James R. Jacob, Jorg W. Eichberg, Robert E. Lanford – 1 December 1989 – Primary chimpanzee hepatocytes were maintained in vitro utilizing a serum‐free medium. Hepatocyte functions were sustained throughout the culture period as demonstrated by the synthesis and secretion of liver‐specific plasma proteins characteristic for differentiated hepatocytes. Hepatocyte cultures established from a chimpanzee chronically infected with human hepatitis B virus exhibited the synthesis and secretion of hepatitis B virus proteins into the medium.

Maria Buti, Rafael Esteban, Rosendo Jardi, Francisco Rodriguez‐Frias, Jose Casacuberta, Juan Ignacio Esteban, Elena Allende, Jaime Guardia – 1 December 1989 – To investigate the presence of serum hepatitis delta virus antigen by immunoblot and its correlation with other markers of active viral replication (intrahepatic hepatitis D antigen, IgM antibody to hepatitis D and serum hepatitis D virus RNA), we studied serum samples from 50 patients with chronic hepatitis D virus infection (38 with and 12 without intrahepatic hepatitis D antigen).

1 December 1989

Goran B. G. Klintmalm, Joseph R. Nery, Bo S. Husberg, Thomas A. Gonwa, Glenn W. Tillery – 1 December 1989 – One hundred four liver transplant recipients were retrospectively reviewed for the incidence of liver allograft rejection, the response to antirejection therapy and the impact of rejection on graft and patient survival. Liver biopsies were performed weekly during episodes of graft dysfunction and to follow response to treatment. Baseline immunosuppression consisted of cyclosporine and low‐dose prednisolone. Rejection was treated with steroids and with OKT3 as rescue.

David J. Stewart – 1 December 1989 – To investigate volume‐regulating processes in the hepatocyte, a rapid and precise method of measuring cell volume in isolated hepatocytes was devised which uses a Coulter Counter equipped with a Channelyzer. Isolated hepatocytes exhibit a volume‐decreasing mechanism (potassium channel) which is triggered by cell volume increases as small as 10%. Cell volume increases in the hepatocyte may be mediated by activity of the Na:H exchanger.

Elizabeth Knobler, Maureen B. Poh‐Fitzpatrick, Donna Kravetz, William R. Vincent, Ursula Muller‐Eberhard, Styliani H. Vicent – 1 December 1989 – Equilibrium constants for the binding of protoporphyrin to serum albumin and hemopexin and liver cytosolic fatty acid‐binding protein of the rat were determined fluorometrically. The experimental equilibrium constant [106M−1 (mean ± S. D.)] values were 8.4 ± 1.3, 10.0 ± 2.4 and 34.0 ± 3.0 for albumin, hemopexin and liver fatty acid‐binding protein, respectively.

Gilles Pomier‐Layrargues, J.‐François Giguère, Joël Lavoie, Bernard Willems, Roger F. Butterworth – 1 December 1989 – Ro 15–1788, a benzodiazepine antagonist, has been advocated as a new treatment for hepatic encephalopathy. This drug is extensively metabolized by the liver in normal subjects. In the present study, we examined Ro 15–1788 disposition in eight healthy controls (Group I), eight cirrhotic patients with moderately impaired liver function (Pugh score >10, Group II) and eight patients with severe liver dysfunction (Pugh score > 10, Group III).

Franklin M. Klion – 1 December 1989

John M. Amatruda, Arthur I. Salhanick – 1 December 1989 – Hepatic steatosis and steatonecrosis occur in non‐alcoholic individuals, usually in a setting of obesity, type II diabetes mellitus, and after jejunoileal bypass. We propose an hypothesis for the pathogenesis of these hepaic lesions based on an observation in peritoneal dialysis patients.

Ranjit Banerjee, Saul Karpen, Miriam Siekevitz, Gabriella Lengyel, Joachim Bauer, George Acs – 1 December 1989 – Tumor necrosis factor‐α is an inducer of acute‐phase protein synthesis in liver cells. The mechanism by which tumor necrosis factor‐α alters gene expression in these cells is largely unknown. In this study, we demonstrate that tumor necrosis factor‐α stimulates human immunodeficiency virus‐1 long terminal repeat‐promoted gene expression in the human hepatoblastoma HepG2 cell line and increased binding of trans‐activating factors to kappa B (kB) DNA sequences.