Mitogen‐activated protein kinase activation in hepatocyte growth factor–stimulated rat hepatocytes: Involvement of protein tyrosine kinase and protein kinase C

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.

Binding of apolipoprotein A‐I and acetaldehyde‐modified apolipoprotein A‐I to liver extracellular matrix

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.

Relationship between serum and hepatic 7S fragments of type IV collagen in chronic liver disease

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.

The effect of long‐term treatment with spironolactone on variceal pressure in patients with portal hypertension without ascites

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.

Zinc supplementation and amino acid‐nitrogen metabolism in patients with advanced cirrhosis

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).

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