Impact of hepatitis B virus basic core promoter mutations on T cell response to an immunodominant HBx‐derived epitope

Silvina Laura Malmassari, Qiang Deng, Hélène Fontaine, Dianne Houitte, François Rimlinger, Valérie Thiers, Bernard Maillere, Stanislas Pol, Marie‐Louise Michel – 26 April 2007 – The hepatitis B X (HBx) protein is a crucial component in HBV infection in vivo and has been implicated in HCC. In this study, we aimed to detect and characterize peripheral HBx‐specific T cells in chronically infected patients at the inactive carrier state of the disease.

Hepatitis B viral factors in HBeAg‐Negative carriers with persistently normal serum alanine aminotransferase levels

Chih‐Lin Lin, Li‐Ying Liao, Chun‐Jen Liu, Ming‐Whei Yu, Pei‐Jer Chen, Ming‐Yang Lai, Ding‐Shinn Chen, Jia‐Horng Kao – 26 April 2007 – Chronic hepatitis B patients with high‐normal serum ALT (levels of 0.5‐1× upper limit of normal) are still at risk of liver disease progression. We thus investigated the correlation between serum ALT level and hepatitis B viral factors in HBeAg‐negative carriers with persistently normal serum ALT level (PNALT).

Tissue factor pathway inhibitor‐2 as a frequently silenced tumor suppressor gene in hepatocellular carcinoma

Chun‐Ming Wong, Yeung‐Lam Ng, Joyce Man‐Fong Lee, Carmen Chak‐Lui Wong, Oi‐Fung Cheung, Chung‐Yiu Chan, Edmund Kwok‐Kwan Tung, Yick‐Pang Ching, Irene Oi‐Lin Ng – 26 April 2007 – In HCC, inactivation of tumor suppressor genes plays a significant role in carcinogenesis. Apart from deletions and mutations, growing evidence has indicated that epigenetic alterations including aberrant promoter methylation and histone deacetylation are also implicated in inactivation of tumor suppressor genes.

Increased activity of hepatic microsomal triglyceride transfer protein and bile acid synthesis in gallstone disease

Juan Castro, Ludwig Amigo, Juan Francisco Miquel, Cecilia Gälman, Fernando Crovari, Alejandro Raddatz, Silvana Zanlungo, Roberto Jalil, Mats Rudling, Flavio Nervi – 26 April 2007 – A strong interrelationship exists between the regulation of bile acid (BA) metabolism and hepatic very low density lipoprotein (VLDL) production. We have recently shown that BA synthesis is increased in gallstone disease.

Met signals hepatocyte survival by preventing Fas‐triggered FLIP degradation in a PI3k‐Akt–dependent manner

Anice Moumen, Alessandro Ieraci, Salvatore Patané, Carme Solé, Joan X. Comella, Rosanna Dono, Flavio Maina – 26 April 2007 – The FasL‐Fas couple is a general death mediator whose activated signals lead to caspase‐8 activation and apoptosis in adult hepatocytes. Suppression of caspase‐8 activation and cell death is a protective mechanism modulated by the FLICE‐Like Inhibitory Protein (FLIP). Although hepatocyte growth factor (HGF) and its receptor Met are known to mediate cell survival in developing livers, the molecular mechanisms involved in this process are poorly understood.

Serum HBV RNA is a predictor of early emergence of the YMDD mutant in patients treated with lamivudine

Tsuyoshi Hatakeyama, Chiemi Noguchi, Nobuhiko Hiraga, Nami Mori, Masataka Tsuge, Michio Imamura, Shoichi Takahashi, Yoshiiku Kawakami, Yoshifumi Fujimoto, Hidenori Ochi, Hiromi Abe, Toshiro Maekawa, Hiroiku Kawakami, Hiromi Yatsuji, Yasuyuki Aisaka, Hiroshi Kohno, Shiomi Aimitsu, Kazuaki Chayama – 26 April 2007 – Lamivudine (LAM) is a nucleoside analogue widely used for the treatment of chronic hepatitis B virus (HBV) infection.

Racial disparities in the management of hospitalized patients with cirrhosis and complications of portal hypertension: A national study

Geoffrey C. Nguyen, Dorry L. Segev, Paul J. Thuluvath – 26 April 2007 – Having complications of portal hypertension is a harbinger of decompensated cirrhosis and warrants consideration for liver transplantation (LT). Racial disparities in LT have been reported. We sought to characterize disparities in the performing of surgical and endoscopic procedures among hospitalized patients with complications of portal hypertension. We queried the Nationwide Inpatient Sample from 1998 to 2003 to identify patients with cirrhosis and complications of portal hypertension.

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