目的 探讨显微血管减压术治疗三叉神经痛的效果,并分析导致面神经损伤的原因.方法 回顾性分析2013年10月至2017年12月贵州医科大学第三附属医院及哈尔滨医科大学第四附属医院神经外科收治的192例显微血管减压术治疗三叉神经痛患者的临床资料,手术实况录像回放,全部患者均采用枕下乙状窦后入路,显微血管减压术,术中游离责任血管,并以Teflon棉球隔离.结果 192例患者中,术后疼痛完全缓解173例,大部分缓解11例,延迟治愈5例,不缓解0例,面神经损伤3 例.对所有患者随访3 ~6 个月,三叉神经痛复发2 例,永久性面神经损伤1 例.结论 显微血管减压术治疗三叉神经痛效果可靠,术中避免导致面神经损伤的不当操作,可以完全或极大程度降低面神经损伤的可能.

目的 探讨夹闭基底动脉分叉部动脉瘤的可行性与手术入路的选择.方法 回顾性分析2007年1月至2010年6月哈尔滨医科大学第四附属医院神经外科收治的9例基底动脉分叉部动脉瘤患者的临床资料.三维数字减影全脑血管造影(3D-DSA)显示动脉瘤位于基底动脉分叉部,囊状,根据3D-DSA显示动脉瘤与后床突的位置关系及动脉瘤顶的指向,7例选择翼点入路,2例选择右侧颞下入路.结果 9例患者均成功夹闭,随访6个月.3例术前合并脑积水的患者中,2例缓解,1例行脑室腹腔分流术.3例动眼神经麻痹的患者中,1例痊愈,2例好转.9例患者中,3例行3D-DSA,6例行CTA复查,未见动脉瘤残留.格拉斯哥预后(GOS)评分5分7例,4分2例.结论 根据基底动脉分叉部动脉瘤瘤颈与后床突的位置关系及瘤顶的指向,选择合理的手术入路,手术夹闭是治疗基底动脉分叉部动脉瘤的一种良好方法.

Objective To evaluate the therapeutic outcome of microsurgery for dural arteriovenous fistulas (DAVF). Methods Clinical data of 6 patients with DAVF underwent microsurgery were analyzed retrospectively, including onset as subarachnoid hemorrhage in 2 patients, cerebral hemorrhage in 2, epilepsy in 1 and exophthalmos in 1. Results All the vascular malformations were resected, and the preoperative symptoms improved to different degree. DSA or CTA examinations were performed in all the patients 6 months after the operation. All the lesions were resected completely, and there was no recurrence or residue of vascular malformation. Six patients were followed up for mean period of 2.1 years, ranged from 1 to 5.5 years. However, there was no newly occurred cerebral hemorrhage or nervous dysfunction during the follow-up period, and the activities of daily living achieved gradeⅠ in 5 patients and gradeⅡ in 1. Conclusion Microsurgery is a safe and effective therapeutic method for DAVF.

Objective To explore the expression level and methylation status of SOX9 gene in human glioma,and find out the relationship between SOX9 and pathological grade of glioma.Methods Totally 113 glioma tissues and 34 normal brain tissues were collected.SOX9 expression was detected by RT-PCR method and methylation status was measured by PCR-MSP.The survival curve was analyzed by Kplan-Meier methods.Results The relative expression level of SOX9 mRNA was 0.203±0.097 and 0.496±0.213 in normal brain tissues and glioma tissue respectively,and significant difference was found between them (P ＜ 0.01).Survival curve showed that the survival time was obviously shorter in patients with high SOX9 gene expression than in those with low expression (P ＜0.01).The noumethylation rate ofSOX9 gene promoter region in glioma tissues were 11.1％ in grade Ⅰ,33.3％ in grade Ⅱ,53.8％ in grade Ⅲ,71.9％ in grade Ⅳ respectively.There was significant difference between high-grade (Ⅲ-Ⅳ) group and low-grade group (Ⅰ-Ⅱ) (P ＜ 0.01).Conclusions The expression ofSOX9 gene upregulate and methylation of SOX9 gene in the promoter region decrease in human glioma.The patient's survival time is closely correlated with expression level ofSOX9 gene.

SOX7 has been recently recognized as a tumor suppressor belonging to the SOX (SRY-related HMG-box) family of a transcription factor. However, its role in human gliomas is unknown. Our study showed that SOX7 expression was significantly downregulated in human gliomas. Statistical analysis showed that SOX7 suppression was associated with higher histological grades of tumors in glioma tissues. SOX7 could suppress tumor properties both in vivo and in vitro, and depletion of the HMG domain abolishes its tumor suppressive roles. In vitro assays demonstrated that SOX7 could downregulate Wnt/β-catenin transcription and decrease the expression of Cyclin D1 and c-Myc, while the mutant SOX7 lost these functions. These results suggested that the HMG-box is a key domain of SOX7 for negatively regulating the Wnt/β-catenin signaling pathway when functioning as a tumor suppressor in a glioma.

With secure and dependable antihypertensive effects, telmisartan is an antihypertensive drug. Telmisartan was reported showing distinct neuroprotective effect in cerebral IR injury but the underlying mechanisms are still unclear. The aim of this study was to evaluate the effect of telmisartan prevents cerebral ischemia-reperfusion (I/R) injury-mediated oxidative stress and inflammation in model rat to explore possible molecular mechanism. Male Sprague-Dawley (SD) rats were used to induce cerebral I/R injury using middle cerebral artery occlusion. 30 SD rats were randomly and evenly divided into 3 groups: Sham, I/R, telmisartan treated ischemia-reperfusion group. The results showed that telmisartan improved neurological impairments, inhibited apoptosis, resisted oxidative stress and inflammation in hippocampus of cerebral I/R injury rats. However, pretreatment with telmisartan inhibited the activation of adrenocorticotropic hormone (ACTH), vasopressin, catecholamine and natriuretic peptides activities in cerebral IR injury rat. These findings confirm the involvement of telmisartan prevents cerebral ischemia-reperfusion injury-mediated oxidative stress and inflammation in model rat.

As a phosphatase, SHP-2 has been identified to be involved in regulating several cell functions, including growth, division, adhesion and motility. Therefore, SHP‑2 may affect the response of glioma to radiotherapy, such as via enhancing angiogenesis. The present study aimed to investigate the function of SHP‑2, a protein tyrosine phosphatase, in the radiosensitivity of glioma. U251, U87 and SHG44 glioma cell lines were transfected with small interfering (si)RNA against SHP‑2 and cell proliferation was assessed using a cell counting kit 8 assay, cell apoptosis was assessed by fluorescence‑activated cell sorting and immunoblotting, cell invasion was determined by an invasion assay, and the vasculogenic mimicry capacity was assessed by a tube formation assay. SHP‑2 siRNA transfection reduced the proliferation and increased apoptosis in the glioma cell lines. Downregulation of SHP‑2 suppressed glioma cell invasion and vasculogenic mimicry. These results demonstrated that no significant difference was observed between glioma tissues and normal brain tissues, however, silencing of SHP‑2 inhibited cell proliferation, invasion and vasculogenic mimicry in the glioma cell lines. SHP‑2 may be a novel therapeutic target for glioma.

Glioma which has strong proliferation and angiogenesis ability is the most common and malignant primary tumor in central nervous system. Pituitary tumor transforming gene (PTTG) is found in pituitary tumor, and plays important role in cell proliferation, cell cycle, cell apoptosis, and angiogenesis. However, the role of PTTG in glioma is still incompletely investigated. Here, we explored the correlation between PTTG and glioma grade, as well as micro-vessel density (MVD). In addition, siRNA was used to silence PTTG expression in glioma cell lines including U87MG, U251, and SHG44. Cell proliferation, apoptosis, invasion, and angiogenesis were studied both in vitro and in vivo. Our results demonstrated that PTTG expression was significantly up-regulated in glioma, and had positive correlation with glioma grade and MVD. Silencing of PTTG inhibited glioma cell proliferation, migration/invasion, and angiogenesis, induced cell apoptosis, suppressed cell invasion, and arrested cell cycle at G0/G1 stage. Silencing of PTTG could also inhibit tumor growth, invasion, and angiogenesis in vivo. Our data indicated that PTTG might be a potential target for glioma treatment.

蛋白酪氨酸磷酸酶家族由130多种蛋白酪氨酸磷酸酶组成,它们和蛋白质酪氨酸激酶家族一起调控蛋白质中酪氨酸残基的磷酸化以及去磷酸化的动态平衡,它们的活性直接决定细胞内蛋白质的磷酸化水平的高低.SHP-2是蛋白酪氨酸磷酸酶家族的一员,在各种细胞和组织中均有广泛的表达,参与多个信号传导通路,介导细胞的生长、分化、迁移、粘附及凋亡等.SHP-2的表达异常会导致多种疾病的产生,但是相关综述较少,同时未见文献报道其在胶质瘤中的作用,因此本文简要介绍SHP-2的结构、功能、信号传导,并阐述了SHP-2与常见疾病的关系.

Glioma is the most common malignant tumor of neurosurgery, which morbidity accounting for 5% of systemic cancer, accounting for 70% of the tumors of children, and showed an increasing trend. High degree of malignant glioma grows rapidly, which has a very strong invasion of glioma.The 5-year survival rate is very low, because it is lack of effective cure. It is very difficult to deal the tumor with surgical resection and very vulnerable to relapse after a relatively poor prognosis, which have done great harm to human health and even life. With the development of molecular biology and biotechnology applications, it has become a new research direction of human cancer treatment to reveal the occurrence of glioma development mechanism and seek effective methods for gene therapy at the gene level. Reynolds and Richards have isolated cell populations from adult mouse striatum which can keep proliferating possessed with multiple differentiation potential and put forward concept of neural stem cells(neural stem cell, NSC). NSC have highly proliferation and self-renewal capacity and migration functions as well as the characteristics of a good fusion with normal brain tissue, which provides a good foundation for gene therapy for glioma.

目的:探讨伴有临床症状的鞍区颗粒细胞瘤(granular cell tumour,GCT)的病理组织学起源及其治疗方法.方法:回顾性分析我院收治的1例具有临床症状的GCT患者的治疗状况和病理结果,并结合近20年来关于GCT病理和治疗的相关文献报道,探讨GCT肿瘤病理组织起源和治疗要点.结果:该患者影像学报告怀疑鞍区炎性肉芽肿,给予抗生素治疗后复查MRI显示鞍区占位较前次无改变,增强MRI可见占位明显强化,诊断良性肿瘤,并采取翼点入路手术切除.术后病理证实为神经垂体颗粒细胞瘤.术后患者头痛缓解,尿量、尿比重、垂体内分泌激素等相关指标相继恢复至正常值.结论:GCT很可能起源于神经组织,伴有临床症状的GCT的治疗首选开颅手术,肿瘤残存的患者,术后不必放射治疗,定期复查即可.

Glioma is one of the most highly angiogenic tumors, and glioma stem cells (GSCs) are responsible for resistance to chemotherapy and radiotherapy, as well as recurrence after operation. Stathmin is substantial for mitosis and plays an important role in proliferation and migration of glioma-derived endothelial cells. However, the relationship between stathmin and GSCs is incompletely understood. Here we isolated GSCs from glioma cell lines U87MG and U251, and then used siRNA targeting stathmin for silencing. We showed that silencing of stathmin suppressed the proliferation, increased the apoptosis rate, and arrested the cell cycle at G2/M phase in GSCs. Silencing of stathmin in GSCs also resulted in inhibited the migration/invasion as well as the capability of vasculogenic mimicry. The susceptibility of GSCs to temozolomide was also enhanced by stathmin silencing. Our findings suggest stathmin as a potential target in GSCs for glioma treatment.

目的 评价显微血管减压术治疗偏头痛的疗效,探讨对顽固性偏头痛患者实施微血管减压术的可行性.方法 对实施显微血管减压术64例偏头痛患者的临床资料进行回顾性分析.结果对顽固性偏头痛患者实行显微血管减压术治愈率为85%,总有效率为97%以上.结论 显微血管减压术以其微小的损伤,良好的疗效成为顽固性偏头痛患者首选治疗方法.

The purpose of this study was to investigate the functions of microRNA-9, which is a tissue-specific microRNA in central nervous system, in the vasculogenic mimicry (VM) of glioma cell lines in vitro and in vivo. Glioma cell lines U87MG, U251 and SHG44 were transfected with microRNA-9 mimic, microRNA-9 inhibitor or scramble sequences. The amount of microRNA-9 and Stathmin (STMN1) mRNA was determined by quantitative real-time PCR, and the protein expression of STMN1 was determined by western blot. Cell proliferation and apoptosis were assessed. The interactions between the 3'UTR of STMN1 and miR-9 was determined by luciferase reporter assay. The VM capacity in vitro was evaluated using VM formation assay, and the rescue experiment of STMN1 was carried out in U251 cells. The in vivo experiment was applied with animal models implanted with U87MG cells.MicroRNA-9 mimic transfection reduced proliferation and increased apoptosis in glioma cell lines (p < 0.05). MicroRNA-9 mimic up-regulated STMN1 mRNA levels but reduced its protein levels (p < 0.05), and luciferase activity of STMN1 was suppressed by microRNA-9 mimic transfection (p < 0.05). Furthermore, microRNA-9 mimic transfection suppressed tumor volume growth, as well as VM both in vitro and in vivo. The cell viability and microtube density were upregulated in U251 cells after STMN1 up-regulation (p < 0.05). STMN1 is a target of microRNA-9, and microRNA-9 could modulate cell proliferation, VM and tumor volume growth through controlling STMN1 expression. MicroRNA-9 and its targets may represent a novel panel of molecules for the development of glioma treatment.

<正>脑出血(intracerebral hemorrhage,ICH)是指非外伤性脑实质内出血,约占所有卒中的15%～20%,是一种常见病、多发病,目前仍缺乏有效的治疗手段[1-2]。为了减轻ICH后二次损伤对患者预后的影响,其形成机制已成为研究热点。目前研究表

目的 探讨天幕裂孔侧方手术中滑车神经保护的方法及可行性.方法 回顾性分析经天幕裂孔侧方手术导致滑车神经损伤的9例患者的临床资料,寻找天幕裂孔侧方手术中损伤滑车神经的原因,并尝试寻找可行的预防措施.结果 9例患者中有4例在随访半年后症状完全消失,5例没有好转,1例失访,5例完全损伤患者中,4例通过有目的 预防损伤,可避免永久性损伤.结论 滑车神经极细且在小脑幕侧方行程又长,天幕裂孔侧方手术时极易损伤,但术中采用综合的预防措施,可大大降低损伤的可能.

Objective To investigate the extent of tumor resection,choice of surgical approach and application of the radiotherapy for petroclival meningiomas.Methods Clinical data of 51 patients with petroclival meningiomas were analyzed retrospectively.The surgical approach was chosen according to the size,location and extension of the tumor and the condition of patients,including subtemporal transtentorial approach in 31 patients,presigmoid approach in 3 and suboccipital-retrosigmoid approach in 17.Results The tumor resection with Simpson grade Ⅰ or Ⅱ was achieved in 40 patients,Simpson grade Ⅲ section in 9 and Simpson grade Ⅳ section in 2.The patients with Simpson grade Ⅲ or Ⅳ resection were underwent radiotherapy after the operation.The complications occurred after the operation,including coma in 8 patients,facial nerve palsy in 7,limb muscle strength decline in 11,oculomotor nerve palsy in 15,abducent nerve palsy in 5 and intracranial infection in 3.One patient died after the operation.Fifty patients were followed up for 6 to 18 months,most preoperative symptoms and postoperative complications were improved to different degree,and no tumor recurrence or residual tumor progression was seen during the follow-up period.Conclusions Total tumor removal is a radical treatment for petroclival meningiomas,however,it usually leads to serious complications.The individualized surgical approach should be chosen for each patient according to the comprehensive situation of patients before the operation.Simpson grade Ⅲ to Ⅳ resection can improve the quality-of-life for patients,and postoperative radiotherapy can control the residual tumor growth and effectively reduce the tumor recurrence.

Objective: To investigate the influence of Stathmin gene silencing on the invasion of glioma-derived microvascular endothelial cells(GDMEC). Methods: Microvascular endothelial cells were isolated from 22 cases of human high grade gliomas, and purified by magnetic beads coated with anti-CD105 antibody(including 8 WHO Ⅲ glioma, 14 WHO Ⅳ glioma, 13 male, 9 female). Stathmin expression was silenced by application of specific siRNA in the high grade GDMEC. The migration of GDMEC were investigated by Transwell. Results: Stathmin gene silencing by RNAi significantly decreased the mRNA and protein expression of Stathmin in the microvascular endothelial cells of high grade GDMEC of glioma(P0.01), moreover, lowered the count of migrated microvascular endothelial cells(P0.01). Conclusion: Stathmin gene silencing by RNAi could inhibit the migration of microvascular endothelial cells of high grade GDMEC of glioma.

Objective To investigate the relationship between the expression of connective tissue growth factor(CTGF) and aggressive of human pituitary adenom,that provides the theoretical basis for the biological treatment of pituitary adenoma. Methods Quantitative real time PCR( qRT-PCR) and Western blot were used to detecte the expression of CTGF in 16 cases of non-invasive pituitary adenoma and 52 cases of invasive pituitary adenoma(IPA) . Results CTGF expression was found in all cases of invasive pituitary adenomas and noninvasive pituitary adenomas. The expression of CTGF in invasive pituitary adenoma was higher than that of in noninvasive pituitary adenoma(P=0. 01) . Conclusions The expression of CTGF in invasive pituitary adenoma is significantly higher than that of in the noninvasive pituitary adenoma and related with the size of pituitary adenoma.