Kwesi N. Tsiquaye, Thomas F. McCaul, Arie J. Zuckerman – 1 July 1985 – A 14‐month old female Pekin duck experimentally infected as an embryo with duck hepatitis B virus via the amniotic route has been a chronic carrier of duck hepatitis B virus with very high (P/N) values of DNA polymerase activity since hatching. All the progeny were, on evaluation for congenital infection, found to be duck hepatitis B virus positive by endogenous DNA polymerase reaction and electron microscopy. These offspring remained persistently viremic throughout the study.

Charles S. Lieber, Maria A. Leo, Ki M. Mak, Leonore M. Decarli, Shinkichi Sato – 1 July 1985 – To determine how choline supplementation affects the liver and whether it can protect against ethanol‐induced liver injury, baboons were fed either normal or choline‐supplemented diets, each with or without ethanol. Eighteen baboons were pair‐fed for 3 to 4 years liquid diets with 50% of total energy as ethanol or isocaloric carbohydrate; ten animals were given our regular diets, whereas in eight the choline content was increased 5‐fold.

Frank L. Iber – 1 July 1985

Leon Schiff – 1 July 1985

Kurt Einarsson, Jon Ahlberg, Bo Angelin, Ingemar Björkhem, Staffan Ewerth – 1 July 1985 – We determined the serum concentrations of cholic, chenodeoxycholic and deoxycholic acids in portal and peripheral venous blood in 9 gallstone‐free patients and 39 patients with cholesterol gallstones during standardized cholecystectomy. An accurate and specific gas chromatographic‐mass spectrometric technique was used.

Yuro Shibayama, Katsuji Nakata – 1 July 1985 – To determine the localization of increased vascular resistance in cirrhotic liver, blood pressures were measured by a direct cannulation method at several key points in the hepatic vascular pathway in normal and cirrhotic rats. Cirrhosis was produced by feeding a choline‐deficient diet. Blood pressures in normal rats were 110 mm H2O in the portal vein, 68 mm H2O in the terminal portal venule, 28 mm H2O in the terminal hepatic venule and 20 mm H2O in the inferior vena cava.

I. Sendama, B. de Hemptinne, L. Lambotte – 1 July 1985 – Aminopyrine demethylation was investigated in rats after a 70% hepatectomy to assess possible parallelism between the recovery of mass and function. Tests were performed by analyzing 14CO2 exhalation from 0.1 μCi per 100 gm of body weight of [dimethylamine‐14C]aminopyrine given intraperitoneally with incremental doses of unlabeled drug.

Bernhard H. Lauterburg, Elizabeth L. Todd, Charles V. Smith, Jerry R. Mitchell – 1 July 1985 – The hepatotoxicity of isoniazid in rats results from the metabolic activation of acetylhydrazine, a metabolite of isoniazid, by the cytochrome P450 monooxygenase system. Inhibition of the drugmetabolizing enzyme system with a compound suitable for clinical use such as cimetidine might therefore prevent liver injury in experimental animals and in patients on isoniazid without interfering with the antituberculous activity of the drug.

Peggy J. Macphee, Vincent J. Dindzans, Lai‐Sum Fung, Gary A. Levy – 1 July 1985 – The acute and chronic effects of mouse hepatitis virus type 3 on the microcirculation of the liver in both semisusceptible C3HeB/FeJ and fully resistant A/J mice were studied. In the C3HeB/FeJ mice, abnormalities of microcirculatory flow were noted as early as 12 hr after infection and by 24 hr, localized avascular foci appeared. Disturbances were characterized by granular blood flow, sinusoidal microthrombi, distortion of sinusoids by edematous hepatocytes and necrotic lesions.

Bruce A. Runyon, Richard L. Morrissey, John C. Hoefs, Frederic A. Wyle – 1 July 1985 – The opsonic activity of 60 ascitic fluids from 47 patients was measured using a standard opsonophagocytic assay. Curve analysis of the opsonic activity compared to the ascitic fluid concentration of total protein, total hemolytic complement, C3 and C4 yielded correlation coefficients of 0.84 (p < 0.001), 0.84 (p < 0.001), 0.94 (p < 0.001) and 0.92 (p < 0.001), respectively. There appeared to be a threshold of concentration for each protein below which there was no killing of bacteria.