唇腭裂患者上颌骨牵引成骨术后发音方式的变化

目的:通过对行颅外支架式上颌骨牵引成骨术(rigidexternaldistraction,RED)唇腭裂患者治疗前后的错误发音数量变化、不同发音部位、不同发音方法以及不同类型错误发音发生特点及其变化评价,分析上颌骨RED对患者发音方式的影响。方法:1999年至2001年行上颌骨RED的唇腭裂术后上颌发育不足患者21例,其中男性13例,女性8例,平均年龄15.05岁。所有患者RED前后进行语音测听并分类。治疗前后错误发音的差异性用非参数检验。结果:RED术后42.9%患者错误发音数较RED前增加,19.0%减少,38.1%无变化。从发音部位,舌尖前音错误发音发生率最高,其次为舌面音。从发音方法,错误发音多发于塞擦音。错误发音类型以咽喉摩擦/爆破音为主,其次为腭化构音和声门爆破音。上颌骨RED后腭化构音累及音节数减少,但咽喉摩擦/爆破音和声门爆破音反而增加,尤其是咽喉摩擦/爆破音。结论:唇腭裂患者经RED前移上颌骨后,会对患者发音方式产生影响,在行语音治疗前需考虑全面。     

骨髓输液在PICU的应用探讨

目的　探讨骨髓输液在PICU的适应证、方法及临床效果。方法　选择PICU危重症建立静脉通道困难患儿 30例 ,采用 7号骨穿针或 7～ 9号头皮针于胫骨粗隆下 1～ 2cm穿刺、固定 ,接入医嘱液体 ,记录穿刺所需时间、入液速度及生命体征变化、并发症等。结果　 2 8例 1次成功 ,2例用头皮针者有堵塞 ,换针后重新穿刺成功 ,穿刺、固定到接入液体平均时间 (30± 10 )s。速率 :一般压力 (8± 3)ml (kg体重·h) ,加压下 (17± 6 )ml (kg体重·h) ,所有病例均达到了医嘱要求。骨髓输液持续时间 3～ 2 2h ,无 1例出现并发症。结论　骨髓输液在PICU危重症抢救中可迅速建立液体通道 ,争取抢救时间。头皮针比骨髓穿刺针易于固定 ,使用更方便     

胫骨平台骨折合并内侧副韧带损伤的诊治体会

[目的]探讨胫骨平台骨折伴膝内侧副韧带损伤的诊断及治疗方法。[方法]回顾性分析本院1996年1月~2005年12月期间收治的52例胫骨平台骨折合并重度内侧副韧带损伤病例,并对有随访的49例(保守治疗21例,手术治疗28例)进行分析。[结果]随访10个月~9年(平均1.7年),按照Schatzker分型:Ⅱ型39例,Ⅲ型6例,Ⅵ型4例。骨折均切开复位内固定,对韧带损伤的治疗分为2组,保守治疗组21例,膝关节功能:优11例,良9例,差1例。手术治疗组28例,Ⅰ期修复19例:优17例,良2例。Ⅱ期修复9例:优5例,良3例,差1例。[结论]胫骨平台骨折合并内侧副韧带损伤Ⅰ期修复效果理想。     

搭建基础平台实现高职医学订单教学

搭建基础平台是改传统三年制医学教学“1＋1＋1”模式为“1＋1”模式，为以“市场为导向，就业为中心”的高职教学进行多向培养提供条件，既拓宽教学渠道，适应市场需求，解决学生就业问题，同时又有利于学校发展，符合教学新模式量展要求。     

肝移植术后胆道并发症的介入治疗

目的 探讨原位肝移植术后胆道并发症的介入治疗疗效。方法 回顾性分析我院2002年6月至2005年9月诊治的173例原位肝移植患者的临床资料。结果 术后出现胆道并发症14例（8．1％），其中胆管狭窄6例．胆管狭窄合并胆漏1例，胆泥淤积或结石3例，肝断面胆漏2例（劈离式肝移植患者），T管拔除后胆漏1例，Oddi括约肌功能失常1例。除1例胆道狭窄再次行肝移植，因发生严重感染导致肝功能衰竭死亡外．其余患者经介入治疗均获得满意的效果。结论 介入治疗是诊断和治疗肝移植术后胆道并发症的首选方法。     

Serial CT findings of Paragonimus infested dogs and the Micro-CT findings of the worm cysts.

OBJECTIVE: To investigate the serial CT findings of Paragonimus westermani infected dogs and the microscopic structures of the worm cysts using Micro-CT. MATERIALS AND METHODS: This study was approved by the committee on animal research at our institution. Fifteen dogs infected with P. westermani underwent serial contrast-enhanced CT scans at pre-infection, after 10 days of infection, and monthly thereafter until six months for determining the radiologic-pathologic correlation. Three dogs (one dog each time) were sacrificed at 1, 3 and 6 months, respectively. After fixation of the lungs, both multi-detector CT and Micro-CT were performed for examining the worm cysts. RESULTS: The initial findings were pleural effusion and/or subpleural ground-glass opacities or linear opacities at day 10. At day 30, subpleural and peribronchial nodules appeared with hydropneumothorax and abdominal or chest wall air bubbles. Cavitary change and bronchial dilatation began to be seen on CT scan at day 30 and this was mostly seen together with mediastinal lymphadenopathy at day 60. Thereafter, subpleural ground-glass opacities and nodules with or without cavitary changes were persistently observed until day 180. After cavitary change of the nodules, the migratory features of the subpleural or peribronchial nodules were seen on all the serial CT scans. Micro-CT showed that the cyst wall contained dilated interconnected tubular structures, which had communications with the cavity and the adjacent distal bronchus. CONCLUSION: The CT findings of paragonimiasis depend on the migratory stage of the worms. The worm cyst can have numerous interconnected tubular channels within its own wall and these channels have connections with the cavity and the adjacent distal bronchus.     

甲磺酸罗比卡因与盐酸罗比卡因用于硬膜外阻滞的效应比较

目的 评价甲磺酸罗比卡因用于硬膜外阻滞的效应和安全性。方法 45例择期行下腹或下肢手术病人,随机分别接受用甲磺酸罗比卡因(8.94 mg/ml,观察组)或盐酸罗比卡因(7.5mg/ml,对照组)施行的硬膜外阻滞。观察两组在感觉阻滞、运动阻滞、镇痛和肌肉松弛方面的效果,同时观察用药前后肝肾功能变化。结果 观察组和对照组感觉阻滞平面达到T6以上的病例分别为84.3％和76％(P>0.05),Bromage≥3级的病例分别90％和92％(P>0.05)。两组感觉阻滞平面固定时间、Bromage达到最大级别时间、最大级别维持时间和运动阻滞维持时间均无显著性差异(P>0.05)。两组镇痛及肌松满意率无显著性差异。观察组术中2例发生低血压,2例发生心动过缓,而对照组仅1例发生低血压。两组术后24 h天冬氨酸氨基转移酶(AST)、天冬氨酸转氨酶(ALT)、尿素氮(BUN)和肌酐(Cr)均在正常范围。结论 甲磺酸罗比卡因与盐酸罗比卡因行硬膜外阻滞的效应基本相同,且无明显毒性。     

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.