Peter Karayiannis, Lidija M. Petrovic, Mark Fry, Duncan Moore, Mike Enticott, Michael J. McGarvey, Peter J. Scheuer, Howard C. Thomas – 1 February 1989 – Three tamarins (Saguinus labiatus), two of which had previously been infected with hepatitis A virus and parenteral non‐A, non‐B hepatitis, were inoculated intravenously with the agent of GB hepatitis. All three animals developed alanine aminotransferase abnormalities 2, weeks after inoculation. Peak alanine aminotransferase levels were recorded 4 weeks postinoculation.

J. Eileen Hay, Albert J. Czaja, Jorge Rakela, Jurgen Ludwig – 1 February 1989 – To determine the nature of unexplained chronic serum aspartate aminotransferase elevations of a mild to moderate degree in asymptomatic patients, we performed systematic clinical, biochemical and histologic examinations in 47 individuals who had been screened for virus‐, alcohol‐or drug‐related disease. Serum aspartate aminotransferase levels ranged from 3‐to 8‐fold normal (mean: 156 ± 7 units per liter) for at least 6 months (mean: 30 ± 6 months).

François Kemeny, Jacqueline Vadrot, Andrew Wu, Claude Smadja, Jonathan L. Meakins, Dominique Franco – 1 February 1989 – The pathological findings of 26 consecutive resections for hepatocellular carcinomas developing in cirrhotic patients were analyzed morphologically with a special interest in the presence of a capsule, vascular extension and satellite nodules. Tumor sizes varied from 2 to 11 cm. There were 20 expanding (76.9%) and six infiltrating tumors. Infiltrating tumors were significantly larger than expanding tumors (p<0.01).

Hidekazu Tsukamoto, Xiao Ping Xi – 1 February 1989 – Centrilobular hypoxia mediated by enhanced hepatic consumption of oxygen has been hypothesized to be a factor of pathogenetic importance in ethanol‐induced liver injury. In the present study, this hypothesis was tested in a rat model which developed alcoholic centrilobular liver necrosis.

Robert L. Carithers – 1 February 1989

David S. Lapointe, Merle S. Olson – 1 February 1989 – Mean transit times for the movement of extracellular and intracellular reference compounds through isolated perfused rat livers were determined during exposure of livers to platelet‐activating factor (AGEPC; 1‐0‐hexa‐decyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine) and the α‐adrenergic agonist phenylephrine, using the multiple indicator dilution technique.

Giorgio Senaldi, Giorgina Mieli‐Vergani, Alexander O. Mowat, Diego Vergani – 1 February 1989

Robert E. Vestal – 1 February 1989

Jay H. Lefkowitch – 1 February 1989 – The etiology of idiopathic portal hypertension (IPH) is not known. To obtain clues to the pathogenesis, an attempt was made to produce a hepatic lesion similar to that in IPH by repeated injections of aggregated killed non‐pathogenic E. coli directly into the portal vein. In the treated dogs, histology of the liver showed dense fibrosis in the portal tract and an aberrant vasculature around the portal area after 1 month. Portal pressure was elevated and middle‐to‐small‐sized portal branches were decreased in number as studied by portography.

1 February 1989