Notices
1 May 1984
1 May 1984
Peter Ferenci, S.Chris Pappas, Peter J. Munson, Ken Henson, E. Anthony Jones – 1 March 1984 – It has previously been shown in an animal model of hepatic encephalopathy (HE) that the number of receptors for the inhibitory neurotransmitter, γ‐aminobutyric acid (GABA), increases and that the number of receptors for the excitatory neurotransmitter, glutamate, decreases.
Hiroshi Murakami, Junsuke Kuriki, Shinichi Kakumu, Kazuhiko Fukui, Nobuo Sakamoto – 1 March 1984 – Hybrid cell lines which secreted antibodies to liver‐specific membrane lipoprotein (LSP) were obtained by immunizing SMA and BALB/c mice with human LSP and fusing their splenocytes with the myeloma cell line P 3‐NSI/l‐Ag 4‐l.
1 March 1984
Gerald Y. Minuk, John Vergalla, Peter Ferenci, E. Anthony Jones – 1 March 1984 – γ‐Aminobutyric acid (GABA) is a potent inhibitory neurotransmitter which is synthesized by the enteric bacterial flora and delivered into portal venous blood. To determine whether the liver is likely to play an important role in regulating serum GABA levels, the uptake and metabolism of [3H]GABA by three populations of cells isolated from rat liver were studied. GABA was specifically taken up by hepatocytes but not by endothelial or Kupffer cells.
Gary C. Kanel, Robert L. Peters – 1 March 1984 – The hepatorenal syndrome, a primary cause of death from acute and chronic liver disease, consists of a functional renal failure whereby examination of the kidney has previously shown no distinct or specific morphologic change. We describe an unusual renal lesion consisting of the reflux of proximal convoluted tubular epithelium into Bowman's space. An autopsy series shows this glomerular change to be present in 71.4% of cases with the hepatorenal syndrome, while only present in 0 to 27.3% in other autopsy categories (p < 0.001).
Bertram I. Cohen, Anil K. Singhal, Richard J. Stenger, Patricia May‐Donath, Judith Finver‐Sadowsky, Charles K. Mcsherry, Erwin H. Mosbach – 1 March 1984 – The prevention of cholesterol cholelithiasis by dietary chenodeoxycholic and ursodeoxycholic acids was studied in the male prairie dog (Cynotttys ludovicianus). Gallstones were induced by administration of a semisynthetic diet containing 0.4% cholesterol for a period of 8 weeks. Groups of 5 or 6 animals received the lithogenic diet with added chenodeoxycholic or ursodeoxycholic acid (0.03% “low dose” or 0.06% “high dose”).