排序方式: 共有50条查询结果,搜索用时 156 毫秒
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目的观察艾司西酞普兰对广泛性焦虑患者疗效及不良反应的影响。方法将100例广泛性焦虑患者随机分为实验组与对照组,每组50例。实验组予艾司西酞普兰片口服15mg/d,对照组予艾司西酞普兰模拟剂15mg/d,两组进行6周的治疗,采用汉密尔顿焦虑量表(HAMA)评价疗效,抗抑郁药副反应评定量表(SERS)评定艾司西酞普兰的不良反应。结果与对照组比较,治疗后实验组HAMA评分明显下降(P〈0.01);实验组治疗的总有效率为70%(35例),对照组为30%(15例),两组比较差异有统计学意义(P〈0.01)。结论艾司西酞普兰对广泛性焦虑患者的疗效显著,安全性高。 相似文献
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目的:通过卡托普利抑制金属基质蛋白酶的活性以提高粘接界面的稳定性。方法:采用不同浓度的卡托普利乙醇溶液和卡托普利乙醇/水溶液对人离体牙牙本质表面进行预处理,通过场发射扫描电镜观察卡托普利预处理对牙本质表面形貌的影响;在此基础上通过两种自酸蚀粘接剂对牙本质进行粘接,表征即刻粘接强度,并通过老化处理,评价卡托普利预处理对粘接持久性的影响。结果:扫描电镜结果提示,卡托普利溶液可以部分去除沾污层并暴露牙本质胶原。基于扫描电镜结果,选择0.15?g/mL卡托普利乙醇溶液(50%乙醇)处理30?s作为预处理条件,通过可乐丽菲露 SE BOND 进行牙本质粘接,即刻微拉伸强度从(30.80±4.70)MPa 提升至(37.48±3.20)MPa(P<0.05);老化处理 1 年后,对照组微拉伸强度显著下降[(22.90±6.82)MPa,P<0.05],而实验组微拉伸强度没有明显的变化[(36.56±5.10)MPa,P>0.05]。用可乐丽菲露 S3 BOND 进行牙本质粘接,对照组的即刻微拉伸强度为(31.33±4.11)MPa,与实验组(34.70±4.07)MPa 差异无统计学意义(P>0.05);老化处理 1 年后,实验组的微拉伸强度高于对照组[分别为(32.36±3.58)MPa和(21.43±6.27)MPa,P<0.05]。结论:卡托普利预处理不仅可以提高自酸蚀粘接的即刻粘接强度,而且改善了粘接的持久性。 相似文献
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创伤后多脏器功能衰竭患者细胞粘附分子和补体激活成分水平的变化及意义 总被引:5,自引:1,他引:5
目的:探讨创伤后多器官功能衰竭(MOF)患者血浆粘附分子和补体活化成分水平的变化及意义。方法:采用酶联免疫吸附法(ELISA)检测36例创伤后MOF患者及31例创伤患者和35例健康人外周血白细胞CD18的变化、血浆可溶性细胞间粘附分子-1(sICAM-1),可溶性血管细胞间粘附分子-1(sVCAM-1)和血浆补体活化片段(sC5b-9)浓度的变化。结果:MOF患者白细胞CD18的表达、sICAM- 相似文献
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假体周围感染(PJI)是全髋关节置换术后灾难性的并发症,目前二期翻修手术对于髋关节PJI仍是最为有效的治疗方法.传统的抗生素骨水泥关节型占位器的植入是二期翻修间隔期控制感染复发的关键,但既往研究中患者于间隔期髋关节功能及生活质量均处于较低水平.骨水泥型假体是较为新颖的二期翻修占位器设计,以PROSTALAC系统为代表的... 相似文献
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目的探讨关节型全抗生素骨水泥间隔物治疗全膝关节置换术(TKA)后假体感染的中长期转归。方法在上海交通大学附属第六人民医院关节外科的假体关节感染资料库中选取从2004年6月至2010年6月,采用关节型抗生素骨水泥间隔物治疗全膝关节假体术后感染患者28例。入选患者男性11例,女性17例;年龄56~87岁,平均(73±7)岁。一期手术彻底清创+取出假体+间隔物植入。术中采用骨水泥制模,植入带抗生素骨水泥关节型间隔物。术后可早期部分负重,关节屈伸活动,选用敏感抗生素治疗6周,感染控制后再植入高限制性假体。根据Delphi标准判别感染是否控制。结果对本组患者随访8(4~12)年。28例中有20例在植入间隔物后接受假体再植入术,随访感染控制率为85%(17/20)。另有8例植入关节型间隔物后未再植入假体,其中2例最终行关节融合术,3例行膝上截肢,另3例感染控制未再植入假体。结合再植入假体和保留间隔物的总体感染控制率(除外截肢)为78.6%(22/28)。间隔期间隔物并发症包括1例间隔物脱位、2例间隔物断裂和1例间隔物从骨端脱出。结论采用关节型全抗生素骨水泥间隔物结合二期翻修治疗TKA后假体周围感染可以取得较高的成功率;但有相当一部分病例在植入间隔物后未再植入假体,在报道总体治疗成功率的时需要考虑这部分病例,并对其最终转归给予关注。 相似文献
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Xiong Q Sun H Zhang Y Nan F Li M 《Proceedings of the National Academy of Sciences of the United States of America》2008,105(8):3128-3133
Noninactivating potassium current formed by KCNQ2 (Kv7.2) and KCNQ3 (Kv7.3) subunits resembles neuronal M-currents which are activated by voltage and play a critical role in controlling membrane excitability. Activation of voltage-gated potassium channels by a chemical opener is uncommon. Therefore, the mechanisms of action are worthy further investigation. Retigabine and zinc pyrithione are two activators for KCNQ channels but their molecular interactions with KCNQ channel remain largely elusive. Here we report that retigabine and zinc pyrithione recognize two different sites of KCNQ2 channels. Their agonistic actions are noncompetitive and allow for simultaneous binding of two different activators on the same channel complex, hence giving rise to combinatorial potentiation with characteristic properties of both openers. Examining their effects on mutant channels, we showed zinc pyrithione is capable of opening nonconductive channels and coapplication of zinc pyrithione and retigabine could restore a disease mutant channel similar to wild type. Our results indicate two independent activator binding sites present in KCNQ channels. The resultant combinatorial potentiation by multiple synthetic chemical openers indicates that KCNQ channels are accessible to various types and combinations of pharmacological regulation. 相似文献
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Ping Deng Zhi-Ping Pang Zhigang Lei Sojin Shikano Qiaojie Xiong Brandon K Harvey Barry London Yun Wang Min Li Zao C Xu 《Journal of cerebral blood flow and metabolism》2011,31(9):1823-1835
Excitotoxicity is the major cause of many neurologic disorders including stroke. Potassium currents modulate neuronal excitability and therefore influence the pathological process. A-type potassium current (IA) is one of the major voltage-dependent potassium currents, yet its roles in excitotoxic cell death are not well understood. We report that, following ischemic insults, the IA increases significantly in large aspiny (LA) neurons but not medium spiny (MS) neurons in the striatum, which correlates with the higher resistance of LA neurons to ischemia. Activation of protein kinase Cα increases IA in LA neurons after ischemia. Cultured neurons from transgenic mice lacking both Kv1.4 and Kv4.2 subunits exhibit an increased vulnerability to ischemic insults. Increase of IA by recombinant expression of Kv1.4 or Kv4.2 is sufficient in improving the survival of MS neurons against ischemic insults both in vitro and in vivo. These results, taken together, provide compelling evidence for a protective role of IA against ischemia. 相似文献