神经导航下经岩骨幕上下联合入路中面神经管的解剖研究

OBJECTIVE: To study the value of neuronavigation in the transpetroal approach, and to provide anatomic data for the protection of the nerves in the facial nerve canal (FNC) during surgeries. METHODS: Simulated surgery through the transpetroal approach was performed on 16 sides of 8 adult cadaver heads with the assistance by neuronavigation. The anatomy of the facial nerve and the relationship of related structures were observed and the distances from the utmost external edge of the mastoid to different segments of the FNC were measured. RESULTS: Neuronavigation was successful with all the FNC, with the mean error of less than 0.9 mm. The FNC could be divided into 3 segments, the labyrinthine, the tympanic and the mastoid segments, stretching 3.6+/-1.2 mm, 11.2+/-2.5 mm and 16.1+/-3.6 mm respectively and with diameters of 1.2+/-0.3 mm, 1.4+/-0.1 mm and 1.7+/-0.2 mm, respectively. CONCLUSION: Neuronavigation may help protect the FNC during surgical procedures, and a thorough knowledge of the anatomic features of the FNC can be significant for preservation of the facial nerves.     

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.     

矢状缝早闭(舟状头)全颅成形术

目的探讨治疗矢状缝早闭(舟状头)畸形的手术方法。方法采用David“‖”形颅缝重建法(6例)、旋转骨瓣截骨法(2例)、梅花颅骨瓣头颅盖成型法(3例)等术式对舟状头进行矫治。结果11例患儿均治愈,外形满意。结论1~3个月舟状头宜采用简单的David“‖”形颅缝重建法进行治疗,3个月以上的患儿可选用浮动颅骨瓣头颅成型术、梅花瓣法颅骨瓣头颅盖成型术等方法进行治疗。     

血红素氧合酶-1与脑出血的继发性损害

自发性脑出血是指非外伤性脑实质出血,发病率高,死亡率高[1],且脑出血后患者多遗留不同程度的神经功能障碍。因此,探讨脑出血后脑组织损伤的病理生理机制对于改善脑出血病情及预后是十分必要的。大量研究表明自发性脑出血后造成的脑损伤存在多种机制[2]:早期血肿机械占位效应、     

基于实验均方误差F值的基因表达数据最佳聚类评判方法研究

目的 近年来产生了一些用于分析基因表达数据的聚类算法，却很少有关于评价聚类算法方法的研究。本研究的目的是尝试建立一个定量的评价基因表达数据聚类结果的方法。方法 本研究提供了一个系统的评价聚类结果的方法，利用我们提出的实验均方误差F值对几个常见的聚类算法进行比较。结果 利用F值对类质量的评价和利用已有的生物学知识对类进行分析的结果一致。结论 实验均方误差F值可以定量地评判用于基因表达数据的聚类算法。     

脑血管意外尿失禁的机制探讨

目的探讨脑血管意外引起尿失禁的可能机制。方法对42例诊断为脑血管意外伴有尿失禁的患者进行尿动力学检查(包括静止期尿道压测定、充盈期及排尿期膀胱尿道功能测定)并按Burney分类进行分析,同时研究病变部位、脑血管意外性质和病变半球侧与尿动力学的关系。结果42例脑血管意外患者中,表现为逼尿肌反射亢进者31例(73.8%):其中外括约肌无抑制性松弛19例(45.2%),逼尿肌-外括约肌不协调3例(7.1%),逼尿肌-外括约肌协调9例(21.4%);逼尿肌反射减低,外括约肌协调者11例(26.2%);无逼尿肌功能正常者。发生膀胱顺应性减低5例(11.9%),发生尿感缺失者11例(26.2%)。初感尿容量(140.00±46.97)ml;膀胱最大容量(293.20±60.71)ml;最大尿道闭合压(65.14±19.83)cmH2O。逼尿肌最大收缩力(Pdetmax)为(60.98±31.11)cmH2O;最大尿流率时逼尿肌压力(Pdet-Qmax)为(35.98±17.46)cmH2O;逼尿肌收缩时间(Tcon)为(86.07±36.09)sec;最大流量(Qmax)为(9.02±5.62)ml/s。中风后尿失禁患者其发病部位多见于基底节、皮层多灶以及额顶叶,脑出血与脑梗塞患者的尿动力学表现无明显差异,左右半球病变对尿动力学也无明显差异。结论脑血管意外后尿失禁的尿动力学异常主要为逼尿肌反射亢进,部分出现逼尿肌反射减弱,但感觉正常,感觉缺失者较少见;外括约肌功能以无抑制性松弛为主,其次为逼尿肌-外括约肌协调,少数出现不协调;较少出现膀胱顺应性降低。     

经直肠超声引导下经会阴125I粒子永久植入治疗前列腺癌的初步经验

目的探讨经直肠超声引导下经会阴125I粒子永久植入治疗前列腺癌的疗效和并发症。方法本组前列腺癌患者5例。年龄61￣83岁,平均70.4岁。临床分期T2bN0M0者2例,T3aN0M0者3例。Gleason评分6分者2例,7分者1例,8分者2例。术前前列腺特异性抗原(PSA)4.5￣17.5ng/ml。T3a期患者植入治疗前先行内分泌治疗。术前制定治疗计划,经直肠超声引导下经会阴125I粒子永久植入操作。术后观察PSA水平变化,连续3次PSA升高即为生化复发,观察术后尿路和直肠并发症发生情况。结果5例患者均术后恢复顺利。术后随访18个月,PSA均明显下降,PSA为0.1ng/ml者3例,0.01ng/ml者1例,0.04ng/m1者1例。5例患者术后均出现不同程度的尿路刺激症状,但6个月后逐渐好转。4例术后出现排便次数增多,术后3个月均好转。未发现尿失禁、直肠溃疡等并发症。结论经直肠超声引导下经会阴125I粒子永久植入治疗前列腺癌的疗效确切,创伤较小。     

微处理器控制的植入式心脏起搏器专用电路研制

介绍了一种基于微处理器的植入式心脏起搏器专用电路设计。该设计采用的技术路线和国外现有技术方案不同，它采用通用微处理器设计，降低了投资风险，缩短了开发周期．特别适合于我国这样的发展中国家。     

不同脑缺血和再灌流过程中大鼠脑组织NO含量的动态变化

采用线栓法制成大鼠大脑中动脉梗塞 ( MCAO)模型 ,依 Hb O2 - NO法测定持续性脑缺血和缺血 /再灌流脑组织内 NO含量的变化 ,以探讨不同脑缺血和再灌流过程中 NO的变化规律及其意义。结果 :缺血 3小时受损脑组织 NO水平即增高 ,再灌流后 NO逐步升高 ,而持续性缺血状态下 NO则表现降低后再升高的变化。虽然两组 NO在 7天时均有明显降低 ,但仍高于缺血前水平。认为持续性脑缺血和缺血 /再灌流情况下 NO的变化规律有所不同 ,与缺血脑组织的缺氧及产生 NO所需底物供应缺乏有关 ,且可能与脑组织的损害密切相关