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Oxide Synthase Gene Polymorphisms (oxide + synthase_gene_polymorphism)

Distribution by Scientific Domains
Medical Sciences50%
Life Sciences50%

Kinds of Oxide Synthase Gene Polymorphisms

  • nitric oxide synthase gene polymorphism
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    Selected Abstracts

    No association between the neuronal nitric oxide synthase gene polymorphism and Alzheimer Disease,

    AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 6 2002
    Ying-Jay Liou
    Abstract Nitric oxide synthase (NOS) has been implicated in the pathogenesis of Alzheimer disease (AD). To examine the role of the neuronal NOS (nNOS) gene in AD, patients (n,=,139) and control subjects (n,=,101) were genotyped for the nNOS dinucleotide polymorphism. No association was demonstrated for AD and this particular nNOS polymorphism. © 2002 Wiley-Liss, Inc. [source]

    Endothelial nitric oxide synthase gene polymorphisms in patients with nontraumatic femoral head osteonecrosis

    JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 8 2006
    Kyung-Hoi Koo
    Abstract As endothelial nitric oxide synthase (eNOS) has beneficial effects on skeletal, vascular, and thrombotic systems, the association between nontraumatic femoral head osteonecrosis (FHON) and eNOS gene polymorphisms was investigated in Korean patients with FHON. Genomic DNA from 103 patients with nontraumatic FHON (idiopathic in 50, steroid-induced in 29, and alcohol abuse in 24) and 103 control subjects matched for gender and age (3-year range) was analyzed for the 27-bp repeat polymorphism in intron 4 and Glu298Asp polymorphism in exon 7. The frequencies of alleles and genotypes were compared between patients and control subjects. The frequency of 4a allele was significantly higher in total patients than control subjects [6.8% vs. 2.4%, p,=,0.0345, odds ratio (OR) 2.931]. In subgroup analysis, the 4a allele significantly increased in patients with idiopathic FHON versus control subjects (9.0% vs. 2.4%, p,=,0.0297, OR 3.976). The frequency of the 4a/b genotype in total patients (13.6% vs. 4.9%, p,=,0.0302, OR 3.083) as well as patients with idiopathic FHON (18.0% vs. 4.9%, p,=,0.0246, OR 4.302) was higher than control subjects. The distribution of Glu298Asp polymorphisms was not significantly different between patients and control subjects. Microstellate polymorphism in intron 4 of eNOS polymorphism was significantly associated with idiopathic FHON in Korean patients. Because 4a allele is associated with lower synthesis of eNOS, these results suggest that carrier state of 4a allele in intron 4 might be a genetic risk factor of FHON and could provide insight into the protective role of nitric oxide in the pathogenesis of FHON. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:1722,1728, 2006 [source]

    Inducible and endothelial constitutive nitric oxide synthase gene polymorphisms in Kawasaki disease

    PEDIATRICS INTERNATIONAL, Issue 2 2003
    Vahid Khajoee
    AbstractBackground: Nitric oxide (NO) is secreted by immune and vascular endothelial cells, and appears to play important roles in the pathophysiology of Kawasaki disease (KD). Thus, genetic variations in NO synthase (NOS) genes may be involved in the development of coronary artery lesions (CAL) in KD. Methods: The present study investigated the association of endothelial constitutive NOS (ecNOS) and inducible NOS (iNOS) gene polymorphisms with the development of CAL in KD in a Japanese population. Results: The genotype distributions of 27-bp tandem repeat polymorphism within intron 4 of ecNOS gene did not show any significant difference between controls and KD patients with or without CAL. In addition, there was no significant association between whole-allele distribution of iNOS gene promoter (penta-repeat CCTTT) polymorphism and KD with or without CAL. Conclusion: These results did not support any association of ecNOS and iNOS gene polymorphisms to the development of CAL in KD patients in a Japanese population. [source]

    Endothelial nitric oxide synthase gene polymorphisms in giant cell arteritis

    ARTHRITIS & RHEUMATISM, Issue 11 2003
    Carlo Salvarani
    Objective To examine potential associations of the Glu/Asp298 polymorphism in exon 7 and the 4a/b polymorphism in intron 4 of the endothelial nitric oxide synthase (eNOS) gene with susceptibility to and clinical expression of giant cell arteritis (GCA), particularly in patients with versus those without ischemic complications. Methods Ninety-one consecutive patients with biopsy-proven GCA, who were residents of Reggio Emilia, Italy, and 133 population-based controls from the same geographic area were genotyped by polymerase chain reaction and allele-specific oligonucleotide techniques for eNOS polymorphisms in exon 7 and intron 4. The patients were separated into 2 subgroups according to the presence or absence of ischemic complications (visual loss and/or jaw claudication and/or aortic arch syndrome). Results The distribution of the Glu/Asp298 genotype differed significantly between GCA patients and controls (corrected P [Pcorr] = 0.003). Carriers of the Asp298 allele (Asp/Asp or Glu/Asp) were significantly more frequent among the GCA patients than among the controls (Pcorr = 0.0002, odds ratio 3.3, 95% confidence interval 1.7,6.3). The distribution of the 4a/b genotype was similar in GCA patients and controls. No significant associations were found when GCA patients with and without ischemic complications were compared. Conclusion Our findings show that the Glu/Asp298 polymorphism of the eNOS gene is associated with GCA susceptibility. [source]