In recent years, animal studies reveal that nNOS derived NO plays a vasoprotective role in the atherosclerosis [11�C14]. nNOS derived NO in nonadrenal, noncholinergic autonomic nerves may activate systemic vasculature and together with eNOS derived NO, dilate peripheral, and cerebral blood vessel [9, 15, download catalog 16] and is also involved in the control of blood pressure [17, 18]. In the cerebral infarction model, NOS1-deficient mice had smaller infarct ratio and milder neurological dysfunction when compared with controls, suggesting that NOS1 is detrimental for cerebral infarction [19, 20]. Thus, nNOS may influence the susceptibility to stroke in a mechanism complementary but different from that of eNOS.The human NOS1 gene was first identified in the neurons of the brain and thus is also known as neural NOS (nNOS) [21].
It has been confirmed that nNOS is expressed in not only the brain and peripheral nitrogen source nerves but also the kidney, heart, muscular skeletal muscles, vascular smooth muscle cells, and endothelial cells. Human NOS1 (nNOS) gene is mapped to 12q24.2, and 240kb in length. It contains 29 exons and 28 introns. To date, few studies have been conducted to investigate the relationship between nNOS gene polymorphism and pathogenesis of IS. Recently, Manso et al. [22] investigated the NOS1 gene polymorphism in a Portuguese population. Their results showed that the NOS1 gene polymorphism (rs1483757, rs7308402, rs2293050, and rs2139733) was closely related to the pathogenesis of IS. Thus, it is necessary to confirm this finding in different populations.
To date, no study has been carried out to explore the relation of NOS gene polymorphism with the pathogenesis of IS in Chinese. This case-control study was undertaken to investigate the association between NOS1 gene polymorphism and IS in Han Chinese of North China. Furthermore, stratification analysis was done according to the gender. Our findings may provide evidence for the prevention of stroke.2. Materials and Methods2.1. SubjectsAcute ischemic stroke patients (n = 413) were recruited from the Department of Neurology of First Affiliated Hospital of China Medical University and NO 202 Hospital of People’s Liberation Army of China. There were 201 males and 212 females. Focal neurological deficits were abrupt and acute and continued for more than 24h. Ischemic stroke was confirmed by brain MRI and/or cranial CT scan.
Transient ischemic attack, cerebral embolism, hemorrhagic infarction, cerebral hemorrhage, and subarachnoid hemorrhage were excluded. In addition, cerebral infarction due to cardiogenic events, arteritis, tumors, drugs, trauma, vascular malformations, hematological diseases, or aneurysm was excluded. Concomitant liver AV-951 and kidney diseases and thyroid disease were not found in these patients. Diagnosis was done by neurologists.