“Toxic memory” via chaperone modification is a potential mechanism for rapid mallory‐denk body reinduction

Pavel Strnad, Guo‐Zhong Tao, Phillip So, Kenneth Lau, Jim Schilling, Yuquan Wei, Jian Liao, M. Bishr Omary – 27 May 2008 – The cytoplasmic hepatocyte inclusions, Mallory‐Denk bodies (MDBs), are characteristic of several liver disorders, including alcoholic and nonalcoholic steatohepatitis. In mice, MDBs can be induced by long‐term feeding with 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine (DDC) for 3 to 4 months or rapidly reformed in DDC‐induced then recovered mice by DDC refeeding or exposure to a wide range of toxins for only 5 to 7 days.

Evaluation of risk factors in the development of hepatocellular carcinoma in autoimmune hepatitis: Implications for follow‐up and screening

Andrew D. Yeoman, Thawab Al‐Chalabi, John B. Karani, Alberto Quaglia, John Devlin, Giorgina Mieli‐Vergani, Adrian Bomford, John G. O'Grady, Phillip M. Harrison, Michael A. Heneghan – 27 May 2008 – Hepatocellular carcinoma (HCC) has traditionally been considered a rare complication of cirrhosis secondary to autoimmune hepatitis (AIH), yet the true incidence remains unknown due to a lack of published data. Consequently, some professional guidelines do not mandate routine surveillance for HCC in this condition.

Inflammatory stress exacerbates lipid accumulation in hepatic cells and fatty livers of apolipoprotein E knockout mice

Kun L. Ma, Xiong Z. Ruan, Stephen H. Powis, Yaxi Chen, John F. Moorhead, Zac Varghese – 27 May 2008 – The prevailing theory in non‐alcoholic fatty liver disease (NAFLD) is the “two‐hit” hypothesis. The first hit mainly consists of lipid accumulation, and the second is subsequent systemic inflammation. The current study was undertaken to investigate whether inflammatory stress exacerbates lipid accumulation in liver and its underlying mechanisms.

Activation of hepatic stellate cells after phagocytosis of lymphocytes: A novel pathway of fibrogenesis

Nidal Muhanna, Sarit Doron, Ori Wald, Amjad Horani, Ahmed Eid, Orit Pappo, Scott L. Friedman, Rifaat Safadi – 16 May 2008 – Increased CD8‐T lymphocytes and reduced natural killer (NK) cells contribute to hepatic fibrosis. We have characterized pathways regulating the interactions of human hepatic stellate cells (HSCs) with specific lymphocyte subsets in vivo and in vitro.

Programmed death 1 expression during antiviral treatment of chronic hepatitis B: Impact of hepatitis B e‐antigen seroconversion

Alexander Evans, Antonio Riva, Helen Cooksley, Sandra Phillips, Smrithi Puranik, Amit Nathwani, Sara Brett, Shilpa Chokshi, Nikolai V. Naoumov – 16 May 2008 – Hyperexpression of the programmed death 1 (PD‐1) molecule is a hallmark of exhausted T‐cells, having a negative impact on T‐cell activation and function.

Long‐term efficacy and safety of adefovir dipivoxil for the treatment of hepatitis B e antigen–positive chronic hepatitis B

Patrick Marcellin, Ting‐Tsung Chang, Seng G. Lee Lim, William Sievert, Myron Tong, Sarah Arterburn, Katyna Borroto‐Esoda, David Frederick, Franck Rousseau – 16 May 2008 – Treatment of 171 patients with hepatitis B e antigen (HBeAg)‐positive chronic hepatitis B (CHB) with adefovir dipivoxil (ADV) 10 mg over 48 weeks resulted in significant histological, virological, serological, and biochemical improvement compared with placebo. The long‐term efficacy and safety of ADV in a subset of these patients was investigated for up to 5 years.

Hyponatremia in cirrhosis: Pathogenesis, clinical significance, and management

Pere Ginès, Mónica Guevara – 16 May 2008 – Hyponatremia is a frequent complication of advanced cirrhosis related to an impairment in the renal capacity to eliminate solute‐free water that causes a retention of water that is disproportionate to the retention of sodium, thus causing a reduction in serum sodium concentration and hypo‐osmolality. The main pathogenic factor responsible for hyponatremia is a nonosmotic hypersecretion of arginine vasopressin (or antidiuretic hormone) from the neurohypophysis related to circulatory dysfunction.

Hepatocellular adenomas: Magnetic resonance imaging features as a function of molecular pathological classification

Hervé Laumonier, Paulette Bioulac‐Sage, Christophe Laurent, Jessica Zucman‐Rossi, Charles Balabaud, Hervé Trillaud – 16 May 2008 – Hepatocellular adenomas (HCAs) are a group of benign tumors forming three molecular pathological subgroups: (1) hepatocyte nuclear factor 1α (HNF‐1α)–inactivated, (2) β‐catenin–activated, and (3) inflammatory. Some HCAs present both β‐catenin activation and inflammation. We analyzed magnetic resonance imaging (MRI) data for correlations between features on imaging and pathological classification of HCAs.

Significant gene expression differences in histologically “Normal” liver biopsies: Implications for control tissue

Tarik Asselah, Ivan Bièche, Ingrid Laurendeau, Michelle Martinot‐Peignoux, Valerie Paradis, Dominique Vidaud, Dominique‐Charles Valla, Pierre Bedossa, Patrick Marcellin, Michel Vidaud – 9 May 2008 – Gene expression technologies allow the analysis of gene networks whose expression is associated with specific pathological conditions compared with normal tissue. We hypothesized that histologically normal tissue obtained in different ways (percutaneous or surgical liver biopsies), usually used as normal controls in gene expression studies, could have different gene expression patterns.

Statins in liver disease: A molehill, an iceberg, or neither?

Curtis K. Argo, Paola Loria, Stephen H. Caldwell, Amedeo Lonardo – 9 May 2008 – A growing number of chronic liver disease patients, especially those with metabolic syndrome–associated nonalcoholic fatty liver disease or hepatitis C virus–associated dysmetabolic syndrome, will take statins to prevent cardiovascular disease. As a result, clinicians will weigh complex issues raised by the interaction of statins with liver metabolism in these disorders.

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