Platelets and platelet‐derived serotonin promote tissue repair after normothermic hepatic ischemia in mice

Antonio Nocito, Panco Georgiev, Felix Dahm, Wolfram Jochum, Michael Bader, Rolf Graf, Pierre‐Alain Clavien – 26 January 2007 – Hepatic ischemia and reperfusion (I/R) leads to the formation of leukocyte–platelet aggregates. Upon activation, platelets generate reactive oxygen species and release proapoptotic and proinflammatory mediators as well as growth factors. In cold hepatic ischemia, adhesion of platelets to endothelial cells mediates sinusoidal endothelial cell apoptosis. Furthermore, platelet‐derived serotonin mediates liver regeneration.

Human and rat bile acid–CoA:amino acid N‐acyltransferase are liver‐specific peroxisomal enzymes: Implications for intracellular bile salt transport

Antonella Pellicoro, Fiona A. J. van den Heuvel, Mariska Geuken, Han Moshage, Peter L. M. Jansen, Klaas Nico Faber – 26 January 2007 – Bile acid–coenzyme A:amino acid N‐acyltransferase (BAAT) is the sole enzyme responsible for conjugation of primary and secondary bile acids to taurine and glycine. Previous studies indicate a peroxisomal location of BAAT in peroxisomes with variable amounts up to 95% detected in cytosolic fractions. The absence or presence of a cytosolic pool of BAAT has important implications for the intracellular transport of unconjugated/deconjugated bile salts.

Mutual changes of thioredoxin and nitrosothiols during biliary cirrhosis: Results from humans and cholestatic rats

Ignazio Grattagliano, Piero Portincasa, Vincenzo O. Palmieri, Giuseppe Palasciano – 26 January 2007 – Cholestasis is associated with changes in NO metabolism and thiol oxidation. Thioredoxin contributes to regulate vascular tone and intracellular redox status by cleaving nitrosothiols and maintaining −SH groups. This study investigated the changes in circulating thioredoxin and nitrosothiols and the relationship with protein sulfhydryls (PSH), hepatic concentrations, hyaluronate, and histology in patients with primary biliary cirrhosis (PBC) and in rats with bile duct ligation (BDL).

Vascular dysfunction in human and rat cirrhosis: Role of receptor‐desensitizing and calcium‐sensitizing proteins

Martin Hennenberg, Jonel Trebicka, Erwin Biecker, Michael Schepke, Tilman Sauerbruch, Jörg Heller – 26 January 2007 – In cirrhosis, vascular hypocontractility leads to vasodilation and contributes to portal hypertension. Impaired activation of contractile pathways contributes to vascular hypocontractility. Angiotensin II type 1 receptors (AT1‐Rs) are coupled to the contraction‐mediating RhoA/Rho‐kinase pathway and may be desensitized by phosphorylation through G‐protein‐coupled receptor kinases (GRKs) and binding of β‐arrestin‐2.

Factors influencing the progression of fibrosis in patients with recurrent hepatitis C after liver transplantation under antiviral therapy: A retrospective analysis of 939 liver biopsies in a single center

Thomas Walter, Jérôme Dumortier, Olivier Guillaud, Valérie Hervieu, Jean‐Yves Scoazec, Olivier Boillot – 26 January 2007 – Recurrent hepatitis C after liver transplantation (LT) is a major problem, since up to 30% of patients develop cirrhosis only 5 years after LT in the absence of antiviral therapy. The aim of this study was to examine the rate of progression of fibrosis and its associated risk factors in patients submitted to an early antiviral treatment post‐LT.

Molecular and functional analysis of occult hepatitis B virus isolates from patients with hepatocellular carcinoma

Teresa Pollicino, Giuseppina Raffa, Lucy Costantino, Antonella Lisa, Cesare Campello, Giovanni Squadrito, Massimo Levrero, Giovanni Raimondo – 26 January 2007 – Occult HBV infection is characterized by the persistence of HBV DNA in the liver of individuals negative for HBV surface antigen (HBsAg). Occult HBV may exist in the hepatocytes as a free genome, although the factors responsible for the very low viral replication and gene expression usually observed in this peculiar kind of infection are mostly unknown.

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