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).

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.

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.

Imad Abou Hashieh, Sylvie Mathieu, André Gerolami – 1 May 1992 – The formation of intracellular lumina with apical differentiation is observed in several cancerous epithelial cell lines including human hepatocarcinoma. This disorder of cell polarization can be induced by the inhibition of cell‐cell communication, a known factor of carcinogenesis.

Manfred J. Müller, Hans U. Lautz, Birgit Plogmann, Mechthild Bürger, Jürgen Körber, Friedrich W. Schmidt – 1 May 1992 – Many clinicians subjectively feel that cirrhotic patients frequently have clinical signs of hypermetabolism. However, it is unknown whether hypermetabolism is a constant feature of chronic liver disease, corresponds to liver destruction and repair or is of prognostic value.

Miquel Bruguera, Josep Llach, Joan Rodés – 1 May 1992 – Eleven patients with chronic intrahepatic cholestasis in whom a liver biopsy specimen showed unexplained bile duct paucity were investigated. Cholestasis developed during the neonatal period in three, at infancy (before 14 yr) in four and after 14 yr in the remaining four patients. In all patients other conditions characterized by chronic cholestasis associated with ductopenia such as primary biliary cirrhosis, primary sclerosing cholangitis, drug‐induced liver disease, sarcoidosis or graft‐vs.‐host disease were excluded.

Gilles Pomier‐Layrargues, Lise Giroux, Bernard Rocheleau, Pierre‐Michel Huet – 1 May 1992 – We recently reported that ritanserin, a 5‐hydroxytryptamine receptor antagonist, induced significant reduction of portal pressure in cirrhotic rats. In this study, we investigated the hemodynamic effects of a combination of propranolol and ritanserin in conscious and unrestrained cirrhotic rats. Heparinized catheters exiting from the neck were placed into the portal vein, inferior vena cava, aorta and left ventricle.

Peter van Eyken, Albert Geerts, Pieter de Bleser, Jean‐Marc Lazou, Raf Vrijsen, Raf Sciot, Eddie Wisse, Valeer J. Desmet – 1 May 1992 – The distribution and the cellular source of the novel extracellular matrix glycoprotein tenascin were studied in normal and fibrotic rat liver. Cryostat sections of normal rat livers, livers of rats treated with intraperitoneal injections of CCl4 and 4‐day‐old and 8‐day‐old primary fat‐storing cell cultures were stained for tenascin and desmin using an immunoperoxidase procedure or a double‐label immunofluorescence technique.

Anna Mae Diehl – 1 May 1992

Kazuhiko Hosoda, Masao Omata, Osamu Yokosuka, Naoya Kato, Masao Ohto – 1 May 1992 – To study the role of hepatitis C virus in non‐A, non‐B chronic hepatitis, 49 liver biopsy samples from 40 patients with non‐A, non‐B chronic hepatitis and 9 control patients were analyzed by complementary DNA/polymerase chain reaction. Two segments of the HCV genome, one in the nonstructural region and the other in the noncoding region, were amplified by two sets of primer pairs.