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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22940
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dc.contributor.authorAngelakopoulou, A.en
dc.contributor.authorShah, T.en
dc.contributor.authorSofat, R.en
dc.contributor.authorShah, S.en
dc.contributor.authorBerry, D. J.en
dc.contributor.authorCooper, J.en
dc.contributor.authorPalmen, J.en
dc.contributor.authorTzoulaki, I.en
dc.contributor.authorWong, A.en
dc.contributor.authorJefferis, B. J.en
dc.contributor.authorManiatis, N.en
dc.contributor.authorDrenos, F.en
dc.contributor.authorGigante, B.en
dc.contributor.authorHardy, R.en
dc.contributor.authorLaxton, R. C.en
dc.contributor.authorLeander, K.en
dc.contributor.authorMotterle, A.en
dc.contributor.authorSimpson, I. A.en
dc.contributor.authorSmeeth, L.en
dc.contributor.authorThomson, A.en
dc.contributor.authorVerzilli, C.en
dc.contributor.authorKuh, D.en
dc.contributor.authorIreland, H.en
dc.contributor.authorDeanfield, J.en
dc.contributor.authorCaulfield, M.en
dc.contributor.authorWallace, C.en
dc.contributor.authorSamani, N.en
dc.contributor.authorMunroe, P. B.en
dc.contributor.authorLathrop, M.en
dc.contributor.authorFowkes, F. G.en
dc.contributor.authorMarmot, M.en
dc.contributor.authorWhincup, P. H.en
dc.contributor.authorWhittaker, J. C.en
dc.contributor.authorde Faire, U.en
dc.contributor.authorKivimaki, M.en
dc.contributor.authorKumari, M.en
dc.contributor.authorHypponen, E.en
dc.contributor.authorPower, C.en
dc.contributor.authorHumphries, S. E.en
dc.contributor.authorTalmud, P. J.en
dc.contributor.authorPrice, J.en
dc.contributor.authorMorris, R. W.en
dc.contributor.authorYe, S.en
dc.contributor.authorCasas, J. P.en
dc.contributor.authorHingorani, A. D.en
dc.date.accessioned2015-11-24T19:29:00Z-
dc.date.available2015-11-24T19:29:00Z-
dc.identifier.issn1522-9645-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22940-
dc.rightsDefault Licence-
dc.subjectAdulten
dc.subjectAgeden
dc.subjectBiological Markers/blooden
dc.subjectBody Mass Indexen
dc.subjectCase-Control Studiesen
dc.subjectCoronary Disease/blood/*geneticsen
dc.subjectDiabetes Mellitus, Type 2/blood/*geneticsen
dc.subjectDiabetic Cardiomyopathies/blood/*geneticsen
dc.subjectFemaleen
dc.subjectGenome-Wide Association Studyen
dc.subjectHumansen
dc.subjectLipids/*blooden
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectPolymorphism, Single Nucleotide/*geneticsen
dc.subjectProspective Studiesen
dc.subjectRisk Factorsen
dc.titleComparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaborationen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1093/eurheartj/ehr225-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/21804106-
heal.identifier.secondaryhttp://eurheartj.oxfordjournals.org/content/33/3/393.full.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2012-
heal.abstractAIMS: To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other risk factors and CHD events. METHODS AND RESULTS: Using two case-control studies, three cross-sectional, and seven prospective studies with up to 25 000 individuals and 5794 CHD events we evaluated associations of 34 genome-wide-association study-identified SNPs with CHD risk and 16 CHD-associated risk factors or biomarkers. The Ch9p21 SNPs rs1333049 (OR 1.17; 95% confidence limits 1.11-1.24) and rs10757274 (OR 1.17; 1.09-1.26), MIA3 rs17465637 (OR 1.10; 1.04-1.15), Ch2q36 rs2943634 (OR 1.08; 1.03-1.14), APC rs383830 (OR 1.10; 1.02, 1.18), MTHFD1L rs6922269 (OR 1.10; 1.03, 1.16), CXCL12 rs501120 (OR 1.12; 1.04, 1.20), and SMAD3 rs17228212 (OR 1.11; 1.05, 1.17) were all associated with CHD risk, but not with the CHD biomarkers and risk factors measured. Among the 20 blood lipid-related SNPs, LPL rs17411031 was associated with a lower risk of CHD (OR 0.91; 0.84-0.97), an increase in Apolipoprotein AI and HDL-cholesterol, and reduced triglycerides. SORT1 rs599839 was associated with CHD risk (OR 1.20; 1.15-1.26) as well as total- and LDL-cholesterol, and apolipoprotein B. ANGPTL3 rs12042319 was associated with CHD risk (OR 1.11; 1.03, 1.19), total- and LDL-cholesterol, triglycerides, and interleukin-6. CONCLUSION: Several SNPs predicting CHD events appear to involve pathways not currently indexed by the established or emerging risk factors; others involved changes in blood lipids including triglycerides or HDL-cholesterol as well as LDL-cholesterol. The overlapping association of SNPs with multiple risk factors and biomarkers supports the existence of shared points of regulation for these phenotypes.en
heal.journalNameEur Heart Jen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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