Miguel A. Icarte, Margarita Pizarro, Luigi Accatino – 1 October 1991 – The hepatic transport of bile salts appears to be adaptively regulated by changes in the bile salt pool size and in the flux of bile salt through the liver. The maximum secretory rate of taurocholate increases or decreases when the bile salt pool size is modified by either oral feeding of cholate or taurocholate (up‐regulation) or prolonged bile salt depletion through a biliary fistula (down‐regulation), respectively.

David Carbone – 1 October 1991 – Human hepatocellular carcinomas (HCC) from patients in Qidong, an area of high incidence in China, in which both hepatitis B virus and aflatoxin B1 are risk factors, were analysed for mutations in p53, a putative tumour‐suppressor gene. Eight of the 16 HCC had a point mutation at the third base position of codon 249. The G→T transversion in seven HCC DNA samples and the G→C transversion in the other HCC are consistent with mutations caused by aflatoxin B1 in mutagenesis experiments. No mutations were found in exons 5, 6, 8 or the remainder of exon 7.

Raymond S. Koff, Melissa P. Upton – 1 October 1991

1 October 1991

Charles L. Mendenhall, Leonard Seeff, Anna Mae Diehl, Saad J. Ghosn, Samuel W. French, Peter S. Gartside, Susan D. Rouster, Zelma Buskell‐Bales, Charles J. Grossman, Gary A. Roselle, Robert E. Weesner, Pedro Garcia‐Pont, Stephen J. Goldberg, Thomas W. Kiernan, Carlo H.

Genevieve Inchauspe, Kenji Abe, Suzanne Zebedee, Marc Nasoff, Alfred M. Prince – 1 October 1991 – Three oligonucleotide primer combinations selected from the 5′ noncoding, the nucleocapsid and the putative nonstructural regions of the hepatitis C virus genome were compared in a nested polymerase chain reaction assay with respect to sensitivity and specificity for the detection of viral RNA in chimpanzeeinfected and human‐infected sera.

Wladimiro Jiménez, Jolanta Gutkowska, Pere Ginés, Vicente Arroyo, Francisca Rivera, Joan Rodés – 1 October 1991 – Patients with cirrhosis and ascites show sodium retention and normal or increased plasma levels of atrial natriuretic factor, a peptide with powerful natriuretic activity.

Stephen Webster, Jeanne Gottstein, Andres T. Blei, Robert Levy – 1 October 1991 – Brain edema and intracranial hypertension are a major cause of death in fulminant hepatic failure. We have shown that brain water measured in rats after hepatic devascularization (portacaval anastomosis followed in 24 to 48 hr by ligation of the hepatic artery) increases with the progression of encephalopathy. In this study, we examined whether intracranial hypertension develops in this model of fulminant hepatic failure.

Robert Safirstein, Marvin F. Levitt – 1 October 1991

1 October 1991