阿立哌唑治疗首发精神分裂症75例临床观察

目的观察阿立哌唑(成都康弘药业集团有限公司生产,商品名为博思清)治疗首发精神分裂症的疗效及安全性,以指导临床合理用药。方法选取2013年4月至2015年11月在我院住院治疗的首发精神分裂症的75例为研究对象,单独采用阿立哌唑进行治疗,临床观察持续8周。采用BPRS评定临床疗效,并记录下不良反应发生情况。结果经阿立哌唑治疗,临床痊愈65例(86.7%),好转6例(8%);无效4例(5.3%),不良反应少且程度轻。结论应用阿立哌唑治疗首发精神分裂症疗效显著,且无明显不良反应发生,患者依从性良好,值得临床推广使用。     

阿立哌唑口腔崩解片与阿立哌唑片治疗精神分裂症对照研究

目的:比较阿立哌唑口腔崩解片与阿立哌唑片治疗精神分裂症的疗效和安全性.方法:将120例精神分裂症患者随机分为研究组(阿立哌唑口腔崩解片治疗组)60例和对照组(阿立哌唑片治疗组)60例.研究组阿立哌唑口腔崩解片10-30mg/d,对照组阿立哌唑片10-30ms/d,疗程均为8周.在治疗前及治疗后第2、4、8周末使用PANSS评定临床疗效、使用TESS评定药物不良反应,进行比较分析.结果:阿立哌唑口腔崩解片的治疗有效率为68.3%.阿立哌唑片的治疗有效率为70.0%,两组疗效无显著性差异,不良反应无显著性差异(P>0.05).结论:阿立哌唑口腔崩解片与阿立哌唑片治疗精神分裂症均有良好的疗效与耐受性,两药差异不显著.     

阿立哌唑与氟哌啶醇治疗精神分裂症对照研究

目的:评估阿立哌唑的临床疗效和不良反应.方法:将75例精神分裂症患者随机分成两组,分别以阿立哌唑和氟哌啶醇治疗,疗程6周,以阳性症状量表和阴性症状量表(PANSS)及副反应量表评定疗效和安全性.结果:两药对精神分裂症均有良好的治疗效果,但阿立哌唑起效较快.阿立哌唑不良反应明显较氟哌啶醇少而轻.结论:阿立哌唑治疗精神分裂症有效、安全.     

阿立哌唑与利培酮治疗精神分裂症对照研究

目的:探讨阿立哌唑与利培酮治疗精神分裂症的疗效和不良反应。方法:应用阿立哌唑与利培酮分别治疗精神分裂症各34例,疗程8周。用阳性与阴性症状量表(PANSS)评定疗效,用治疗中出现的症状量表(TESS)评定药物不良反应。结果:两组PNSS总评分治疗前后差异有显著性。阿立哌唑组总有效率82.3%,利培酮组为82.3%,两者相同(P>0.05)。不良反应发生率:阿立哌唑组为19.82%,利培酮组为25.32%,阿立哌唑组低于利培酮组,差异有显著性(P<0.05)。结论:阿立哌唑与利培酮对精神分裂症有疗效好,且疗效相同。但不良反应少,是一种安全、有效的抗精神药。     

阿立哌唑治疗老年精神分裂症的疗效和安全性观察

目的:观察阿立哌唑治疗老年精神分裂症的临床疗效和安全性。方法:70例老年精神分裂症患者随机分为以下2组:阿立哌唑组[男性17例,女性18例,年龄(66.2±2.4)岁]和氟哌啶醇组[男性18例,女性17例,年龄(65.4±2.4)岁]。阿立哌唑组和氟哌啶组的起始剂量分别为5~10mg/d和2mg/d,之后视病情分别调整为(12.8±3.3)mg/d和(7.3±3.6)mg/d,共治疗8周。采用阳性症状与阴性症状量表(PANSS)评定临床疗效,用不良反应症状量表(TESS)评定不良反应。结果:阿立哌唑组与氟哌啶醇组的有效率分别为88.6%和85.7%,2组比较差异无统计学意义(P>0.05)。阿立哌唑组不良反应少而轻微。结论:阿立哌唑为治疗老年精神分裂症的有效安全药物。     

阿立哌唑与利培酮治疗精神分裂症的系统评价

目的:评价阿立哌唑与利培酮治疗精神分裂症的疗效及发生不良反应的差异。方法:检索国内关于阿立哌唑与利培酮对照研究治疗精神分裂症的文献,应用系统评价方法对查阅到的14篇文献进行评估。结果:阿立哌唑与利培酮的疗效比较无显著性差异(χ2=0.02,P>0.05,OR=1.04,95%CI(0.80～1.35))。利培酮组发生肌张力增高、静坐不能、震颤、体重增加、月经紊乱、溢乳等不良反应比阿立哌唑组多,有显著性差异(χ2=14.96～65.37,P<0.05～0.001)。结论:阿立哌唑与利培酮的疗效相当,但阿立哌唑不良反应的发生率较低。     

阿立哌唑治疗精神分裂症的多中心随机双盲对照试验

目的:评价阿立哌唑治疗精神分裂症的疗效及安全性。方法:采用多中心随机双盲双模拟、阳性药平行对照的方法。以利司哌酮(昔名利培酮)为对照,受试者分别口服阿立哌唑10~30 mg.d-1与利司哌酮2~6 mg.d-1,疗程42 d。结果:共收集精神分裂症病人222例,其中阿立哌唑组111例与利司哌酮组111例。治疗结束时,2组PANSS总分与BPRS总分较治疗前均显著降低(P<0.01);PANSS总分减分率阿立哌唑组(65±s28)%,利司哌酮组为(67±26)%,差异无显著意义(P>0.05)。临床总有效率:阿立哌唑组为77.0%,利司哌酮组为79.2%,2组比较差异无显著意义(P>0.05)。阿立哌唑组常见的不良反应为:静坐不能、震颤、失眠、心动过速,不良反应较利司哌酮组少。结论:阿立哌唑治疗精神分裂症的疗效与利司哌酮相似,不良反应较利司哌酮为少,是一种安全而有效的抗精神病药。     

阿立哌唑与氯氮平对慢性精神分裂症患者疗效及脂质指标的影响比较

目的分析阿立哌唑与氯氮平对慢性精神分裂症患者的治疗效果及脂质指标的影响。方法80例慢性精神分裂症患者,随机分为阿立哌唑组和氯氮平组,每组40例。阿立哌唑组患者给予口服阿立哌唑治疗,氯氮平组患者给予口服氯氮平治疗。比较两组患者的临床疗效、不良反应发生率及治疗前后的脂代谢指标水平。结果阿立哌唑组患者的临床治疗总有效率为95.00%,高于氯氮平组的80.00%,差异有统计学意义(P<0.05)。阿立哌唑组患者治疗前后的甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平组内比较,差异无统计学意义(P>0.05);氯氮平组患者治疗前后的TC、LDL-C、HDL-C水平组内比较,差异无统计学意义(P>0.05);氯氮平组治疗后的TG高于治疗前,且高于阿立哌唑组,差异有统计学意义(P<0.05)。阿立哌唑组患者的不良反应发生率为7.50%,低于对照组的27.50%,差异有统计学意义(P<0.05)。结论氯氮平对慢性精神分裂症患者的脂代谢指标有明显影响,但阿立哌唑对脂代谢指标无明显影响,且相比氯氮平疗效更加显著,不良反应更少,临床安全性更好,临床可将其作为慢性精神分裂症患者的首选药物进行应用。     

阿立哌唑联用西酞普兰治疗精神分裂症的临床疗效观察

目的研究阿立哌唑(博思清)联用西酞普兰与单用阿立哌唑治疗精神分裂症的临床疗效及安全性。方法 60例精神分裂症患者首次使用阿立哌唑治疗后随机分成两组分别给予阿立哌唑和阿立哌唑联用西酞普兰治疗8周,并用PANSS量表评价临床疗效,TESS量表评价不良反应。结果两组之间疗效有显著差异,阿立哌唑联用西酞普兰组患者病情好转更彻底,阴性症状消失,更用利于回归社会,而继续单用阿立哌唑组虽然精神症状消失,但患者整天精神不佳,不想干活,不良反应相对较多(P<0.05)。结论阿立哌唑联用西酞普兰疗效显著,副作用小,患者耐受性好。     

阿立哌唑与利培酮治疗女性精神分裂症的Meta分析

目的:评价阿立哌唑与利培酮治疗女性精神分裂症的疗效及安全性。方法:应用循证医学方法对符合标准的12项研究进行分析,评价阿立哌唑与利培酮治疗女性精神分裂症的疗效及安全性的差异。结果:阿立哌唑与利培酮治疗女性精神分裂症的显效率和有效率差异均无统计学意义(P>0.05),但在副作用评定中显示,锥体外系反应、体质量增加和泌乳及月经紊乱阿立哌唑显著低于利培酮(P<0.00001)。结论:阿立哌唑与利培酮均是治疗女性精神分裂症的良好药物,但在副作用方面存在差异。     

Nachweis einiger Heilmittel in der Kniegelenksynovialflüssigkeit

Zusammenfassung Mittels Gaschromatographie und Dünschichtchromatographie wiesen die Autoren 11 Substanzen nach, welche durch Injektion oder nach Verabreichung per os in die Kniegelenksynovialflüssigkeit eindrangen. In ihrer Aufstellung konnten sie eine direkte Beziehung zwischen Struktur sowie chemischphysikalischen Eigenschaften der Substanz und ihrer Fähigkeit, aus dem Blut in die Kniegelenksynovialflüssigkeit einzudringen, nicht nachweisen, außer der Tatsache, daß Substanzen mit starker Affinität zu Eiweißstoffen erst in höheren Dosen nachweisbar waren.     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Emerging drugs for epilepsy

Epilepsy affects ≤ 1% of the world's population. Antiepileptic drugs (AEDs) are the mainstay of treatment, although more than a third of patients are not rendered seizure free with existing medications. Uncontrolled epilepsy is associated with increased mortality and physical injuries, and a range of psychosocial morbidities, posing a substantial economic burden on individuals and society. Limitations of the present AEDs include suboptimal efficacy and their association with a host of adverse reactions. Continued efforts are being made in drug development to overcome these shortcomings employing a range of strategies, including modification of the structure of existing drugs, targeting novel molecular substrates and non-mechanism-based drug screening of compounds in traditional and newer animal models. This article reviews the need for new treatments and discusses some of the emerging compounds that have entered clinical development. The ultimate goal is to develop novel agents that can prevent the occurrence of seizures and the progression of epilepsy in at risk individuals.     

盐酸达泊西汀中甲磺酸甲酯、甲磺酸乙酯及甲磺酸异丙酯的顶空毛细管GC-ECD法测定

建立了衍生化顶空毛细管气相色谱-电子捕获检测器(ECD)法测定盐酸达泊西汀中的甲磺酸甲酯(MMS)、甲磺酸乙酯(EMS)和甲磺酸异丙酯(IMS).应用碘化钠衍生技术,使用PW-5毛细管柱,载气为氮气,ECD检测,程序升温.MMS、EMS和IMS分别在0.03～0.30、0.05～0.50和0.05～0.50 μg/ml浓度范围内线性关系良好,平均回收率分别为63.5％、100.3％和96.2％,最低检测限分别为0.30、0.50和0.50 ng/ml.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.