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).

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.

Liver endothelial cells promote LDL‐R expression and the uptake of HCV‐like particles in primary rat and human hepatocytes

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.

Do alcohol‐metabolizing enzyme gene polymorphisms increase the risk of alcoholism and alcoholic liver disease?

Elias Zintzaras, Ioannis Stefanidis, Mauro Santos, Francesc Vidal – 26 January 2006 – Case–control studies that have investigated the association between alcoholism and alcohol‐induced liver damage and the ADH2, ADH3, CYP2E1, and ADLH2 polymorphisms have reported controversial or inconclusive results. Thus, we conducted a meta‐analysis of 50 association studies of the above polymorphisms.

CD4+ T cells contribute to postischemic liver injury in mice by interacting with sinusoidal endothelium and platelets

Andrej Khandoga, Marc Hanschen, Julia S. Kessler, Fritz Krombach – 26 January 2006 – The mechanisms by which T cells contribute to the hepatic inflammation during antigen‐independent ischemia/reperfusion (I/R) are not fully understood. We analyzed the recruitment of T cells in the postischemic hepatic microcirculation in vivo and tested the hypothesis that T cells interact with platelets and activate sinusoidal endothelial cells, resulting in microvascular dysfunction followed by tissue injury.

Subscribe to