Epithelial‐to‐mesenchymal transitions in the liver

Steve S. Choi, Anna Mae Diehl – 20 November 2009 – The outcome of liver injury is dictated by the effectiveness of repair. Successful repair (i.e., regeneration) results in replacement of dead epithelial cells with healthy epithelial cells, and reconstructs normal hepatic structure and function. Liver regeneration is known to involve replication of surviving mature hepatocytes and bile duct cells. This review discusses recent evidence for other mechanisms that might also replace dead hepatic epithelial cells and repair liver damage, particularly during chronic injury.

The heat shock protein inhibitor Quercetin attenuates hepatitis C virus production

Oscar Gonzalez, Vanessa Fontanes, Santanu Raychaudhuri, Rachel Loo, Joseph Loo, Vaithilingaraja Arumugaswami, Ren Sun, Asim Dasgupta, Samuel W. French – 20 November 2009 – The hepatitis C viral (HCV) genome is translated through an internal ribosome entry site (IRES) as a single polyprotein precursor that is subsequently cleaved into individual mature viral proteins. Nonstructural protein 5A (NS5A) is one of these proteins that has been implicated in regulation of viral genome replication, translation from the viral IRES and viral packaging.

Mechanistic insights into immunomodulation by hepatic stellate cells in mice: A critical role of interferon‐γ signaling

Horng‐Ren Yang, Hong‐Shuie Chou, Xiaodong Gu, Lianfu Wang, Kathleen E. Brown, John J. Fung, Lina Lu, Shiguang Qian – 20 November 2009 – The liver is considered to be an immune‐privileged organ that favors the induction of tolerance. The underlying mechanisms are not completely understood. Interestingly, liver transplants are spontaneously accepted in several animal models, but hepatocyte transplants are acutely rejected, suggesting that liver nonparenchymal cells may effectively protect the parenchymal cells from immune attack.

Treatment of insulin resistance with metformin in naïve genotype 1 chronic hepatitis C patients receiving peginterferon alfa‐2a plus ribavirin

Manuel Romero‐Gómez, Moisés Diago, Raúl J. Andrade, José L. Calleja, Javier Salmerón, Conrado M. Fernández‐Rodríguez, Ricard Solà, Javier García‐Samaniego, Juan M. Herrerías, Manuel De la Mata, Ricardo Moreno‐Otero, Óscar Nuñez, Antonio Olveira, Santiago Durán, Ramón Planas, Spanish TRIC‐1 (Treatment of Resistance to Insulin in Hepatitis C Genotype 1) group – 20 November 2009 – Insulin resistance affects sustained virological response (SVR) in chronic hepatitis C.

Public health impact of antiviral therapy for hepatitis C in the United States

Michael L. Volk, Rachel Tocco, Sameer Saini, Anna S.F. Lok – 20 November 2009 – Despite dramatic improvements in antiviral therapy for hepatitis C, there is reason to believe that the uptake of antiviral therapy remains limited. The aims of this study were to determine the number of patients being treated with antiviral therapy in the U.S., to estimate the public health impact of these treatment patterns, and to identify barriers to treatment for patients with hepatitis C.

Cyclin‐dependent kinase 1 plays a critical role in DNA replication control during rat liver regeneration

Delphine Garnier, Pascal Loyer, Catherine Ribault, Christiane Guguen‐Guillouzo, Anne Corlu – 20 November 2009 – Liver regeneration is a unique process to restore hepatic homeostasis through rapid and synchronous proliferation of differentiated hepatocytes. Previous studies have shown that hepatocyte proliferation is characterized by high expression levels of the “mitotic” cyclin‐dependent kinase 1 (Cdk1) during S‐phase compared to other mammalian cells.

Activation of the complement system in human nonalcoholic fatty liver disease

Sander S. Rensen, Yanti Slaats, Ann Driessen, Carine J. Peutz‐Kootstra, Jeroen Nijhuis, Rudi Steffensen, Jan Willem Greve, Wim A. Buurman – 20 November 2009 – Activation of the innate immune system plays a major role in nonalcoholic fatty liver disease (NAFLD). The complement system is an important component of innate immunity that recognizes danger signals such as tissue injury.

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