Colchicine clearance is impaired in alcoholic cirrhosis

Jonathan A. Leighton, Michael K. Bay, Alma L. Maldonado, Steven Schenker, K. Vincent Speeg – 1 December 1991 – Colchicine may have benefit in primary biliary cirrhosis and alcoholic liver disease. It is currently used in patients with impaired liver function, yet little is known about its elimination in such patients. Colchicine clearance in the rat is significantly impaired in various models of liver disease. To study this in human beings, colchicine pharmacokinetics were compared in normal subjects and patients with alcoholic cirrhosis.

Investigation of the role of polymorphisms at the alcohol and aldehyde dehydrogenase loci in genetic predisposition to alcohol‐related end‐organ damage

Christopher P. Day, Rumaisa Bashir, Oliver F. W. James, Margaret F. Bassendine, David W. Crabb, Holly R. Thomasson, Ting‐Kai Li, Howard J. Edenberg – 1 November 1991 – Little is known about factors determining individual susceptibility to the physical complications of alcohol abuse but genetically determined differences in ethanol metabolism may be important. The oxidative metabolism of alcohol is catalyzed by alcohol and aldehyde dehydrogenase.

Azathioprine hepatotoxicity after liver transplantation

Martina Sterneck, Russell Wiesner, Nancy Ascher, John Roberts, Linda Ferrell, Jurgen Ludwig, John Lake – 1 November 1991 – We report the first two cases of apparent azathioprine hepatotoxicity occurring after liver transplantation. The two patients exhibited jaundice, elevated serum transaminase activities and histopathological features of sinusoidal congestion and centrilobular hepatocellular degeneration 17 and 61 days after transplantation. After withdrawal of azathioprine, liver test results improved immediately in both patients.

Transport of free fatty acid and triglyceride in anhepatic rats

Steven H. Quarfordt, Eliana Defaria, Barry A. Landis, R. Randal Bollinger, Yasuo Yamaguchi – 1 November 1991 – Without a liver the fractional plasma removal of free fatty acid is one third and chylomicron triglyceride one half of that in the intact rat. The intestine of the anhepatic rat converted enteral fatty acid to plasma triglyceride but was unable to do the same for plasma free fatty acid.

Detection of proliferating liver cells in various diseases by a monoclonal antibody against DNA polymerase‐α: With special reference to the relationship between hepatocytes and sinusoidal cells

Shuichi Seki, Hiroki Sakaguchi, Nobuyoshi Kawakita, Atsushi Yanai, Tetsuo Kuroki, Yasuhiro Mizoguchi, Kenzo Kobayashi, Takeyuki Monna – 1 November 1991 – Proliferating cells in liver specimens from patients with various diseases were detected by use of a monoclonal antibody against human DNA polymerase‐α, which is present in the nuclei of cells in the G1, S, M and G2 phases of the mitotic cell cycle and absent in the G0 phase, to clarify the kinetics and morphological characteristics of these cells.

Localization of CYP1A1 and CYP1A2 messenger RNA in normal human liver and in hepatocellular carcinoma by in situ hybridization

Ross A. McKinnon, Pauline de la M. Hall, Linda C. Quattrochi, Robert H. Tukey, Michael E. McManus – 1 November 1991 – To better characterize the precise cellular distribution of CYP1A gene products in man, we have undertaken Northern‐blot and in situ hybridization analyses of CYP1A expression in human liver. Using riboprobes transcribed from both CYP1A1 and CYP1A2 complementary DNAs to probe a series of Northern blots of 23 human liver messenger RNA samples, CYP1A1 expression was demonstrated in 11 samples and CYP1A2 expression was evident in 22 samples.

Histochemical demonstration of sinusoidal γ‐glutamyltransferase activity by substrate protection fixation: Comparative studies in rat and guinea pig liver

António José Lanca, Yedy Israel – 1 November 1991 – Most histochemical methods for the detection of an enzymatic activity are preceded by tissue fixation with chemical agents that partially inactivate the enzymes. It is well known that substrates exert a marked protection against fixative‐induced inactivation.

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