Cellular responses in experimental liver injury: Possible cellular origins of regenerative stem‐like progenitor cells
William B. Coleman, D. Hunter Best – 19 April 2005
William B. Coleman, D. Hunter Best – 19 April 2005
Gaspare Maria Pendino, Andrea Mariano, Pasquale Surace, Carmelo Antonio Caserta, Maria Teresa Fiorillo, Angela Amante, Stefania Bruno, Carmelo Mangano, Irene Polito, Fulvia Amato, Rodolfo Cotichini, Tommaso Stroffolini, Alfonso Mele, ACE Collaborating Group – 19 April 2005 – Serum biochemical liver tests (LTs) (ALT, AST, GGT) and platelet counts are often used to screen for chronic liver disease. Population‐based data on abnormal LTs in Mediterranean areas are lacking.
Hartmut Jaeschke, Cathleen Cover, Mary Lynn Bajt – 19 April 2005
Juan A. Pineda, Manuel Romero‐Gómez, Fernando Díaz‐García, José A. Girón‐González, José L. Montero, Julián Torre‐Cisneros, Raúl J. Andrade, Mercedes González‐Serrano, José Aguilar, Manuela Aguilar‐Guisado, José M. Navarro, Javier Salmerón, Francisco J. Caballero‐Granado, José A. García‐García – 30 March 2005 – The impact of human immunodeficiency virus (HIV) coinfection on the survival of patients with hepatitis C virus (HCV)‐related end‐stage liver disease (ESLD) is unknown.
Priska Kaufmann, Michael Török, Anya Hänni, Paul Roberts, Rodolfo Gasser, Stephan Krähenbühl – 29 March 2005 – Treatment with benzarone or benzbromarone can be associated with hepatic injury. Both drugs share structural similarities with amiodarone, a well‐known mitochondrial toxin. Therefore, we investigated the hepatotoxicity of benzarone and benzbromarone as well as the analogues benzofuran and 2‐butylbenzofuran. In isolated rat hepatocytes, amiodarone, benzarone, and benzbromarone (20 μmol/L) decreased mitochondrial membrane potential by 23%, 54% or 81%, respectively.
John T. Brooling, Jean S. Campbell, Claudia Mitchell, George C. Yeoh, Nelson Fausto – 29 March 2005 – Hepatocytes and intrahepatic progenitor cells (oval cells) have similar responses to most growth factors but rarely proliferate together. Oval cells constitute a reserve compartment that is activated when hepatocyte proliferation is inhibited. Interferon γ (IFN‐γ) increases in liver injury that involves oval cell responses, but it is not upregulated during liver regeneration after partial hepatectomy.
Jorge A. Marrero, Robert J. Fontana, Ashley Barrat, Frederick Askari, Hari S. Conjeevaram, Grace L. Su, Anna S. Lok – 28 March 2005 – Currently there is no consensus as to which staging system is best in predicting the survival of patients with hepatocellular carcinoma (HCC). The aims of this study were to identify independent predictors of survival and to compare 7 available prognostic staging systems in patients with HCC. A total of 239 consecutive patients with cirrhosis and HCC seen between January 1, 2000, and December 31, 2003, were included.
Suheeta Roy, Hideyuki Hyogo, Suresh K. Yadav, Michele K. Wu, Linda A. Jelicks, Joseph D. Locker, Philippe G. Frank, Michael P. Lisanti, David L. Silver, David E. Cohen – 25 March 2005 – Human obesity is associated with abnormal hepatic cholesterol homeostasis and resistance to leptin action. Because leptin administration to rodents promotes the biliary elimination of plasma cholesterol, this study was designed to elucidate a pathophysiological role for leptin during the development of obesity. We fed mice diets containing high or low saturated fat contents.
Mary Pat McAndrews, Karl Farcnik, Peter Carlen, Andrei Damyanovich, Mirela Mrkonjic, Susan Jones, E. Jenny Heathcote – 25 March 2005 – Neurocognitive morbidity has been reported in individuals with chronic hepatitis C virus (HCV) infection, but the magnitude of such dysfunction in the absence of disease‐correlated factors known to affect the central nervous system (e.g., substance abuse, cirrhosis, depression, interferon treatment) and the impact of any such change on functioning is unclear.
Tadashi Ikegami, Yasushi Matsuzaki, Sugano Fukushima, Junichi Shoda, Jean Luc Olivier, Bernard Bouscarel, Naomi Tanaka – 25 March 2005 – Phospholipase A2 IIA (PLA2IIA), which plays a crucial role in arachidonic acid metabolism and in inflammation, is upregulated under various pathological conditions, including in the gallbladder and gallbladder bile from patients with multiple cholesterol gallstones, in the liver and kidney of rats with cirrhosis, as well as in the colonic tissue of animals treated with a chemical carcinogen.