Henk J. Blom, Peter Ferenci, Georg Grimm, Sing H. Yap, Albert Tangerman – 1 March 1991 – Mixed disulfides of methanethiol represent a relative estimate for an exposure to methanethiol. The concentrations of methanethiol‐mixed disulfides, methionine, 4‐methylthio‐2‐oxobutyrate and ammonia were measured in patients with different stages of hepatic encephalopathy, in patients with chronic kidney failure and in healthy subjects. In patients with hepatic encephalopathy, the mean serum concentrations of all these compounds were elevated.

Yoshimichi Haruna, Norio Hayashi, Kazuhiro Katayama, Nobukabu Yuki, Akinori Kasahara, Yutaka Sasaki, Hideyuki Fusamoto, Takenobu Kamada – 1 March 1991 – The X protein can act on the enhancer of hepatitis B virus in an in vitro system and elevate the transcriptional level of hepatitis B virus. However, because no relationship had been reported between X protein expression and hepatitis B virus replication in patients with chronic hepatitis B, we focused on its expression in the liver in comparison with markers of hepatitis B virus replication.

Chien‐Jen Chen, Kung‐Yee Liang, Ah‐Seng Chang, Yo‐Chi Chang, Sheng‐Nan Lu, Yun‐Fan Liaw, Wen‐Yu Chang, Maw‐Chang Sheen, Tong‐Ming Lin – 1 March 1991 – Independent and interactive effects related to the development of hepatocellular carcinoma were assessed using a community‐based case‐control study for hepatitis B virus, habitual alcohol drinking, cigarette smoking, peanut consumption and history of hepatocellular carcinoma among the immediate family.

Devorah Gurantz, Claudio D. Schteingart, Lee R. Hagey, Joseph H. Steinbach, Thomas Grotmol, Alan F. Hofmann – 1 March 1991 – Using the isolated perfused rat and hamster liver, the relationship between bile flow, bile acid secretion rate and bile acid biotransformation after the injection of a small, bolus dose of radioactive ursodeoxycholate or of its C23 homolog, norursodeoxycholate, was examined. Ursodeoxycholate was promptly secreted into bile mostly as amino acid conjugates; <3% was secreted in unchanged form in the rat and <2% in the hamster.

Z. Reno Vlahcevic, Douglas M. Heuman, Phillip B. Hylemon – 1 March 1991

Adrian M. Di Bisceglie, Jay H. Hoofnagle – 1 March 1991

Adrian Greenstein – 1 March 1991

S. Chris Pappas – 1 March 1991

Beat Meyer, Hesheng Luo, Mario Bargetzi, Eberhard L. Renner, Georg A. Stalder – 1 March 1991 – Hepatic drug metabolism is decreased in patients with severe liver disease, but it is unclear to what extent this is due to altered hepatic blood flow or reduced intrinsic metabolic capacity. In this study we quantitated in needle‐biopsy specimens the intrinsic capacity of liver tissue from 67 patients with mild liver disease (n = 36), chronic active hepatitis (n = 16) and cirrhosis (n = 15) to metabolize two model compounds in vitro.

Horng‐I Yeh, G. D. V. Van Rossum – 1 March 1991 – We have studied the mechanism by which liver Golgi apparatus maintains the acidity of its contents, using a subcellular fraction from rat liver highly enriched in Golgi marker enzymes. Proton accumulation (measured by quenching of acridine‐orange fluorescence) and anion‐dependent ATPase were characterized and compared. Maximal ATPase and proton accumulation required ATP; GTP and other nucleotides gave 10% to 30% of maximal activity. Among anions, Cl− and Br− approximately doubled the activities; others were much less effective.