盐酸多柔比星的高效毛细管电泳法分析

用高效毛细管电泳法测定盐酸多柔比星的含量。考察不同试验条件下盐酸多柔比星的胶束动电毛细管电泳行为。选择５０ｍｍｏｌ／Ｌ十二烷基硫酸钠，５０ｍｍｏｌ／Ｌ硼 溶液（ｐＨ８．７）含１０％乙腈为运行缓冲液，以β－萘磺酸钠为内标，于２３１ｎｍ波长处测定。在０．１７～０．８５ｇ／Ｌ的范围内呈良好的线性关系，ｒ＝０．９９９４，重现性实验ＲＳＤ为２．５％（ｎ＝５）。     

氟罗沙星注射剂治疗40例尿路感染的临床疗效

目的：比较氟罗沙星与氧氟星注射剂治疗尿路的感染的临床疗效。方法：将８０例尿路感染病例随机分为两组，分别应用氟罗沙星（０．２￣０．４ｇ／ｄ）和氧氟沙星（０．２￣０．４ｇ／ｄ）。结果：氟罗沙星组和氧氟沙星组的总有效率分别为８５％和８０％，细菌清除率分别为９２．５％和８７．５％，两组间无显著差异（Ｐ〉０．０５）。不良反应发生率分别为１２．５％和７．５％（Ｐ〈０．０５）。结论：氟罗生注射剂治疗尿路感染用药     

氟罗沙星与环丙沙星治疗细菌性感染的比较

目的：评价氟罗沙星注射液对细菌性感染的疗效及安全性。方法：１６２例病人随机分为氟罗沙星治疗组、环丙沙星对照组各６１例和氟罗沙星开放组４０例。氟罗沙星治疗和开放组用氟罗沙星０．２～０．４ ｇ,静脉滴注,ｑｄ;环丙沙星对照组用环丙沙星,０．２～０．４ ｇ,静脉滴注,ｂｉｄ;疗程均为 ７～１４ｄ。结果：氟罗沙星注射液治疗总有效率为 ９３．１％（９３／１０１）与环丙沙星相当,治疗组有效率为９２％（５６／６１）与对照组８２％（５０／６１）相似（Ｐ＞０．０５）;但前者的细菌清除率（９４％）高于后者（８６％, Ｐ＜０． ０５）;不良反应发生率氟罗沙星（６％）也与环丙沙星（８％）相似（Ｐ＞０．０５）。结论：氟罗沙星注射液对细菌性感染有效而安全。     

脂必妥对大鼠高脂血症模型血脂水平的影响

目的：研究脂必妥的降脂疗效。方法：通过对大鼠腹腔注射脂酶抑制剂——１０％泰洛沙泊溶液（３ｍＬ／ｋｇ）后７ｍｉｎ，分别用脂必妥２．５９，１．２９，０．６５ｇ／ｋｇ，及洛伐他汀１０ｍｇ／ｋｇ灌胃给药。结果：脂必妥２．５９ｇ／ｋｇ组及洛伐他汀组（１０ｍｇ／ｋｇ）的胆固醇（ＴＣ）值分别降低３３％（Ｐ＜０．０１）及３１％（Ｐ＜０．０１），组间比较Ｐ＞０．０５；低密度脂蛋白胆固醇（ＬＤＬ－ｃｈ）值分别降低５０％（Ｐ＜０．０１）及４４％（Ｐ＜０．０１）；脂必妥１．２９ｇ／ｋｇ组亦能降低ＴＣ及ＬＤＬ－ｃｈ值１８％（Ｐ＜０．０５）及２６％（Ｐ＜０．０５）；小剂量０．６５ｇ／ｋｇ的脂必妥仅能降低ＴＣ１４％（Ｐ＜０．０５）；各组对三酰甘油（ＴＧ）值均无显著降低作用（Ｐ＞０．０５）。结论：脂必妥有显著降低血脂过多大鼠ＴＣ及ＬＤＬ－ｃｈ值的作用。     

甲苯磺酸托氟沙星胶囊溶出度测定方法的研究

本文报道用盐酸液（０．１ｍｏｌ／Ｌ）作溶剂，以转篮法测定甲苯磺酸托氟沙星胶囊的溶出度，按本实验测得的吸收系数（Ｅ_（１ｃｍ）~（１％））为７３８计算主药的溶出量。本法简便、灵敏、准确，甲苯磷酸托氟沙星的平均回收率为１００．２％，ＲＳＤ＝０．４５％（ｎ＝８）。     

盐酸林可霉素口服液在人体内药动学和生物利用度

８名健康受试者一次口服盐酸林可霉素的口服液和片剂两种剂型后，用高效液相－电化学（ＨＰＬＣ－ＥＤ）法测定盐酸林可霉素的血药浓度，其血药浓度符合一室模型。结果盐酸林可霉素口服液和片剂主要药动学参数分别为：Ｃ_(ｍａｘ)：５．０±０．５ｍｇ／Ｌ和４．３±０．６ｍｇ／Ｌ；Ｔｍａｘ：２．１６±０．２１ｈ和２．３±０．６ｈ；ＡＵＣ：３７±７（ｍｇ·ｈ）／Ｌ和３６±７（ｍｇ·ｈ）／Ｌ。盐酸林可霉素口服液对片剂的相对生物利用度为１０４±５％，可认为口服液与片剂生物等效。     

盐酸伊达比星的半合成研究

以柔红霉索为原料，经八步反应制得盐酸伊达比星，总收率为24．2％。本法具有反应路线短，反应条件温和，操作简单等优点，适合工业化生产。     

高效液相色谱法测定定喘止咳胶囊中三组分的含量

用反相高效液相色谱法在ＯＤＳ柱上以甲醇－０．１ｍｏｌ／Ｌ磷酸二氢钾液（ｐＨ３．０）－０．０２ｍｏｌ／Ｌ庚烷磺酸钠液（５８．５：３５．５：６）为流动相，采用时间程序设定检测波长，选用醋酸洗必泰为内标物对定喘止咳胶囊中氨茶碱、盐酸溴己新和扑尔敏进行了分离和含量测定，方法简便，准确，各组份的线性关系良好，平均回收率：氨茶碱９９．８％，ＲＳＤ１．２７％；盐酸溴己新９９．５％，ＲＳＤ１．２９％；扑尔敏９６．４％，ＲＳＤ１．２９％（ｎ＝６）。     

HPLC法同时测定呋麻滴鼻液中二组分的含量

本文采用高效液相色谱法，以扑尔敏为内标，ＵＶ检测波长为２５７ｎｍ，以ＹＷＧ－Ｃ１８为固定相，甲醇－０．０１ｍｏｌ／Ｌ磷酸二氢钾（ｐＨ３．０）为流动相，同时测定呋麻滴鼻液中呋喃西林和盐酸麻黄素的含量。方法简便、快速准确。各组分与内标具有良好的线性关系和分离度。平均回收率（ｎ＝５）及相对标准偏差为：呋喃西林（９９．４３±０．３５）％，盐酸麻黄素（９９．１４±０．７５）％。     

高效液相色谱法测定双扑伪麻片中扑热息痛、盐酸伪麻黄碱、扑尔敏的含量

用高效液相色谱法,同时分离测定双扑伪麻片中扑热息痛、盐酸伪麻黄碱和扑尔敏的含量．线性范围：扑热息痛０２０～０８０ｇ／Ｌ,ｒ＝０９９９５;盐酸伪麻黄碱００１２～００４８ｇ／Ｌ,ｒ＝０９９９６;扑尔敏００００７２～０００２８８ｇ／Ｌ,ｒ＝０９９９２．平均回收率（ｘ±ｒｓｄ）％分别为：扑热息痛（１００２±１７）％;盐酸伪麻黄碱（９９６±１４）％;扑尔敏（９８４±２６）％．     

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.