Predicting the discharge status after liver transplantation at a single center: A new approach for a new era

Dympna M. Kelly, Renee Bennett, Nancy Brown, Judy McCoy, Derek Boerner, Changhong Yu, Bijan Eghtesad, Wael Barsoum, John J. Fung, Michael W. Kattan – 27 March 2012 – The aim of this study was to develop a tool for preoperatively predicting the need of a patient to attend an extended care facility after orthotopic liver transplantation (OLT).

Cost‐effectiveness of boceprevir or telaprevir for untreated patients with genotype 1 chronic hepatitis C

Calogero Cammà, Salvatore Petta, Marco Enea, Raffaele Bruno, Fabrizio Bronte, Vincenza Capursi, Americo Cicchetti, Giorgio L. Colombo, Vito Di Marco, Antonio Gasbarrini, Antonio Craxì, on behalf of the WEF Study Group – 27 March 2012 – Randomized controlled trials (RCTs) show that triple therapy (TT) with peginterferon alpha, ribavirin, and boceprevir (BOC) or telaprevir (TVR) is more effective than peginterferon‐ribavirin dual therapy (DT) in the treatment of previously untreated patients with genotype 1 (G1) chronic hepatitis C (CHC).

Cyclin E1 controls proliferation of hepatic stellate cells and is essential for liver fibrogenesis in mice

Yulia A. Nevzorova, Jörg‐Martin Bangen, Wei Hu, Ute Haas, Ralf Weiskirchen, Nikolaus Gassler, Sebastian Huss, Frank Tacke, Piotr Sicinski, Christian Trautwein, Christian Liedtke – 27 March 2012 – Liver fibrogenesis is associated with the transition of quiescent hepatocytes and hepatic stellate cells (HSCs) into the cell cycle. Exit from quiescence is controlled by E‐type cyclins (cyclin E1 [CcnE1] and cyclin E2 [CcnE2]). Thus, the aim of the current study was to investigate the contribution of E‐type cyclins for liver fibrosis in man and mice.

Impaired intrahepatic natural killer cell cytotoxic function in chronic hepatitis C virus infection

Stefania Varchetta, Dalila Mele, Stefania Mantovani, Barbara Oliviero, Eleonora Cremonesi, Serena Ludovisi, Giuseppe Michelone, Mario Alessiani, Riccardo Rosati, Marco Montorsi, Mario U. Mondelli – 20 March 2012 – Hepatitis C virus (HCV) persistence in the host results from inefficiencies of innate and adaptive immune responses. Most studies addressing the role of innate immunity concentrated on peripheral blood (PB) natural killer (NK) cells, whereas only limited information is available on intrahepatic (IH) NK cells.

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