Role of intracellular calcium in superoxide‐induced hepatocyte injury

Masaru Murata, Morito Monden, Koji Umeshita, Hiroshi Nakano, Toshio Kanai, Mitsukazu Gotoh, Takesada Mori – 1 May 1994 – The mechanisms of hepatocyte injury caused by exogenous superoxide were investigated with the use of cultured rat hepatocytes. Cell viability, cytosolic free calcium concentration and cell surface structure were observed. Superoxide was produced by adding hypoxanthine and xanthine oxidase to the buffer. Cytosolic free calcium concentration was calculated by means of ratio imaging of fura 2 fluorescence with multiparameter digitized microscopy.

Ultrastructural location of human hepatocyte growth factor in human liver

Hiroki Sakaguchi, Shuichi Seki, Hirohito Tsubouchi, Yasushi Daikuhara, Yoshiyuki Niitani, Kenzo Kobayashi – 1 May 1994 – Human hepatocyte growth factor has been purified from the plasma of patients with fulminant liver failure, but where this factor is produced in organs or cells of subjects with liver diseases is unknown. Therefore, we used a monoclonal antibody to human hepatocyte growth factor to stain cells in three normal and 29 diseased liver tissues by immunohistochemical techniques.

The distribution of calcium salt precipitates in the core, periphery and shell of cholesterol, black pigment and brown pigment gallstones

Howard S. Kaufman, Thomas H. Magnuson, Henry A. Pitt, Peter Frasca, Keith D. Lillemoe – 1 May 1994 – Calcium bilirubinate, palmitate, carbonate and phosphate have been identified in the cores of cholesterol and pigment gallstones, suggesting a role for precipitated calcium salts in the early events of gallstone formation. Previous studies that compared the calcium salt contents of cholesterol and pigment stones required destruction of gallstone structure.

Hepatocellular Na+/H+ exchange is activated early, transiently and at a posttranscriptional level during rat liver regeneration

Andreas Dällenbach, Ulrich Marti, Eberhard L. Renner – 1 May 1994 – In hepatocytes in vitro, Na+/H+ exchange, an important regulator of intracellular pH, is activated by epidermal growth factor, but its activity during liver regeneration in vivo is unknown. We therefore compared activity and regulation of Na+/H+ exchange in hepatocytes isolated after two‐thirds partial hepatectomy or sham surgery, respectively, by measuring intracellular pH (fluorimetry) and steady state Na+/H+ exchange mRNA levels (Northern blotting).

Presinusoidal and proximal intrasinusoidal confluence of hepatic artery and portal vein in rat liver: Functional evidence by orthograde and retrograde bivascular perfusion

Yuji Watanabe, Gerhard P. Püschel, Andreas Gardemann, Kurt Jungermann – 1 May 1994 – The site of confluence of the artery and the portal vein in the liver still appears to be controversial. Anatomical studies suggested a presinusoidal or an intrasinusoidal confluence in the first, second or even final third of the sinusoids. The objective of this investigation was to study the problem with functional biochemical techniques.

Hepatic artery and portal vein vascularization of normal and cirrhotic rat liver

Ibrahim Kassissia, Antoine Brault, P.‐Michel Huet – 1 May 1994 – The hepatic artery and portal vein vascularization of seven normal and seven cirrhotic rats was evaluated by means of the multiple‐indicator dilution technique using the flow‐limited model analysis. Injected 15‐μm microspheres were all trapped by the liver in normal and cirrhotic rats after portal vein and hepatic artery injections, ruling out the presence of intrahepatic shunts larger than 15 μm.

The canadian multicenter double‐blind randomized controlled trial of ursodeoxycholic acid in primary biliary cirrhosis

E. Jenny Heathcote, Karen Cauch‐Dudek, Valery Walker, Robert J. Bailey, Laurence M. Blendis, Cameron N. Ghent, Pina Michieletti, Gerald Y. Minuk, S. Chris Pappas, Linda J. Scully, Urs P. Steinbrecher, Lloyd R. Sutherland, C. Noel Williams, Helga Witt‐Sullivan, Lawrence J. Worobetz, Ruth A. Milner, Ian R. Wanless – 1 May 1994 – Ursodeoxycholic acid, a dihydroxyl bile acid normally present in human beings in minimal amounts, becomes incorporated into the bile salt pool when taken orally. In cholestasis, bile acids are retained in the liver and are hepatotoxic.

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