胫骨高位截骨手术并发症23例次分析

[目的] 探讨胫骨高位截骨手术并发症的发生情况，并提出预防和治疗措施。[方法]2000年1月～2004年10月采用胫骨高位截骨术治疗膝骨关节炎合并内翻畸形患者126人，21人发生手术并发症，男4例，女17例；年龄48～64岁，平均61岁。术前拍摄站立膝关节正位X线片，测量股骨一胫骨角，计算截骨角度，采用外侧闭合胫骨高位截骨术矫正膝内翻畸形。[结果] 术后随访6～12个月，平均7．5个月。共21名患者发生各类并发症23例次．发生率为16．7％。其中发生胫骨骨折4例，腓总神经麻痹3例，出现深静脉血栓形成5例，膝内翻复发病例6例，内固定失败4例（其中2例合并膝内翻复发），感染1例。[结论] 降低胫骨高位截骨手术并发症需要术者熟悉局部解剖和精确的术前设计，提高手术技巧及完善的围手术期护理。     

微创经皮肾镜取石术治疗上尿路结石

目的 探讨微创经皮肾镜取石术治疗上尿路结石的有效性和安全性.方法上尿路结石患者368例,平均年龄57岁.其中输尿管上段结石116例,结石大小(2.1±0.8)cm;肾结石252例,结石大小(4.6±1.4)cm,其中非鹿角形结石190例,结石大小(3.2±1.1)cm,鹿角形结石62例,结石大小(7.6±1.6)cm.均采用微创经皮肾穿刺,输尿管镜下气压弹道或联合钬激光碎石治疗,对结石清除率和并发症等进行统计分析.结果 368例患者中单通道取石356例(96.7%),双通道12例(3.3%).一期取石344例(93.5%),二期取石24例(6.5%).总结石取净率为88.6%(326/368).平均手术时间73 min.一期取净结石者住院时间4～8 d,平均6 d.术后发热14例(3.8%);输血5例(1.4%);2例肾结石术后出血严重者经输血及超选择性肾动脉栓塞后治愈.结论 微创经皮肾镜取石术损伤小、住院时间短、术中出血及并发症少、结石清除率高、可重复取石,是治疗上尿路结石有效的微创手段.     

Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke.

Bone marrow stromal cells (MSCs) increase vascular endothelial growth factor (VEGF) expression and promote angiogenesis after stroke. Angiopoietin-1 (Ang1) and its receptor Tie2 mediate vascular integrity and angiogenesis as does VEGF and its receptors. In this study, we tested whether MSC treatment of stroke increases Ang1/Tie2 expression, and whether Ang1/Tie2 with VEGF/ vascular endothelial growth factor receptor 2 (VEGFR2) (Flk1), in combination, induced by MSCs enhances angiogenesis and vascular integrity. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAo) and treated with or without MSCs. Marrow stromal cell treatment significantly decreased blood-brain barrier (BBB) leakage and increased Ang1, Tie2, and occludin (a tight junction protein) expression in the ischemic border compared with MCAo control. To further test the mechanisms of MSC-induced angiogenesis and vascular stabilization, cocultures of MSCs with mouse brain endothelial cells (MBECs) or astrocytes were performed. Supernatant derived from MSCs cocultured with MBECs significantly increased MBEC expression of Ang1/Tie2 and Flk1 compared with MBEC alone. Marrow stromal cells cocultured with astrocytes also significantly increased astrocyte VEGF and Ang1/Tie2 expression compared with astrocyte culture alone. Conditioned media from MSCs alone, and media from cocultures of MSCs with astrocytes or MBECs, all significantly increased capillary tube-like formation of MBEC compared with control Dulbecco's modified Eagle's medium media. Inhibition of Flk1 and/or Ang1 significantly decreased MSC-induced MBEC tube formation. Knockdown of Tie2 expression in MBECs significantly inhibited MSC-induced tube formation. Our data indicate MSC treatment of stroke promotes angiogenesis and vascular stabilization, which is at least partially mediated by VEGF/Flk1 and Ang1/Tie2.     

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。     

腰椎间盘突出症早期手术并发症的回顾性分析

腰椎间盘突出是腰腿痛的主要原因,因患病率高,手术开展较为普及,关于其手术后并发症的相关报导也逐渐增多。为了进一步了解这些并发症的发生原因,我们将1993年2月至2004年12月手术治疗腰椎间盘突出症768例中所发生的74例早期并发症进行回顾性分析,针对手术的危险因素提出相应的     

氧化应激诱导神经细胞凋亡与c-Myc、Fas-FasL、核因子-κB关系的研究

目的　探讨氧化应激诱导神经细胞凋亡与c -Myc、Fas -FasL、核因子 -κB(NF -κB)蛋白表达的关系。　方法　将分离培养的新生SD大鼠大脑皮质神经细胞分为 :A组 (对照组 )、B组 (缺氧处理 )、C组 (低浓度H2 O2 处理 )、D组 [缺氧 +超氧化物歧化酶 (SOD)处理 ]、E组 (H2 O2 +SOD处理 ) ,利用琼脂糖凝胶电泳、末端脱氧核苷酸介导的X -dUTP缺口末端标记法 (TUNEL)、流式细胞仪测定细胞凋亡 ,免疫组织化学方法 (SP法 )测定细胞c -Myc、Fas -FasL、NF -κB蛋白表达。结果　B组和C组神经细胞凋亡率分别为A组的 6倍和 8倍 (P <0 .0 1) ;A组c -Myc、Fas-FasL、NF -κB阴性表达 ,其余各组均有阳性表达 ;SOD在降低B组和C组细胞c-Myc、Fas-FasL、NF -κB表达强度的同时 ,细胞凋亡率也随之降低。　结论　氧化应激诱导神经细胞凋亡可能与NF -κB的激活 ,启动凋亡相关基因c -Myc、Fas -FasL有关。     

腹腔注射高渗盐水对下丘脑室旁核加压素能神经元的兴奋作用

目的探讨外周高渗刺激激活下丘脑室旁核(PVN)神经元的细胞类别。方法以腹腔注射高渗盐水作为外周高渗刺激。细胞外记录PVN神经元单位放电的变化，并用免疫细胞化学方法观察PVN中los的表达及los表达阳性神经元的性质。结果腹腔注射高渗盐水使PVN的位相型放电神经元兴奋，PVN内los表达明显增加，特别是PVN大细胞中大量的los阳性神经元同时表达精氨酸加压索(AVP)。结论外周高渗刺激能够激活PVN内的加压索(VP)能神经元。     

经导管封闭治疗小儿继发孔房间隔缺损

目的探讨应用经导管封闭治疗小儿房间隔缺损的临床效果.方法 16例ASD患儿.男6例,女10例;年龄2～14(8±4)岁,体重10～40(23±9)Kg.先行右心导管用球囊导管测量ASD大小,选择适合的封堵器,在X线及超声引导下释放封堵器堵闭ASD,术后随访疗效,追踪残余分流率和并发症.结果应用此法封闭16例ASD,全部成功.手术时间为(70±30)血n,透视时间(13±8)min,术中无明显并发症.术后随访右房、右室径较术前明显缩小,恢复正常(P＜0.05);无残余分流发生.结论经导管封闭治疗小儿房间隔缺损术具有创伤小,成功率高,安全性好的优点,但其长期疗效需进一步随访观察.     

诱导型一氧化氮合酶在前列腺增生组织中表达的研究

目的：探讨诱导型一氧化氮合酶(iNOS)与前列腺增生(BPH)病理生理变化的关系。方法:用免疫组化法检测10例正常和30例有膀胱出口梗阻的BPH患者膀胱和前列腺组织中iNOS的表达。结果：BPH组前列腺组织中iNOS呈阳性染色，主要分布于前列腺的上皮细胞及上皮下组织中，间质平滑肌组织中均为阴性；对照组的膀胱壁、膀胱颈部和前列腺组织中均无iNOS阳性染色。结论：iNOS仅在BPH患者前列腺组织中有特异性表达，提示它参与了前列腺增生的病理生理过程。