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.

W. Ray Kim, Terry M. Therneau, Joanne T. Benson, Walter K. Kremers, Charles B. Rosen, Gregory J. Gores, E. Rolland Dickson – 26 January 2006 – The usual method of estimating survival probabilities, namely the Kaplan‐Meier method, is suboptimal in the analysis of deaths on the transplant waiting list. Death, transplantation, and withdrawal from list must all be considered.

Jesús M. Banales, Fabián Arenas, Carlos M. Rodríguez‐Ortigosa, Elena Sáez, Iker Uriarte, R. Brian Doctor, Jesús Prieto, Juan F. Medina – 26 January 2006 – Canalicular bile is modified along bile ducts through reabsorptive and secretory processes regulated by nerves, bile salts, and hormones such as secretin. Secretin stimulates ductular cystic fibrosis transmembrane conductance regulator (CFTR)–dependent Cl− efflux and subsequent biliary HCO3− secretion, possibly via Cl−/HCO3− anion exchange (AE).

Winnie Yeo, Philip J. Johnson – 26 January 2006

Amelia Mazzone, Pamela Tietz, John Jefferson, Richard Pagano, Nicholas F. LaRusso – 26 January 2006 – Canalicular bile is formed by the osmotic filtration of water in response to osmotic gradients generated by active transport at the apical and basolateral plasma membrane domains of hepatocytes. We recently demonstrated that mixed plasma membrane fractions isolated from rat hepatocyte couplets contain lipid microdomains (“rafts”) enriched in cholesterol and sphingolipids and AQP8 and 9.

Yaakov Nahmias, Monica Casali, Laurent Barbe, Francois Berthiaume, Martin L. Yarmush – 26 January 2006 – Low‐density lipoprotein (LDL) is an important carrier of plasma cholesterol and triglycerides whose concentration is regulated by the liver parenchymal cells. Abnormal LDL regulation is thought to cause atherosclerosis, while viral binding to LDL has been suggested to facilitate hepatitis C infection. Primary hepatocytes quickly lose the ability to clear LDL during in vitro culture.

Cosimo Colletta, Carlo Smirne, Carlo Fabris, Pierluigi Toniutto, Mario Pirisi – 26 January 2006