Meta‐analysis using individual participant data is the gold standard for diagnostic studies
Ming‐Hua Zheng, Ke‐Qing Shi, Yu‐Chen Fan, Yong‐Ping Chen – 12 January 2011
Ming‐Hua Zheng, Ke‐Qing Shi, Yu‐Chen Fan, Yong‐Ping Chen – 12 January 2011
Emilio Ramos, Léon Kautz, Richard Rodriguez, Michael Hansen, Victoria Gabayan, Yelena Ginzburg, Marie‐Paule Roth, Elizabeta Nemeth, Tomas Ganz – 12 January 2011 – In response to iron loading, hepcidin synthesis is homeostatically increased to limit further absorption of dietary iron and its release from stores. Mutations in HFE, transferrin receptor 2 (Tfr2), hemojuvelin (HJV), or bone morphogenetic protein 6 (BMP6) prevent appropriate hepcidin response to iron, allowing increased absorption of dietary iron, and eventually iron overload.
Diego F. Calvisi, Maria M. Simile, Sara Ladu, Maddalena Frau, Matthias Evert, Maria L. Tomasi, Maria I. Demartis, Lucia Daino, Maria A. Seddaiu, Stefania Brozzetti, Francesco Feo, Rosa M. Pascale – 12 January 2011 – Up‐regulation of the v‐Myb avian myeloblastosis viral oncogene homolog‐like2 B‐Myb (MYBL2) gene occurs in human hepatocellular carcinoma (HCC) and is associated with faster progression of rodent hepatocarcinogenesis.
Frank Tacke, Christian Trautwein – 12 January 2011 – In the classical form of alpha1‐antitrypsin (AT) deficiency, a point mutation in AT alters the folding of a liver‐derived secretory glycoprotein and renders it aggregation‐prone. In addition to decreased serum concentrations of AT, the disorder is characterized by accumulation of the mutant alpha1‐antitrypsin Z (ATZ) variant inside cells, causing hepatic fibrosis and/or carcinogenesis by a gain‐of‐toxic function mechanism. The proteasomal and autophagic pathways are known to mediate degradation of ATZ.
Rachael Turner, Oswaldo Lozoya, Yunfang Wang, Vincenzo Cardinale, Eugenio Gaudio, Gianfranco Alpini, Gemma Mendel, Eliane Wauthier, Claire Barbier, Domenico Alvaro, Lola M. Reid – 12 January 2011 – Livers are comprised of maturational lineages of cells beginning extrahepatically in the hepato‐pancreatic common duct near the duodenum and intrahepatically in zone 1 by the portal triads.
12 January 2011
12 January 2011
Martin Wagner, Gernot Zollner, Michael Trauner – 12 January 2011 – Nuclear receptors are ligand‐activated transcriptional regulators of several key aspects of hepatic physiology and pathophysiology. As such, nuclear receptors control a large variety of metabolic processes including hepatic lipid metabolism, drug disposition, bile acid homeostasis, as well as liver regeneration, inflammation, fibrosis, cell differentiation, and tumor formation. Derangements of nuclear receptor regulation and genetic variants may contribute to the pathogenesis and progression of liver diseases.
Alessia Omenetti, Lee M. Bass, Robert A. Anders, Maria G. Clemente, Heather Francis, Cynthia D. Guy, Shannon McCall, Steve S. Choi, Gianfranco Alpini, Kathleen B. Schwarz, Anna Mae Diehl, Peter F. Whitington – 12 January 2011 – Biliary atresia (BA) is notable for marked ductular reaction and rapid development of fibrosis. Activation of the Hedgehog (Hh) pathway promotes the expansion of populations of immature epithelial cells that coexpress mesenchymal markers and may be profibrogenic.
Won‐Il Jeong, Ogyi Park, Yang‐Gun Suh, Jin‐Seok Byun, So‐Young Park, Earl Choi, Ja‐Kyung Kim, Hyojin Ko, Hua Wang, Andrew M. Miller, Bin Gao – 12 January 2011 – Activation of innate immunity (natural killer [NK] cell/interferon‐γ [IFN‐γ]) has been shown to play an important role in antiviral and antitumor defenses as well as antifibrogenesis. However, little is known about the regulation of innate immunity during chronic liver injury.