Survivin在食管癌中的表达及其与bcl-2表达关系的相关研究

目的 探讨Survivin在食管癌组织中的表达及其与bc1-2蛋白表达的相关性。方法应用免疫组织化学SP法，检测Survivin、bc1-2蛋白在68例食管癌组织和20例正常食管组织中的表达。结果 Survivin蛋白在正常食管组织中低表达或不表达，68例食管癌组织中，49例表达阳性，占72．1％。Survivin蛋白表达与分化程度、淋巴结转移密切相关（P〈0．05）。食管癌组织bc1-2蛋白表达阳性、阴性组中，Survivin蛋白阳性表达率分别为94．7％（36／38）和43．3％（13／30），两者比较．差异有统计学意义（P〈0．05）。Survivin蛋白表达与bc1-2蛋白表达密切相关。结论 Survivin在食管癌组织中表达上调，通过抑制细胞凋亡，在食管癌的发生中起到重要作用；凋亡相关基因bc1-2的上调与Survivin的表达可能在食管癌变中起协同作用。     

脊髓栓系神经源性膀胱的MRI表现

目的:分析脊髓栓系神经源性膀胱的MRI特征，评价MRI在脊髓栓系神经源性膀胱诊断中的价值。资料与方法:对32例经MRI检查的脊髓栓系神经源性膀胱患者资料进行回顾性分析。结果:脊髓栓系神经源性膀胱的MRI表现呈现一定的特征，主要表现为脊髓圆锥低位，膀胱壁的1处或多处局限性增厚并结节状隆起。结论:MRI可为临床脊髓栓系神经源性膀胱的诊断提供可靠的依据。     

Expression of CⅡTA Gene in Five Human Malignant Hematological Cell Lines and Its Significance

The role of MHC class Ⅱ transactivator (CⅡTA) in constitutive or IFN-γ inducib|e expression of HLA molecules in human malignant hematological cell lines was investigated. The expression of HLA molecules and CⅡTA protein was detected by Western blot, immunohistochemistry and flow cytometry. The expression of CⅡTA gene was determined by RT-PCR. The capability of peripheral blood T cell reaction stimulated by tumor cells was monitored by mixed lymphocyte reaction. It was found that the HLA Ⅱ-positive tumor cells expressed the CⅡTA quite well, andthe expression of HLA Ⅰ＋Ⅱ was increased in the tumor cells with constitutive or inducible expression of CⅡTA after induced by IFN-γ. The tumor cells which did not express CⅡTA after in-duced by IFN-γ were not response to the expression of HLA Ⅱ promoted by IFN-γ. It suggests a correlation between the inability of some malignant hematological cell lines in response to IFN-γ for HLA expression and the deficiency in the inducible expression of CⅡTA, indicating CⅡTA might take part in the regu|ation of HLA Ⅰ＋Ⅱ expression in the tumor cells, which might p|ay an important role in tumor immunologic escape.     

不同剂量左旋多巴对帕金森病大鼠行为学影响

目的观察不同剂量左旋多巴治疗帕金森病（PD）的效果,并进一步探讨合理使用左旋多巴治疗PD的剂量。方法采用6-OHDA脑立体定向注射术建立大鼠PD模型,采用行为学观察法观察3种不同剂量左旋多巴[按体重10、50、100mg/（kg.d）]作用不同时间（1、3、5、7d）对PD大鼠黑质细胞毒性作用后的行为学变化以及停止左旋多巴治疗后7d各项指标的变化。结果与对照组比较,小剂量组大鼠旋转圈数随左旋多巴使用剂量和时间增加而减少,中、大剂量组大鼠旋转圈数随左旋多巴使用剂量和时间增加而增加;各组大鼠旋转启动时间随左旋多巴使用剂量和时间增加而减少,最高转速及持续时间则随使用剂量增加而增加。结论应尽可能以小剂量、间隔使用左旋多巴治疗PD。     

腕关节融合钢板内固定术的临床疗效

目的评价腕关节融合钢板内固定术的临床疗效。方法2000年7月-2004年12月，采用腕关节融合钢板内固定术治疗创伤性腕关节炎21例。随访内容包括腕关节疼痛程度、手指关节活动度、握力和x线片。根据Buck—Gramcko／Lohrnanrm评分表评价腕关节总体功能，DASH调查表评价腕关节融合术对患者日常活动及生活质量的影响。结果术后21例获得随访，平均随访时间为20个月。术后患侧腕部疼痛值平均为1．5（术前4．5），12例掌指关节和lO例拇指指间关节出现轻微背伸功能障碍，腕部握力为30kg（健侧为38kg）。x线片示腕关节全部骨性融合。Buck—Gramcko／Lohmanrm评分值为8．7，其中优5例、良10例，中6例。DASH值为32，DASH调查表结果表明腕关节融合术后部分日常活动受限。结论腕关节融合钢板内固定成功率高，腕关节疼痛明显减轻，但术后腕关节部分功能丧失。     

FK506和RS-61443对大鼠异体肢体移植的联合免疫抑制作用

目的　通过大鼠异体肢体移植模型 ,旨在分析 FK5 0 6和 RS- 6 14 4 3对大鼠异体肢体移植中急性排斥反应的免疫抑制作用。　方法　选择雄性 Wistar和 SD大鼠为供、受体 ,以 FK5 0 6和 RS- 6 14 4 3为免疫抑制剂 ,对照组为术后不用药组 ,实验组根据用药剂量和药物不同分为 6组 ,各组用药时间均为 5周 (每日 1次共 2周 ,然后每周 2次共 3周 ) ,进行了 10 1例异体肢体移植动物实验。观察大鼠一般情况、移植肢体排斥反应及存活时间。　结果　对照组肢体平均存活时间为 (7.0 0± 0 .78)天 ;实验组 1～ 6组移植肢体平均存活时间分别为 (17.0 8± 4 .5 0、2 3.2 0± 5 .0 5、11.19±2 .2 8、16 .33± 1.83、13.33± 3.2 2和 5 8.76± 6 .81)天。　结论　 FK5 0 6和 RS- 6 14 4 3能抑制大鼠同种异体肢体移植术后急性移植排斥反应的发生 ,并能延长移植肢体的存活时间。     

脊髓损伤后中枢性疼痛的实验模型和机制研究进展

中枢性疼痛(central pain,CP)是脊髓损伤(spi-nal cord injury,SCI)的顽固性合并症,为患者主观上感到损伤平面以下皮肤痛觉消失区一种以自发痛为主的疼痛,发生率为11%~94%,严重者为5%~30%。近年来其发生率逐年增高,使很多患者陷于抑郁、药物成瘾、甚至自杀的悲惨境地。许多疼痛     

Effect of N-tosyl-L-phenylalanylchloromethyl Ketone on Tumor Necrosis Factor-alpha -induced NF-κB Activation and Apoptosis in U937 Cell Line

Summary: To investigate the effect of N-tosyl-L-phenylalanylchloromethyl ketone (TPCK) on tumor necrosis factor-alpha-induced NF-κB activation and apoptosis in U937 cell line, changes and subcellular localization of NF-κB/p65 and IκB-α were observed by fluorescencemicroscopy and expression and degradation of IκB-α by flow cytometry. The apoptosis of U937 cells was measured by flow cytometry and electrophoresis of DNA. Immunolfluorescence assay showed that NF-κB/p65,IκB-α only localized in cytoplasm. After TNF-α stimulation, p65 was localized only in nuclei, and IκB-α was only localized in cytoplasm and decreased. The changes of TNF-α stimulation were specifically inhibited by TPCK. Flow cytometry also revealed the downregulation of IκB-α protein during TNF-α-induced apoptosis and the down-regulation was specifically inhibited by TPCK. Flow cytometry also showed the apoptosis of U937 cells after TNF-α induction. DNA ladder can be detected in cells treated by TNF-α. It is concluded that degradation of IκB-α protein and NF-κB/p65 translocation occur during TNF-α-induced apoptosis of U937 cells, suggesting the activation of NF-κB.TPCK-sensitive protease plays an important role in the degradation of IκB-α protein induced by TNF-α in U937 cells. TPCK sensitive protease also plays an important role in the apoptosis of U937 cells induced by TNF-α.