The stable repression of mesenchymal program is required for hepatocyte identity: A novel role for hepatocyte nuclear factor 4α

Laura Santangelo, Alessandra Marchetti, Carla Cicchini, Alice Conigliaro, Beatrice Conti, Carmine Mancone, Jessica A. Bonzo, Frank J. Gonzalez, Tonino Alonzi, Laura Amicone, Marco Tripodi – 7 March 2011 – The concept that cellular terminal differentiation is stably maintained once development is complete has been questioned by numerous observations showing that differentiated epithelium may undergo an epithelial‐to‐mesenchymal transition (EMT) program.

Interleukin‐32: A new proinflammatory cytokine involved in hepatitis C virus‐related liver inflammation and fibrosis

Alexander R. Moschen, Teresa Fritz, Andrew D. Clouston, Ilka Rebhan, Oliver Bauhofer, Helen D. Barrie, Elizabeth E. Powell, Soo‐Hyun Kim, Charles A. Dinarello, Ralf Bartenschlager, Julie R. Jonsson, Herbert Tilg – 4 March 2011 – Interleukin 32 (IL‐32) is a recently described proinflammatory cytokine that activates p38 mitogen‐activated protein kinase (MAPK) and nuclear factor kappa B (NF‐κB), thereby inducing proinflammatory cytokines such as IL‐1β and tumor necrosis factor alpha (TNF‐α). We investigated the role of IL‐32 in patients with chronic hepatitis C virus (HCV) infection.

Meta‐analysis of the influence of I148M variant of patatin‐like phospholipase domain containing 3 gene (PNPLA3) on the susceptibility and histological severity of nonalcoholic fatty liver disease

Silvia Sookoian, Carlos J. Pirola – 4 March 2011 – Our objective was to estimate the strength of the effect of the I148M (rs738409 C/G) patatin‐like phospholipase domain containing 3 (PNPLA3) variant on nonalcoholic fatty liver (NAFLD) and disease severity across different populations. We performed a systematic review by a meta‐analysis; literature searches identified 16 studies.

High predictive accuracy of an unbiased proteomic profile for sustained virologic response in chronic hepatitis C patients

Keyur Patel, Joseph E. Lucas, J. Will Thompson, Laura G. Dubois, Hans L. Tillmann, Alexander J. Thompson, Diane Uzarski, Robert M. Califf, Martin A. Moseley, Geoffrey S. Ginsburg, John G. McHutchison, Jeanette J. McCarthy, for the MURDOCK Horizon 1 Study Team – 4 March 2011 – Chronic hepatitis C (CHC) infection is a leading cause of endstage liver disease. Current standard‐of‐care (SOC) interferon‐based therapy results in sustained virological response (SVR) in only one‐half of patients, and is associated with significant side effects.

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