Chris J. Dickinson – 1 May 1992 – An outbreak of hepatitis A virus (HAV) infection in a neonatal intensive care unit (NICU) provided the opportunity to examine the duration of HAV excretion in infants and the mechanisms by which HAV epidemics are propagated in NICUs. The outbreak affected 13 NICU infants (20%), 22 NICU nurses (24%), 8 other staff caring for NICU infants, and 4 household contacts; 2 seropositive infants (primary cases) received blood transfusions from a donor with HAV infection.

Lois Roth, Raymond D. Harbison, Robert C. James, Thomas Tobin, Stephen M. Roberts – 1 May 1992 – Cocaine‐induced hepatotoxicity has been reported in human beings and is well documented in mice. One interesting feature of this toxicity that appears to be common to both species is an apparent shift in the intraacinar site of necrosis under circumstances known to alter cocaine metabolism. However, the evidence in human subjects is limited, and studies elucidating the mechanism of this phenomenon cannot be performed in human beings.

Maria Alfonsina Desiderio – 1 May 1992 – Experiments performed in different models of hepatic regeneration at the time of maximal DNA synthesis, determined by thymidine kinase activity assay, demonstrated that spermidine N8‐acetyltransferase activity increased 48 hr after CCl4 administration (2‐fold), 72 hr after CCl4 plus phenobarbital (3‐fold) and 24 hr after partial hepatectomy (4.5‐fold).

John C. Deutsch, Mieko M. Iwahashi, Eileen M. Sutherland, John Mapoles, Francis R. Simon – 1 May 1992 – The uptake of tri‐hydroxy conjugated bile salts by hepatocytes is principally by a sodium‐dependent carrier. We examined the uptake kinetics of the high‐specific‐activity, hydroxylated, conjugated bile salt 125I‐labeled cholyl‐glycyl‐tyrosine, to determine whether this synthetic bile salt was transported by the sodium‐dependent bile salt system. 125I‐labeled cholyl‐glycyl‐tyrosine was synthesized, and its transport kinetics were studied in freshly cultured rat hepatocytes.

1 May 1992

Etienne M Sokal, Joelle Mostin, Jean Paul Buts – 1 May 1992 – Liver cell functional heterogeneity has been shown to persist in toxic CCl4 cirrhosis in growing rats, but the zonation observed in cirrhotic nodules may be different in other types of cirrhosis. To investigate this possibility, we looked at the zonal activities of two microsomal enzymes, glucose‐6‐phosphatase and NADPH dehydrogenase, in cirrhotic nodules from growing rats with chronic cholestasis. Zonal activities were measured by quantitative cytochemistry and microdensitometry.

Kensaku Hata, David H. van Thiel, Ronald B. Herberman, Theresa L. Whiteside – 1 May 1992 – Liver‐derived lymphocytes were isolated from 73 liver biopsy specimens obtained from patients with chronic active liver disease and from six samples of normal liver. Mean absolute numbers (±S.E.M) of liver‐derived lymphocytes recovered from needle biopsy specimens by mild enzymatic digestion of the liver tissue varied from 0.7 ± 0.3 × 10/mm in allografts being rejected to 8.9 ± 0.9 × 10/mm in chronic non‐A, non‐B hepatitis.

Lluis Viladomiu, Joan Genescà, Juan I. Esteban, Helena Allende, Antonio González, Juan Carlos López‐Talavera, Rafael Esteban, Jaime Guardia – 1 May 1992 – To assess the efficacy of interferon‐α in acute hepatitis C, 28 patients with acute posttransfusion hepatitis were randomized to receive 3 million units of recombinant interferon‐α three times weekly for 12 wk or no treatment. Biochemical, histological and serological parameters were monitored during 1 yr of follow‐up.

K. Vincent Speeg, Alma L. Maldonado, Julie Liaci, Donna Muirhead – 1 May 1992 – The multidrug resistance transport protein is a normal constituent of the liver canalicular membrane, although its function has not been defined in vivo. Colchicine, a multidrug resistance substrate, is eliminated mainly by the liver. Cyclosporine reverses multidrug resistance in vitro, presumably by inhibiting the multidrug resistance transporter. This study assesses biliary colchicine elimination and the effect of cyclosporine on this process.

Russell H. Wiesner – 1 May 1992 – Background. In primary biliary cirrhosis the hepatic lesions may result, at least in part, from the intracellular accumulation of potentially toxic endogenous bile acids. Preliminary work suggests that the administration of ursodiol (also called ursodeoxycholic acid), a hydrophilic bile acid without hepatotoxicity, leads to improvement in the condition of patients with primary biliary cirrhosis.