Notice
1 May 1986
The relationship between glucagon and prostaglandin f in stimulating canine hepatic bile flow
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.
The sodium retention of cirrhosis: A reappraisal
Murray Epstein – 1 March 1986
Critical commentary
E. L. Forker, B. A. Luxon – 1 March 1986
Studies of gene transcription and translation in regenerating rat liver
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.
Value of ascitic lipids in the differentiation between cirrhotic and malignant ascites
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.
Ultrastructure of experimental cocaine hepatotoxicity
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.
Epidemiology of hepatitis b e antigen and antibody in mentally retarded hbsag carriers
Ghanshyam Lohiya, Sunita Lohiya, Vinh Trong Ngo, Ramona Crinella – 1 March 1986 – Screening for HBeAg and anti‐HBe was performed on 133 carriers of HBsAg in aninstitution for the mentally retarded. By radioimmunoassay, the prevalences of HBeAg and anti‐HBe were determined to be 16 and 78%, respectively. HBeAg prevalence was significantly different in the following pairs of carriers: 70% in blacks, 10% in whites, and 35% incarriers with Down's syndrome, 8% in carriers without Down's syndrome.