Addition of simvastatin to cold storage solution prevents endothelial dysfunction in explanted rat livers

Lucia Russo, Jorge Gracia‐Sancho, Héctor García‐Calderó, Giusi Marrone, Juan Carlos García‐Pagán, Guillermo García‐Cardeña, Jaime Bosch – 26 October 2011 – Pathophysiological alterations in the endothelial phenotype result in endothelial dysfunction. Flow cessation, occurring during organ procurement for transplantation, triggers the endothelial dysfunction characteristic of ischemia/reperfusion injury, partly due to a reduction in the expression of the vasoprotective transcription factor Kruppel‐like Factor 2 (KLF2).

Plasma cells and the chronic nonsuppurative destructive cholangitis of primary biliary cirrhosis

Toru Takahashi, Tomofumi Miura, Junichiro Nakamura, Satoshi Yamada, Tsutomu Miura, Masahiko Yanagi, Yasunobu Matsuda, Hiroyuki Usuda, Iwao Emura, Koichi Tsuneyama, Xiao‐Song He, M. Eric Gershwin – 26 October 2011 – There has been increased interest in the role of B cells in the pathogenesis of primary biliary cirrhosis (PBC). Although the vast majority of patients with this disease have anti‐mitochondrial antibodies, there is no correlation of anti‐mitochondrial antibody titer and/or presence with disease severity.

Quantitative liver function tests improve the prediction of clinical outcomes in chronic hepatitis C: Results from the hepatitis C antiviral long‐term treatment against cirrhosis trial

Gregory T. Everson, Mitchell L. Shiffman, John C. Hoefs, Timothy R. Morgan, Richard K. Sterling, David A. Wagner, Shannon Lauriski, Teresa M. Curto, Anne Stoddard, Elizabeth C. Wright, the HALT‐C Trial Group – 26 October 2011 – Risk for future clinical outcomes is proportional to the severity of liver disease in patients with chronic hepatitis C virus (HCV). We measured disease severity by quantitative liver function tests (QLFTs) to determine cutoffs for QLFTs that identified patients who were at low and high risk for a clinical outcome.

Claudin‐1 involved in neonatal ichthyosis sclerosing cholangitis syndrome regulates hepatic paracellular permeability

Brigitte Grosse, Doris Cassio, Nadya Yousef, Céline Bernardo, Emmanuel Jacquemin, Emmanuel Gonzales – 26 October 2011 – Neonatal ichthyosis and sclerosing cholangitis (NISCH) syndrome is a liver disease caused by mutations of CLDN1 encoding Claudin‐1, a tight‐junction (TJ) protein. In this syndrome, it is speculated that cholestasis is caused by Claudin‐1 absence, leading to increased paracellular permeability and liver injuries secondary to paracellular bile regurgitation. We studied the role of claudin‐1 in hepatic paracellular permeability.

Thrombocytopenia, splenomegaly, and portal blood flow in patients who have undergone liver transplantation for cirrhosis

Daniel Eyraud, Benjamin Granger, Christian Ionescu, Silvia Fratéa, Sabine Darnat, Jean‐Christophe Vaillant, Jean‐Michel Siksik, Laurent Hannoun, Pierre Coriat – 17 October 2011 – The platelet count (PC), the spleen size (SS), and the portal blood flow (PBF) have been independently studied in the perioperative period after orthotopic liver transplantation (OLT) for cirrhosis, but these parameters have not been described and analyzed in combination.

Hepatitis E virus (HEV)‐specific T‐cell responses are associated with control of HEV infection

Pothakamuri Venkata Suneetha, Sven Pischke, Verena Schlaphoff, Jan Grabowski, Paraskevi Fytili, Anna Gronert, Birgit Bremer, Antoaneta Markova, Jerzy Jaroszewicz, Christoph Bara, Michael P. Manns, Markus Cornberg, Heiner Wedemeyer – 17 October 2011 – Hepatitis E virus (HEV) infection is usually self‐limited but may lead to acute hepatitis and rarely to fulminant hepatic failure. Persistent HEV infections have recently been described in organ transplant recipients receiving immunosuppressive medications, suggesting that HEV is controlled by adaptive immune responses.

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