发音器官运动障碍矫治结合构音训练治疗脑瘫儿童言语障碍疗效分析

目的：通过对发音器官运动障碍矫治和构音训练治疗脑瘫儿童言语障碍，探讨有效治疗脑瘫儿童言语障碍的方法。方法：采用点穴、按摩等手法对发音器官运动障碍进行矫治结合构音训练治疗128例被诊断伴有言语障碍的住院脑瘫患儿,并进行治疗前后发音器官运动功能评定、言语功能评定。结果：显效48例、有效65例，总有效率达88．28％，其中言语语言达正常化者13例治疗效果与患儿的年龄、言语障碍类型等有关。结论：发音器官运动障碍矫治和构音训练相结合是治疗脑瘫儿童言语障碍的重要手段．早期治疗效果更好。     

危重病患者心肌损伤与前炎细胞因子释放的关系

目的 :探讨前炎细胞因子释放在危重病患者继发性心肌损伤中的作用。方法 :98例入住综合 ICU(GICU)的患者均进行急性生理学和慢性健康状况 (APACHE )评分 ;抽取入院 <2 4、4 8和 12 0小时的静脉血 ,检测肌钙蛋白 I(CTn I)、肌酸激酶同工酶 (CK MB)、白介素 1β(IL 1β )和肿瘤坏死因子α(TNFα)含量。结果 :本组患者继发性心肌损伤发生率为 2 1.4 %。APACHE 评分心肌损伤组为 (18.9± 6 .8)分 ,高于非心肌损伤组 (12 .7± 8.9)分 ,P<0 .0 1。心肌损伤组血清 CTn I呈持续增高 ,无明显高峰 ;血清 CTn I与前炎细胞因子的曲线走势非常相似 ,显示有一定的相关性。生存组与死亡组间 CTn I与前炎细胞因子在各时间点上均存在显著差异。与 CK MB相比 ,CTn I对心肌损伤判断的特异性和灵敏性更高。结论 :急性心肌损伤的发生与前炎细胞因子的过度释放有一定关系。     

回输的血小板在体内清除机制研究进展

生理学，病理学方面的研究发现血小板在体内清除主要发生在肝脏和脾脏，但衰老和损伤的血小板被体内清除系统识别和清除的机制还并不清楚。这一机制研究的深入将有助于解决血小板低温保存后体内存活期短．不能较长期发挥作用的难题，为血小板保存提出新的策略。本文就血小扳回输体内后的清除机制，包括P-选择蛋白，GPIbα及其受体Mac-1和内源性金属蛋白酶在血小板清除进程中的作用等的研究进展作一综述。     

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??OBJECTIVE To investigate the effect of verbascoside on iron deposition of astrocyte cell overexpressing heme oxygenase-1 gene, and to seek new drug in treating Alzheimer??s disease. METHODS Primary cultured astrocyte cells of rats were cultured and purified in vitro. With gene recombination and transfer techniques, transfect HO-1 gene into primary cultured astrocyte cells.HO-1 transfected astrocyte were then treated by different concentrations of verbascoside.Proliferation of cell was measured by CCK-8 assay and expression of HO-1 protein was analyzed by Western blotting. Iron deposition was also visualized by Perl??s Prussian blue stain. RESULTS Immunofluorescence staining showed that most of the cells were GFAP-postitive and the purity was over 95%. The expression of HO-1 protein was increased in HO-1 injury model of astrocyte. Treatment of verbascoside with variable concentration caused the decrease of HO-1 protein expression more or less and reduction of iron deposition in transfected cells(20 ??mol??L^-1reducing 47.69%,40 ??mol??L^-1 reducing 51.63%). CONCLUSION Verbascoside could enhance astrocyte cell resistance against injury induced by overexpression of heme oxygenase-1 gene.     

丹参胶囊在欧盟药品注册中的可读性测试研究和实践

药品说明书是载明药品信息的法定文件,对指导公众合理用药起着至关重要的作用。在欧美药品的申报体系和指南中,均要求申请者在药品上市前必须完成药品说明书可读性测试研究,以保证说明书内容通俗易懂,指导公众合理安全用药,避免用药不当可能导致的风险。由于审评理念和标准的差距,目前中国在新药评审的过程中缺乏药品说明书可读性测试研究的要求、法规和指南。以国内申报欧盟成功的品种丹参胶囊注册上市实践为案例,分析欧盟对于药品说明书可读性测试研究的要求,以期为我国建立和实施药品说明书可读性研究的管理思路提供借鉴和参考。     

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??OBJECTIVE To study the protective effect of donepezil on L-glutamic acid-induced injury and the effects on Na⁺ currents and NMDA receptor-mediated currents in neurons. METHODS Cortical and hippocampal neurons were isolated from postnatal 12 h Wistar rats and were cultured for 8-12 d. The protective effect of donepezil on L-glutamic acid-induced injury in neurons was investigated by MTT cell viability assay, and selective Na⁺ channel blocker TTX and selective NMDA receptor blocker MK-801 were taken as positive drugs. The effects of donepezil on Na⁺ and NMDA receptor-mediated current in hippocampal and cortical neurons was studied by using manual patch clamp. RESULTS Donepezil and MK-801 showed protective effects on L-glutamic acid-induced injury model, and TTX can slightly enhance the protective effect of MK-801. 1 ??mol??L^-1 donepezil slightly inhibited Na⁺ currents and NMDA receptor-mediated currents of hippocampal and cortical neurons and 10 ??mol??L^-1 donepezil showed obviously inhibiting effects on Na⁺ currents and NMDA receptor-mediated currents of hippocampal and cortical neurons. CONCLUSION Donepezil can protect neurons from glutamic acid damage, and its mechanism is related to inhibiting current of Na⁺ channel and NMDA receptor channel.     

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??OBJECTIVE To establish a new dissolution method of Ligustrazine Phosphate Pills, which provides reference for revising the quality standard. METHODS The dissolution media were hydrochloric acid solution(pH 1.2), acetate buffer solution(pH 4.5), phosphate buffer solution(pH 6.8) and water. The dissolution curves of six batches of Ligustrazine Phosphate Pills in the four kinds of dissolution media were compared to establish the dissolution method. Apparatus 2 was used for the new method of dissolution test,using 500 mL water as the dissolution medium,at the rate of 75 r??min^-1. The dissolution solution was taken at 20 min and analyzed by HPLC. The dissolution limit was set at 80%. RESULTS The dissolution curves of the six batches of samples were similar in the four kinds of dissolution media. The pills were dissolved completely within 15 min. CONCLUSION The determination method is highly reproducible, accurate and reliable, which can objectively reflect the dissolution of ligustrazine phosphate pills, and provides a basis for the reasonable unification and revision of the dissolution test of the current quality standard.     

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??OBJECTIVE To study the influence and mechanism of bioactive ingredients of Ligusticum chuanxiong Hort. on the transport of gastrodin based on cell culture model in vitro. METHODS Cell toxicity of gastrodin, ligustilide, senkyunolide ?? and senkyunolide A were detected by MTT assay. The transport mechanism of gastrodin and the influence of ligustilide, senkyunolide ?? and senkyunolide A on the transport of gastrodin were studied in MDCK-MDR1 monolayer cells. The changed expressions of P-gp caused by ligustilide, senkyunolide ?? and senkyunolide A were analyzed by Western blotting.RESULTS Gastrodin showed relatively poor absorption in MDCK-MDR1 cells for its apparent permeability coefficients were less than 1??10^-6 cm??s^-1. P-gp inhibitor made the P_app(B??A)/P_app(A??B) of gastrodin reduced from 1.29 to 0.79, which indicated that the transport of gastrodin was influenced by P-gp. In the presence of ligustilide(30 ??g??mL^-1) or senkyunolide ??(120 ??g??mL^-1), the P_app(A??B) of gastrodin in MDCK-MDR1 were significantly increased(P<0.01). In the presence of senkyunolide A(120 ??g??mL^-1), the P_app(A??B) of gastrodin in MDCK-MDR1 were markedly increased(P<0.05). High, medium and low dose of ligustilide, senkyunolide A and senkyunolide ?? could significantly inhibit the expression of P-gp protein.CONCLUSION The results indicate that the transport mechanism of gastrodin might be passive diffusion as the dominating process with the active transportation mediated mechanism involved. Ligustilide, senkyunolide A and senkyunolide ?? increase the transport of gastrodin attribute to down-regulate P-gp expression.