G Marchesini, A Fabbri, G Bianchi, M Brizi, M Zoli – 1 May 1996 – Zinc deficiency is common in cirrhosis and has been involved in the altered nitrogen metabolism. In this study, we measured the effects of zinc supplementation on the dynamics of amino acid‐derived urea synthesis in cirrhosis with mild or latent encephalopathy. The hepatic conversion of amino acids into urea was studied in eight patients with advanced cirrhosis under controlled conditions of substrate availability (continuous alanine infusion), before and after 3‐month oral zinc sulfate supplementation (600 mg/d).

F Nevens, P Lijnen, H VanBilloen, J Fevery – 1 May 1996 – The effect of spironolactone on esophageal variceal pressure (VP) in patients without ascites was investigated. VP was assessed using a noninvasive endoscopic gauge. Spironolactone was administered during a 6‐week period at a dosage of 100 mg/d. This treatment decreased VP from 16.8 ± 1.9 (SD) to 14.1 ± 2.7 mm Hg (P < .001) in a group of 12 patients and from 18.6 ± 2.1 to 13.7 ± 4.1 mm Hg (P < .01) in another group of 8 patients who still had high VP despite chronic intake of propranolol.

T Suou, S Yamada, K Hosho, N Yoshikawa, H Kawasaki – 1 May 1996 – We evaluated the mechanism of increased serum concentrations of the 7S fragment of the N‐terminal domain of type IV collagen (7S collagen) in chronic liver disease. We measured the concentrations of hepatic‐free and deposited 7S collagens after extraction with Tris‐HCl buffer and bacterial collagenase, then compared them with the serum levels in 8 normal controls and 48 patients with chronic liver disease.

V Paradis, P Mathurin, V Ratziu, T Poynard, P Bedossa – 1 May 1996 – Apolipoprotein A‐I (Apo A‐I), a protein produced mainly by hepatocytes, is decreased in the sera of alcoholic patients with liver fibrosis and cirrhosis. To explain this decrease, we investigated possible interactions between liver extracellular matrix (ECM) and Apo A‐I. Using a solid‐phase binding assay, we evaluated the binding of Apo A‐I to the different liver matrix components.

G Kullak‐Ublick, T Gerloff, B Hagenbuch, F Berr, P J Meier, B Stieger – 1 May 1996 – A phospholipid translocating protein from rat liver has been expressed in Xenopus laevis oocytes.

L S Friedman – 1 May 1996

J Cordoba – 1 May 1996

T Adachi, S Nakashima, S Saji, T Nakamura, Y Nozawa – 1 May 1996 – Hepatocyte growth factor (HGF) stimulated mitogen‐activated protein (MAP) kinases and MAP kinase kinase in primary cultured rat hepatocytes. Inhibitors for protein kinase C (PKC), Ro31‐8425, H‐7, and calphostin C, reduced HGF‐induced MAP kinase activity. A PKC activator, phorbol myristate acetate (PMA), induced MAP kinase activation in a concentration‐dependent manner. Protein tyrosine kinase (PTK) inhibitors, genistein, and ST638 also inhibited HGF‐induced MAP kinase activation.

A M Tiggelman, W Boers, A F Moorman, P A J de Boer, C M Van der Loos, J P Rotmans, R A Chamuleau – 1 May 1996 – α2‐Macroglobulin (α2M) in the rat is a strong‐reacting acute‐phase protein with potent protease‐inhibiting and cytokine‐binding properties. Production of α2M is ascribed mainly to liver parenchymal cells. In the present study, we investigated, by means of immunohistochemistry and in situ hybridization, whether fibrosis in the rat liver induced by Schistosoma mansoni eggs leads to local production of α2M.

Luca S. Belli, Enrico Silini, Alberto Alberti, Giorgio Bellati, Claudio Vai, Ernesto Minola, Gianfranco Rondinara, Luciano De Carlis, Margherita Asti, Domenico Forti, Gaetano Ideo – 1 May 1996 – Several genotypes of hepatitis C virus (HCV) have been recently identified by phylogenetic analysis, but their clinical relevance in the liver transplant setting is unknown. We evaluated the incidence and course of recurrent hepatitis C after transplantation in 50 patients who underwent transplantation for HCV‐related liver disease.