Fuel homeostasis and carnitine metabolism in rats with secondary biliary cirrhosis

Stephan Krahenbuhl, Eric P. Brass – 1 November 1991 – Energy metabolism is abnormal in patients and experimental animals with liver cirrhosis. To help better understand the abnormalities, fuel homeostasis and carnitine metabolism were studied in fed and 24‐hr‐starved rats with secondary biliary cirrhosis induced by bile duct ligation for 4 wk. Plasma ketone body concentrations were decreased by 67% in starved, bile duct–ligated rats compared with control rats.

Failure to detect hepatitis C virus genome in human secretions with the polymerase chain reaction

Henry H. Hsu, Teresa L. Wright, Daniel Luba, Mary Martin, Stephen M. Feinstone, Gabriel Garcia, Harry B. Greenberg – 1 November 1991 – Although hepatitis C infection has been clearly demonstrated to be transmitted through blood products or blood contamination, most cases of sporadic hepatitis C infection are unassociated with parenteral risk factors, and it is unclear how infection might be acquired by nonparenteral means. One potential mode of nonparenteral transmission is through body secretions.

Kupffer cells from carbon tetrachloride–injured rat livers produce chemotactic factors for fibroblasts and monocytes: The role of tumor necrosis factor‐α

Juan Armendariz‐Borunda, Jerome M. Seyer, Arnold E. Postlethwaite, Andrew H. Kang – 1 November 1991 – Conditioned media from cultured Kupffer and mononuclear macrophagic cells obtained 48 hr after CCl4 administration to rats contains chemotactic factors for human skin fibroblasts and human monocytes. The chemotactic mediator for fibroblasts was approximately 17 kD and was more prominent at early stages of culture. It induced a dose‐dependent chemotactic response in fibroblasts.

Effects of single ethanol administration on hepatic ornithine decarboxylase induction and polyamine metabolism

Takashi Tanaka, Yoshihiro Sukegawa, Shuhei Nishiguchi, Tetsuo Kuroki, Kenzo Kobayashi, Isao Matsui‐Yuasa, Shuzo Otani, Takashi Toda, Takeyuki Monna – 1 October 1991 – The effects of a single ethanol administration on ornithine decarboxylase induction, polyamine metabolism and DNA synthesis in rat liver after partial hepatectomy were studied. Ethanol given 1 hr before partial hepatectomy at the dose of 2, 3 or 5 gm/kg body wt inhibited the increase in ornithine decarboxylase activity and that in the putrescine level in the liver 4 hr after partial hepatectomy.

Estrogen and progesterone receptors in the gallbladders from patients with gallstones

Franco O. Ranelletti, Mauro Piantelli, Everardo Zanella, Arnaldo Capelli, Attilio M. Farinon – 1 October 1991 – Cytosolic receptors for estrogen and progesterone were assayed in 50 gallbladders from 29 women and 21 men who had cholecystectomies because of choleithiasis. High‐affinity (equilibrium dissociation constant, KD = 0.46 ± 0.23 nmol/L of 24 cases) estrogen receptors were detected in 20 of 29 gallbladders from women (range = 1.6 to 32 fmol/mg protein; mean ± S.D. = 10.9 ± 8.1), whereas in men only 4 of 21 specimens contained detectable estrogen receptors.

Dietary fish oil effects on biliary lipid secretion and cholesterol gallstone formation in the African green monkey

Martin W. Scobey, Fred L. Johnson, John S. Parks, Lawrence L. Rudel – 1 October 1991 – We studied two groups of adult male African green monkeys to assess the effects of dietary fish oil on biliary lipid secretion and cholesterol gallstone formation. One group was fed 0.8 mg cholesterol/kcal and 42% of calories as fat with half of the fat calories derived from lard; the other group was fed a similar diet except for the isocaloric substitution of menhaden oil for lard. After 21/2 to 3 yr, necropsies were performed and the presence of gallstones was determined.

Urinary excretion of lithocholic acid and its conjugates by the bile duct–ligated rat

Joanna M. Little, Piotr Zimniak, Anna Radominska, Roger Lester, Paul Lehman – 1 October 1991 – The 3‐O‐glucuronide of lithocholic acid has been shown to be a potent cholestatic agent in rats. However, even after the onset of lithocholic acid glucuronide–induced cholestasis, little of the administered material was recovered in urine.

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