目的 总结重型颅脑损伤并发交感神经功能亢进(PSH)的治疗经验.方法 回顾性分析2015年1月至2019年12月收治的78例重型颅脑损伤并发PSH的临床资料.结果 出院时,恢复良好39例,植物生存10例,阵发性出汗6例,阵发性血压增高5例,阵发性皮肤潮红3例;死亡15例(19.2％).存活63例随访3个月,与出院时无明显变化.结论 PSH为重型颅脑损伤常见的并发症,脑损伤越重,发生PSH的可能性越大;并发PSH病人预后较差.早期诊断,及时根据临床类型进行积极的针对性治疗,可有效降低病人的致残率和病死率.

目的 探讨胼周动脉动脉瘤(PAA)治疗方法及临床疗效.方法 回顾性分析2012年6月至2020年3月收治的42例PAA的临床资料.25例采用夹闭术治疗,17例行血管内栓塞治疗.结果 所有动脉瘤均成功完成夹闭或栓塞,夹闭术后并发症发生率为(48.0％,12/25),栓塞术后并发症发生率(17.6％,3/17).42例术后临床随访3～12个月,中位数6个月;夹闭术治疗25例末次随访改良Rankin量表(mRS)评分0～2分17例,3～6分8例;预后良好率为68.0％(17/25);栓塞治疗的17例末次随访mRS评分0～2分14例,3～6分3例;预后良好率为82.4％(14/17).42例术后影像随访4～21个月,中位数9个月;夹闭术后复发率为12.0％(3/25),栓塞术后复发率为5.9％(1/17).结论 夹闭术与血管内栓塞是治疗破裂PAA的有效方法,临床上需结合病人具体情况选择个体化的治疗方式以提高治疗效果.

目的 探讨矢状窦旁脑膜瘤术后脑出血及脑水肿形成原因及治疗.方法 回顾性分析12例矢状窦旁脑膜瘤术后并发脑出血及脑水肿的临床资料.结果 9例术后复查CT示脑水肿,加强脱水利尿治疗后好转;2例术后复查CT示瘤腔内少量出血伴重度脑水肿,激素治疗并加强脱水治疗后好转;1例术后复查CT示脑内血肿伴中线结构移位,开颅血肿清除术治疗,术后有轻偏瘫及癫痫,经功能锻炼后肌力在Ⅲ～Ⅳ级.结论 术中静脉损伤可能是矢状窦旁脑膜瘤术后脑出血及脑水肿的主要原因之一,术前充分影像学评估、术中按临床分型充分保护静脉、术后规范化管理,可降低术后脑出血和脑水肿发生率.

目的 探讨前交通动脉动脉瘤夹闭术后并发中枢性尿崩症(CDI)的危险因素.方法 回顾性分析2009年1月～2018年1月显微夹闭术治疗的154例前交通动脉动脉瘤的临床资料;采用多因素logistic回归分析法筛选术后并发CDI的危险因素.结果 154例中,术后并发CDI 13例(8.4％).多因素logistic回归分析结果显示术中动脉瘤破裂是术后并发CDI的独立危险因素(OR=15.642;95％CI 1.035～236.447;P=0.047].结论 前交通动脉动脉瘤夹闭术中,如果发生动脉瘤破裂,临床应注意防治CDI.

Objective To explore the application of spiral CT angiography and three- dimensional reconstruction( 3D-CTA) in the microsurgery of tumors in deep brain. Methods The clinical data of 27 patients with tumors in deep brain,treated by microsurgery assisted with 3D- CTA,were analyzed retrospectively to evaluate the preoperative 3D reconstruction effect and the effect after operation. Results The preoperative 3D images of all tumors can clearly demonstrate the site,size,shape and adjacent vessels and bone,which were in accord with the facts observed during the operation. In the 27 cases,23 patients achieved gross total resection,3 patients achieved subtotal resection and 1 patients achieved partial resection; After the operation,25 patients relieved or remain the same,while 2 patients became worsen. No dead case occurred. 22 cases were good during the follow up 1 month after the operation. Conclusion 3D-CTA can provide 3D images of tumor and adjacent vessels and the skull, which can also be subject to adjustment, measurement and Simulation of operation approach. It provides a visual basis for individual treatment of the tumors in deep brain to choose the best operation approach and reduce the intraoperative risk.

目的:构建含人类疱疹病毒6A亚型DR7基因的慢病毒,研究DR7基因表达对神经胶质瘤细胞U87增殖、迁移、侵袭能力的影响。方法:PCR扩增DR7基因,克隆至慢病毒载体pLenti6.3-MCS-IRES2-EGFP,构建pLenti6.3-DR7-IRES2-EGFP重组慢病毒载体,经293T细胞包装重组病毒转染至神经胶质瘤细胞U87,经blasticidin筛选建立稳定表达株,通过细胞增殖实验、细胞周期实验、细胞划痕及Transwell实验研究稳定表达DR7基因对U87细胞的增殖、迁移及侵袭能力的影响。结果:成功构建了pLenti6.3-DR7-6×His-IRES2-EGFP慢病毒表达载体,筛选了稳定表达DR7基因的U87-DR7-EGFP细胞株,CCK-8细胞增殖实验显示,稳定表达DR7基因的U87-DR7-EGFP细胞与阴性对照细胞U87-NC-EGFP、U87细胞相比,细胞增殖活性明显增高,差异具有统计学意义（P＜0.001）。细胞周期检测发现U87-DR7-EGFP细胞S、G2/M期细胞所占比例多于U87-NC-EGFP、U87细胞:S期的比例分别为（34.73±1.12）%、（24.89±0.93）%、（25.39±0.96）%,差异具有统计学意义（P＜0.001）;G2/M期分别为（17.35±1.61）%、（11.36±1.50）%、（13.17±1.95）%,差异具有统计学意义（P＜0.05）。细胞划痕实验表明,U87-DR7-EGFP细胞愈合能力明显强于U87-NC-EGFP、U87细胞,划痕6 h愈合率分别为:（33.55±2.83）%、（23.50±3.18）%、（22.03±1.47）%,差异具有统计学意义（P＜0.01）;划痕12 h愈合率分别为（70.50±5.39）%、（53.60±4.67）%、（55.09±2.83）%,差异具有统计学意义（P＜0.001）。Transwell实验表明,U87-DR7-EGFP细胞的穿膜数量明显多于U87-NC-EGFP、U87细胞,分别为:（543.00±22.94）、（387.00±15.63）、（412.00±20.30）个,差异具有统计学意义（P＜0.001）。结论:人类疱疹病毒6A亚型DR7基因表达能在体外促进人神经胶质瘤细胞U87增殖、迁移及侵袭,提示其在神经胶质瘤的发生和发展中可能起一定作用。

Objective To discuss the reasonable preoperative risk assessment,clinical classification and surgical approaches for the petroclival tumors.Methods The clinical data of 62 patients with petroclival tumors treated by microsurgery were analyzed retrospectively.On the basis of the imaging characteristics and clinical features,62 cases with petroclival tumors were classified,preoperatively evaluated in terms of the risk for surgery.The outcomes of different surgical approaches for pertroclival tumors were compared.Results Gross total resection was achieved in 38(61%) cases,of whom 3 cases were via extended pterional approach,8 cases via subtemporal transtentorial approach,6 cases via transpetrosal presigmoid approach and 21 cases via retrosigmoid approach.The new cranial nerve deficits occurred in 26(42%) patients after operation.No dead case occurred.Conclusion Surgical approaches should be chosen according to the preoperative risk assessment and classification of the tumors.Relatively simple and minimally invasive surgical approaches such as presigmoid approach or subtemporal transtentorial approach should be chosen for those with high risk in the preoperative risk assessment.

Objective To study the clinical characteristics of tumors at the place between pons and oblongata,the methods of microsurgical treatment,and treatment for complications of microsurgery.Methods The 23 patients undergoing surgical treatment of tumors originated from pons and medullary were reviewed retrospectively.Preoperative clinical presentation and lesion characteristics,adopted surgical approach and complications were analyzed.Results All cases in this group were accepted microsurgical treatment.Numbers of total resection,subtotal resection,and partial resection of tumors were 15,4 and 4,respectively.Cases of glioma,cavernous malformation,hemangioblastoma,and lymphoma were 15,3,4 and 1,respectively.Perioperative complications of worsening original symptoms,new neurological symptoms,intracranial infection,and neurogenic pulmonary edema and bulbar paralysis occupied 6,4,1,1,respectively.There was no death in perioperative.Conclusions There are many kinds of tumors at the place between pons and oblongata,and many patients had severe perioperative complications.Appropriate surgical indications and approaches,microsurgical operation,the prevention and treatment to the postoperative complications,contribute to improve the treatment effect of tumors at the place of pons and oblongata.

Glioblastoma is one of the most malignant brain tumors. Current treatments for glioblastoma usually make poor responses, and novel treatment strategies are extremely imperative. Cytochalasin E was reported to inhibit angiogenesis and tumor growth in some studies, but its effects on gliomas are still unknown. In this study, we found cytochalasin E inhibits U87 human glioblastoma cell growth in a very low concentration range of 10(-8) to 10(-6) M in a time and concentration dependent manner, and the IC50 were 1.17 +/- 032 x 10(-7) M for 48 h treatment, 6.65 +/- 1.12 x 10(-8) M for 72 h and 3.78 +/- 130 x 10(-8) M for 96 h. We also found cytochalasin E induces cell-cycle G2/M phase arrest (72 h-treatment of 10(-6) M cytochalasin E caused 56.2 +/- 6.1% cells arrest in G2/M phase) and cell apoptosis (96 h-treatment of 10(-6) M cytochalasin E induced 24.1 +/- 4.2% cells apoptosis). Thus, cytochalasin E is proposed as a potential agent for glioblastoma chemotherapy.

To examine the effects of anisomycin on glioma cells and the related mechanisms in vitro. The U251 and U87 human glioblastoma cell lines were tested. The growth of the cells was analyzed using a CCK-8 cell viability assay. Apoptosis was detected using a flow cytometry assay. The expression of proteins and phosphorylated kinases was detected using Western blotting. Treatment of U251 and U87 cells with anisomycin (0.01–8 μmol/L) inhibited the cell growth in time- and concentration-dependent manners (the IC50 values at 48 h were 0.233±0.021 and 0.192±0.018 μmol/L, respectively). Anisomycin (4 μmol/L) caused 21.5%±2.2% and 25.3%±3.1% of apoptosis proportion, respectively, in U251 and U87 cells. In the two cell lines, anisomycin (4 μmol/L) activated p38 MAPK and JNK, and inactivated ERK1/2. However, neither the p38 MAPK inhibitor SB203580 (10 μmol/L) nor the JNK inhibitor SP600125 (10 μmol/L) prevented anisomycin-induced cell death. On the other hand, anisomycin (4 μmol/L) reduced the level of PP2A/C subunit (catalytic subunit) in a time-dependent manner in the two cell lines. Treatment of the two cell lines with the PP2A inhibitor okadaic acid (100 nmol/L) caused marked cell death. Anisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit. The regulation of PP2A/C exression by anisomycin provides a clue to further study on its role in glioma therapy.

Although sEH inhibitors are well studied in inflammatory and cardiovascular diseases, their effects on gliomas are unclear. In this study, we investigated the effects of t-AUCB, a more potent and selective sEH inhibitor, on U251 and U87 human glioblastoma cell lines and the HepG2 human hepatocellular carcinoma cell line. Our results showed that t-AUCB efficiently inhibited sEH activities in all three cell lines (the inhibition rate was more than 80% in each) and suppressed U251 and U87 cell growth in a dose-dependent manner, but exhibited no cell growth inhibition on HepG2. We detected high levels of phosphorylated NF-κB-p65 (Ser536) in t-AUCB-treated U251 and U87 cells, and then found that the NF-κB inhibitor PDTC can completely abolish t-AUCB-induced growth inhibition. This indicated that t-AUCB suppresses U251 and U87 cell growth by activating NF-κB-p65. Moreover, we found that t-AUCB induces cell-cycle G0/G1 phase arrest by regulating Cyclin D1 mRNA and protein levels and CDC2 (Thr161) phosphorylation level. We propose to further test this promising reagent for its anti-glioma activity in clinical relevant orthotopic brain glioma models.

SP600125 is a well studied inhibitor of c-Jun N-terminal kinase (JNK). Its direct biochemical effects on JNK-inactive tumor cells are usually ignored. In this study, we investigated the effects of SP600125 on JNK-inactive U251 human glioblastoma cells. Our results demonstrate that, 20 microM or more SP600125 can induce significant cell growth inhibition and cell-cycle G2/M phase arrest in U251 cells. Interestingly, we also found that SP600125 can stop the duplicated chromosomes from separating into two cells and the karyokinesis progression. Our study opened up a new perspective for further studies involved in JNK inhibitors or anti-glioma therapy.

Objective To investigate the effect of midazolam and fentanyl on etomidate-induced myoclonus. Methods A total of 128 patients scheduled for surgery under genaral anesthesia were randomly divided into 5 groups according to the different sequence and dose of anesthetics during anesthesia induction. Midazolam 0. 05 mg/kg, etomidate 0. 25 mg/kg and fentanyl 3μg/kg was used in group Ⅰ, fentanyl 3 μg/kg, etomidate 0. 25 mg/kg, midazolam 0.05 rng/kg in group H,midazoIam 0. 05 mg/kg, fentanyl 3 μg/kg, etomidate 0. 25 mg/kg in group Ⅲ, midazolam 0. 08 mg/kg, etomidate 0. 25 mg/kg, fentanyl 3 μg/kg in group Ⅳ, etomidate 0. 25 mg/kg, midazolam 0. 05 mg/kg, fentanyl 3 μg/kg in group Ⅴ as the control After the injection of etomidate, the scales and positive incidences of myoclonus were observed within 2 minutes. Results The positive incidences of myoclonus were 68. 18% in group Ⅰ, 41.67% in group Ⅱ, 21.88% in group Ⅲ, 21.74% in group Ⅳ, and 59. 26% in group Ⅴ, respectively. Compared with group Ⅴ, groups of Ⅲ and Ⅳ had lower positive incidences and scales (P < 0. 05), whereas groups of Ⅰ and Ⅱ had no statistical changes in positive incidences and scales. Conclusion Using midazolarn, fentanyl, and etomidate consequently may reduce the occurrence of etornidate-induced myoclonus during anesthesia induction.