乳腺癌新辅助化疗后动态增强MRI表现与病理反应性相关性研究

目的探讨乳腺癌新辅助化疗后动态增强MRI（DCE—MRI）表现的形态学和时间信号强度曲线（TIC）类型与病理学反应性的关系。方法45例乳腺癌患者经新辅助化疗结束后行乳腺DCE—MR检查及手术治疗。应用AW4．2图像工作站观察残余肿瘤强化的形态和TIC类型（共3型）。由病理科医师对乳腺癌化疗后手术标本的病理反应性进行评估，分为1～5级，5级为病理完全缓解，4级和5级为组织学显著反应。分析病理反应性级别与DCE—MRI残余强化的TIC类型、形态的关系，统计方法采用精确概率法。结果45例中病理反应性5级7例，4级16例，3级16例，1和2级共6例。20例I型曲线中组织学显著反应者占70．0％（14／20），而6例Ⅲ型曲线均为组织学反应不显著者。TIC类型在不同的病理反应级别分布差异有统计学意义（P=0．001）。组织学显著反应且有残余强化者共18例，其中非肿块性强化11例。残余强化的肿块（非肿块）形态表现在不同病理反应性分级中分布差异有统计学意义（P=0．012）。结论乳腺癌新辅助化疗后DCE—MRI的形态及血液动力学表现特点与化疗后病理反应性相关。非肿块性强化和I型TIC与组织学显著反应有关。     

UVA1对人体皮肤成纤维细胞的影响及临床应用

UVA1作用于皮肤成纤维细胞,使其凋亡增加、酶活性及细胞因子的分泌改变,造成真皮层损伤,还可促进伤口愈合,被用于治疗某些与皮肤成纤维细胞增生相关的皮肤病,如硬皮病、瘢痕疙瘩及增生性瘢痕等。本文就UVA1对皮肤成纤维细胞的影响及其在皮肤病治疗中的应用作以综述。     

脊髓损伤后热休克蛋白27、表皮脂肪酸结合蛋白和金属蛋白酶组织抑制因子-1的基因表达及甲基强的松龙对其表达的影响

目的研究脊髓损伤后热休克蛋白27(HSP27)、表皮脂肪酸结合蛋白(FABPs)和金属蛋白酶组织抑制因子-1(TIMP-1)的基因表达及甲基强的松龙(MP)对其表达的影响.方法SD大鼠30只.随机分为假手术组、单纯脊髓损伤组(损伤组)及脊髓损伤+大剂量MP治疗组(MP组),每组10只.应用改良的Allen's打击法致T8脊髓损伤.MP组大鼠伤后即刻从尾静脉内注射大剂量MP(30mg/kg).损伤后24h切取损伤平面上下0.5cm的脊髓组织,进行RT-PCR反应,检测HSP27、FABPs和TIMP-1的基因表达.结果术后24h假手术组HSP27、FABPs和TIMP-1的基因表达相对丰度分别为0.0643±0.0152、0.6413±0.1005和0.7091±0.0577;损伤组上述三个因子的表达升高,分别为1.0013±0.3861、1.2187±0.2851和0.8971±0.1092,与假手术组比较差异有显著性(P＜0.01、P＜0.05、P＜0.05);MP组上述三个因子的表达继续升高,分别为1.2858±0.1384、1.7122±0.1766和1.2081±0.1093,与损伤组比较差异有显著性(P＜0.05、P＜0.01和P＜0.01).结论脊髓损伤后,邻近损伤处的脊髓组织中HSP27、FABPs及TIMP-1的基因表达显著增高,大剂量MP能进一步促进三个因子表达,发挥组织保护作用.     

针刺对急性心肌缺血大鼠血清NO、血浆ET-1、NO/ET-1比值的影响

目的探讨针刺华佗夹脊穴改善急性心肌缺血的作用机制。方法采用大剂量盐酸异丙肾上腺素(ISO.100mg/kg)皮下注射建立大鼠急性心肌缺血模型。选健康SD大鼠40只,随机分为针刺治疗组、针刺预防组、模型组和空白对照组。观察针刺左侧胸4、胸5夹脊穴及左侧足三里穴对急性心肌缺血大鼠血清一氧化氮(NO)、血浆内皮素-1(ET-1)及NO/ET-1比值及ECG的影响。结果针刺治疗能够提高急性心肌缺血大鼠血清NO的含量,降低其血浆ET-1的含量,从而提高NO/ET-1比值。结论针刺华佗夹脊穴具有改善急性心肌缺血大鼠的血管内皮功能,在一定程度上纠正内皮功能紊乱的作用。针刺预防的上述作用不明显。     

抗地高辛人源小分子抗体的获取

目的 从大容量噬菌体抗体库中筛选人源性抗地高辛抗体,并构建双体抗体.方法 以固相化的地高辛对构建的大容量噬菌体抗体库进行筛选,3～4轮后挑取克隆用酶联免疫吸附测定方法鉴定其特异性,对抗地高辛阳性抗体克隆进行DNA指纹分析及测序分析.选取活性好的克隆进行改造,构建双体抗体.结果 在抗体库的筛选过程中可见到明显的富集现象,获得了4株可与地高辛特异性结合的人源抗体,经DNA指纹分析及测序分析证明为不同克隆基因,阳性克隆的可变区基因轻链均属于λ第一亚群,重链分别属于第三和第四亚群.选取4号克隆进行基因改造,构建双体抗体表达载体,获得了活性较好的双体抗体.结论 利用噬菌体抗体技术获得了人源性抗地高辛抗体,并改造成应用前景较好的双体抗体,可能为临床诊断及治疗洋地黄类药物中毒提供具有实用价值的人源抗体.     

管状膨体聚四氟乙烯用于组织工程支架材料的动物实验研究

目的：研究膨体聚四氟乙烯(ePTFE)植入动物体内后与机体的关系。方法：管状膨体聚四氟乙烯两端闭合，内充DMEM培养液，埋入家兔皮下，观察宿主生命情况，于术后1、2、4、6周取出标本，行大体及光镜下观察。结果：家兔在植入膨体聚四氟乙烯材料及DMEM培养液后存活情况良好，DMEM培养液在1周时即已完全无色透明；4周时膨体聚四氟乙烯与周围组织有粘连，6周时粘连紧密；光镜下观察，各时间点材料间隙均可见着色，1周时可见少量淋巴细胞浸润，无血管及组织细胞。材料内壁未见细胞附着。结论：植入膨体聚四氟乙烯材料及少量DMEM培养液对宿主动物存活无影响；管内外液体可相互交通，管状膨体聚四氟乙烯可作为组织工程化尿道的支架材料。     

交锁髓内钉治疗下肢长管状骨骨折的效果

①目的 探讨交锁髓内钉治疗下肢长管状骨骨折的效果。②方法 应用交锁髓内钉治疗下肢长管状骨骨折56例，随访8～26个月，观察治疗结果。③结果 56例病人术后对位、对线均满意，股骨骨折平均愈合时间为19．9周，胫骨骨折平均愈合时间为17．7周，2例延迟愈合。无主钉或锁钉断裂．无肢体短缩、功能障碍发生。④结论 交锁髓内钉是治疗下肢长管状骨骨折的一种理想、可靠的内固定方法，其疗效满意，值得临床推广应用。     

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.     

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.