奥扎格雷钠联合依达拉奉治疗急性脑梗死临床观察

目的观察奥扎格雷钠联合依达拉奉治疗急性脑梗死的临床疗效。方法选择本院急性脑梗死患者66例,随机分为对照组和治疗组,在常规治疗的基础上,前者给予奥扎格雷钠治疗,后者给予奥扎格雷钠联合依达拉奉治疗,2周后观察两组的临床疗效和神经功能缺损评分。结果对照组有效率为73．3％,治疗组有效率为91．7％,两组比较差异有统计学意义（P〈0．05）;治疗组神经功能缺损评分较对照组明显降低,两组比较差异有统计学意义（P〈0．05）。结论奥扎格雷钠联合依达拉奉治疗急性脑梗死安全有效,优于单用奥扎格雷钠治疗,值得临床推广应用。     

奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效观察

目的探讨依达拉奉和奥扎格雷钠治疗脑梗死的疗效。方法选择诊断明确的急性脑梗死患者138例。治疗组给予依达拉奉联合奥扎格雷钠治疗,对照组给予丹参及胞二磷胆碱治疗。治疗前及14d后,按临床神经功能缺损程度评分标准,进行临床疗效评定。结果治疗14d后治疗组神经功能缺损评分明显低于对照组,总有效率明显高于对照组。结论奥扎格雷钠联合依达拉奉治疗脑梗死安全有效。     

依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效观察

目的观察依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效。方法98例急性脑梗死患者随机分为治疗组与对照组,在常规治疗的基础上,治疗组联合应用依达拉奉和奥扎格雷钠,对照组单独使用奥扎格雷钠,疗程14d,以美国国立卫生研究院卒中量表（NIHSS）和Barthel指数（BI）为指标,评价疗效。结果治疗14d后患者临床神经功能缺损程度改善治疗组优于对照组（P〈0．05）,3个月时治疗组日常生活活动能力优于对照组。结论依达拉奉联合奥扎格雷钠治疗急性脑梗死比单用奥扎格雷钠疗效好,无明显副反应。     

奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效观察

目的：观察奥扎格雷钠联合依达拉奉治疗急性脑梗死的临床疗效。方法：以本院收治的110例急性脑梗死患者为研究对象,随机分为观察组和对照组各55例,其中观察组给予奥扎格雷钠联合依达拉奉治疗,对照组则单独应用奥扎格雷钠进行治疗,2周为1个疗程,此外两组均给予常规的对症支持治疗。治疗后对患者进行神经功能缺损评分并比较两组的疗效。结果：观察组总有效率为96．4％,对照组总有效率为78．2％。两组差异有统计学意义（P〈0．05）;治疗前后观察组神经功能缺损评分改善情况也明显优于对照组,差异亦有统计学意义（P〈0．05）。结论：奥扎格雷钠联合依达拉奉治疗急性脑梗死疗效可靠,能明显改善神经功能的损伤,适合临床上广泛应用。     

依达拉奉联合奥扎格雷钠治疗进展性脑梗死的临床分析

目的观察依达拉奉联合奥扎格雷钠治疗进展性脑梗死的疗效和安全性。方法140例进展性脑梗死患者随机分为治疗组、对照组,各70例。治疗组给予依达拉奉和奥扎格雷钠静脉点滴,对照组给予奥扎格雷钠静脉点滴,并对临床疗效、治疗前后神经功能缺损评分比较。结果依达拉奉联合奥扎格雷钠组总有效率88．6％,对照组总有效率71．4％。与对照组比较,差异有统计学意义（P〈0．01）。结论依达拉奉联合奥扎格雷钠治疗进展性脑梗死能有效地改善神经功能,安全有效,值得推崇。     

依达拉奉联合奥扎格雷钠治疗急性脑梗死的临床疗效观察

目的观察依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效及安全性。方法将我院收治的84例急性脑梗死患者随机分为治疗组42例和对照组42例,在常规治疗的基础上,治疗组联合应用依达拉奉和奥扎格雷钠,对照组则单独使用奥扎格雷钠,14d为一个疗程,14d后进行疗效评价。结果治疗组总有效率为90.5%,对照组总有效率为64.3%,两组相比较有统计学差异（P〈0.05）;治疗14d后患者神经功能缺损评分比较,治疗组明显优于对照组（P〈0.05）,且两组均无明显不良反应。结论依达拉奉联合奥扎格雷钠治疗急性脑梗死疗效显著、安全性高,无明显不良反应,值得临床推广使用。     

急性脑梗死应用依达拉奉联合奥扎格雷钠治疗的疗效观察

目的分析急性脑梗死应用依达拉奉联合奥扎格雷钠治疗的疗效。方法回顾性分析2012年12月至2014年12月本院收治的69例急性脑梗死患者临床资料,按不同治疗方案分为两组,对照组33例行奥扎格雷钠治疗,研究组36例在其基础上行依达拉奉治疗,观察两组疗效及神经功能缺损评分。结果对照组神经功能的缺损评分显著高于研究组,差异具统计学意义(P<0.05)。结论急性脑梗死应用依达拉奉和奥扎格雷钠治疗的疗效显著。     

奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效观察

目的探讨奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效与安全性。方法将207例急性脑梗死患者随机分为观察组69例和对照A组69例、对照B组69例。观察组给予奥扎格雷钠联合依达拉奉治疗,对照A组给予奥扎格雷钠治疗,对照B组给予依达拉奉治疗。治疗前及治疗14d后对3组患者的凝血指标及临床神经功能缺损程度评分（NDS）进行评定,比较疗效及安全性。结果治疗14d后观察组的临床疗效明显优于对照A组和对照B组（P〈0．05）,血小板、凝血指标均在正常范围内。结论应用奥扎格雷钠联合依达拉奉治疗急性脑梗死,两药具有起到叠加互助有效作用,且没有明显不良反应,值得基层医院大力推广应用。     

依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效观察

目的观察依达拉奉联合奥扎格雷钠治疗急性脑梗死的有效性和安全性。方法选择符合标准的急性脑梗死患者102例,治疗组患者52例,给予常规治疗+奥扎格雷钠+依达拉奉联合治疗,对照组患者50例仅给予常规治疗+奥扎格雷钠治疗,治疗14d后比较疗效。结果治疗组总有效率为92.3%,对照组总有效率为88.0%,差异有统计学意义(P<0.05);神经功能缺损评分与对照组比较,差异有统计学意义(P<0.05),治疗期间未见严重不良反应。结论依达拉奉与奥扎格雷钠联合治疗急性脑梗死有协同效果,优于奥扎格雷钠单药治疗,安全性好。     

依达拉奉联合奥扎格雷钠治疗进展性脑梗死患者的疗效分析

目的讨论依达拉奉联合奥扎格雷钠治疗进展性脑梗死患者的疗效。方法回顾性分析62例进展性脑梗死患者的临床资料,采用数字单双号的模式分为对照组与治疗组,每组31例。对照组应用依达拉奉治疗,治疗组则采用依达拉奉联合奥扎格雷钠治疗,比较两组患者治疗后两周的神经功能缺损量表。结果治疗组在治疗1、2周后的神经功能缺损量表评分都明显优于对照组,差异具有统计学意义（P〈0.05）。结论采用依达拉奉联合奥扎格雷钠治疗进展性脑梗死患者,能够有效抑制脑血管痉挛情况进,促进患者的脑功能逐渐恢复。     

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.