组织工程小血管摩擦力测量方法的研究与应用

目的设计一套用于组织工程小血管内壁摩擦力测量的装置并对组织工程血管的材料进行初步的测量,以验证装置的可靠性和相关结论。方法根据血液动力学的原理,对血管的力学模型进行分析,确定组织工程血管内皮细胞摩擦力的测量方法,从而设计完成整套装置并对弹性元件进行测量,并进行组织工程降解材料聚羟基乙酸PGA构成的管状支架进行摩擦力的测量。结果设计完成了测量组织工程血管内壁摩擦力的实验装置,弹性元件的牵拉力与位移的关系呈良好的线性关系。聚羟基乙酸PGA管状支架的摩擦力随流速的增加而增加。结论测量组织工程血管内壁摩擦力的实验装置是可行的,聚羟基乙酸PGA管状支架的摩擦力与流速基本呈现线性关系。     

关节镜下人工韧带重建前交叉韧带的临床初步体会

目的探讨关节镜下应用LARS人工韧带重建前交叉韧带的可行性及近期疗效. 方法用法国产LARS人工韧带对16例前交叉韧带(anterior cruciate ligament,ACL)损伤行关节镜下ACL重建术.等距点钻胫骨、股骨骨道,将肌腱拉入骨道,韧带游离部分位于关节腔内,拉紧后2枚螺钉固定韧带,合并损伤同期处理. 结果手术时间51～86 min,平均64 min.术后无滑膜炎、韧带断裂、活动明显受限等并发症.16例均随访1.5～6个月,平均3.8月.按照IKDC评分标准:术前C级6例,D级10例;术后A级6例,B级9例, C级1例(χ2=6.264,P<0.05).Lysholm膝关节功能评分术前36～76分,(63.7±7.3)分;术后86～97分,(94.8±9.6)分(t=10.356,P<0.05). 结论关节镜下LARS人工韧带重建ACL,操作简便,可使膝关节获得即时稳定性,早期康复锻炼,最大限度的防止关节功能受限,近期疗效满意.     

前列腺癌新辅助治疗临床分析（附32例报告）

目的 总结32例前列腺癌患者新辅助治疗（NHT）的作用。方法 32例前列腺癌患者中药物去势17例，手术去势15例，并联合抗雄激素治疗3个月，统计NHT前后前列腺癌体积、肿瘤大小、PSA、FSH、LH和睾酮水平变化。结果 2组NHT后前列腺体积明显变小、肿瘤变小、变软，甚至消失，PSA和睾酮明显下降，药物去势组睾酮水平在耻骨后前列腺癌根治术（RRP）术后2～3个月可恢复正常，而手术去势组RRP术后睾酮呈持续低水平。结论 NHT可明显缩小前列腺体积，降低PSA，有利于手术操作。药物去势对内分泌影响是可逆的，而手术去势内分泌改变不可逆。     

红景天对高原去势大鼠骨质疏松症的血清IL-6、TNF-α和尿DPD影响

目的:探讨高原高寒地区低氧环境去势大鼠骨质疏松症与血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和尿脱氧吡啶酚(DPD)的关系及红景天预防骨质疏松的作用。方法:选用Wistar雌性大白鼠75只,分别摘除卵巢或假性去卵巢。分为A组(假手术组),B组(切除卵巢组),C组(切除卵巢 尼尔雌醇组),D组(切除卵巢 红景天混合饲料组),E组(切除卵巢 红景天浸液组)。每组15只,术后在海拔3100m青海海北州地区饲养,术后3个月处死,应用放免方法测定血清IL-6、TNF-α和化学发光法测定尿中DPD含量。结果:B组血清IL-6、TNF-α和尿DPD含量显著高于A、C、D、E组。C、D、E组血清IL-6、TNF-α和尿DPD含量与A组比较差异无显著性统计学意义。结论:红景天的抗高原骨质疏松症的作用可能与降低血清IL-6、TNF-α含量和尿中DPD浓度有关。     

Flavonoids modulate monocarboxylate transporter-1-mediated transport of gamma-hydroxybutyrate in vitro and in vivo.

The objective of this study was to determine the effects of flavonoids on the in vitro monocarboxylate transporter 1 (MCT1)-mediated transport and in vivo disposition of the drug of abuse, gamma-hydroxybutyrate (GHB). The uptake of GHB in rat MCT1 gene-transfected MDA-MB231 cells was significantly decreased in the presence of the flavonoids apigenin, biochanin A, chrysin, diosemin, fisetin, genistein, hesperitin, kaempferol, luteolin, morin, narigenin, phloretin, and quercetin, but was not affected by the flavonoid glycosides phloridzin and rutin. The IC(50) values for luteolin, morin, and phloretin were 0.41 +/- 0.14, 6.41 +/- 2.01, and 2.57 +/- 0.48 microM, with the inhibition mechanism for luteolin being competitive. [(3)H]Kaempferol and [(3)H]biochanin A did not exhibit MCT1-mediated uptake, suggesting that these flavonoids are not substrates for MCT1. The combination of luteolin and phloretin inhibited the uptake of GHB in a synergistic manner; however, the combination of luteolin and morin was antagonistic. GHB 1000 mg/kg was administered to rats by i.v. bolus, with or without the concomitant administration of luteolin 10 mg/kg i.v. After luteolin treatment, the renal and total clearances of GHB were significantly increased, probably because of inhibition of the MCT1-mediated renal reabsorption of GHB, and the sleep time significantly decreased (121 +/- 5 min versus 165 +/- 10 min) compared with control rats. Overall, the results of this study indicate that flavonoids from food or herbal products may significantly alter the pharmacokinetics and pharmacodynamics of MCT substrates.     

先天性胃壁肌层缺损诊治体会

目的 探讨提高新生儿先天性胃壁肌层缺损治愈率的方法。方法 总结分析近年来收治的本症11例患儿(均经过病理检验证实)的临床及相关资料。结果 11例患儿中，8例存活，其中7例为近十年的病例。1例死亡，2例放弃治疗，均为十年以前的病例。在存活者中，经追踪观察及消化道造影检查，残胃有明显代偿性生长，患儿生长发育未受到明显的影响。结论 早期发现、及时手术、控制感染、术后营养、支持治疗，其预后良好。     

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.     

首例中国可视化人体心脏三维重建及临床意义

目的 对首例中国数字化可视人体的心脏进行三维重建，为心脏疾病的影像学诊断和外科手术提供三维解剖学依据。方法 将首例中国数字化可视人体心脏部分的薄层断面(层厚1．0mm)输入SGI工作站，经数据分割、对位重建、平滑处理和三维显示等步骤，完成对心脏结构的三维重建。结果 本研究完整地重建出了心脏结构，重建的结构能够以多结构、多彩色实体模型方式显示，可显示心脏内部各结构的空间位置和毗邻关系，可在三维空间伴置上绕任意轴旋转任意角度。结论 重建出的三维图像清晰地显示了心脏内部和整体的结构，实现了心脏的二维可视化。     

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.