Participation of small intraportal stem cells in the restitutive response of the liver to periportal necrosis induced by allyl alcohol

Leonid Yavorkovsky, Eva Lai, Zoran Ilic, Stewart Sell – 1 June 1995 – To determine the involvement of different hepatocyte populations in response to periportal injury, the restitutive response to allyl alcohol (AA) injury was examined.

DNA damage and donor livers: Disease unbidden?

Kathleen Schwarz – 1 June 1995 – Endogenous DNA adducts may contribute to the etiology of human genetic disease and cancer. One potential source of endogenous DNA adducts is lipid peroxidation, which generates mutagenic carbonyl compounds such as malondialdehyde. A sensitive mass spectrometric method permitted detection and quantitation of the major malondialdehyde‐DNA adduct, a pyrimidopurinone derived from deoxyguanosine. DNA from disease‐free human liver was found to contain 5400 adducts per cell, a frequency comparable to that of adducts formed by exogenous carcinogens.

Protective effect of hepatocyte growth factor on interferon‐gamma—induced cytotoxicity in mouse hepatocytes

Masahiko Morita, Yoshifumi Watanabe, Toshihiro Akaike – 1 June 1995 – We examined the interactive effect of several cytokines (interleukin‐1 beta [IL‐1β], tumor necrosis factor alpha [TNF‐α], interferon gamma [IFN‐γ], IL‐6, IFN‐α/B, and hepatocyte growth factor [HGF]) presumably involved in hepatitis, on primary cultured murine hepatocytes. Among these cytokines, only IFN‐γ induced LDH release from hepatocytes in both time‐ and dose‐dependent fashions. The cytotoxic effect was inhibited by antiserum—containing anti‐mouse IFN‐γ monoclonal antibodies (R4‐6A2).

Permissiveness of kupffer cells for simian immunodeficiency virus (SIV) and morphological changes in the liver of rhesus monkeys at different periods of SIV infection

Yury Persidsky, Anne‐Marie Steffan, Jean‐Louis Gendrault, Bruno Hurtrel, Stefan Berger, Cathy Royer, Hans‐Jochen Stutte, Elizabeth Muchmore, Anne‐Marie Aubertin, André Kirn – 1 May 1995 – The pathogenesis of liver injury, which remains unclear in the course of human immunodeficiency virus infection, can be investigated in simian immunodeficiency virus—infected macaques, which develop an immunodeficiency disease resembling human acquired immune deficiency syndrome (AIDS).

Effects of hepatocyte growth factor on the growth and metabolism of human hepatocytes in primary culture

María José Gómez‐Lechón, José Castelli, Isabel Guillén, Enrique o'Connor, Toshikazu Nakamura, Ricardo Fabra, Ramón Trullenque – 1 May 1995 – The effect of recombinant human hepatocyte growth factor (h‐rHGF), a potent mitogen for hepatocytes, was investigated in primary cultures of human hepatocytes. Here, we describe a series of experiments to investigate the kinetics of its mitogenic action, as well as its metabolic effects on cultured human hepatocytes.

Glutathione conjugation of bromosulfophthalein in relation to hepatic glutathione content in the rat in vivo and in the perfused rat liver

C. A. Wilco Snel, K. Sandy Pang, Gerard J. MulderD – 1 May 1995 – The relation between the rate of glutathione (GSH) conjugation and hepatic GSH content was studied in the rat in vivo and the in situ single‐pass‐perfused rat liver preparation with bromosulfophthalein (BSP) as the model substrate. The biliary excretion of the BSP‐GSH conjugate and the hepatic GSH content were monitored simultaneously during intravenous infusions with BSP in the rat in vivo, and during liver perfusions with BSP‐containing perfusion medium.

Ursodeoxycholic acid therapy in primary biliary cirrhosis

David E. J. Jones, Oliver F. W. James, Margaret F. Bassendine – 1 May 1995 – Background/Aims: A double‐blind, placebo‐controlled trial of ursodeoxycholic acid (UDCA) was conducted in 180 patients with primary biliary cirrhosis (PBC) to define the efficacy and safety of UDCA. Efficacy was assessed by time to treatment failure defined as death; liver transplantation; histological progression; development of varices, ascites, or encephalopathy; doubling of total serum bilirubin levels; progression of fatigue or pruritus; drug toxicity; or voluntary withdrawal.

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