复方维A酸凝胶的制备及质量控制

目的：研制复方维A酸凝胶。方法：以卡波姆－940为凝胶基质，三乙醇胺调pH值，制备复方维A酸凝胶，采用联立方程组新解法进行凝胶定量分析。结果：pH值为6.5-7.5，测得3批样品含量分别为标示量的101.03%,100.78%,99.87%;RSD分别为0.65%,0.54%,0.78%，且凝胶稳定无变化，无刺激性。结论：本方法组方合理，稳定性好，可用于痤疮的治疗。     

红蓝光联合复方维A酸红霉素凝胶治疗痤疮疗效观察

目的：探讨红蓝光联合复方维A酸红霉素凝胶治疗痤疮的疗效。方法将228例患者随机分为治疗组（114例）和对照组（114例）。对照组：每晚外用复方维A酸红霉素凝胶。治疗组：红蓝光交替照射联合复方维A酸红霉素凝胶治疗。两组均治疗8周,在治疗后8、12周对两组患者进行疗效判定及比较。结果治疗组有效率为80.70%,对照组为56.14%,两组比较差异有统计学意义（P〈0.05）。结论红蓝光交替照射联合复方维A酸凝胶治疗痤疮疗效安全肯定。     

异维A酸红霉素凝胶治疗痤疮54例临床观察

目的观察异维A酸红霉素凝胶治疗痤疮的临床疗效。方法 108痤疮患者,随机分为对照组和研究组,各54例。对照组给予维A酸软膏,研究组应用异维A酸红霉素凝胶。对比两组效果。结果治疗后两组总有效率比较,研究组(94.4%)优于对照组(75.9%),差异具有统计学意义(P<0.05)。结论异维A酸红霉素凝胶治疗痤疮的临床疗效确切,值得临床应用推广。     

异维A酸红霉素凝胶治疗痤疮的疗效观察

目的:观察异维A酸红霉素凝胶治疗轻、中度寻常痤疮的疗效。方法:将50例轻、中度面部寻常痤疮患者按面部左右侧分为2组,治疗组:左侧面部外用异维A酸红霉素凝胶,每晚1次;对照组:右侧面部外用维胺脂维E乳膏,每晚1次。比较第6周和第8周2组疗效。结果:治疗第6周时,治疗组与对照组的有效率分别为70%、42%(P<0.05);治疗第8周时,治疗组与对照组的有效率分别为82%、76%(P>0.05);对于炎性皮损,在治疗第6、8周时,2组疗效差异有统计学意义(P<0.05)。结论:异维A酸红霉素凝胶治疗轻、中度痤疮疗效确切,起效较维胺脂维E乳膏快。当皮损以炎性丘疹为主时,异维A酸红霉素凝胶疗效优于维胺脂维E乳膏。     

异维A酸红霉素凝胶联合过氧苯甲酰凝胶治疗中、重度痤疮

目的观察异维A酸红霉素凝胶联合过氧苯甲酰凝胶治疗中、重度痤疮的疗效。方法将201例Ⅱ～Ⅳ度寻常痤疮患者随机分为2组,治疗组106例,对照组95例。治疗组予异维A酸红霉素凝胶联合过氧苯甲酰凝胶,对照组给予异维A酸红霉素凝胶治疗。每2周随访1次,观察疗效及不良反应,8周后进行治疗评定。结果治疗组痊愈率和有效率(58.49%、96.23%)高于对照组(36.84%、88.42%)。结论异维A酸红霉素凝胶联合过氧苯甲酰凝胶治疗中、重度痤疮较单纯外用异维A酸红霉素凝胶疗效好。     

异维A酸红霉素凝胶在寻常痤疮中的应用

目的评价异维A酸红霉素凝胶治疗寻常型痤疮的疗效及安全性。方法 90例寻常痤疮每晚清洁皮肤,干燥后外用异维A酸红霉素凝胶,8周为一疗程。结果痊愈率为25%,总有效率为88.3%,10例患者在治疗中出现脱屑,干燥,红斑或烧灼感,均较轻微,未经处理继续用药或者暂停用药后消失。结论异维A酸红霉素凝胶治疗轻中度寻常痤疮安全有效。     

痤疮露Ⅱ号搽剂的质量控制研究

目的制备痤疮露Ⅱ号搽剂并建立其质量控制方法。方法以乳糖酸红霉素为主药制备痤疮露Ⅱ号搽剂,采用紫外分光光度法在482 nm波长处测定乳糖酸红霉素的含量。结果制剂为无色透明液体,乳糖酸红霉素质量浓度的线性范围为16～48μg/mL(r=0.999 8),平均回收率为99.75%,RSD为1.29%(n=6)。结论本制剂制备工艺简便可行,疗效显著,质量稳定可控。     

维A酸霜的研制

目的：研究维A酸霜制备和质量控制的方法。方法：采用一阶导数光谱法测定维A酸的含量，结果：维A酸的平均回收率为99．7％（RSD＝1．1％），结论：该制剂制备工艺合理，擀控方法简便、可行。     

反相高效液相色谱法测定消痤凝胶中3种成分含量

目的建立测定消痤凝胶中替硝唑、氯霉素和维A酸含量的反相高效液相色谱法。方法采用反相高效液相色谱法，以不同的色谱条件分别测定。以C18为分析柱测定替硝唑和氯霉素，其流动相为甲醇：0.3%三乙胺水溶液（用冰醋酸调节pH值至4.5）：乙腈（20：65：15）；检测波长：290 nm；流速：1.0 mL·min 1；柱温：25 ℃。测定维A酸的流动相为甲醇：水：冰醋酸（98：2：0.01）；检测波长：350 nm；流速：1.0 mL·min 1；柱温：25 ℃。结果替硝唑和氯霉素的浓度与峰面积的线性范围分别是9.99～99.90 mg·L 1和19.65～196.50 mg·L 1，平均加样回收率分别为100.1%（RSD＝1.2%），100.3%（RSD＝0.9%）；维A酸浓度与峰面积的线性范围分别是0.98～9.80 mg·L 1；平均加样回收率分别为101.0%（RSD＝1.7%）。结论该法可用于该制剂的含量测定。     

维A酸霜的研制

目的　研究制定维A酸霜制备和质量控制的方法。方法　采用一阶导数光谱法测定维A酸的含量。结果　维A酸的平均回收率为 99.7% (RSD =1 1% )。结论　该制剂制备工艺合理 ,质控方法简便、可行     

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.