Robin D. Hughes, Christopher D. Gove, Roger Williams, Hirohita Tsubouchi, Yasushi Daikuhara – 1 February 1990

Rowen K. Zetterman – 1 February 1990

Elspeth M. Jack, Philip Bentley, Francoise Bieri, Samar F. Muakkassah‐Kelly, Willy Stäubli, Joseph Suter, Felix Waechter, Luis M. Cruz‐Orive – 1 February 1990 – Gamma‐glutamyltranspeptidase‐positive hepatocyte foci were produced in female rats given a single dose of diethylnitrosamine neonatally after birth and, after weaning, a diet containing phenobarbitone for 30 wk. The nucleator method, a new stereological approach, provided an efficient, unbiased estimate of mean cell volume in focal lesions and extrafocal areas.

David Kershenobich, Marcos Rojkind, Alfonso Quiroga, Jorge Alcocer‐Varela – 1 February 1990 – Lymphocyte and monocyte function was investigated in eight patients with primary biliary cirrhosis and in age‐matched and sex‐matched controls. In three of the eight cirrhotic patients, two were in the late stage of the disease (stage III) and concanavalin A‐induced suppressor cell function was markedly decreased; it returned to normal levels after 1 mo of treatment consisting of 5 mg per week of orally administered colchicine.

Yasushi Shiratori, Mitsugu Tanaka, Kenji Hai1, Tateo Kawase, Shuichiro Shiina, Tsuneaki Sugimoto – 1 February 1990 – Although administration of 100 mg galactosamine caused severe hepatic injury in C3H/HeN mice, splenectomy reduced the grade of this hepatotoxicity. However, this hepatic injury was scarcely detected in the endotoxin‐resistant C3H/HeJ mice. In addition, in contrast to high lethality in C3H/HeN mice with a combined administration of galactosamine and endotoxin, splenectomy rendered C3H/HeN mice slightly resistant to this treatment.

Shashi Kumar, Rudolf E. Stauber, Judith S. Gavaler, Michael H. Basista, Vincents J. Dindzans, Robert R. Schade, Mordechai Rabinovitz, Ralph E. Tarter, Robert Gordon, Thomas E. Starzl, David H. Van Thiel – 1 February 1990 – Alcohol abuse is the most common cause of end‐stage liver disease in the United States, but many transplant centers are unwilling to accept alcoholic patients because of their supposed potential for recidivism, poor compliance with the required immunosuppression regimen and resulting failure of the allograft.

Arie J. Zuckerman – 1 February 1990 – A random‐primed complementary DNA library was constructed from plasma containing the uncharacterized non‐A, non‐B hepatitis (NANBH) agent and screened with serum from a patient diagnosed with NANBH. A complementary DNA clone was isolated that was shown to encode an antigen associated specifically with NANBH infections. This clone is not derived from host DNA but from an RNA molecule present in NANBH infections that consists of at least 10,000 nucleotides and that is positive‐stranded with respect to the encoded NANBH antigen.

Fernando Corrales, Carmen Cabrero, Maria A. Pajares, Pablo Ortiz, Antonio Martin‐Duce, Jose M. Mato – 1 February 1990 – Catalytically active human and rat liver S‐adenosylmethionine synthetase exists mainly in tetramer and dimer form. In liver biopsy samples from cirrhotic patients a marked reduction in total S‐adenosylmethionine synthetase activity and a specific loss of the tetrameric form of the enzyme exist. We have investigated the possible role of sulfhydryl groups in maintaining the structure and activity of S‐adenosylmethionine synthetase.

Masaki Matsuoka, Martin Y. Zhang, Hidekazu Tsukamoto – 1 February 1990 – A high‐fat diet has previously been shown to be a key factor for induction of alcoholic liver fibrosis in a rat model of intragastric ethanol infusion. To explore a possible mechanism by which the high‐fat diet facilitated such an effect, the present study examined how the high‐fat diet with or without ethanol affected proliferation and collagen formation of hepatic lipocytes, perisinusoidal cells that have been suggested to be involved in liver fibrogenesis.

Ramesh A. Bhat, Paul P. Ulrich, Girish N. Vyas – 1 February 1990 – Based on the diversity of nucleotide sequences of cloned hepatitis B virus DNA genomes, we have predicted possible replication of genetic variants of human hepatitis B virus. This prediction is exemplified by studies of a chronic carrier of HBsAg/adw2, who lacked anti‐HBc but carried exceedingly high levels of hepatitis B virus DNA in serum.