Decline in native kidney function in liver transplant recipients is not associated with BK virus infection

Muna Salama, Neil Boudville, David Speers, Garry P. Jeffrey, Paolo Ferrari – 24 November 2008 – BK virus (BKV) infection is an established cause of allograft dysfunction in renal transplant recipients. The relationship between BKV infection and chronic kidney disease (CKD) post–orthotopic liver transplantation (OLT) is not well understood. This study aimed to determine the prevalence of BKV infection, its relationship to CKD and renal function loss over time in patients receiving OLT.

Hepatitis C virus therapy in liver transplant recipients: Response predictors, effect on fibrosis progression, and importance of the initial stage of fibrosis

Bruno Roche, Mylene Sebagh, Maria Laura Canfora, Teresa Antonini, Anne‐Marie Roque‐Afonso, Valerie Delvart, Faouzi Saliba, Jean‐Charles Duclos‐Vallee, Denis Castaing, Didier Samuel – 24 November 2008 – Antiviral therapy after liver transplantation (LT) using interferon (IFN) and ribavirin (RBV) can achieve a sustained virological response (SVR) rate ranging from 20% to 45%. The aims of our study were to assess efficacy and tolerability of therapy, effect on fibrosis progression and the importance of the initial fibrosis stage to outcome.

The membrane protein ATPase class I type 8B member 1 signals through protein kinase C zeta to activate the farnesoid X receptor

Tamara Frankenberg, Tamir Miloh, Frank Y. Chen, Meena Ananthanarayanan, An‐Qiang Sun, Natarajan Balasubramaniyan, Irwin Arias, Kenneth D. R. Setchell, Frederick J. Suchy, Benjamin L. Shneider – 24 November 2008 – Prior loss‐of‐function analyses revealed that ATPase class I type 8B member 1 [familial intrahepatic cholestasis 1 (FIC1)] posttranslationally activated the farnesoid X receptor (FXR). Mechanisms underlying this regulation were examined by gain‐of‐function studies in UPS cells, which lack endogenous FIC1 expression.

Selenoprotein P expression is controlled through interaction of the coactivator PGC‐1α with FoxO1a and hepatocyte nuclear factor 4α transcription factors

Bodo Speckmann, Philippe L. Walter, Lirija Alili, Roland Reinehr, Helmut Sies, Lars‐Oliver Klotz, Holger Steinbrenner – 24 November 2008 – Selenoprotein P (SeP), the major selenoprotein in plasma, is produced mainly by the liver, although SeP expression is detected in many organs. Recently, we reported stimulation of SeP promoter activity by the forkhead box transcription factor FoxO1a in hepatoma cells and its attenuation by insulin. Here, we demonstrate that this translates into fine‐tuning of SeP production and secretion by insulin.

Local accumulation and activation of regulatory Foxp3+ CD4 TR cells accompanies the appearance of activated CD8 T cells in the liver

Petra Bochtler, Petra Riedl, Ivan Gomez, Reinhold Schirmbeck, Jörg Reimann – 24 November 2008 – Only small populations of nonactivated, nonproliferating Foxp3+ CD4 regulatory T cell (TR) cells are found in the nonparenchymal cell compartment of the mouse liver while liver‐draining celiac nodes contain expanded, activated TR cell populations (similar to other lymph nodes). Liver Foxp3+ CD4 TR cells suppress activation of T cell responses.

Transplantation‐mediated alloimmune thrombocytopenia: Guidelines for utilization of thrombocytopenic donors

Geraldine C. Diaz, Joan Prowda, Irene J. Lo, Gowthami M. Arepally, Neal Evans, Yvonne Wheeless, Benjamin Samstein, James V. Guarrera, John F. Renz – 24 November 2008 – Transplantation‐mediated alloimmune thrombocytopenia (TMAT) is donor‐derived thrombocytopenia following solid‐organ transplantation. To date, no clear consensus on the appropriateness of organ utilization from cadaver donors with a history of idiopathic thrombocytopenia purpura (ITP) has emerged.

Cell culture–produced hepatitis C virus does not infect peripheral blood mononuclear cells

Svetlana Marukian, Christopher T. Jones, Linda Andrus, Matthew J. Evans, Kimberly D. Ritola, Edgar D. Charles, Charles M. Rice, Lynn B. Dustin – 24 November 2008 – Hepatitis C virus (HCV) replicates primarily in the liver, but HCV RNA has been observed in association with other tissues and cells including B and T lymphocytes, monocytes, and dendritic cells. We have taken advantage of a recently described, robust system that fully recapitulates HCV entry, replication and virus production in vitro to re‐examine the issue of HCV infection of blood cell subsets.

Histological changes in HCV antibody–positive, HCV RNA–negative subjects suggest persistent virus infection

Matthew Hoare, William T. H. Gelson, Simon M. Rushbrook, Martin D. Curran, Tracy Woodall, Nicholas Coleman, Susan E. Davies, Graeme J. M. Alexander – 24 November 2008 – It is unclear whether hepatitis C virus (HCV) has been eradicated or persists at a low level in HCV antibody–positive HCV RNA–negative individuals. The natural history and liver histology are not well characterized. One hundred seventy‐two HCV antibody–positive, serum HCV RNA–negative patients underwent diagnostic liver biopsy between 1992 and 2000 and were followed a median 7 years (range, 5–12).

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