Reassessment of the algorithm for prediction of liver fibrosis in patients with features of the metabolic syndrome
Fabrice Lainé, Claude Bendavid, Jeff Morcet, Michéle Perrin, Catherine Massart, Yves Deugnier – 26 January 2006
Noninvasive diagnosis of cirrhosis in chronic hepatitis C based on standard laboratory tests
Carolin Lackner, Gerd Struber, Csilla Bankuti, Bernd Bauer, Rudolf E. Stauber – 26 January 2006
Does nucleolin bind the NF kappa B DNA binding motif?
Lori R. Bernstein – 26 January 2006
Tightly regulated induction of the adhesion molecule necl‐5/CD155 during rat liver regeneration and acute liver injury
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.
The sources of parenchymal regeneration after chronic hepatocellular liver injury in mice
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.
Proteasome inhibition induces hepatic stellate cell apoptosis
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.
Deaths on the liver transplant waiting list: An analysis of competing risks
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.
Bicarbonate‐rich choleresis induced by secretin in normal rat is taurocholate‐dependent and involves AE2 anion exchanger
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).
Diagnosis, prevention and management of hepatitis B virus reactivation during anticancer therapy
Winnie Yeo, Philip J. Johnson – 26 January 2006
Isolation and characterization of lipid microdomains from apical and basolateral plasma membranes of rat hepatocytes
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.