To investigate whether four single nucleotide polymorphisms (SNPs) rs2293054 [Ile734Ile], rs1047735 [His902His], rs2293044 [Val1353Val], rs2682826 (3'UTR) of nitric oxide synthase 1 (NOS1) are associated with the development and clinical phenotypes of ischemic stroke.
We enrolled 120 ischemic stroke patients and 314 control subjects. Ischemic stroke patients were divided into subgroups according to the scores of the National Institutes of Health Stroke Survey (NIHSS, <6 and ≥6) and Modified Barthel Index (MBI, <60 and ≥60). SNPStats, SNPAnalyzer, and HelixTree programs were used to calculate odds ratios (ORs), 95% confidence intervals (CIs), and p-values. Multiple logistic regression models were performed to analyze genetic data.
No SNPs of the
These results suggest that NOS1 may be related to the clinical phenotypes of ischemic stroke in Korean population.
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To investigate the effect of enhanced external counterpulsation (EECP) on plasma nitric oxide (NO), Endothelin 1 (ET1), high sensitive C-reactive protein (HSCRP) and quality of life (QoL) in patients with coronary artery disease (CAD).
We conducted a pilot randomized clinical trial in order to evaluate plasma NO, ET1, HSCRP and QoL before and after twenty sessions of EECP (group A) and cardiac rehabilitation (CR, group B) in 42 patients with CAD (21 in each group).
Forty-two patients (33 male and 9 female) were included in the study. The mean age was 58.2±10 years. The mean HSCRP was 1.52±0.7 in the EECP group and it was reduced to 1.27±0.4 after intervention. The reduction in HSCRP was not statistically significant in EECP and CR groups with p=0.33 and p=0.27, respectively. There was not significant improvement of NO, ET1, and QoL in the EECP and CR groups shortly after therapy (p>0.05).
Although the short-term EECP treatment in CAD patients improved HSCRP, NO, ET1, and QoL compared with the baseline those improvements are not statistically significant. Further studies are necessary with large study groups and more sessions.
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Objective: To investigate the neuropathic changes induced by nucleus pulposus and possible role of nitric oxide (NO) in the pathogenesis of painful radiculopathy.
Method: Autologous nucleus pulposus was harvested from the rat coccygeal intervertebral disc and grafted to the sciatic nerve. Pain behavior, neurophysiologic and pathologic changes were compared between autografted and sham operated group during 14-day-period. Western immunoblotting and immunohistochemistry with anti-nitrotyrosine mouse monoclonal antibody were used to compare the NO production and nerve damage in autografted and sham operated nerve tissues.
Results: Mechanical allodynia and thermal hyperalgesia were observed 2 days after autograft of nucleus pulposus and persisted during 14-day-period (p＜0.05). Motor nerve conduction latency was delayed and compound muscle action potential amplitude was decreased 5 days after autograft (p＜0.05). Histologically, nucleus pulposus induced severe inflammatory reaction with fibroblast proliferation and foamy macrophage infiltration, which were persisted during 14-day- period. More nitrated proteins were detected consistently in nerve tissues with autograft of nucleus pulposus and immunohistochemical staining of nitrotyrosine was prominent around foamy macrophages.
Conclusion: These data suggest that nucleus pulposus induce mechanical allodynia, thermal hyperalgesia and nerve dysfunction through inflammatory reaction with macrophage infiltration. NO and NO related tissue injury may play an important role in the pathogenesis of painful radiculopathy.
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