阿加曲班对实验性大鼠脑出血周围组织神经元损伤的保护作用

目的研究阿加曲班对大鼠实验性大脑内出血的脑保护作用及其可能机制。方法选择SD大鼠60只,按随机数字法分为假手术组(1 2只)、脑出血组(12只)和阿加曲班治疗组(治疗组,36只)。治疗组又按注射阿加曲班1.0、1.5、2.0 mg/kg剂量分为治疗1组(12只)、治疗2组(12只)和治疗3组(12只)。观察应用阿加曲班前后脑出血大鼠神经功能缺损变化情况;应用免疫组织化学和Western blot法,观察阿加曲班干预前后大鼠大脑血肿周围组织中神经元烯醇化酶(NSE)、胶质纤维酸性蛋白(GFAP)阳性神经元数目的变化,以及NSE、诱导型一氧化氮合酶和GFAP表达水平的变化。结果与假手术组和治疗组比较,脑出血组大鼠血肿周围组织中NSE阳性神经元数目明显减少,GFAP阳性神经元数目明显增多,差异有统计学意义(P0.05,P0.01)。与脑出血组比较,治疗组大鼠血肿周围组织中NSE表达水平明显升高,而诱导型一氧化氮合酶及GFAP表达水平明显降低,差异有统计学意义(P0.05,P0.01)。结论阿加曲班可以有效拮抗大鼠脑出血血肿周围组织中NSE的丢失,其机制可能与阿加曲班降低神经元活性氧含量以及抑制炎性反应等作用有关。     

脑静脉及静脉窦血栓形成27例临床特点与影像学分析

目的分析脑静脉及静脉窦血栓形成（CVT）的临床特点及治疗方法。方法回顾性分析27例CVT患者的病因、临床表现、脑脊液检查、影像学特征、治疗及预后。结果CVT可见于各个年龄段,以中青年女性多见。妊娠、感染、免疫性疾病等为常见病因,部分病例病因不明。早期表现多为头痛,可伴有癫痫发作和各种神经功能缺损的症状和体征,脑脊液压力明显升高。典型病例颅脑CT可见到病变静脉窦高密度影或伴有脑水肿和脑出血。MRI平扫可见病变静脉窦内异常信号。磁共振静脉成像或数字减影血管造影（DSA）可见病变静脉窦显影欠佳或不显影。经抗凝、降低颅内压等对症治疗,病情好转21例,恶化3例,死亡2例,转院治疗1例。结论CVT的临床表现多样且缺乏特异性,关注患者是否存在CVT发生的高危因素,尽早行颅脑CT、MRI或DSA检查以明确诊断,DSA是CVT诊断的金标准。明确诊断后积极抗凝治疗的同时,应根据病因进行针对性治疗。     

神经生长因子、Noggin基因转染对骨髓间充质干细胞分化的影响

目的 研究外源性神经生长因子(NGF]、Noggin转染骨髓间充质干细胞(BMSCs)的可行性,并观察基因修饰的细胞向神经元方向的分化情况.方法 采用贴壁法分离纯化BMSCs,通过细胞表面标志及成脂诱导鉴定细胞.Ad-GFP-NGF、Ad-GFP-Noggin单独及联合转染BMSCs.通过Westernblot、免疫细胞化学观察目的 蛋白表达.通过免疫组化观察转染后BMSCs向神经元方向分化情况.结果贴壁法获得的细胞具有BMSCs表型,能分化为脂肪细胞.未转染组和Ad-GFP转染组少量表达NGF,不表达Noggin.NGF、Noggin单独及联合转染BMSCs均能高效表达目的 蛋白.NGF、Noggin转染的BMSCs可分化为具有神经元形态,并表达神经丝蛋白(NF-H)的细胞,联合转染组NF-H阳性细胞比例最高.结论 贴壁法能有效纯化BMSCs,Ad-GFP-NGF、Ad-GFP-Noggin单独及联合转染BMSCs安全并能高效表达目的 蛋白,NGF、Noggin转染的BMSCs 体外培养能向神经元样细胞方向分化,两种蛋白联合修饰能增强这种分化作用.     

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.     

脑静脉及静脉窦血栓形成27例临床特点与影像学分析

目的 分析脑静脉及静脉窦血栓形成(CVT)的临床特点及治疗方法.方法 回顾性分析27例CVT患者的病因、临床表现、脑脊液检查、影像学特征、治疗及预后.结果 CVT可见于各个年龄段,以中青年女性多见.妊娠、感染、免疫性疾病等为常见病因,部分病例病因不明.早期表现多为头痛,可伴有癫痫发作和各种神经功能缺损的症状和体征,脑脊液压力明显升高.典型病例颅脑CT可见到病变静脉窦高密度影或伴有脑水肿和脑出血.MRI平扫可见病变静脉窦内异常信号.磁共振静脉成像或数字减影血管造影(DSA)可见病变静脉窦显影欠佳或不显影.经抗凝、降低颅内压等对症治疗,病情好转21例,恶化3例,死亡2例,转院治疗1例.结论 CVT的临床表现多样且缺乏特异性,关注患者是否存在CVT发生的高危因素,尽早行颅脑CT、MRI或DSA检查以明确诊断,DSA是CVT诊断的金标准.明确诊断后积极抗凝治疗的同时,应根据病因进行针对性治疗.     

水通道蛋白AQP4研究进展

水通道蛋白（Aquapofins,AQPs）是一个同源、四聚体结构的水通道蛋白家族,主要功能是运输水分,另外AQP3、AQP7和AQP9等水通道蛋白属于水甘油膜孔蛋白质,还可运输甘油和各类小的极性分子。脑组织中的水通道蛋白主要为水通道蛋白4（aquapofin-4,AQP4）,是1994年Jung等利用水通道蛋白家族的同源性克隆分离出来的,在中枢神经系统分布最为丰富,可能是脑脊液重吸收、渗透压调节,脑水肿形成等生理、病理过程的分子生物学基础。因此,研究AQP4可为脑水肿及水代谢疾病提供分子水平的理论依据,同时为临床治疗脑水肿及水代谢疾病提供一种新途径。     

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.     

全血灌流免疫吸附治疗被动转移型实验性自身免疫性重症肌无力的研究

目的观察全血灌流免疫吸附治疗实验性自身免疫性重症肌无力(EAMG)的疗效。方法用重症肌无力患者血清中的免疫球蛋白(IgG)建立急性EAMG模型,并进行全血灌流免疫吸附治疗,观察其疗效。结果以球形纤维素为载体色氨酸为配基的吸附剂治疗2h,能清除49.85%±2.55%的致病抗体,肌无力症状显著改善;重复神经电刺激实验CMAP衰减率从21.875±3.226(3Hz)、22.250±2.815(5Hz)和24.375±1.685(10Hz)恢复到17.875±1.642(P<0.05)、18.750±1.388(P<0.05)和23.250±1.388;单纤维肌电图示MCD值也从23.125±2.997(3Hz)、26.375±4.172(5Hz)和30.375±4.470(10Hz)显著性地缩短至19.250±1.488(P<0.05)、21.750±2.375(P<0.05)和26.125±2.031(P<0.05)MEPP波幅(μV)也从30.54±3.74显著增加至40.43±3.45(P<0.01),频率(次/s)从17.18±2.87显著增加至18.74±2.75(P<0.01);单位面积的神经肌肉接头数从9.825±3.401增加至10.900±2.879(P<0.05)。结论全血灌流免疫吸附治疗能有效清除被动转移型重症肌无力动物体内致病抗体,并相应改善临床症状,提高神经肌肉电传导功能,增加神经肌肉接头处nAChR数量,为临床重症肌无力的血液净化治疗提供了新措施。     

帕金森病治疗指南

帕金森病的命名是出于对詹姆斯·帕金森的敬意,他的经典论文“短论震颤麻痹”发表于1817年,首次描述了该病的临床特征。帕金森病是一与年龄相关的神经退变性疾病,平均发病年龄为60岁。据     

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.