The inhibition of neutrophil elastase ameliorates mouse liver damage due to ischemia and reperfusion

Yoichiro Uchida, Maria Cecilia S. Freitas, Danyun Zhao, Ronald W. Busuttil, Jerzy W. Kupiec‐Weglinski – 29 July 2009 – Neutrophils are considered crucial effector cells in the pathophysiology of organ ischemia/reperfusion injury (IRI). Although neutrophil elastase (NE) accounts for a substantial portion of the neutrophil activity, the function of NE in liver IRI remains unclear. This study focuses on the role of NE in the mechanism of liver IRI.

Increased incidence of cytomegalovirus infection in high‐risk liver transplant recipients receiving valganciclovir prophylaxis versus ganciclovir prophylaxis

Kevin T. Shiley, Leanne B. Gasink, Todd D. Barton, Patrice Pfeiffenberger, Kim M. Olthoff, Emily A. Blumberg – 29 July 2009 – Optimal measures for the prevention of cytomegalovirus (CMV) in high‐risk orthotopic liver transplant (OLT) patients are unknown. The charts of high‐risk OLT recipients with 12 months of follow‐up who were transplanted over a 44‐month period were reviewed. The incidence of CMV disease in CMV‐seropositive donor/CMV‐seronegative recipient patients receiving valganciclovir or ganciclovir prophylaxis was compared.

ABO‐incompatible deceased donor liver transplantation in the United States: A national registry analysis

Zoe A. Stewart, Jayme E. Locke, Robert A. Montgomery, Andrew L. Singer, Andrew M. Cameron, Dorry L. Segev – 29 July 2009 – In the United States, ABO‐incompatible liver transplantation (ILT) is limited to emergent situations when ABO‐compatible liver transplantation (CLT) is unavailable. We analyzed the United Network for Organ Sharing database of ILT performed from 1990‐2006 to assess ILT outcomes for infant (0‐1 years; N = 156), pediatric (2‐17 years; N = 170), and adult (> 17 years; N = 667) patients.

De novo bile salt transporter antibodies as a possible cause of recurrent graft failure after liver transplantation: A novel mechanism of cholestasis

Verena Keitel, Martin Burdelski, Zsuzsanna Vojnisek, Lutz Schmitt, Dieter Häussinger, Ralf Kubitz – 29 July 2009 – Progressive familial intrahepatic cholestasis type 2 (PFIC‐2) is caused by mutations of the bile salt export pump (BSEP [ABCB11]), an ATP‐binding cassette (ABC)‐transporter exclusively expressed at the canalicular membrane of hepatocytes. An absence of BSEP from the canalicular membrane causes cholestasis and leads to liver cirrhosis, which may necessitate liver transplantation in early childhood.

MicroRNAs involved in tumor suppressor and oncogene pathways: Implications for hepatobiliary neoplasia

Justin L. Mott – 29 July 2009 – MicroRNAs are a class of small regulatory RNAs that function to modulate protein expression. This control allows for fine‐tuning of the cellular phenotype, including regulation of proliferation, cell signaling, and apoptosis; not surprisingly, microRNAs contribute to liver cancer biology. Recent investigations in human liver cancers and tumor‐derived cell lines have demonstrated decreased or increased expression of particular microRNAs in hepatobiliary cancer cells.

Individualized treatment strategy according to early viral kinetics in hepatitis C virus type 1–infected patients

Thomas Berg, Viola Weich, Gerlinde Teuber, Hartwig Klinker, Bernd Möller, Jens Rasenack, Holger Hinrichsen, Tilman Gerlach, Ulrich Spengler, Peter Buggisch, Heike Balk, Myrga Zankel, Konrad Neumann, Christoph Sarrazin, Stefan Zeuzem – 29 July 2009 – Individualized treatment on the basis of early viral kinetics has been discussed to optimize antiviral therapy in chronic hepatitis C virus (HCV) infection. Individually tailored reduction in treatment duration in HCV type 1–infected patients represents one possible strategy.

MicroRNA‐23b cluster microRNAs regulate transforming growth factor‐beta/bone morphogenetic protein signaling and liver stem cell differentiation by targeting Smads

Charles E. Rogler, Lauretta LeVoci, Tammy Ader, Aldo Massimi, Tatyana Tchaikovskaya, Raquel Norel, Leslie E. Rogler – 29 July 2009 – Transforming growth factor‐beta / bone morphogenetic protein (TGFβ/BMP) signaling has a gradient of effects on cell fate choice in the fetal mouse liver. The molecular mechanism to understand why adjacent cells develop into bile ducts or grow actively as hepatocytes in the ubiquitous presence of both TGFβ ligands and receptors has been unknown. We hypothesized that microRNAs (miRNAs) might play a role in cell fate decisions in the liver.

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