Two different subtypes of antimitochondrial antibodies are associated with primary biliary cirrhosis: Identification and characterization by radioimmunoassay and immunoblotting

Michael Manns, Guido Gerken, Apostolos Kyriatsoulis, Christian Trautwein, Konrad Reske, Karl‐Hermann Meyer Zum Büschenfelde – 1 September 1987 – Antimitochondrial antibodies from patients with primary biliary cirrhosis react with different mitochondrial polypeptides as demonstrated by Western blots.

Primary biliary cirrhosis: Associations with class II major histocompatibility complex antigens

Gregory J. Gores, S. Breanndan Moore, Lloyd D. Fisher, Frank C. Powell, E. Rolland Dickson – 1 September 1987 – Tissue injury in primary biliary cirrhosis is thought to be mediated by immune mechanisms. Various Class II antigens of the major histocompatibility complex are associated with autoimmune diseases and their differing clinical manifestations. Thus, the aim of this study was to examine the relationship between primary biliary cirrhosis, its clinical manifestations and serologically defined Class II antigens (HLA‐DR and HLA‐DQ).

Acinar redistribution and heterogeneity in transport of the organic cation rhodamine B in rat liver

Ineke Braakman, Geny Martha Maria Groothuis, Dirk Klaas Fokke Meijer – 1 September 1987 – We studied a possible acinar heterogeneity in the transport of organic cations, using rhodamine B as model compound. Employing perfusions of isolated rat livers in the ante‐ and retrograde mode and quantitative fluorescence microscopy, Zones 1 and 3 were shown to be equally efficient in taking up rhodamine B. Ten minutes after injection in an antegrade perfusion, 95% of the dose was localized in the portal half of the acinus.

The association of hepatic glycogen depletion with hyperammonemia in cirrhosis

Udaya M. Kabadi – 1 September 1987 – Hyperammonemia is a well‐recognized metabolic abnormality which occurs in cirrhotic patients with advanced liver dysfunction. We recently documented that hyperglucagonemia that occurs as a result of hepatic glycogen depletion may be responsible for this hyperammonemia by promoting gluconeogenesis to provide glucose as a fuel for functioning of several organ systems. Thus, hepatic glycogen depletion may be the initial process responsible for hyperammonemia.

Prevention of recurrence of esophageal varices after endoscopic injection sclerotherapy with ethanolamine oleate

Seigo Kitano, Nobuhiro Koyanagi, Yasunori Iso, Hidefumi Higashi, Keizo Sugimachi – 1 September 1987 – Endoscopic injection sclerotherapy was given to 155 patients with esophageal varices mainly related to non‐alcoholic liver cirrhosis. The formation of a superficial ulcer in the lower esophagus was achieved in 141 (91.0%) of the 155 patients, with an average of 4.1 sessions of endoscopic injection sclerotherapy during an average time of 4.9 weeks.

Mallory bodies and intermediate filaments: Of mice and men

Helmut Denk – 1 September 1987 – Livers from 12 mice fed griseofulvin for 4 to 6 months were perfused in situ with a detergent solution to extract lipid membranes leaving the cytoskeleton intact. Seven control mice were similarly studied. After 30 to 120 minutes perfusion, liver samples were examined by scanning electron microscopy and transmission electron microscopy. By light microscopy, Mallory bodies (MBs) were observed in pericentral hepatocytes. These were confirmed by transmission electron microscopy. Intermediate filaments (IFs) were observed in close apposition to MBs.

Glycoside conjugation in microsomes from hepatic and renal carcinoma of man

Heidrun Matern, Heinz‐Herbert Fiebig, Siegfried Matern – 1 September 1987 – Human hepatoma which had been xenografted into nude mice have been estimated for their ability to catalyze glucuronic acid and glucose conjugation of endogenous compounds and p‐nitrophenol. The xenobiotic p‐nitrophenol was glucuronidated with a comparable rate in microsomes from human hepatoma, human liver and host liver.

Lack of hepatic transferrin receptor expression in hemochromatosis

Raf Sciot, Alan C. Paterson, Joost J. Van Den Oord, Valeer J. Desmet – 1 September 1987 – The major part of hepatocellular iron is derived from uptake of transferrin‐bound iron by means of nonspecific fluid‐phase endocytosis and specific, saturable binding on high‐affinity transferrin receptors. We investigated the expression of transferrin receptors on hepatocytes in liver biopsies of 22 cases of hemochromatosis (21 primary hemochromatosis and 1 secondary hemochromatosis), using immunohistochemical demonstration of the human transferrin receptor with the specific monoclonal antibody OKT9.

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