Jean‐Claude Homberg, Nisen Abuaf, Olivier Bernard, Shamsul Islam, Fernando Alvarez, Samir H. Khalil, Raoul Poupon, François Darnis, Victor‐Georges Lévy, Patrick Grippon, Pierre Opolon, Jacques Bernuau, Jean‐Pierre Benhamou, Daniel Alagille – 1 November 1987 – Sixty‐five patients with histologically proven chronic active hepatitis of unknown cause but associated with the antiliver/kidney microsome antibody type 1, confirmed by immunofluorescence and immunoprecipitation, were selected as forming a special entity.

Edward L. Krawitt, Alan E. Kilby, Richard J. Albertini, Moses S. Schanfield, Bettejayne F. Chastenay, Phillip C. Harper, Ruth M. Mickey, Timothy L. McAuliffe – 1 November 1987 – The strategy of assigning a surrogate phenotype, defined as the presence of antinuclear and/or antismooth muscle antibodies to disease‐free first degree relatives of index cases was used to search for a postulated disease susceptibility gene in autoimmune chronic active hepatitis.

Douglas Stevenson, Jiing‐Huey Lin, Myron J. Tong, G. June Marshall – 1 November 1987 – A continuous adherent cell line was established from a hepatocellular carcinoma of an HBsAg‐positive Italian male. This cell line, designated Tong/HCC, has been grown in a hormone‐supplemented medium for more than 18 months. The cell line secretes HBsAg, α‐fetoprotein, albumin and α1‐antitrypsin. α‐Fetoprotein production is enhanced by the addition of hydrocortisone and appears to be glucocorticoid concentration‐dependent.

Bernhard H. Lauterburg – 1 November 1987 – An increased influx and/or a decreased extrusion of calcium across the plasma membrane resulting in an increase in cytosolic‐free calcium could play an important role in the initiation of irreversible cell injury. Therefore, the translocation of calcium across the plasma membrane was probed in the perfused rat liver using multiple indicator dilution methodology.

Thomas C. Mahl – 1 November 1987

Mark L. Batshaw – 1 November 1987 – Twenty‐two patients with inherited hyperammonemic syndromes are presented. These patients represent 22 different families. The diagnosis was based mainly on family history, blood ammonium levels, acid base balance, urinary orotic acid, urinary and plasma amino acids and organic acids. The final diagnosis was confirmed by determination of liver enzyme activity. In 12 patients (54%), the first clinical manifestations were noticed after the neonatal period; 7 patients (31%) were diagnosed after infancy, and 8 (23%) after the age of 8 years.

Chia‐Ming Chu, Wei‐Chue Shyu, Ruey‐Wen Kuo, Yun‐Fan Liaw – 1 November 1987 – It has been suggested that cytotoxic T cells are involved in the recognition and lysis of the infected hepatocytes in chronic hepatitis B virus infection, and that the target antigen is probably HBcAg which is displayed on the hepatocyte membrane during active viral replication. However, studies in other viral infection have demonstrated that cytotoxic T cells recognize viral antigen on the infected cells only in the context of HLA class I antigens.

Kunihiko Ohnishi, Yuichi Tanabe, Munemasa Ryu, Kaichi Isono, Yoshikazu Yamamoto, Sadahito Usui, Yoshiaki Hiyama, Nobuaki Goto, Shosuke Iwama, Shujiro Sugita, Fumio Nomura, Kunio Okuda – 1 November 1987 – A total of 100 patients with small hepatocellular carcinoma, ⩽5 cm in diameter, seen during the last 8 years were analyzed retrospectively for survival time in relation to treatment and Child's grading.

Robert G. Paul, Stanford T. Roodman, Deborah A. Paul, Robert P. Perrillo – 1 November 1987 – The density of HLA Class I antigen on peripheral blood mononuclear cells was evaluated by flow cytometry in the following groups of patients: 41 HBsAg carriers; 12 individuals with chronic non‐A, non‐B hepatitis, and 4 with acute hepatitis B. Fourteen of the carriers were positive for antibody to human immunodeficiency virus, and all were negative for antibody to delta agent. Elevated levels of Class I antigen were observed in only 19% of patients with chronic hepatitis B virus infection alone.

Hans P. Dienes, Thomas Hütteroth, Georg Hess, Stefan C. Meuer – 1 November 1987 – The present knowledge of the inflammatory reaction occurring in situ during hepatitis B favors a T cell‐dependent MHC‐restricted immune response. However, the reports in the literature are primarily based on the application of monoclonal antibodies directed at different lymphocyte subsets which discern only lymphocytic phenotypes and do not reflect the actual situation adequately.