Preservation solutions in liver transplantation: What are the options?
Bijan Eghtesad, Federico Aucejo, John J. Fung – 30 January 2006
Bijan Eghtesad, Federico Aucejo, John J. Fung – 30 January 2006
30 January 2006
Thierry Poynard, Mona Munteanu, Yen Ngo, Mercedes Torres, Yves Benhamou, Dominique Thabut, Vlad Ratziu – 26 January 2006
Keyur Patel, Suzanne Norris, Lauralynn Lebeck, Anne Feng, Michael Clare, Stephen Pianko, Bernard Portmann, Lawrence M. Blatt, James Koziol, Andrew Conrad, John G. McHutchison – 26 January 2006 – Patients infected with HIV‐1 who are heterozygous at HLA class I loci present greater variety of antigenic peptides to CD8+ cytotoxic T lymphocytes, slowing progression to AIDS. A similar broad immune response in chronic hepatitis C (CHC) infection could result in greater hepatic injury.
Fabrice Lainé, Claude Bendavid, Jeff Morcet, Michéle Perrin, Catherine Massart, Yves Deugnier – 26 January 2006
Carolin Lackner, Gerd Struber, Csilla Bankuti, Bernd Bauer, Rudolf E. Stauber – 26 January 2006
Lori R. Bernstein – 26 January 2006
Briana M. Erickson, Nancy L. Thompson, Douglas C. Hixson – 26 January 2006 – TuAg1/TagE4, the rat ortholog of the human poliovirus receptor CD155, is expressed on a high percentage of rat hepatocellular carcinomas. Recent studies have shown that TuAg1/TagE4/CD155 is a member of the nectin family of immunoglobulin (Ig)‐like cell adhesion molecules, designated necl‐5. Necl‐5 is present at exceedingly low levels in adult epithelial tissues but is upregulated in primary cultures of rat hepatocytes, suggesting that disruption of liver architecture triggers its expression.
Pamela Vig, Francesco P. Russo, Robert J. Edwards, Paul J. Tadrous, Nicholas A. Wright, Howard C. Thomas, Malcolm R. Alison, Stuart J. Forbes – 26 January 2006 – After liver injury, parenchymal regeneration occurs through hepatocyte replication. However, during regenerative stress, oval cells (OCs) and small hepatocyte like progenitor cells (SHPCs) contribute to the process. We systematically studied the intra‐hepatic and extra‐hepatic sources of liver cell replacement in the hepatitis B surface antigen (HBsAg‐tg) mouse model of chronic liver injury.
Akira Anan, Edwina S. Baskin‐Bey, Steven F. Bronk, Nathan W. Werneburg, Vijay H. Shah, Gregory J. Gores – 26 January 2006 – Induction of hepatic stellate cell (HSC) apoptosis attenuates hepatic fibrosis, and, therefore, mechanisms to induce HSC cell death are of therapeutic interest. Proteasome inhibitors induce apoptosis in transformed cells, especially those cells dependent upon nuclear factor kappa B (NF‐κB) activation. Because stimulated HSCs also trigger NF‐κB activation, the aim of this study was to determine if proteasome inhibitors induce HSC apoptosis.