Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity

Luigi E. Adinolfi, Michele Gambardella, Augusto Andreana, Marie‐françoise Tripodi, Riccardo Utili, Giuseppe Ruggiero – 30 December 2003 – The role of steatosis in the progression of liver damage in chronic hepatitis C (CHC) was studied. Enrolled were 180 consecutive liver biopsy‐proven CHC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and steatosis, body mass index (BMI; kg/m2), distribution of body fat, HCV genotype, and levels of HCV RNA.

The phenobarbital response enhancer module in the human bilirubin UDP‐glucuronosyltransferase UGT1A1 gene and regulation by the nuclear receptor CAR

Junko Sugatani, Hiroyuki Kojima, Akiko Ueda, Satoru Kakizaki, Kouichi Yoshinari, Qi‐Hui Gong, Ida S. Owens, Masahiko Negishi, Tatsuya Sueyoshi – 30 December 2003 – The UDP‐glucuronosyltransferase, UGT1A1, is the critical enzyme responsible for detoxification of the potentially neurotoxic bilirubin by conjugating it with glucuronic acid. For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver. We have now delineated the PB response activity to a 290‐bp distal enhancer sequence (−3483/−3194) of the UGT1A1 gene.

Zinc mesoporphyrin represses induced hepatic 5‐aminolevulinic acid synthase and reduces heme oxygenase activity in a mouse model of acute hepatic porphyria

Macé M. Schuurmans, Francine Hoffmann, Raija L. Lindberg, Urs A. Meyer – 30 December 2003 – Zinc mesoporphyrin (ZnMP) is a potent inhibitor of heme oxygenase (HO) and represses 5‐aminolevulinic acid synthase (ALAS). These properties make it a potential candidate for treatment of inducible acute hepatic porphyrias, diseases characterized by neurovisceral symptoms, and massive ALAS induction.

Tauroursodeoxycholic acid inserts the apical conjugate export pump, Mrp2, into canalicular membranes and stimulates organic anion secretion by protein kinase C–dependent mechanisms in cholestatic rat liver

Ulrich Beuers, Manfred Bilzer, Anila Chittattu, Gerd A. Kullak‐Ublick, Dietrich Keppler, Gustav Paumgartner, Frank Dombrowski – 30 December 2003 – Ursodeoxycholic acid (UDCA) exerts anticholestatic effects by undefined mechanisms. Previous work suggested that UDCA stimulates biliary exocytosis via Ca++‐ and protein kinase C (PKC)‐dependent mechanisms.

Central venulitis in pediatric liver allografts

Alyssa M. Krasinskas, Eduardo D. Ruchelli, Elizabeth B. Rand, Jesse L. Chittams, Emma E. Furth – 30 December 2003 – Central venulitis (CV), a distinct histologic lesion described in adult liver transplants, can occur with acute portal tract rejection or in isolation (ICV). Possible etiologies include immunosuppressive drug toxicity, acute cellular rejection, viral hepatitis, ischemic injury, and recurrent disease.

Repopulation of mouse liver with human hepatocytes and in vivo infection with hepatitis B virus

Maura Dandri, Martin R. Burda, Eva Török, Joerg M. Pollok, Alicja Iwanska, Gunhild Sommer, Xavier Rogiers, Charles E. Rogler, Sanjeev Gupta, Hans Will, Heiner Greten, Joerg Petersen – 30 December 2003 – Mice containing livers repopulated with human hepatocytes would provide excellent in vivo models for studies on human liver diseases and hepatotropic viruses, for which no permissive cell lines exist.

Resistance to fulminant hepatitis and carcinogenesis conferred by overexpression of retinoblastoma protein in mouse liver

Toshiaki Ichihara, Yoshinori Komagata, Xiao‐Li Yang, Tadayoshi Uezato, Katsuhiko Enomoto, Kenji Koyama, Jun‐ichi Miyazaki, Toshihiro Sugiyama, Naoyuki Miura – 30 December 2003 – Previously, retinoblastoma (Rb) transgenic mice were produced under the control of the Rb gene promoter and showed dwarf characteristics. Here, we created transgenic mice, in which the human Rb gene was controlled by the hepatocyte nuclear factor‐1 gene promoter/enhancer and was expressed primarily in the liver. The liver of these novel transgenic mice was normally developed.

Ursodeoxycholic acid administration in patients with cholestasis of pregnancy: Effects on primary bile acids in babies and mothers

Giuseppe Mazzella, Rizzo Nicola, Azzaroli Francesco, Simoni Patrizia, Bovicelli Luciano, Miracolo Anna, Simonazzi Giuliana, Colecchia Antonio, Nigro Giovanni, Mwangemi Constance, Festi Davide, Roda Enrico – 30 December 2003 – Little is known about the effects on the fetus of ursodeoxycholic acid (UDCA) treatment for intrahepatic cholestasis of pregnancy (ICP). Twenty ICP patients were given UDCA at 1.5 to 2 g/d, to our knowledge the highest dosage yet reported.

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