Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18664
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dc.contributor.authorMarkoula, S.en
dc.contributor.authorGiannopoulos, S.en
dc.contributor.authorAsproudis, I.en
dc.contributor.authorKostoulas, C.en
dc.contributor.authorNikas, A.en
dc.contributor.authorBagli, E.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorGeorgiou, I.en
dc.date.accessioned2015-11-24T18:54:16Z-
dc.date.available2015-11-24T18:54:16Z-
dc.identifier.issn1090-0535-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18664-
dc.rightsDefault Licence-
dc.subjectAge Factorsen
dc.subjectAgeden
dc.subjectAged, 80 and overen
dc.subjectAlanineen
dc.subjectAllelesen
dc.subjectAngiotensinogen/*geneticsen
dc.subjectConfidence Intervalsen
dc.subjectCysteineen
dc.subjectDNA Transposable Elementsen
dc.subjectFemaleen
dc.subjectGene Deletionen
dc.subjectGenetic Predisposition to Diseaseen
dc.subjectGenotypeen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectMethionineen
dc.subjectMiddle Ageden
dc.subjectOdds Ratioen
dc.subjectOptic Neuropathy, Ischemic/*geneticsen
dc.subjectPeptidyl-Dipeptidase A/*geneticsen
dc.subjectPolymorphism, Geneticen
dc.subjectReceptor, Angiotensin, Type 1/*geneticsen
dc.subjectRenin-Angiotensin System/*geneticsen
dc.subjectSex Factorsen
dc.subjectThreonineen
dc.titleRenin-angiotensin-aldosterone system genes and nonarteritic anterior ischemic optic neuropathyen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/21633717-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2011-
heal.abstractPURPOSE: Recent literature suggests a genetic component for non-arteritic anterior ischemic optic neuropathy (NAION). We examined the association of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene, of the M235T polymorphism of the angiotensinogen gene, and of the A1166C polymorphism of the angiotensin II type 1 receptor gene with NAION. METHODS: Forty-seven patients with NAION and 76 controls, age- and gender-matched, were recruited and genotyped for renin-angiotensin-aldosterone system (RAAS) genes. Genotypes were determined by polymerase chain reaction and restriction enzyme analysis. NAION and control groups were compared in regard to the prevalence of renin-angiotensin-aldosterone system polymorphisms, and further stratified by age and gender. RESULTS: NAION occurrence was not associated with the M235T polymorphism of the angiotensinogen gene and the A1166C polymorphism of the angiotensin II, type 1 receptor gene. Regarding the angiotensin-converting enzyme insertion/deletion polymorphism, our findings suggest that the II genotype could be a risk factor for NAION in younger male patients when compared to all cases and controls (p=0.033, odds ratio=5.71, confidence interval=1.152 C28.35 and p=0.03, odds ratio=5.33, confidence interval=1.17 C24.31 respectively). Furthermore I allele was present in all male patients younger than 55 years, making this allele a likely predisposing factor for NAION in young males. CONCLUSIONS: Since NAION may occur when compromised watershed microcirculation is combined with insufficient autoregulation of systematic circulation, polymorphisms of genes involved in systematic circulation, such as the RAAS genes, may be associated with NAION occurrence. Large-scale, multicentered, controlled prospective studies are needed to further explore the effects of RAAS polymorphisms or other genetic factors on NAION susceptibility.en
heal.journalNameMol Visen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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