脑泰营养素治疗帕金森病临床疗效观察

[目的]考察脑泰营养素对帕金森病(PD)临床症状的控制和改善。[方法]选择PD病人41例,随机分为治疗组和对照组,对照组采用美多巴治疗,治疗组在此基础上加用脑泰营养素。分别比较两组治疗前后Hoehn-Yahr(H-Y)分级和改良Webster量表评分变化及两组间的疗效差异。[结果]与对照组比较,治疗组的H-Y分级和改良Webster量表评分明显减少(P<0.05),总有效率明显提高(P<0.05)。[结论]在使用美多巴的基础上加用脑泰营养素治疗PD,可明显增强疗效。     

Somatostatin infusion withdrawal in the diagnosis of childhood growth hormone deficiency

OBJECTIVE: An evaluation of growth hormone (GH) testing for GH deficiency (GHD) in childhood is confounded by the lack of a world-wide consensus on the definition of GHD. Although a single GH test remains the most powerful biochemical tool in the evaluation of a child with growth failure, the test remains far from ideal. Withdrawal of somatostatin (SS) infusion is followed by a rebound rise of GH thought to be mediated by endogenous GH-releasing hormone (GHRH) function. This study was designed to compare the GH response to 90 min SS infusion in children with normal GH secretion versus children with GH deficiency. METHODS: Ten children with GHD and 10 healthy controls (NC) have been evaluated for GH response to somatostatin infusion withdrawal (SSIW) and compared with response of two provocative tests, glucagon plus propranolol test and L-Dopa test. All children received constant infusion of somatostatin for 90 min (3 microg/kg per h, Stilamin, Serono, Aubonne, Switzerland). In order to determine GH, blood samples were obtained 90 min before the SS infusion and 0, 15, 30, 45, 60, 75, and 90 min after the cessation of infusion. RESULTS: Growth hormone peak levels with SSIW were significantly lower in GH deficient children than in healthy children (2.5 +/- 1.2 ng/dL, vs 21.9 +/- 5.3 ng/dL, respectively, P < 0.01). No adverse effects were observed during or after somatostatin infusion. CONCLUSION: In the present study, SSIW elicited a significant GH rise in healthy children but not in children with GH deficiency. Although further controlled studies using more data are necessary to expand these findings, the results suggested that children with GH deficiency can be reliably discriminated from healthy children by SSIW.     

阳离子脂质体介导BFGF/GFP基因对药物性耳蜗损害的防治作用

目的 探讨阳离子脂质体(天然碱性脂SA)携带碱性成纤维细胞生长因子/绿色荧光蛋白(bFGF/GFP)基因在豚鼠耳蜗中的表达,以及对庆大霉素所致耳蜗损害的防治作用。方法 将36只豚鼠分为3组,预防组右耳园窗注入SA-bFGF/GFP复合物后次日肌肉注射庆大霉素150mg.Kg~(-1).d~(-1)8天,治疗组先用庆大霉素8d后次日右耳给药,对照组单用庆大霉素8d。分别于实验前后及处死前行听觉脑干诱发电位(ABR)测试。荧光显微镜下观察耳蜗GFP的表达;用耳蜗琥珀酸脱氢酶染色铺片,扫描电镜观察毛细胞的缺失情况。结果 荧光显微镜下见双侧耳蜗均有GFP表达。预防和治疗组处死前的双耳ABR阈值与对照组比较差异有显著意义(P<0.01,P<0.05),耳蜗内外毛细胞缺失数与对照组比较差异有显著意义(P<0.01,P<0.05)。结论 SA脂质体介导的bFGF/GFP基因单耳给药双侧耳蜗均有高效表达,并对庆大霉素所致的耳蜗损害有防治作用。     

Basic fibroblast growth factor protects auditory neurons and hair cells from noise exposure and glutamate neurotoxicity

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PGP 9.5在SD大鼠肠神经节细胞成熟度评价中的作用

目的 研究肠神经节细胞成熟度评价的方法和特异性抗体的作用，探讨PGP9．5对研究先天性肠神经系统发育异常疾病的意义。方法 40只不同年龄的SD大鼠：胎龄15d(E15)，20d(E20)，生后9d(P9)，成年的SD大鼠各10只。取标本，甲醛固定石蜡包埋切片，常规处理后用HE染色和PGP9．5、CathePsin D、NSE的免疫组化染色，通过观察免疫染色阳性定位和定性情况和测量节细胞的平均最大直径，分析肠神经节细胞的发育和成熟状况。结果 PGP9．5染色阳性率达100％；NSE在E15中全部阴性，在E20和P9中皆呈弱阳性反应；而CathpinD 只在大脑中反应阳性。肠神经节细胞尺寸测量结果E20，P9和成年各年龄组间差异有显著性意义(P＜0．01)；PGP9．5所显示的节细胞形成良好的成熟与幼稚的染色形态——成熟的节细胞脑浆颗粒清晰、细胞核淡染、核仁明显，末成熟的节细胞则胞浆胞核浓染、结构不清、无明显的核仁。结论 PGP9．5在肠神经节细胞中的成熟与幼稚的不同染色形态可特征性地评价肠神经节细胞的成熟度。实验提示，PGP9．5的免疫组化技术评价肠神经节细胞成熟度是一种可靠而简便的方法，在各种人类肠神经系统发育异常性疾病的形态学研究和临床诊治中有重要的实践意义。     

RNA干扰对人神经母细胞瘤VEGF-A表达的抑制作用

目的 构建VEGF-A的短发夹RNA真核表达载体,并通过其介导的RNA干扰抑制人神经母细胞瘤细胞株SH-SY5Y VEGF-A的表达.方法 根据VEGF-A的cDNA序列合成两对寡核苷酸片段,退火后分别插入真核表达载体组成重组质粒psc001、psc002,对重组质粒进行PCR、测序鉴定验证并经Western Blot筛选,然后将筛选所得的质粒转染人神经母细胞瘤细胞株SH-SY5Y.转染48h后行Annexin V和PI双重标记流式细胞仪检测转染细胞凋亡情况,ELISA检测VEGF-A蛋白的表达水平.结果 PCR和测序证实寡核苷酸片段已成功插入质粒psc001、psc002中,流式细胞仪检测结果 显示转染的外源基因未引起显著的神经母细胞瘤细胞凋亡,ELISA结果 显示转染后细胞株SH-SYSY的VEGF-A蛋白表达受到显著抑制(P<0.05).结论 成功构建人VEGF-A的短发卡RNA真核表达载体,转染人神经母细胞瘤SH-SY5Y细胞后能显著抑制VEGF-A的表达,但没有引起显著的细胞凋亡(P0.05).     

电刺激促进后肢缺血大鼠VEGFmRNA和蛋白的表达

目的：观察电刺激对后肢缺血大鼠VEGF的调节。方法：采用SD大鼠股浅动脉结扎法制备后肢缺血模型，应用RT-PCR和免疫组化方法检测电刺激对后肢缺血大鼠VEGFmRNA和蛋白表达的影响。结果：刺激频率为25Hz，强度为0.1V不引起肌肉收缩。缺血模型建立7d后连续电刺激7d，VEGFmRNA的表达刺激组比非刺激组增加3倍，VEGF蛋白增加两倍。结论：电刺激可促进后肢缺血大鼠VEGFmRNA和蛋白的表达，从而实现非分子的治疗性血管生成作用。     

甘草酸两种异构体治疗肾综合征出血热的疗效观察

目的 :比较甘草酸两种异构体治疗肾综合征出血热 (HFRS)的临床效果。方法 :HFRS患者78例 ,随机分为A、B两组。A组加用甘草酸α体制剂 (甘利欣 )静脉滴注 ,B组加用甘草酸β 体制剂 (美能 )静脉滴注。观察两组越期率等多项临床指标并进行比较。结果 :两组治疗后 ,除丙氨酸氨基转移酶复常时间无差异外 ,其余观察指标均存在显著性差异 ,B组疗效优于A组 (P<0 01)。结论 :临床治疗HFRS ,甘草酸 β体制剂疗效显著优于甘草酸α体制剂     

治疗阿尔采末病的药物靶点:β-分泌酶

近年来的研究表明,β-淀粉样蛋白(Aβ)是老年斑的主要成分,有明显的神经细胞毒性作用,在阿尔采末病(AD)的发病过程中发挥了重要作用,因此降低脑中Aβ的生成量是治疗AD的策略。Aβ是由β-和γ-分泌酶裂解其前体蛋白(APP)而生成,其中β-分泌酶(BACE)是启动Aβ形成的关键限速酶,因此BACE是开发治疗AD药物的一个具有吸引力的作用靶点。该文就近来对β-分泌酶的研究作一综述。     

PPAR-γ的激动剂抑制肺癌细胞生长的实验研究

目的　研究肺癌细胞上过氧化物酶体增生物激活受体γ(PPAR γ)的表达及其经配体 (激动剂 )活化后抑制肺癌细胞生长的机制。方法　以RT PCR和Westernblot检测肺癌细胞上PPAR γ的表达 ,并通过MTT和细胞计数检测经PPAR γ的激动剂作用后的细胞增殖情况 ,以TUNEL检测细胞的凋亡情况。结果　两种细胞上均有PPAR γ的表达 ;PPAR γ的配体作用后明显抑制细胞生长 ,且与时间和剂量有关 ;经配体活化的PPAR γ能诱导细胞凋亡 ,使其增殖受抑。结论　作为肺癌治疗的新靶点———PPAR γ在肺癌细胞上表达 ,且经配体活化后能通过诱导凋亡而抑制肺癌细胞的生长 ,从而为未来肺癌的治疗提供了新的途径