Interpretation of positive transcription‐mediated amplification test results from polymerase chain reaction–negative samples obtained after treatment of chronic hepatitis C

Chihiro Morishima, Timothy R. Morgan, James E. Everhart, Elizabeth C. Wright, Minjun C. Apodaca, David R. Gretch, Mitchell L. Shiffman, Gregory T. Everson, Karen L. Lindsay, William M. Lee, Anna S. F. Lok, Jules L. Dienstag, Marc G. Ghany, Teresa M. Curto, HALT‐C Trial Group – 28 October 2008 – The Siemens VERSANT® transcription‐mediated amplification (TMA) assay is extremely sensitive for the detection of hepatitis C virus (HCV) RNA in serum.

Alcohol‐induced alterations in hepatic microtubule dynamics can be explained by impaired histone deacetylase 6 function

Blythe D. Shepard, Rohan A. Joseph, George T. Kannarkat, Tara M. Rutledge, Dean J. Tuma, Pamela L. Tuma – 28 October 2008 – We have been using polarized, hepatic WIF‐B cells to examine ethanol‐induced liver injury. These cells polarize in culture and maintain numerous liver‐specific activities including the ability to metabolize alcohol. Previously, we found that microtubules were more highly acetylated and more stable in ethanol‐treated WIF‐B cells and that increased microtubule acetylation required ethanol metabolism and was likely mediated by acetaldehyde.

Differentiation therapy of hepatocellular carcinoma in mice with recombinant adenovirus carrying hepatocyte nuclear factor‐4α gene

Chuan Yin, Yong Lin, Xin Zhang, Yue‐Xiang Chen, Xin Zeng, Hai‐Yan Yue, Jun‐Liang Hou, Xing Deng, Jun‐Ping Zhang, Ze‐Guang Han, Wei‐Fen Xie – 28 October 2008 – Previous studies have shown that hepatocyte nuclear factor‐4α (HNF4α) is a central regulator of differentiated hepatocyte phenotype and forced expression of HNF4α could promote reversion of tumors toward a less invasive phenotype. However, the effect of HNF4α on cancer stem cells (CSCs) and the treatment of hepatocellular carcinoma (HCC) with HNF4α have not been reported.

Intrahepatic levels of CXCR3‐associated chemokines correlate with liver inflammation and fibrosis in chronic hepatitis C

Marija Zeremski, Lydia M. Petrovic, Luis Chiriboga, Queenie B. Brown, Herman T. Yee, Milan Kinkhabwala, Ira M. Jacobson, Rositsa Dimova, Marianthi Markatou, Andrew H. Talal – 28 October 2008 – Chemokines, chemotactic cytokines, may promote hepatic inflammation in chronic hepatitis C virus (HCV) infection through the recruitment of lymphocytes to the liver parenchyma.

Alpha‐lipoic acid decreases hepatic lipogenesis through adenosine monophosphate‐activated protein kinase (AMPK)‐dependent and AMPK‐independent pathways

Keun‐Gyu Park, Ae‐Kyung Min, Eun Hee Koh, Hyoun Sik Kim, Mi‐Ok Kim, Hye‐Sun Park, Yong‐Deuk Kim, Tae‐Seung Yoon, Byoung Kuk Jang, Jae Seok Hwang, Jae Bum Kim, Hueng‐Sik Choi, Joong‐Yeol Park, In‐Kyu Lee, Ki‐Up Lee – 28 October 2008 – Fatty liver is common in obese subjects with insulin resistance. Hepatic expression of sterol regulatory element binding protein‐1c (SREBP‐1c), which plays a major role in hepatic steatosis, is regulated by multiple factors, including insulin, adenosine monophosphate–activated protein kinase (AMPK), liver X receptors (LXRs), and specificity protein 1.

Translocation of iron from lysosomes into mitochondria is a key event during oxidative stress‐induced hepatocellular injury

Akira Uchiyama, Jae‐Sung Kim, Kazuyoshi Kon, Hartmut Jaeschke, Kenichi Ikejima, Sumio Watanabe, John J. Lemasters – 28 October 2008 – Iron overload exacerbates various liver diseases. In hepatocytes, a portion of non‐heme iron is sequestered in lysosomes and endosomes. The precise mechanisms by which lysosomal iron participates in hepatocellular injury remain uncertain. Here, our aim was to determine the role of intracellular movement of chelatable iron in oxidative stress‐induced killing to cultured hepatocytes from C3Heb mice and Sprague‐Dawley rats.

Rab4 facilitates cyclic adenosine monophosphate–stimulated bile acid uptake and Na+‐taurocholate cotransporting polypeptide translocation

Christopher M. Schonhoff, Krishna Thankey, Cynthia R.L. Webster, Yoshiyuki Wakabayashi, Allan W. Wolkoff, M. Sawkat Anwer – 28 October 2008 – Cyclic adenosine monophosphate (cAMP) stimulates hepatic bile acid uptake by translocating sodium‐taurocholate (TC) cotransporting polypeptide (Ntcp) from an endosomal compartment to the plasma membrane. Rab4 is associated with early endosomes and involved in vesicular trafficking. This study was designed to determine the role of Rab4 in cAMP‐induced TC uptake and Ntcp translocation.

The angiogenic makeup of human hepatocellular carcinoma does not favor vascular endothelial growth factor/angiopoietin‐driven sprouting neovascularization

Wenjiao Zeng, Annette S.H. Gouw, Marius C. van den Heuvel, Peter J. Zwiers, Pieter E. Zondervan, Sibrand Poppema, Nong Zhang, Inge Platteel, Koert P. de Jong, Grietje Molema – 28 October 2008 – Quantitative data on the expression of multiple factors that control angiogenesis in hepatocellular carcinoma (HCC) are limited. A better understanding of the mechanisms underlying angiogenesis in HCC will improve the rational choice of anti‐angiogenic treatment.

Is there a meaningful serum hepatitis B virus DNA cutoff level for therapeutic decisions in hepatitis B e antigen–negative chronic hepatitis B virus infection?

George V. Papatheodoridis, Emanuel K. Manesis, Spilios Manolakopoulos, Ioannis S. Elefsiniotis, John Goulis, John Giannousis, Antonios Bilalis, Georgia Kafiri, Dimitrios Tzourmakliotis, Athanasios J. Archimandritis – 28 October 2008 – The diagnosis of hepatitis B e antigen (HBeAg)‐negative chronic hepatitis B indicating therapeutic intervention currently requires serum hepatitis B virus (HBV) DNA ≥2,000 IU/mL.

Evaluation of previously nonscreened hereditary hemorrhagic telangiectasia patients shows frequent liver involvement and early cardiac consequences

Rodica Gincul, Gaetan Lesca, Bénédicte Gelas‐Dore, Nathalie Rollin, Martine Barthelet, Sophie Dupuis‐Girod, Franck Pilleul, Sophie Giraud, Henri Plauchu, Jean‐Christophe Saurin – 28 October 2008 – Hereditary hemorrhagic telangiectasia (HHT) is a genetic disease characterized by cutaneous, mucosal, and sometimes visceral arteriovenous malformations. Severe hepatic manifestations have been characterized in a subgroup of patients, but few data are available in previously nonscreened patients. We prospectively evaluated liver involvement and its cardiac consequences in such patients.

Subscribe to