Long‐term outcome of Japanese patients with type 1 autoimmune hepatitis

Kaname Yoshizawa, Akihiro Matsumoto, Tetsuya Ichijo, Takeji Umemura, Satoru Joshita, Michiharu Komatsu, Naoki Tanaka, Eiji Tanaka, Masao Ota, Yoshihiko Katsuyama, Kendo Kiyosawa, Masanori Abe, Morikazu Onji – 15 February 2012 – The long‐term outcome of patients with autoimmune hepatitis (AIH) in Japan has not been well‐defined. The aim of this study was to clarify the outcome of this disease over a long follow‐up period compared with that of the general Japanese population as well as that among patients. A total of 203 AIH patients were enrolled for a mean follow‐up period of 131 months.

Specific immunization strategies against oxidized low‐density lipoprotein: A novel way to reduce nonalcoholic steatohepatitis in mice

Veerle Bieghs, Patrick J. van Gorp, Sofie M.A. Walenbergh, Marion J. Gijbels, Fons Verheyen, Wim A. Buurman, David E. Briles, Marten H. Hofker, Christoph J. Binder, Ronit Shiri‐Sverdlov – 15 February 2012 – Nonalcoholic steatohepatitis (NASH) is characterized by hepatic lipid accumulation combined with inflammation, which can ultimately progress into cirrhosis. Recently, we demonstrated that deletion of scavenger receptors (SRs) CD36 and SR‐A in hematopoietic cells reduced hepatic inflammation.

Source and characterization of hepatic macrophages in acetaminophen‐induced acute liver failure in humans

Charalambos Gustav Antoniades, Alberto Quaglia, Leonie S. Taams, Ragai R. Mitry, Munther Hussain, Robin Abeles, Lucia A. Possamai, Matthew Bruce, Mark McPhail, Christopher Starling, Bart Wagner, Adrian Barnardo, Sabine Pomplun, Georg Auzinger, William Bernal, Nigel Heaton, Diego Vergani, Mark R. Thursz, Julia Wendon – 15 February 2012 – Acetaminophen‐induced acute liver failure (AALF) is associated with innate immunity activation, which contributes to the severity of hepatic injury and clinical outcome.

Fatty liver index, gamma‐glutamyltransferase, and early carotid plaques

Michaela Kozakova, Carlo Palombo, Marco Paterni Eng, Jacqueline Dekker, Allan Flyvbjerg, Asimina Mitrakou, Amalia Gastaldelli, Ele Ferrannini, ; and the RISC Investigators – 15 February 2012 – An association between fatty liver and carotid atherosclerosis has been established; however, it is not clear whether this relationship is a consequence of shared conventional risk factors or whether it is determined by specific circulating factors originating from liver or adipose tissue.

Oxidative stress, Nrf2 and keratin up‐regulation associate with Mallory‐Denk body formation in mouse erythropoietic protoporphyria

Amika Singla, David S. Moons, Natasha T. Snider, Elizabeth R. Wagenmaker, V. Bernadene Jayasundera, M. Bishr Omary – 15 February 2012 – Mallory‐Denk bodies (MDBs) are hepatocyte inclusions commonly seen in steatohepatitis. They are induced in mice by feeding 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine (DDC) for 12 weeks, which also causes porphyrin accumulation. Erythropoietic protoporphyria (EPP) is caused by mutations in ferrochelatase (fch), and a fraction of EPP patients develop liver disease that is phenocopied in Fechm1Pas mutant (fch/fch) mice, which have an inactivating fch mutation.

Modulation of regulatory T‐cell activity in combination with interleukin‐12 increases hepatic tolerogenicity in woodchucks with chronic hepatitis B

Itziar Otano, Lester Suarez, Javier Dotor, Manuela Gonzalez‐Aparicio, Julien Crettaz, Cristina Olagüe, Africal Vales, Jose Ignacio Riezu, Esther Larrea, Francisco Borras, Alberto Benito, Ruben Hernandez‐Alcoceba, Stephan Menne, Jesús Prieto, Gloria González‐Aseguinolaza – 15 February 2012 – Regulatory T cells (Treg) play a critical role in the modulation of immune responses to viral antigens in chronic viral hepatitis. Woodchucks (Marmota monax) infected with the woodchuck hepatitis virus (WHV) represent the best animal model for chronic hepatitis B virus (HBV) infection.

Proteome and computational analyses reveal new insights into the mechanisms of hepatitis C virus–mediated liver disease posttransplantation

Deborah L. Diamond, Alexei L. Krasnoselsky, Kristin E. Burnum, Matthew E. Monroe, Bobbie‐Jo Webb‐Robertson, Jason E. McDermott, Matthew M. Yeh, Jose Felipe Golib Dzib, Nathan Susnow, Susan Strom, Sean C. Proll, Sarah E. Belisle, David E. Purdy, Angela L. Rasmussen, Kathie‐Anne Walters, Jon M. Jacobs, Marina A. Gritsenko, David G. Camp, Renuka Bhattacharya, James D. Perkins, Robert L. Carithers, Iris W. Liou, Anne M. Larson, Arndt Benecke, Katrina M. Waters, Richard D. Smith, Michael G.

Dysregulation of innate immunity in hepatitis C virus genotype 1 IL28B‐unfavorable genotype patients: Impaired viral kinetics and therapeutic response

Susanna Naggie, Anu Osinusi, Antonios Katsounas, Richard Lempicki, Eva Herrmann, Alexander J. Thompson, Paul J. Clark, Keyur Patel, Andrew J. Muir, John G. McHutchison, Joerg F. Schlaak, Martin Trippler, Bhavana Shivakumar, Henry Masur, Michael A. Polis, Shyam Kottilil – 13 February 2012 – Recent studies have shown that a single‐nucleotide polymorphism upstream of the interleukin‐28B (IL28B) gene plays a major role in predicting therapeutic response in hepatitis C virus (HCV)‐infected patients treated with pegylated interferon (PEG‐IFN)/ribavirin.

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