Don C. Rockey, Jacquelyn J. Maher, William R. Jarnagin, Giulio Gabbiani, Scott L. Friedman – 1 September 1992 – Hepatic lipocytes (perisinusoidal, Ito cells) are the primary matrix‐producing cells in liver fibrosis. During liver injury they undergo activation, a process characterized by cell proliferation and increased fibrogenesis. We and others have established a culture model in which in vivo features of lipocyte activation can be mimicked by cells grown on plastic.

Michael A. E. Ramsay, A. W. Paulsen, Thomas H. Swygert – 1 September 1992

G. Michael Taylor, Robert D. Goldin, Peter Karayiannis, Howard C. Thomas – 1 September 1992 – An in situ hybridization method using radiolabeled oligonucleotide probes was developed to study primary sites of hepatitis A virus replication in an experimental animal model of infection. Hepatitis A genomic sequences were demonstrated in hepatocytes of four marmosets with acute hepatitis A by use of antisense probes. In two of these animals, staining was also found when a sense probe was used, which is consistent with active replication in the hepatocytes.

Adrian M. di Bisceglie, Michiko Shindo, Tse‐Ling Fong, Michael W. Fried, Mark G. Swain, Nora V. Bergasa, Constantine A. Axiotis, Jeanne G. Waggoner, Yoon Park, Jay H. Hoofnagle – 1 September 1992 – Interferon‐α therapy is of proven efficacy in chronic hepatitis C, but it is not universally effective and may be associated with intolerable side effects. Ribavirin is a nucleoside analog with a broad spectrum of antiviral action. We conducted an uncontrolled pilot study of ribavirin therapy in 13 patients with chronic hepatitis C.

Raymond S. Koff, Herbert L. Bonkovsky, Richard Lambrecht – 1 September 1992

Raymond S. Koff – 1 September 1992

J. Michael Henderson, G. Thomas Gilmore, Gregory J. Mackay, John R. Galloway, Thomas F. Dodson, Michael H. Kutner – 1 September 1992 – Liver blood flow and systemic hemodynamics were measured intraoperatively in 34 patients after liver transplantation. Ultrasound transit‐time flow probes measured hepatic arterial and portal venous flow over 10 to 75 min 1 to 3 hr after reperfusion. Cardiac output was measured by thermodilution. Mean cardiac output was 9.5 ± 2.8 L/min; the mean total liver blood flow of 2,091 ± 932 ml/min was 23% ± 11% of cardiac output.

Tian‐Jun Huang, Jayanta Roy Chowdhury, Pulak Lahiri, Purna C. Yerneni, Vasudeva R. Bommineni, Irwin M. Arias, Namita Roy Chowdhury – 1 September 1992 – Hepatic bilirubin excretion requires UDP‐glucuronosyltransferase–mediated glucuronidation. Patients with type I Crigler‐Najjar syndrome and mutant rats (Gunn strain) inherit deficiency of UDP‐glucuronyltransferase activity toward bilirubin as an autosomal recessive trait and, as a result, exhibit marked nonhemolytic unconjugated hyperbilirubinemia throughout postnatal life.

Paul D. Berk – 1 September 1992

Takechika Fujii, Michimori Kohno, Chisato Hirayama – 1 August 1992 – Urinary 15N‐ammonia and 15N‐urea were measured by gas chromatography‐mass spectrometry after the intravenous administration of 15N‐ammonia (0.2 μmol/kg/hr) to 6 volunteers and 11 patients with cirrhosis. Urinary 15N‐nitrogen excretion as ammonia and urea was measured during the 210‐min infusion period, and urea synthesis and ammonia conversion to amino acids were analyzed with a three‐compartment model using the nonlinear least‐squares method.