Altered expression of heme oxygenase‐1 in the livers of patients with portal hypertensive diseases

Nobuya Makino, Makoto Suematsu, Yoshiaki Sugiura, Hiroyasu Morikawa, Susumu Shiomi, Nobuhito Goda, Tsuyoshi Sano, Yuji Nimura, Keizo Sugimachi, Yuzuru Ishimura – 30 December 2003 – This study was designed to determine changes in expression of heme oxygenase (HO)‐1, the stress‐inducible and carbon monoxide–producing enzyme, in normotensive and portal hypertensive human livers. GTS‐1, a monoclonal antibody against rat HO‐1 cross‐reacted with the human HO‐1 and blocked its enzyme activity, allowing us to examine the activity and localization of HO‐1.

Efficacy and safety of pegylated (40‐kd) interferon α‐2a compared with interferon α‐2a in noncirrhotic patients with chronic hepatitis C

K. Rajender Reddy, Teresa L. Wright, Paul J. Pockros, Mitchell Shiffman, Gregory Everson, Robert Reindollar, Michael W. Fried, Preston P. Purdum, Donald Jensen, Coleman Smith, William M. Lee, Thomas D. Boyer, Amy Lin, Simon Pedder, Jean DePamphilis – 30 December 2003 – Administration of interferon (IFN) 3 times weekly in patients with chronic hepatitis C (CHC) is associated with low sustained responses, which may be, in part, related to this regimen's inability to maintain IFN concentrations sufficient to suppress viral replication.

Nomenclature for antiviral‐resistant human hepatitis B virus mutations in the polymerase region

Lieven J. Stuyver, Stephen A. Locarnini, Anna Lok, Douglas D. Richman, William F. Carman, Jules L. Dienstag, Raymond F. Schinazi – 30 December 2003 – There is currently no universally accepted numbering convention for the antiviral drug‐related resistance mutations in the reverse transcriptase (rt) domain of the human hepatitis B virus (HBV) polymerase. The published inconsistencies have resulted from different HBV genotypes. A standardized numbering system for HBV polymerase is proposed.

Combination of interferon and ribavirin in chronic hepatitis C: Re‐treatment of nonresponders to interferon

Adrian M. Di Bisceglie, Judy Thompson, Nancy Smith‐Wilkaitis, Elizabeth M. Brunt, Bruce R. Bacon – 30 December 2003 – Chronic infection with hepatitis C virus (HCV) may result in cirrhosis, liver failure, and hepatocellular carcinoma. A minority of patients have a sustained response to antiviral therapy, and nonresponders remain at risk of developing progressive liver disease. We conducted a randomized, controlled trial of therapy with the combination of interferon (IFN) and ribavirin in patients with chronic hepatitis C who had not responded to an initial course of therapy with IFN alone.

Rat hepatic stellate cells contribute to the acute‐phase response with increased expression of α1(I) and α1(IV) collagens, tissue inhibitor of metalloproteinase‐1, and matrix‐metalloproteinase‐2 messenger RNAs

Natalia Nieto, Jose A. Dominguez‐Rosales, Luis Fontana, Adriana Salazar, Juan Armendariz‐Borunda, Patricia Greenwel, Marcos Rojkind – 30 December 2003 – The acute‐phase response (APR) represents a systemic reaction of the organism to multiple nonspecific inflammatory stimuli. In general, it is protective for the host, and hepatocytes are the main cells responding with alterations in the expression of a set of liver‐specific proteins named the acute‐phase proteins.

Bile acid‐induced rat hepatocyte apoptosis is inhibited by antioxidants and blockers of the mitochondrial permeability transition

Baruch Yerushalmi, Rolf Dahl, Michael W. Devereaux, Eric Gumpricht, Ronald J. Sokol – 30 December 2003 – The accumulation of hydrophobic bile acids plays a role in the induction of apoptosis and necrosis of hepatocytes during cholestasis. The aim of this study was to determine in freshly isolated rat hepatocytes the roles of oxidant stress and the mitochondrial permeability transition (MPT) in bile acid‐induced apoptosis.

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