Gerald W. Peskin – 1 March 1986

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.

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.

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.

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

Murray Epstein – 1 March 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.

Simon Gelman, Fumio Nomura, Hitoshi Hatano, Kunihiko Ohnishi, Kunio Okuda – 1 January 1986

J. P. Vinel, J. Cassigneul, M. Levade, J. J. Voigt, J. P. Pascal – 1 January 1986 – Seventy‐two consecutively admitted patients with biopsy‐proven alcoholic cirrhosis and a bleeding episode endoscopically proven to originate from ruptured esophageal varices were studied. Hemodynamic assessment was performedwithin 48 hr of admission using the transjugular approach.

1 January 1986