Graves病骨生化标志的变化初探

目的 探讨Graves患者骨生化标志的改变。方法 对38例Graves患者进行血AKP、Ca、P、ICTP、DPD、BGP、U-HOP/Cr及BMD测定。结果 Graves组的BMD显著低于正常对照组(P<0.01),Ca、ICTP、DPD、BCP、U-HOP/Cr显著高于对照组,Graves组的BMD与ICTP和DPD,BGP有很好的相关性(r=0.36,r=0527、r=0.401)。结论 Graves组骨吸收增加,骨形成减少。     

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.     

老年人与青年人皮肤血流量比较研究

目的 判定增龄对皮肤血流量的影响。方法 用PIM2-LDPI检测皮肤血流量。结果 老年组前额、左手指背、命门穴部位皮肤血流量分别为:(1.94±0.86)V,(1.92±0.52)V和(0.71±0.19)V,与青年组比较差异无显著性。但是,老年男性在命门穴的皮肤血流量明显高于青年男性(P<0.05),老年女性前额的皮肤血流量明显降低(P<0.01)。男性比女性的皮肤血流量高。结论 皮肤血流量的差异无年龄相关性,男性组的皮肤血流量比女性组高。     

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、     

甲醛固定源同种异体骨移植材料的体外实验研究

OBJECTIVE: To conduct an in vitro study to assess the preliminary possibility of using formalin-fixed, instead of fresh, human bone tissues for allografting. METHODS: Fresh cadaveric bone tissues were fixed by formalin for more than 6 months and dissected into 5 mmx5 mmx5 mm pieces and 5 mmx5 mmx40 mm sticks, followed by chemical treatments to prepare the allograft bone materials. When alls treatments were completed, the bone grafts were centrifuged and their properties and cellular compatibility assessed in comparison with the currently used bone grafts clinically. RESULTS: The residual formaldehyde of the fixed allograft bone material was much below the controlled level and no significant differences were noted between the bone graft materials tested in regard to the chemical and mechanical properties and biocompatibility. CONCLUSION: This material we have prepared may meet the clinical demands for bone grafting, with good biocompatibility and less chance for infection by pathological agents.     

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。     

多效蛋白在大肠癌恶性化过程中的作用

目的了解多效蛋白在大肠癌中的表达情况 ,以及对大肠癌恶性化的影响。方法采用RT PCR和免疫组化染色 ,对 2 4例大肠癌组织和 19例大肠癌癌旁组织的多效蛋白mRNA表达情况进行分析。结果 2 4例大肠癌组织和 19例癌旁正常组织中表达多效蛋白mRNA的各有 18例。多效蛋白不但表达在肿瘤细胞 ,还表达在其他间质细胞中。大肠癌组织中多效蛋白的表达明显高于癌旁正常组织 (34%vs.9% ,P <0 0 5 )。 (94 % )大肠癌多效蛋白mRNA主要由内源性多效蛋白转录 ,且表达在肿瘤的 4个分期中 ,而人类内源性逆转录病毒 多效蛋白仅融合转录在Ⅲ、Ⅳ期肿瘤上 (31% )。结论多效蛋白尤其是人类内源性逆转录病毒 多效蛋白与大肠癌的恶性化有关。     

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。