Cytochrome P4502E1 sensitizes to tumor necrosis factor alpha–induced liver injury through activation of mitogen‐activated protein kinases in mice

Defeng Wu, Arthur Cederbaum – 26 February 2008 – The goal of this study was to evaluate the role of mitogen‐activated protein kinase (MAPK) in cytochrome P4502E1 (CYP2E1) potentiation of lipopolysaccharide or tumor necrosis factor alpha (TNF‐α)–induced liver injury. Treatment of C57/BL/6 mice with pyrazole (PY) plus lipopolysaccharide (LPS) induced liver injury compared with mice treated with PY or LPS alone. The c‐Jun N‐terminal kinase (JNK) inhibitor SP600125 or p38 MAPK inhibitor SB203580 prevented this liver injury.

Optical analysis of computed tomography images of the liver predicts fibrosis stage and distribution in chronic hepatitis C

Manuel Romero‐Gómez, Emilio Gómez‐González, Ana Madrazo, Marina Vera‐Valencia, Luis Rodrigo, Ramón Pérez‐Alvarez, Rosa Pérez‐López, Victor M. Castellano‐Megias, Manuel Nevado‐Santos, Juan C. Alcón, Ricard Solá, José M. Pérez‐Moreno, José M. Navarro, Raúl J. Andrade, Javier Salmerón, Manuel Fernández‐López, Rafael Aznar, Moisés Diago – 26 February 2008 – This study was undertaken to evaluate an image processing method for assessing liver fibrosis in conventional computed tomography (CT) scans in patients with chronic hepatitis C.

Serum aminotransferase activity and mortality risk in a United States community

Tae Hoon Lee, W. Ray Kim, Joanne T. Benson, Terry M. Therneau, L. Joseph Melton – 26 February 2008 – Serum aminotransferase [such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT)] is commonly used as an indicator of liver disease. The aim of the study was to determine the degree to which aminotransferase results are associated with increased mortality at the population level.

Interferon regulatory factor‐3 activation, hepatic interferon‐stimulated gene expression, and immune cell infiltration in hepatitis C virus patients

Daryl T.‐Y. Lau, Penny Mar Fish, Mala Sinha, David M. Owen, Stanley M. Lemon, Michael Gale – 26 February 2008 – Interferon regulatory factor‐3 (IRF‐3) activation directs α/β interferon production and interferon‐stimulated gene (ISG) expression, which limits virus infection.

Autophagy activation by rapamycin eliminates mouse Mallory‐Denk bodies and blocks their proteasome inhibitor‐mediated formation

Masaru Harada, Shinichiro Hanada, Diana M. Toivola, Nafisa Ghori, M. Bishr Omary – 21 February 2008 – The proteasomal and lysosomal/autophagy pathways in the liver and other tissues are involved in several biological processes including the degradation of misfolded proteins. Exposure of hepatocyte cell lines to proteasome inhibitors (PIs) results in the formation of inclusions that resemble Mallory‐Denk bodies (MDBs). Keratins are essential for MDB formation and keratin 8 (K8)‐overexpressing transgenic mice are predisposed to MDB formation.

Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease

Winston Dunn, Ronghui Xu, Jeffrey B. Schwimmer – 21 February 2008 – People at risk for coronary heart disease are often at risk for nonalcoholic fatty liver disease (NAFLD). The association of modest wine consumption with NAFLD has not been studied and the recommendation of wine for patients at risk for both diseases is controversial. The aim is to test the hypothesis that modest wine consumption is associated with decreased prevalence of NAFLD.

S‐adenosylmethionine inhibits lipopolysaccharide‐induced gene expression via modulation of histone methylation

Ainhoa Iglesias Ara, Meng Xia, Komal Ramani, José M. Mato, Shelly C. Lu – 21 February 2008 – We previously showed that S‐adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)‐induced tumor necrosis factor α (TNFα) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor κ B nuclear binding. However, the exact molecular mechanism or mechanisms of the inhibitory effect were unclear. While SAMe is a methyl donor, MTA is an inhibitor of methylation.

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