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.

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.

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.

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).

Byers W. Shaw – 1 May 1996

Cameron N. Ghent, William J. Wall – 1 May 1996

Kevork M. Peltekian, Leonard Makowka, Roger Williams, Laurence M. Blendis, Gary A. Levy, Prostaglandins in Liver Transplantation Research Group – 1 May 1996 – Prostaglandins (PG) are involved in the regulation of many physiological processes in the liver and play a major role in the pathophysiology and treatment of liver diseases. In addition to their effects on cell growth and immune function, PGs have shown cytoprotective effects on hepatocytes in various toxic, ischemic, and infectious models of liver injury.

1 May 1996

A O Williams, A D Knapton – 1 May 1996 – Hepatic silicosis, cirrhosis, liver cell adenoma, and carcinomas developed in nude mice (NCr‐Nu) given quartz by the subcutaneous and intraperitoneal routes. Syrian golden hamsters (15:16 EHS:cr) given quartz by both routes developed extensive fibrosis and cirrhosis and had higher morbidity and mortality rates after 3 months. Crystalline silica (quartz) induces fibrosis, adenomas, and carcinomas in the lungs of Fisher 344 rats, but certain strains of mice and hamsters are resistant to quartz‐induced pulmonary carcinogenesis.

P Martin‐Sanz, M J Diaz‐Guerra, M Casado, L Bosca – 1 May 1996 – Incubation of primary cultures of fetal hepatocytes with lipopolysaccharide (LPS) elicited the expression of nitric oxide (NO) synthetase as well as antagonized the apoptotic cell death evoked by treating the cells with transforming growth factor β1 (TGF‐β1). In addition to LPS, exposure of the cells to chemical NO donors also protected against apoptotic cell death when assayed at concentrations in the low micromolar range.