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李贞贞 《国际泌尿系统杂志》2015,(4)
糖尿病肾病( Diabetic nephropathy,DN)是糖尿病最常见、最严重的并发症之一。 DN发病机制复杂,是在遗传背景的基础上多因素综合作用的结果。长期高血糖是导致DN的始动因素,其诱导的氧化应激及炎症反应相互作用,最终导致DN的发生。针对这两个靶点通路的治疗将成为DN治疗领域的新热点。 相似文献
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目的 探讨屈光不正性弱视类型及初始治疗的年龄对近立体视功能的影响.方法 采用颜氏立体图对门诊的121例3~9岁屈光不正性弱视儿童的立体视功能进行治疗前后(6月)的对比分析,观察弱视程度的不同及屈光类型的不同对患儿立体视治疗前后的影响及不同开始治疗年龄对近立体视发育的影响.结果 屈光不正性弱视儿童有不同程度的近立体视,具有正常近立体视锐度比例为22.92%.以散光性屈光不正为主,高度远视者近立体视较差,开始治疗的年龄越小,近立体视功能发育越好,疗效越好,不同年龄组治疗效果间有统计学意义;不同程度的屈光不正性弱视患者治愈后近立体视锐度也存在差异,轻度 、中度弱视较重度弱视立体视功能发育较好,治疗后预后好,重度弱视的立体视功能预后较差,差异有统计学意义.结论 屈光不正性弱视中高度远视对视功能影响较大,开始治疗年龄越小,立体视发育预后较好.开始治疗年龄较晚的立体视发育相对较差.散光型弱视儿童立体视功能明显好于高度远视组儿童(屈光参差除外),重度弱视有一部分视力提高后立体视仍未发育,在弱视治疗的后期要注意双眼视觉的恢复. 相似文献
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Objective To investigate the effect of sodium nitroprusside (SNP) on hippocampal neuronal nitricoxide synthase (nNOS)expression after focal cerebral ischemia-reperfusion in rats and the mechanism of neuroprotective effect of SNP. Method 108 male SD rats weighting 250 g-300 g were randomly divided into 3 groups (n=36). Focal ischemia-reperfusion was established by occlusion of middle cerebral artery (MCA ).Control group (C): in which sham operation was performed; Ischemia-reperfusion group (I): after sodium chloride(5 μl) was injected into the lateral cerebral ventricle using microsyringe, MCA was occluded for 2 h; SNP group (S): SNP (0.055 mg/kg, 5μl ) was injected into the lateral cerebral ventricle using microsyringe, then MCA was occluded for 2 h. The experimental groups were further divided into 3 subgroups(n=12) according to the reperfusion time: 2 h, 6 h and 12 h. Neurological function score were tested before reperfusion; Pathological changes were observed by HE staining; The hippocampal tissue were obtained for detection of nNOS protein expression by immuno-histochemistry technique and nNOS mRNA expression by RT-PCR technique. Results Neuronal mortality in every subgroup of group I and S increased significantly compared with that in group C(P<0.05); Compared with that in 2 h(43.8 ± 2.1),6h (73.9±4.7) subgroup of group I, neuronal mortality in 2 h (36.5 ±1.2), 6h (42.6 ± 1.9) subgroup of group S decreased significantly (P<0.05); There were more nNOS mRNA expression in every subgroup of group I and S compared with that in group C (P<0.05),nNOS mRNA expression in 2 h (0.428 3 ± 0.000 4), 6 h (0.482 7 ± 0.005 2 )subgroup of group S decreased compared with that in 2 h (0.472 1 ±0.011 5), 6h(0.744 2±0.011 6)subgroup of group I(P<0.05); The expression of nNOS protein in other subgroup of group I and S increased except that in 6 h subgroup of group S(P<0.05); Compared with that in 2 h(0.265 8 ± 0.000 5), 6 h(0.284 0 ± 0.013 4) subgroup of group I, the expression of nNOS protein in 2 h (0.251 4 ±0.001 1), 6h (0.258 9 ±0.004 0) subgroup of group S decreased (P<0.05). Conclusion SNP coμld attenuate the focal cerebral ischemia/reperfusion injury and the possible mechanism may be related to the inhibition of nNOS expvession. 相似文献
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