Mordechai Rabinovitz, Judith S. Gavaler, Robert H. Kelly, David H. Van Thiel – 1 July 1992 – Primary hemochromatosis is a genetically determined autosomal recessive disorder characterized by the excessive accumulation of body iron, most of which is deposited in the parenchymal cells of various organs.
Paul K. Vreugdenhil, Diane C. Marsh, Folkert O. Belzer, James H. Southard – 1 July 1992 – We used an isolated‐hepatocyte model to study how hypothermic storage (simulating liver preservation) affects metabolism after prolonged preservation. Rat hepatocytes were stored in the University of Wisconsin solution for up to 72 hr. After each day of storage, protein synthesis, urea synthesis, ATP content and lactate dehydrogenase release were determined in rewarmed (37° C) and oxygenated hepatocytes.
Frederick Askari, James Wilson – 1 July 1992 – An approach involving retroviral‐mediated gene therapy for the treatment of neoplastic disease is described. This therapeutic approach is called “virus‐directed enzyme/prodrug therapy” (VDEPT). The VDEPT approach exploits the transcriptional differences between normal and neoplastic cells to achieve selective killing of neoplastic cells. We now describe development of the VDEPT approach for the treatment of hepatocellular carcinoma.
Andrew Mason, Boris Yoffe, Christine Noonan, Mary Mearns, Carolyn Campbell, Amanda Kelley, Robert P. Perrillo – 1 July 1992 – In this study, peripheral‐blood mononuclear cells from patients with chronic hepatitis B and spontaneous or therapy‐induced disappearance of HBsAg were examined for HBV DNA. Samples were evaluated by in situ hybridization and polymerase chain reaction both before and after clearance of HBsAg.
Masakatsu Uchihara, Namiki Izumi, Chifumi Sato, Fumiaki Marumo – 1 July 1992 – Endothelin is a newly discovered potent vasoconstrictor peptide. To explain the clinical significance of endothelin in patients with chronic liver diseases, we measured the plasma concentration of endothelin in patients with chronic hepatitis (n = 15), cirrhosis with ascites (n = 8) and cirrhosis without ascites (n = 12), and we compared the findings with the plasma concentration of endothelin in normal controls (n = 14).
Yasuaki Ito, Hideyuki Hiraishi, Mahnaz Razandi, Akira Terano, Takashi Harada, Kevin J. Ivey – 1 July 1992 – Reactive oxygen metabolites have been reported to be important in the pathogenesis of ischemia/reperfusion‐induced and alcohol‐and druginduced liver injuries. We investigated the role of superoxide dismutase, cellular and extracellular, in preventing reactive oxygen metabolite–induced cytotoxicity in cultured rat hepatocytes. Cells were exposed to reactive oxygen metabolites enzymatically generated by hypoxanthine‐xanthine oxidase.
Alastair J. Strain – 1 July 1992 – Incubation of fetal rat hepatocytes (FRH) with transforming growth factor β1 (TGF‐β1) resulted in growth arrest and a biphasic effect on epidermal growth factor (EGF) receptor. After 2 h of exposure, EGF receptor (EGFR) was reduced by 43%. From 6 to 24 h, TGF‐β1 exposure resulted in progressive increase in EGFR up to 74% over control. The increased binding was due to increase in high affinity EGF binding sites. FRH grown in medium containing EGF exhibited down‐regulated EGFR with loss of high affinity EGF binding sites.
Giuseppe Torgano, Maurizio Vecchi, Eliana Arosio, Daniela Santambrogio, Guido Ronchi, Giorgio Annoni, Maurizio Tomasini, Ettore Contessini, Roberto De Franchis – 1 July 1992 – Little is known about the distribution of IgG‐bearing cell subpopulations in normal liver and their possible changes in disease conditions. We developed an immunohistochemical method that proved suitable and accurate for the identification and characterization of IgG‐bearing cells and their subpopulations in liver specimens. The method uses specific monoclonal antibodies on serial mirror liver sections.
Professor Giulio Marchesini, Elisabetta Bugianesi, Giampaolo Bianchi, Andrea Fabbri, Elisabetta Marchi, Marco Zoli, Emilio Pisi – 1 July 1992 – A block in the transsulfuration pathway has previously been suggested in cirrhosis on the basis of increased fasting methionine concentrations, decreased methionine elimination and low levels of methionine end products. To date, methionine elimination has never been studied under controlled steady‐state conditions, and the relation of the severity of liver disease to impaired methionine metabolism has not been clarified.