低氧增强SY5Y培养细胞内nPKCε的膜转位

目的:通过观察低氧刺激对培养SY5Y神经母细胞瘤细胞内nPKCε和nPKCθ膜转位激活的影响,以探讨两者是否参与细胞低氧预适应的发生。方法:利用本室建立的体外培养SY5Y细胞低氧刺激模型,并应用SDS-聚丙烯酰胺凝胶电泳(SDS-PAGE)、蛋白印记(Western-Blot)等方法,半定量分析SY5Y细胞内nPKCε、nPKCθ的膜转位水平。结果:SY5Y细胞经低氧刺激后,随刺激时间(0.5、2、4、6、8、12和24h)的延长,nPKCε在胞浆内的含量逐渐减少,而胞膜成分中的含量则明显增加,且于低氧刺激2h后的增高水平具有统计学显著意义(P<0.001);然而,nPKCθ在正常情况下只存在于胞膜成分内,且其含量不随低氧刺激时间的增加而改变(P>0.1)。结论:nPKCε可能参与了细胞低氧耐受的发生。     

鞘内注射治疗髓母细胞瘤研究进展

髓母细胞瘤是儿童原发中枢神经系统最常见的恶性肿瘤,约占儿童颅内肿瘤的20%。髓母细胞瘤主要累及小脑蚓部,具有很强的脑脊液播散倾向,目前仍以手术为主结合化疗及放疗的综合治疗为主要治疗方式。其原发部位及脑脊液播散特点,使得鞘内注射成为特殊治疗手段,但是患儿却要长期忍受此种方式给生理和心理造成的巨大影响,因而积极寻求既能靶向杀伤肿瘤细胞、毒副反应又小的新的辅助治疗手段更具临床意义。     

抑制血管细胞黏附分子-1表达对大鼠颈动脉内膜切除术后再狭窄的影响

Objective To evaluate the inhibitory effects of VCAM-1 siRNA on VCAM-1 protein expression and restenosis following carotid endarterectomy in rats. Methods Lentivirus-based VCAM-1 siRNA was constructed and its efficacy of blocking VCAM-1 protein expression in endothelial cells and carotids was identified by Western blot. Doppler ultrasonography and morphometric analysis were performed to measure the degree of restenosis. Results VCAM-1 siRNA decreased the protein expression of VCAM-1 in cultured endothelial cells and carotids. Treatment of VCAM-I siRNA showed a significant reduction in the restenosis and manifested as an increased blood velocity and linear diameter as compared with control siRNA (P < 0. 05) . Morphometric analysis showed that the ratio of intima to media area (I/M) increased significantly in CEA group (3.99 ± 0. 65) versus sham-operated group (0. 35 ± 0. 13) (P < 0. 05). Furthermore, VCAM-1 siRNA resulted in an evident decrease in the neointimal area (1.79 ± 0. 43) as compared with that of the control siRNA (4. 33 ± 0. 59) (P < 0. 05). Conclusion VCAM-1 plays an important role in pathogenesis of restenosis after carotid endarterectomy. VCAM-1 siRNA blocks VCAM-1 protein expression and alleviates the restenosis following carotid endarterectomy in rats.     

抑制血管细胞黏附分子-1表达对大鼠颈动脉内膜切除术后再狭窄的影响

目的 通过VCAM-1 siRNA(小分子干扰RNA)抑制血管细胞黏附分子(VCAM-1)的表达,观察对大鼠颈动脉内膜切除术(CEA)后再狭窄的影响.方法 构建VCAM-1特异性的siBNA并与慢病毒载体连接;在体外培养的大鼠血管内皮细胞中,应用蛋白印迹的方法 验证VCAM-1 siRNA抑制VCAM-1表达的有效性;大鼠颈动脉内膜切除后局部给予VCAM-1 siRNA,通过蛋白印迹方法 观察VCAM-1表达量变化,应用超声检测和形态学测定,分析术后再狭窄程度的变化.结果 VCAM-1siRNA可以降低VCAM-1蛋白在血管内皮细胞及颈动脉组织中的表达量(P<0.05);VCAM-1 siRNA可减轻再狭窄程度,增加术后管腔内径和局部血流速度,与对照siRNA相比差异有统计学意义(P<0.05);形态学测定分析血管内膜与中膜面积比(I/M),假手术、内膜切除(CEA)组分别为0..5±0.13、3.99±0.65.CEA后再狭窄明显,与假手术组间的差异有统计学意义(P<0.05);CEA联合对照siRNA及CEA联合VCAM-1 siRNA的I/M值分别为4.33±0.59、1.79±0.43,VCAM-1 siRNA可以明显减轻再狭窄的程度,两组间的差异有统计学意义(P<0.05).结论 VCAM-1参与颈动脉内膜切除术后再狭窄的发生,通过VCAM-1 siRNA抑制VCAM-1的表达可以防治再狭窄.     

缓释VEGF的可吸收性微管在TMR中的应用研究

目的 :观察血管内皮细胞生长因子结合缓释技术 ,促机械性TMR管道内血管生成的作用。方法 :利用机械钻在家兔左室前壁进行心肌钻孔 ,形成透室壁性心肌管道 ,实验组心肌管道内放入含VEGF及肝素的可吸收性多孔缓释微管 ;对照组放入不含VEGF及肝素的可吸收性多孔缓释微管。动物于术后8周处死 ,利用组织切片染色法 ,对照观察实验组和对照组TMR管道内血管生成状况。结果 :实验组TMR管道内血管生成的密度 /数量为 9.2 4± 0 .46条 /10× 4倍 ;对照组为 1.98± 0 .87条 /10× 4倍 ,两者具有非常显著性差异 ,P <0 .0 0 1。结论 :VEGF通过可吸收性多孔微管的缓释作用 ,对管道内血管的再生与重建具有非常明显的促进作用。     

抑制血管细胞黏附分子-1表达对大鼠颈动脉内膜切除术后再狭窄的影响

Objective To evaluate the inhibitory effects of VCAM-1 siRNA on VCAM-1 protein expression and restenosis following carotid endarterectomy in rats. Methods Lentivirus-based VCAM-1 siRNA was constructed and its efficacy of blocking VCAM-1 protein expression in endothelial cells and carotids was identified by Western blot. Doppler ultrasonography and morphometric analysis were performed to measure the degree of restenosis. Results VCAM-1 siRNA decreased the protein expression of VCAM-1 in cultured endothelial cells and carotids. Treatment of VCAM-I siRNA showed a significant reduction in the restenosis and manifested as an increased blood velocity and linear diameter as compared with control siRNA (P < 0. 05) . Morphometric analysis showed that the ratio of intima to media area (I/M) increased significantly in CEA group (3.99 ± 0. 65) versus sham-operated group (0. 35 ± 0. 13) (P < 0. 05). Furthermore, VCAM-1 siRNA resulted in an evident decrease in the neointimal area (1.79 ± 0. 43) as compared with that of the control siRNA (4. 33 ± 0. 59) (P < 0. 05). Conclusion VCAM-1 plays an important role in pathogenesis of restenosis after carotid endarterectomy. VCAM-1 siRNA blocks VCAM-1 protein expression and alleviates the restenosis following carotid endarterectomy in rats.     

外展神经鞘瘤一例

患者 男,59岁.因间断头痛,右侧耳鸣伴听力下降2年余,头痛加重1周入院.查体:右耳听力70 dB,吞咽及咳嗽反射稍差,饮水呛咳,余未见异常.头部CT示后颅窝等密度影,内听道未见明显扩大.头部MRI示桥前池囊实性占位病变,呈混杂信号影,增强后实性部分强化明显(图1a).考虑神经鞘瘤可能性大.入院后,全麻下行右侧枕下乙状窦后入路,术中见病变囊性部分含淡黄色囊液,实性部分呈灰红色,质软,血供中等,包膜完整;肿瘤与外展神经脑池段粘连紧密,Dorello管口处二者融为一体,镜下近全切除肿瘤,外展神经解剖保留.术后复查MRI示病变切除满意(图1b).术后右眼外展轻度受限.病理结果:神经鞘瘤.结合术中所见及术后病理明确诊断为外展神经鞘瘤.     

脊髓原发性Rosai-Dorfman病一例

Rosai—Doffman病（Rosai—Doffman disease,RDD）,即窦组织细胞增生性巨淋巴结病,是一种原发良性组织细胞增生性疾病,具有特殊的组织病理学特点。该病变通常累及淋巴结,临床表现为颈部无痛性淋巴结肿大,多伴有发热、     

幕下及椎管内肿瘤伴发软脑膜转移癌引发癫痫六例报告

癫痫一般由幕上病变引起,幕下及椎管内病变几乎不会发生癫痫,但是,幕下及椎管内肿瘤伴发软脑膜转移癌(leptomeningeal metastasis,LM)时,转移灶可散布于幕上,则有可能引起癫痫发作[1-3].我科2009年9月至201 1年12月收治5例小脑髓母细胞瘤和1例马尾原始神经外胚层肿瘤(primitiveneuroectodermal tumors,PNET),6例均伴有LM且发生癫痫,现报告如下.     

抑制血管细胞黏附分子-1表达对大鼠颈动脉内膜切除术后再狭窄的影响

Objective To evaluate the inhibitory effects of VCAM-1 siRNA on VCAM-1 protein expression and restenosis following carotid endarterectomy in rats. Methods Lentivirus-based VCAM-1 siRNA was constructed and its efficacy of blocking VCAM-1 protein expression in endothelial cells and carotids was identified by Western blot. Doppler ultrasonography and morphometric analysis were performed to measure the degree of restenosis. Results VCAM-1 siRNA decreased the protein expression of VCAM-1 in cultured endothelial cells and carotids. Treatment of VCAM-I siRNA showed a significant reduction in the restenosis and manifested as an increased blood velocity and linear diameter as compared with control siRNA (P < 0. 05) . Morphometric analysis showed that the ratio of intima to media area (I/M) increased significantly in CEA group (3.99 ± 0. 65) versus sham-operated group (0. 35 ± 0. 13) (P < 0. 05). Furthermore, VCAM-1 siRNA resulted in an evident decrease in the neointimal area (1.79 ± 0. 43) as compared with that of the control siRNA (4. 33 ± 0. 59) (P < 0. 05). Conclusion VCAM-1 plays an important role in pathogenesis of restenosis after carotid endarterectomy. VCAM-1 siRNA blocks VCAM-1 protein expression and alleviates the restenosis following carotid endarterectomy in rats.