白细胞介素-6与脑胶质瘤关系的研究

目的:通过观察人脑胶质瘤细胞是否可以自发分泌白细胞介素-6(interleukin-6,IL-6),为进一步探讨IL-6在脑胶质瘤发生、发展中的可能作用提供线索。方法:对4例脑胶质瘤病人的手术标本进行原代细胞培养,分不同时相收获上清,并对其上清进行IL-6活性检测。结果:各组上清中均有IL-6活性,IL-6生物活性以D_(0～6)上清活性最高(1.131U/L),D_(0～6)上清活性最低(0.18U/L)。人脑胶质瘤细胞受细菌脂多糖刺激后,分泌IL-6的能力略有增强。IL-6单克隆抗体可中和脑胶质瘤上清对B9.9细胞的增殖作用。结论:原代培养的人脑胶质瘤细胞可自发分泌IL-6。     

神经导航下颅内病变活检术

我科自2002年9月至2005年6月在神经导航引导下对17例颅内病变性质不明确的患者进行了活检术,取得了满意的效果,现报告如下.     

经翼点入路显微切除侧裂区胶质瘤18例分析

目前，手术是治疗脑胶质瘤首选且有效的方法。侧裂区胶质瘤周围血管丰富，肿瘤被额颞叶覆盖，切除难度较大，而术后并发症较多，2001～2004年我们共收治侧裂区胶质瘤18例，均经翼点入路行显微手术切除术，术后效果满意。现报告如下。     

微创疗法治疗脑室出血108例临床观察

2000年3月～2006年6月,我们采用微创疗法治疗脑室出血108例,效果较好.现报告如下. 临床资料:本组男63例,女45例.年龄18～82岁,平均51.5岁.均经颅CT证实为脑室出血铸型.     

人脑胶质瘤CXCL12基因的甲基化分析研究

Objective To detect the methylation status of CXCL12 gene and the mRNA expression of CXCL12, CXCR4 and DNA methyhransferases (DNMTs) in glioma, and to analyze the methylation regulation and mechanism of CXCL12/CXCR4 signaling axis in the malignant progress of glioma. Methods The mRNA expression of CXCL12, CXCR4, DNMT1, DNMT3A and DNMT3B was detected by the semi - quantitative RT - PCR and real - time PCR in 76 gliomas and 10 normal brain tissues. The methylation status of CXCL12 in glioma was also studied by the methylation specific PCR. Results ( 1 ) The mRNA expression of CXCR4 in glioma increased with WHO grades. (2) Methylation of CXCL12 was detected in 34. 2% ( 26/76 ) of gliomas, but the methylation rate decreased with WHO grades. ( 3 ) Epigenetic inactivation of CXCL12 mainly happened in low- grade gliomas, and the CXCL12 mRNA levels were closely related to its methylation status. (4) The expression levels of these three DNMT genes were significantly higher in the CXCL12 - methylated gliomas than in the CXCL12 - unmethylated ones. Conclusion The CXCR4 gene may be a marker of aggressive biological behavior of glioma. The CXCL12 promoter hypermethylation is detected mainly in low - grade gliomas. And the methylaiton of CXCL12 gene cause the down - regulation of its mRNA levels in low - grade gliomas. The high expressions of DNMT1、DNMT3A and DNMT3B may be the potential mechanism of CXCL12 methylation.     

高浓度谷氨酸对原代培养人脑胶质瘤细胞生长抑制和凋亡的影响

目的探讨高浓度谷氨酸对人脑胶质瘤原代培养细胞的生长抑制和凋亡诱导作用。方法在体外对新鲜的人脑胶质瘤标本进行原代培养；不同浓度的谷氨酸作用不同时间后，进行形态学观察噻唑蓝（MTT）法检测生长抑制率；流式细胞仪Armexin V-FITC／PI双染法检测凋亡率。结果原代人脑胶质瘤细胞短期培养成功。高浓度谷氨酸对培养细胞有明显的抑制作用，并且存在一定的剂量依赖关系。当谷氨酸的浓度为25～50mmol／L时，可明显诱导培养细胞凋亡，并且凋亡率随药物浓度增加和时间延长而增高；当谷氨酸浓度达100mmol／L以上时，细胞则主要以坏死为主。结论以酶消化法可成功对人脑胶质瘤细胞进行体外原代培养；在一定的浓度范围内，高浓度谷氨酸能明显的抑制原代培养人脑胶质瘤细胞生长，并诱导其凋亡。     

人胶质细胞源性神经营养因子在肌萎缩性脊髓侧索硬化症小鼠模型基因治疗中的作用

目的 探讨人胶质细胞源性神经营养因子(GDNF)基因治疗在肌萎缩性脊髓侧索硬化症(ALS)中的作用。方法 ALS小鼠随机分成AdCMVlacz对照组和AdCMVgdnf治疗组各12只。第9周肌肉注射AdCMVgdnf或AdCMVlacz病毒。第10周测试运动能力,并记录发病时间和生存时间。利用ELISA和免疫组织化学检测骨骼肌肉和脊髓中GDNF的表达,对脊髓运动神经元细胞数目和腓肠肌质量变化进行定量分析。结果 ① AdCMVgdnf治疗组ALS小鼠注射部位肌肉中GDNF水平为(6589.0±325.0)pg/mg,而对照组为（75.3±18.9） pg/mg,治疗组高于对照组近100倍（P＜0.01）。② 对照组的腓肠肌质量为（88.6±14.5)mg,治疗组为（174.9±18.7）mg,差异有统计学意义（P＜0.01）。③ 治疗组脊髓运动神经元细胞中GDNF较对照组明显增加,并且神经元细胞数目也明显增加（P＜0.01）。④与对照组的发病时间（96.2±5.8）d比较,治疗组为（123.0±6.9 ）d,差异有统计学意义（P＜0.01）。与对照组生存期(127.3±4.6) d比较,治疗组为（155.2±4.1） d,差异有统计学意义（P＜0.01）。结论 AdCMVgdnf基因治疗对ALS小鼠脊髓运动神经元有保护作用,缓解肌肉萎缩,改善神经运动功能,延缓疾病的发生和延长生存期。     

颅内肿瘤危险因素的病例对照研究

目的  探讨颅内肿瘤的危险因素和保护因素。方法  采用成组设计病例对照研究方法,对264例原发性颅内肿瘤患者和273例对照进行问卷调查,应用非条件Logistic回归模型推断暴露因素与颅内肿瘤的关系。结果  单因素和多因素Logistic回归分析结果表明,源于配偶的被动吸烟、源于同事的被动吸烟、职业性接触汽（柴）油和经常接触农药可增加患颅内肿瘤的危险性,其OR值及95%CI分别为1.777(1.103,2.861)、1.911(1.095,3.334)、4.298(1.008,18.314)和1.728(1.000,3.049)。饮酒和啤酒酒精摄入量＜9mL/d可降低患颅内肿瘤的危险性,其OR值及95%CI分别为0.297(0.108,0.821)和0.216(0.046,1.024)。结论  颅内肿瘤的危险因素为源于配偶及同事的被动吸烟、职业性接触汽（柴）油和经常接触农药;保护因素为饮酒和啤酒酒精摄入量＜9mL/d。     

鼻窦内窥镜下激光切除听神经鞘瘤并保留面神经1例报告

我院于1996—03—07在鼻窦内窥镜下激光切除1例听神经鞘瘤并完全保留面神经,取得满意效果,现报告如下.1 病例报告病人男性,23岁.因左眼闭合不紧、口角歪斜6年,左耳听力下降伴行走不稳2月余于1996—02—26入院.神经系统检查:神志清楚,左眼球水平震颤,左面部浅感觉减退,左眼裂大于右眼裂,左鼻唇沟浅,露齿偏右.左耳听力下降.饮水呛咳.左侧肢体肌力Ⅳ级,左侧共济运动差,闭目难立征( ),左侧巴彬斯基征( ).CT扫描显示:左侧     

人脑胶质瘤CXCL12基因的甲基化分析研究

Objective To detect the methylation status of CXCL12 gene and the mRNA expression of CXCL12, CXCR4 and DNA methyhransferases (DNMTs) in glioma, and to analyze the methylation regulation and mechanism of CXCL12/CXCR4 signaling axis in the malignant progress of glioma. Methods The mRNA expression of CXCL12, CXCR4, DNMT1, DNMT3A and DNMT3B was detected by the semi - quantitative RT - PCR and real - time PCR in 76 gliomas and 10 normal brain tissues. The methylation status of CXCL12 in glioma was also studied by the methylation specific PCR. Results ( 1 ) The mRNA expression of CXCR4 in glioma increased with WHO grades. (2) Methylation of CXCL12 was detected in 34. 2% ( 26/76 ) of gliomas, but the methylation rate decreased with WHO grades. ( 3 ) Epigenetic inactivation of CXCL12 mainly happened in low- grade gliomas, and the CXCL12 mRNA levels were closely related to its methylation status. (4) The expression levels of these three DNMT genes were significantly higher in the CXCL12 - methylated gliomas than in the CXCL12 - unmethylated ones. Conclusion The CXCR4 gene may be a marker of aggressive biological behavior of glioma. The CXCL12 promoter hypermethylation is detected mainly in low - grade gliomas. And the methylaiton of CXCL12 gene cause the down - regulation of its mRNA levels in low - grade gliomas. The high expressions of DNMT1、DNMT3A and DNMT3B may be the potential mechanism of CXCL12 methylation.