Delai Zhao, Arthur Zimmermann, Larisa V. Kuznetsova, Anthony M. WheatleyD – 1 May 1995 – The aim of this study was to investigate the long‐term consequences of non‐rearterialization of the graft in rat liver transplantation. Liver transplantation with (AOLT) and without graft rearterialization (NOLT) was performed in anesthetized male Lewis rats. Quantitative morphometry and semiquantitative histopathology of the liver were performed at various times after operation. Volume fractions of tissue components were determined.

Clare Selden, Denis Calnan, Neil Morgan, Hervey Wilcox, Edward Carr, Humphrey J. F. Hodgson – 1 May 1995 – Histidinemia in mice and in humans is an autosomal recessive disorder of histidine metabolism that leads to high‐histidine levels in both plasma and urine and is caused by a lack of hepatic histidine‐α‐deaminase (histidase). We have used a novel approach to hepatocellular transplantation to effect a complete phenotypic cure of histidinemia in a mouse model.

Antonio Diez‐Ruiz, Gernot P. Tilz, Francisco Gutierrez‐Gea, Blas Gil‐Extremera, Christian Murr, Helmut Wachter, Dietmar Fuchs – 1 April 1995 – Alcohol‐induced cirrhosis (AC) is accompanied by disturbances of immune function and cytokine production.

Ariane Mallat, Anne‐Marie Preaux, Sylvie Blazejewski, Jean Rosenbaum, Daniel Dhumeaux, Philippe Mavier – 1 April 1995 – During the course of ongoing liver fibrogenesis, Ito cells acquire myofibroblastic features, proliferate, and synthesize increased amounts of extracellular matrix components. Interferon (IFN) alfa and IFN gamma have been shown to elicit antiproliferative and/or antifibrogenic effects in various cell cultures of mesenchymal origin.

Daniell B. Hill, Jack Schmidt, Steven I. Shedlofsky, Donald A. Cohen, Craig J. McClain – 1 April 1995 – Tumor necrosis factor‐α(TNF‐α) is a mediator of liver injury. The objective of this study was to develop an in vitro model of TNF‐mediated liver cell injury using the Hep G2 cell line. Hep G2 cells normally are insensitive to TNF cytotoxicity, but they were rendered susceptible, or sensitized, to TNF cytotoxicity by inhibitors of RNA and protein synthesis.

Robert S. Britton, Kyle E. Brown – 1 April 1995 – Hereditary haemochromatosis is characterised by iron overload that may lead to tissue damage. Free iron is a potent promoter of hydroxyl radical formation that can cause increased lipid peroxidation and depletion of chain‐breaking antioxidants. We have therefore assessed lipid peroxidation and antioxidant status in 15 subjects with hereditary haemochromatosis and age/sex matched controls. Subjects with haemochromatosis had increased serum iron (24.8 (19.1–30.5) vs. 17.8 (16.1–19.5) μmol/L, P = 0.021) and % saturation (51.8 (42.0–61.6) vs.

Raymond S. Koff – 1 April 1995

Raymond S. Koff – 1 April 1995

Hitoshi Ikeda, Kenji Fujiwara – 1 April 1995 – Ito cells are the primary matrix‐producing cells in the liver. In hepatic fibrosis in vivo or culture on plastic, these cells undergo activation, a process characterized by cell proliferation, fibrogenesis, and smooth muscle α‐actin expression. The cytosolic‐binding proteins of cyclosporin A (CsA) and FK506 accelerate folding of various proteins including collagen and become inactivated by binding to those agents. CsA is shown to inhibit collagen synthesis in cultured fibroblasts.

1 April 1995