis. In situ hybridization revealed that in the normal liver the cellular distribution of mdr transcripts and protein is restricted to hepatocytes and that a gradient, highest in zone 1 and lowest in zone 3, exists in the level of the mdr transcripts in the liver acinus.

Samy A. Azer, Michael Murray, Geoffrey C. Farrell, Neill H. Stacey – 1 November 1993 – Because some patients with cirrhosis have serum transaminase levels within the normal range, a prospective study was undertaken to determine whether the concentration of individual serum bile acids would be a sensitive indicator of development of cirrhosis. The choline‐deficient rat has been used as a model for study of these changes. Using high‐performance liquid chromatography, we measured the concentrations of individual serum bile acids at 3, 6, 10, 20 and 30 wk of dietary intake.

Franziska Oberhammer, Wilfried Bursch, Roman Tiefenbacher, Gertraud Fröschl, Margit Pavelka, Tonio Purchio, Rolf Schulte‐Hermann – 1 November 1993 – In previous studies we showed that transforming growth factor‐β1 induces apoptosis in hepatocyte cultures and regressing livers, the mature form being more potent than the transforming growth factor‐β1 latency‐associated protein. In this study we addressed the question of whether apoptosis can be induced within a short time after administration of transforming growth factor‐β1.

Xiaoli Ma, Enrique Baraona, Charles S. Lieber – 1 November 1993 – Because ethanol inhibits mitochondrial fatty acid oxidation, with substantial accumulation of fatty acids in the livers of female (but not male) rats, and induces microsomal activities, we assessed possible changes in ω‐oxidation. To study this, we pair‐fed 24 male and 24 female littermate rats of the same age liquid diets containing 36% of energy either as ethanol or as additional carbohydrate for 4 wk. In controls, the microsomal ω‐hydroxylation of lauric acid was 28% greater in female than in male rats (p < 0.05).

1 November 1993

Mieko Matsui, Minoru Nakamura, Hiromi Ishibashi, Kichiko Koike, Jiro Kudo, Yoshiyuki Niho – 1 November 1993 – Peripheral B lymphocytes from a patient with primary biliary cirrhosis were infected with Epstein‐Barr virus, and Epstein‐Barr virus–transformed B lymphocytes producing large amounts of IgG antibodies to pyruvate dehydrogenase complex were selected, expanded and fused with the human‐mouse heteromyeloma cell line F3B6.