BACKGROUND: Our aim in the present study was to determine whether endothelial NO synthase gene (ecNOS) polymorphisms are associated with myocardial infarction (MI). METHODS: Forty chromosomes from patients with MI were screened for polymorphisms of the ecNOS gene using polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis and sequencing. Ten polymorphisms were detected: three in the 5' flanking sequence at positions -1474, -924 and -788, two in coding sequences 774C --> T (silent) and G894 --> T (Glu-298 --> Asp) and five in introns 2, 11, 12, 22 and 23. Five hundred and thirty-one patients with MI and 610 control subjects recruited in France and Northern Ireland in the ECTIM study were genotyped for these polymorphisms. RESULTS: Glu-298 homozygotes were more frequent among patients with MI than in control subjects in the French population [OR = 1.47 (1.03-1.97), P < 0.009], but no such difference was observed in Northern Ireland. No significant difference between cases and control subjects was detected for the other polymorphisms. Our search for a possible association of the combination of ecNOS polymorphisms with MI by logistic regression analysis was also negative. CONCLUSIONS: We have explored a set of polymorphisms of the ecNOS gene in a large case-control study of MI and found that the polymorphisms were not consistently associated with MI.
BACKGROUND: Our aim in the present study was to determine whether endothelial NO synthase gene (ecNOS) polymorphisms are associated with myocardial infarction (MI). METHODS: Forty chromosomes from patients with MI were screened for polymorphisms of the ecNOS gene using polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis and sequencing. Ten polymorphisms were detected: three in the 5' flanking sequence at positions -1474, -924 and -788, two in coding sequences 774C --> T (silent) and G894 --> T (Glu-298 --> Asp) and five in introns 2, 11, 12, 22 and 23. Five hundred and thirty-one patients with MI and 610 control subjects recruited in France and Northern Ireland in the ECTIM study were genotyped for these polymorphisms. RESULTS:Glu-298 homozygotes were more frequent among patients with MI than in control subjects in the French population [OR = 1.47 (1.03-1.97), P < 0.009], but no such difference was observed in Northern Ireland. No significant difference between cases and control subjects was detected for the other polymorphisms. Our search for a possible association of the combination of ecNOS polymorphisms with MI by logistic regression analysis was also negative. CONCLUSIONS: We have explored a set of polymorphisms of the ecNOS gene in a large case-control study of MI and found that the polymorphisms were not consistently associated with MI.
Authors: Ruth Fricker; Christiane Hesse; Johanna Weiss; Yorki Tayrouz; Michael M Hoffmann; Kristina Unnebrink; Ulrich Mansmann; Walter E Haefeli Journal: Br J Clin Pharmacol Date: 2004-08 Impact factor: 4.335
Authors: Mohamed Z Gad; Mohamed F Abdel Rahman; Ingy M Hashad; Sahar M Abdel-Maksoud; Nabil M Farag; Khaled Abou-Aisha Journal: Genet Test Mol Biomarkers Date: 2012-06-25
Authors: Leah R MacClellan; Timothy D Howard; John W Cole; O Colin Stine; Wayne H Giles; Jeffery R O'Connell; Marcella A Wozniak; Barney J Stern; Braxton D Mitchell; Steven J Kittner Journal: Stroke Date: 2009-08-06 Impact factor: 7.914
Authors: M G Colombo; M G Andreassi; U Paradossi; N Botto; S Manfredi; S Masetti; G Rossi; A Clerico; A Biagini Journal: Heart Date: 2002-06 Impact factor: 5.994