Cellular theories of aging as related to the liver
J. Fred Dice – 1 May 1985 – The age‐associated decjline in function of several organs, including the liver, may be caused by mechanisms operating on the cellular level. Fibroblasts and several other cell types derived from normal individuals have limited lifespans in culture, and several abnormalities described for senescent cultured fibroblasts also apply to hepatocytes and other cell types obtained from aged organisms.
El enfermo icterico, 5th edition. By Horacio Jinich. pp. 239 ± xv. Mexico: Interamericana, 1983
Eugene R. Schiff, Hector Serrano – 1 May 1985
Natural history of chronic hepatitis B virus infection in taiwan: Studies of hepatitis B virus DNA in serum
Chia‐Ming Chu, Peter Karayiannis, Martin J. F. Fowler, Jon Monjardino, Yun‐Fan Liaw, Howard C. Thomas – 1 May 1985 – Hepatitis B virus DNA (HBV DNA) in serum was measured by a Spot hybridization technique in a consecutive series of 79 cases with chronic HBV infection from Taiwan. HBV DNA was found in 96.3% (52/54) of HBeAg‐positive, 66% (2/3) with neither HBeAg or anti‐HBe and in 63.6% (14/22) of anti‐HBe positive patients. The levels of HBV DNA in the HBe‐Ag‐positive patients were significantly higher than in the anti‐HBe positive patients (median, 944 vs. 58 pg per ml, p < 0.001).
The effect of the combination of nitroglycerin and propranolol on splanchnic and systemic hemodynamics in a portal hypertensive rat model
Richard J. Kroeger, Roberto J. Groszmann – 1 May 1985 – Present investigations support major contributions from increases in both portal blood flow and portal vascular resistance in the mechanism that maintains portal hypertension. β‐Adrenergic blockers have been shown to reduce the elevated portal blood flow component. The possibility that nitroglycerin administration could reduce the elevated portal vascular resistance component is investigated here. Portal hypertension was induced in rats by a calibrated constriction of the portal vein.
Suppression of T helper function: An immunoregulatory effect of rosette inhibitory factor in hepatitis B virus infection
Gary E. Sanders, Robert P. Perrillo – 1 May 1985 – The potential immunoregulatory effects of rosette inhibitory factor (RIF) were evaluated using lymphocyte subpopulations defined by monoclonal antibodies (OKT4, OKT8). Initial experiments indicated that RIF inhibits E‐rosette formation by T cells that provide helper/inducer function (OKT4+). Subsequently, experiments were done to assess if RIF had an inhibitory effect on in vitro immunoglobulin and anti‐HBs production. These studies used peripheral blood mononuclear cells from convalescent and hepatitis B‐vaccinated donors.
Evidence for a channel for the electrogenic transport of chloride ion in the rat hepatocyte
Christine E. Bear, Connie N. Petrunka, Steven M. Strasberg – 1 May 1985 – Chloride is the major inorganic anion in bile but its mechanism of passage from blood to bile is uncertain. Specific membrane channels account for most net inorganic anion flux in other cell types such as the proximal tubular cell and red blood cell; disulfonic stilbenes inhibit anion movement through these channels. Therefore, we have sought the presence of similar channels in the hepatocyte.
Hepatic (Na+, K+)‐ATPase: A current view of its structure, function and localization in rat liver as revealed by studies with monoclonal antibodies
Hyam L. Leffert, Dale B. Schenk, Jeffrey J. Hubert, Harold Skelly, Mark Schumacher, Reginald Ariyasu, Mark Ellisman, Katherine S. Koch, Gilbert A. Keller – 1 May 1985
Ranitidine‐acetaminophen interaction: Effects on acetaminophen‐induced hepatotoxicity in fischer 344 rats
Thomas B. Leonard, D. Gwyn Morgan, John G. Dent – 1 May 1985 – Cimetidine has been shown to protect against acetaminophen‐mediated hepatotoxicity in both rats and mice. In contrast to cimetidine, ranitidine recently has been determined to potentiate the hepatotoxic action of acetaminophen in Fischer 344 rats. The present studies were designed to characterize this ranitidine‐acetaminophen interaction. Acetaminophen administration (750 mg per kg, p.o.) to F344 rats produced maximal hepatic necrosis, 24 hr after treatment, as assessed by SGPT activity and histopathology.