Suchergebnisse

L'objectif de cet article est de tester l'existence d'une relation entre la structure industrielle (spécialisation, diversité, concurrence locale et taille des firmes), le salaire et les investissements directs étrangers d'une part, et la performance productive des entreprises manufacturières en termes de valeur ajoutée, d'autre part. Pour cinq secteurs industriels répartis sur 138 délégations du littoral tunisien et observés sur la période 1998-2004, les résultats d'estimation d'un modèle en données de panel non cylindré montrent que la spécialisation, la diversification et la concurrence locale sont toutes bénéfiques pour le développement industriel. Les résultats révèlent également que les entreprises de grande taille sont les plus productives et que les investissements directs étrangers ont un effet négatif sur la valeur ajoutée des secteurs manufacturiers.

International Liver Disease Genetics Consortium. ; Cirrhosis likely shares common pathophysiological pathways despite arising from a variety of liver diseases. A recent GWAS identified rs641738, a polymorphism in the MBOAT7 locus, as being associated with the development of alcoholic cirrhosis. Here we explore the role of this variant on liver inflammation and fibrosis in two cohorts of patients with chronic hepatitis C. In 2,051 patients, rs641738 associated with severe hepatic inflammation and increased risk of fibrosis, as well as fast fibrosis progression. At functional level, rs641738 associated with MBOAT7 transcript and protein levels in liver and blood, and with serum inflammatory, oxidative stress and macrophage activation markers. MBOAT7 was expressed in immune cell subsets, implying a role in hepatic inflammation. We conclude that the MBOAT7 rs641738 polymorphism is a novel risk variant for liver inflammation in hepatitis C, and thereby for liver fibrosis. ; M.E., M.W.D. and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1053206) and Project grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432). H.G. received support from The NOVO Nordisk Foundation the Danish Strategic Research Council (10-092797). U.S. and J.N. are supported by DFG SFB-TR57 and the Hector-Foundation (M63). K.T. is supported by Scholarship from the Egyptian government.

International Liver Disease Genetics Consortium (ILDGC). ; Hepatocarcinogenesis is tightly linked to liver fibrosis. Recently, two GWAS variants, MICA rs2596542 and DEPDC5 rs1012068 were identified as being associated with the development of HCV-induced hepatocellular carcinoma (HCC) in Japanese patients. The role of these variants on hepatic inflammation and fibrosis that are closely associated with HCC development is not known, nor are the biological mechanisms underlying their impact on the liver. Here, we demonstrate in 1689 patients with chronic hepatitis C (CHC) (1,501 with CHC and 188 with HCV-related HCC), that the MICA (T) allele, despite not being associated with HCC susceptibility, is associated with increased fibrosis stage (OR: 1.47, 95% CI: 1.05–2.06, p = 0.02) and fibrosis progression rate (hazards ratio: 1.41, 95% CI: 1.04–1.90, p = 0.02). The DEPDC5 variant was not associated with any of these phenotypes. MICA expression was down-regulated in advanced fibrosis stages. Further, (T) allele carriage was associated with lower MICA expression in liver and serum. Transforming growth factor-β1 (TGF-β1) expression suppresses MICA expression in hepatic stellate cells. Our findings suggest a novel mechanism linking susceptibility to advanced fibrosis and subsequently indirectly to HCC, to the level of MICA expression through TGF-β1-dependent mechanisms. ; M.E., C.L., M.D. and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (APP1053206, APP1149976) and Project grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432). U.S. and J.N. are supported by DFG SFB-TR57 and the Hector-Foundation (M63). R.E. and K.T. are supported by a scholarship from the Egyptian government. A.B. is supported by an Australian Government Research Training Program (RTP) scholarship. ; Peer reviewed