Acetaminophen hepatotoxicity and targeted rescue: A model for specific chemotherapy of hepatocellular carcinoma

George Y. Wu, Catherine H. Wu, Mark I. Rubin – 1 September 1985 – We have taken advantage of the presence of hepatic receptors for galactose‐terminal (asialo‐)glycoproteins to achieve targeted rescue of differentiated hepatocytes from acetaminophen‐induced toxicity in vitro. To accomplish this, a conjugate was formed by covalent coupling of N‐acetylcysteine (an acetaminophen antagonist) to galactose‐terminal (asialo‐)fetuin.

Polycythemia and the budd‐chiari syndrome: Study of serum erythropoietin and bone marrow erythroid progenitors

Victor Georges Levy, Agnès Ruskone, Claude Baillou, Diana Thierman‐Duffaud, Albert Najman, Georges Albert Boffa – 1 September 1985 – The mechanism of polycythemia associated with the Budd‐Chiari syndrome is unknown. Erythropoiesis in 10 patients with Budd‐Chiari syndrome was studied in an attempt to distinguish prior unrecognized polycythemia vera from secondary polycythemia.

Time course and mechanism of alterations in proton relaxation during liver regeneration in the rat

H. Dirk Sostman, John C. Gore, M. Wayne Flye, G. Allan Johnson, Robert J. Herfkens – 1 July 1985 – We studied the proton T1 and T2, water and lipid content of regenerating rat liver from 1 to 7 days after 70% hepatectomy. Liver from normal and sham‐operated animals and splenic tissue from all animals were studied as controls. In vivo proton spectroscopy and imaging of liver was performed in a separate group of control and posthepatectomy rats. The T2 of regenerating liver, but not of sham or normal control liver, was prolonged.

Liver disease activity and hepatitis B virus replication in chronic delta antigen‐positive hepatitis B virus carriers

Stephanos J. Hadziyannis, Morris Sherman, Harvey M. Lieberman, David A. Shafritz – 1 July 1985 – Delta antigen is currently thought to reflect superinfection of the liver with a defective RNA virus (delta agent), requiring helper function from hepatitis B virus for its replication.

Hereditary chronic conjugated hyperbilirubinemia in mutant rats caused by defective hepatic anion transport

Peter L. M. Jansen, Wilbert H. Peters, Wouter H. Lamers – 1 July 1985 – A mutant rat strain is described with autosomal recessive conjugated hyperbilirubinemia. Transport of conjugated bilirubin and tetrabromosulfophthalein from liver to bile is severely impaired whereas uptake of organic anions from plasma to liver is normal. During the first 10 days of life, serum bilirubin levels are 147 ± 11 μmoles per liter with 68.7% diconjugates and 27.9% monoconjugates. In adult rats, serum bilirubin is 33 ± 8 μmoles per liter with 81.8% diconjugates and 12.1% monoconjugates vs.

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