Multiple effects of silymarin on the hepatitis C virus lifecycle

Jessica Wagoner, Amina Negash, Olivia J. Kane, Laura E. Martinez, Yaakov Nahmias, Nigel Bourne, David M. Owen, Joe Grove, Claire Brimacombe, Jane A. McKeating, Eve‐Isabelle Pécheur, Tyler N. Graf, Nicholas H. Oberlies, Volker Lohmann, Feng Cao, John E. Tavis, Stephen J. Polyak – 23 May 2010 – Silymarin, an extract from milk thistle (Silybum marianum), and its purified flavonolignans have been recently shown to inhibit hepatitis C virus (HCV) infection, both in vitro and in vivo. In the current study, we further characterized silymarin's antiviral actions.

Serum hepatitis B surface antigen and hepatitis B e antigen titers: Disease phase influences correlation with viral load and intrahepatic hepatitis B virus markers

Alexander J.V. Thompson, Tin Nguyen, David Iser, Anna Ayres, Kathy Jackson, Margaret Littlejohn, John Slavin, Scott Bowden, Edward J. Gane, William Abbott, George K.K. Lau, Sharon R. Lewin, Kumar Visvanathan, Paul V. Desmond, Stephen A.

Roles of hypoxia‐inducible factor‐1α (HIF‐1α) versus HIF‐2α in the survival of hepatocellular tumor spheroids

Heidi Menrad, Christian Werno, Tobias Schmid, Ekaterini Copanaki, Thomas Deller, Nathalie Dehne, Bernhard Brüne – 23 May 2010 – Hypoxia‐inducible factors (HIFs) provoke adaptation to hypoxic stress occurring in rapidly growing tumor tissues. Therefore, overexpression of HIF‐1 or HIF‐2 is a common feature in hepatocellular carcinoma but their specific function is still controversially discussed. To analyze HIF function in hypoxia‐induced cell death we created a stable knockdown of HIF‐1α and HIF‐2α in HepG2 cells and generated tumor spheroids as an in vitro hepatocellular carcinoma model.

CX3CR1 and vascular adhesion protein‐1‐dependent recruitment of CD16+ monocytes across human liver sinusoidal endothelium

Alexander I. Aspinall, Stuart M. Curbishley, Patricia F. Lalor, Chris J. Weston, Miroslava Blahova, Evaggelia Liaskou, Rebecca M. Adams, Andrew P. Holt, David H. Adams – 23 May 2010 – The liver contains macrophages and myeloid dendritic cells (mDCs) that are critical for the regulation of hepatic inflammation. Most hepatic macrophages and mDCs are derived from monocytes recruited from the blood through poorly understood interactions with hepatic sinusoidal endothelial cells (HSECs). Human CD16+ monocytes are thought to contain the precursor populations for tissue macrophages and mDCs.

Sustained virologic response prevents the development of esophageal varices in compensated, Child‐Pugh class A hepatitis C virus–induced cirrhosis. A 12‐year prospective follow‐up study

Savino Bruno, Andrea Crosignani, Corinna Facciotto, Sonia Rossi, Luigi Roffi, Alessandro Redaelli, Roberto de Franchis, Piero Luigi Almasio, Patrick Maisonneuve – 23 May 2010 – The incidence of de novo development of esophageal varices (EV) in patients with compensated liver cirrhosis has been determined by few studies in the short term and never in the long term.

Right atrial pressure is not adequate to calculate portal pressure gradient in cirrhosis: A clinical‐hemodynamic correlation study

Vincenzo La Mura, Juan G. Abraldes, Annalisa Berzigotti, Eva Erice, Alexandra Flores‐Arroyo, Juan Carlos García‐Pagán, Jaime Bosch – 23 May 2010 – Hepatic venous pressure gradient (HVPG), the difference between wedge and free hepatic venous pressure, is the preferred method for estimating portal pressure. However, it has been suggested that hepatic atrial pressure gradient (HAPG)—the gradient between wedge hepatic venous pressure and right atrial pressure (RAP)—might better reflect variceal hemodynamics.

Inhibitory role of peroxisome proliferator‐activated receptor gamma in hepatocarcinogenesis in mice and in vitro

Jun Yu, Bo Shen, Eagle S. H. Chu, Narci Teoh, Kin‐Fai Cheung, Chung‐Wah Wu, Shiyan Wang, Cleo N. Y. Lam, Hai Feng, Junhong Zhao, Alfred S. L. Cheng, Ka‐Fai To, Henry L. Y. Chan, Joseph J. Y. Sung – 23 May 2010 – Although peroxisome proliferator‐activated receptor gamma (PPARγ) agonist have been shown to inhibit hepatocellular carcinoma (HCC) development, the role of PPARγ in hepatocarcinogenesis remains unclear. We investigated the therapeutic efficacy of PPARγ against HCC.

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