Adrian M. Di Bisceglie, Jay H. Hoofnagle – 1 May 1986 – In an attempt to establish a model of the healthy carrier state in hepatitis B virus (HBV) infections, transgenic mice expressing HBV genes were produced. Fertilized one‐cell eggs were microinjected with subgenomic fragments of HBV DNA containing the coding regions for the HBV surface antigen (HBsAg) and pre‐S and×antigens. Either the normal (HBV) or metallothionein promoters were used to obtain expression of the HBV genes. There was no evidence of viral replication or tissue pathology.

John Polio – 1 May 1986

1 May 1986

D. L. Kaminski, Y. G. Deshpande – 1 March 1986 – Both glucagon and prostaglandin F2α have been shown to stimulate a chloride‐rich choleresis in dogs. This study was performed to ascertain the interrelationship between glucagon and prostaglandin F2α in stimulating bile flow. The experiments were performed using dogs with chronic biliary and gastric fistulas. Initially, the effects of prostaglandin F2α on serum glucagon levels were evaluated. Glucagon administration increased bile volume andchloride secretion as did prostaglandin F2α.

Murray Epstein – 1 March 1986

E. L. Forker, B. A. Luxon – 1 March 1986

Brian E. Huber, Carole A. Heilman, Peter J. Wirth, Mark J. Miller, Snorri S. Thorgeirsson – 1 March 1986 – Specific transcriptional and translational products associated with regenerating liver were analyzed by differential hybridization to a cDNA library and by two‐dimensional electrophoresis of hepatic proteins, respectively.

Dieter Jüngst, Alexander L. Gerbes, Robert Martin, Gustav Paumgartner – 1 March 1986 – Ascitic fluid concentrations of cholesterol, triglycerides and phospholipids, were compared with ascitic fluid total protein in 40 patients with chronic liver disease, 51patients with various neoplasms and 1 patient with cardiac failure. Seven patients withboth chronic liver disease and malignancy were considered separately. The first 54 patients (23 cirrhotic and 31 with malignancy) were used to determine median values and ranges and to define the most suitable cutoff concentrations between both groups.

Marcia R. Gottfried, Michelle W. Kloss, Doyle Graham, Elmer J. Rauckman, Gerald M. Rosen – 1 March 1986 – Cocaine is a potent hepatotoxin in mice. It is converted in the liver by a minor oxidative pathway to the active metabolite, norcocaine nitroxide. Previous studies have shown evidence of a lipid peroxidative mechanism of toxicity, including increased conjugated diene absorption by hepatic microsomal lipids following a single 60 mg per kg i.p. dose of cocaine in DBA/2Ha mice.

Gerald W. Peskin – 1 March 1986