鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

护理干预对老年高血压患者血压控制效果的影响

目的探讨护理干预对老年高血压患者血压控制效果的影响。方法选取本院2011年1月-2012年8月收治的老年高血压患者148例,随机分为两组,对照组74例患者采用常规护理,观察组74例患者采用护理干预,护理时间为1个月,比较两组患者护理前后的舒张压和收缩压。结果护理后,观察组与对照组患者的舒张压和收缩压均明显降低,观察组患者的舒张压和收缩压均明显低于对照组,观察组血压控制率（82．4％）明显高于对照组（67．6％）,差异均有统计学意义（P〈0．05）。结论护理干预可以明显改善老年高血压患者的血压状况,降低舒张压和收缩压,是一种有效的血压控制方法,值得临床推广使用。     

脑静脉及静脉窦血栓形成的临床分析

目的 探讨脑静脉及脑静脉窦血栓形成(CVT)的诊断及治疗策略.方法 对23例确诊为脑静脉及脑静脉窦血栓形成的患者的病因、临床表现、影像学特征、治疗方法及预后进行回顾性分析.结果 23例患者中,经降颅压、抗炎及抗凝等对症及支持治疗后,19例好转出院,3例死亡,1例自动出院.结论 脑静脉及脑静脉窦血栓病因复杂,临床表现无特异性,确诊须行MRL/MRV或DSA检查.早期给予抗凝及溶栓治疗可获得较好效果.     

特发性快速眼动期睡眠行为障碍与多系统萎缩的相关性研究进展

特发性快速眼动期睡眠行为障碍(iRBD)是潜在的α-突触核蛋白病的最有力的标志物之一。大量文献记录了多系统萎缩(MSA)中iRBD的高发率,iRBD作为MSA前驱期的特征性改变,其在MSA进展中的作用也引起研究者们的关注。目前,还没有正式的前驱期MSA的诊断标准,iRBD为识别潜在的前驱期MSA患者提供了手段。认知能力通常保持相对完整,色觉异常较少,保留嗅觉会出现较严重的泌尿系统症状,这些临床特征可以帮助判定iRBD患者向MSA的转化。本文就iRBD的流行病学特点、在MSA中临床特征、与MSA进展、预后和转化的关系等进行综述,以期进一步了解iRBD与MSA的关系,为MSA前驱期的预防、诊断和治疗提供帮助。     

护理干预对2型糖尿病并发心血管病患者的影响

目的探讨护理干预对2型糖尿病并发心血管病患者的影响。方法选取本院2011年2月-2012年8月收治的2型糖尿病并发心血管病患者96例,随机分为两组,48例患者采用常规护理为对照组,另外48例患者采用护理干预为观察组,护理疗程为1个月,比较两组患者护理前后的血糖、心电图及血压异常情况。结果护理后,观察组与对照组的血糖、心电图及血压异常率均明显降低,观察组血糖异常率（37．5％）、心电图异常率（12．5％）、血压异常率（27．1％）均明显低于对照组（60．4％、31．2％、47．9％）,差异均有统计学意义（P〈0．05）。结论有效的护理干预可以明显改善2型糖尿病并发心血管病患者的血糖状况、心电图情况、血压状况。临床疗效显著,值得临床推广使用。     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.