Hepatitis C virus core protein stimulates hepatocyte growth: Correlation with upregulation of wnt‐1 expression

Takayoshi Fukutomi, Yonghong Zhou, Shigenobu Kawai, Hidetoshi Eguchi, Jack R. Wands, Jisu Li – 19 April 2005 – Hepatitis C virus (HCV) core protein has been implicated in the development of human hepatocellular carcinoma (HCC). Here we report that expression of HCV core protein by transient transfection increased cell proliferation, DNA synthesis, and cell cycle progression in Huh‐7 cells, a human HCC‐derived cell line. Culture supernatant from transfected cells also harbored a growth‐promoting effect.

HIV coinfection shortens the survival of patients with hepatitis C virus‐related decompensated cirrhosis

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.

Differential regulation of rodent hepatocyte and oval cell proliferation by interferon γ

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.

Mechanisms of benzarone and benzbromarone‐induced hepatic toxicity

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.

Prognosis of hepatocellular carcinoma: Comparison of 7 staging systems in an American cohort

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.

Small gallstones, preserved gallbladder motility, and fast crystallization are associated with pancreatitis

Niels G. Venneman, Willem Renooij, Jens F. Rehfeld, Gerard P. vanBerge‐Henegouwen, Peter M. N. Y. H. Go, Ivo A. M. J. Broeders, Karel J. van Erpecum – 25 March 2005 – Acute pancreatitis is a severe complication of gallstones with considerable mortality. We sought to explore the potential risk factors for biliary pancreatitis.

Late liver‐related mortality from complications of transfusion‐acquired hepatitis C

Hiroshi Kamitsukasa, Hideharu Harada, Hideo Tanaka, Michiyasu Yagura, Hajime Tokita, Akira Ohbayashi – 25 March 2005 – Although several cohort studies have been reported in individuals with chronic hepatitis C virus (HCV) infection, little is known about liver‐related mortality among the elderly. We conducted a cohort study in 302 patients with tuberculosis sequelae who had received a blood transfusion at a young age and had subsequently been treated at a chest clinic.

Fibrosis correlates with a ductular reaction in hepatitis C: Roles of impaired replication, progenitor cells and steatosis

Andrew D. Clouston, Elizabeth E. Powell, Meagan J. Walsh, Michelle M. Richardson, A. Jake Demetris, Julie R. Jonsson – 25 March 2005 – The mechanisms for progressive fibrosis and exacerbation by steatosis in patients with chronic hepatitis C (HCV) are still unknown. We hypothesized that proliferative blockade in HCV‐infected and steatotic hepatocytes results in the default activation of hepatic progenitor cells (HPC), capable of differentiating into both biliary and hepatocyte lineages, and that the resultant ductular reaction promotes portal fibrosis.

Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells

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.

Prevalence and significance of neurocognitive dysfunction in hepatitis C in the absence of correlated risk factors

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.

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