Darius Moradpour, Josef Altorfer, Renata Flury, Peter Greminger, Christa Meyenberger, Res Jost, Martin Schmid – 1 December 1994 – We describe a 33‐yr‐old pregnant woman in whom a primary biliary cirrhosis—like syndrome developed after 2 wk of chlorpromazine therapy. The clinical course was characterized by severe jaundice lasting 22 mo, intense pruritus, fever, steatorrhea, high alkaline phosphatase levels and hypercholesterolemia.

Antonio Follo, Jose María Llovet, Miquel Navasa, Ramón Planas, Xavier Forns, Anna Francitorra, Antoni Rimola, Miguel Angel Gassull, Vicente Arroyo, Joan Rodés – 1 December 1994 – Although spontaneous bacterial peritonitis is considered a precipitating factor of renal impairment in cirrhosis, no study specifically addressing this problem has been reported. This study was aimed at assessing the incidence, clinical course, predictive factors and prognosis of renal impairment in cirrhotic patients with peritonitis.

Bruno Christ Phd., Annegret Nath, Peter C. Heinrich, Kurt Jungermann – 1 December 1994 – The influence of recombinant human interleukin‐6, the major mediator of the inflammatory response in liver, on the glucagon‐ and insulin‐dependent induction of the phosphoenolpyruvate carboxykinase and glucokinase gene, respectively, was monitored on the level of gene transcription, mRNA abundance and enzyme activity in cultured rat hepatocytes.

Stephan Krähenbühl, Sven Fischer, Christine Talos, Professor Jürg Reichen – 1 December 1994 – The effect of ursodeoxycholate and tauroursodeoxycholate on the toxicity of lipophilic bile acids (chenodeoxycholate and lithocholate) on the function of the electron transport chain was investigated in isolated rat liver mitochondria. At a concentration of 30 μmol/L, both chenodeoxycholate and lithocholate reduced state 3 oxidation rates and respiratory control ratios of L‐glutamate, succinate and duroquinol.

Daniel Martinez‐Fong, Jerald E. Mullersman, Anthony F. Purchio, Juan Armendariz‐Borunda, Antonio Martinez‐Hernandez M.D. – 1 December 1994 – The basic approach in targeted gene delivery relies on the formation of a complex between a vector and a molecule that will be selectively internalized by the target cells. In the case of hepatocytes, asialoglycoproteins are convenient targeting molecules because of the high affinity and avidity of the hepatocyte galactose receptor.

Allan Cooper – 1 December 1994 – The atherogenic macromolecule lipoprotein(a) [Lp(a)] has resisted in vivo analyses partly because it is found in a limited number of experimental animals. Although transgenic mice expressing human apolipoprotein (a) [apo(a)] have previously been described, they failed to assemble Lp(a) particles because of the inability of human apo(a) to associate with mouse apolipoprotein B (apoB). We isolated a 90‐kilobase P1 phagemid containing the human apoB gene and with this DNA generated 13 lines of transgenic mice of which 11 expressed human apoB.

Harold O. Conn – 1 December 1994 – An inverse relation is known to link blood potassium with renal synthesis and the release of ammonia. Given the liability of hyperammonemia for precipitating hepatic encephalopathy (HE), 28 patients affected by stage I HE were equally divided into two groups and maintained up to their death at the highest (5.4–5.5 mEq/l) or the lowest (3.5–3.6 mEq/l) normokalemia levels.

1 December 1994

Judith A. Marlett, Kathryn B. Hosig, Nicholas W. Vollendorf, Fred L. Shinnick, Valerie S. Haack, Jon A. Story – 1 December 1994 – Nine normolipidemic young men consumed a constant diet for 2 mo into which oat bran was incorporated during the second month so that we might test the hypotheses that oats lower serum cholesterol concentrations by decreasing bile acid and fat absorption and increasing bile acid synthesis. Bile acid kinetics were determined by measuring the 13C enrichment of serum cholic and chenodeoxycholic acids.

Fumio Nomura, Kunihiko Ohnishi, Hidetaka Terabayashi, Toshiaki Nakai, Kazumasa Isobe, Kazuhiro Takekoshi, Kunio Okuda – 1 December 1994 – Increased plasma ammonia levels in patients with advanced cirrhosis have been attributed to reduced conversion of enteric ammonia to urea by the diseased liver and to entry of enteric ammonia into systemic circulation by way of portal‐systemic shunts. Because single‐pass extraction is high for portal venous ammonia, reduction of portal blood supply to hepatocytes may have detrimental effects on the hepatic extraction of ammonia.