GC测定甲苯咪唑中的残留溶剂

目的 采用顶空气相色谱法测定甲苯咪唑原料药中的有机溶剂残留量。方法 以DMF-H₂O（2︰1）溶液为样品溶剂,选用PerkinElmer气相色谱仪,配备顶空进样器和FID检测器,Agilent DB-624毛细管柱为分析柱,外标法测定。结果 甲醇、乙醇、异丙醇、三氯甲烷和甲苯分别在18.7~224,46.9~562,46.9~562,1.50~17.9,2.81~33.8 μg·mL^-1内线性关系良好（r>0.999）;各组分检出限分别为0.19,0.10,0.11,0.18,0.08 μg·mL^-1;各组分回收率为90.0%~110.0%。结论 该方法准确、灵敏、可靠,可用于甲苯咪唑有机残留溶剂的测定。     

高效液相色谱法测定长春西汀注射液中长春西汀的含量

目的 建立测定长春西汀注射液中长春西汀含量的高效液相色谱法。方法 色谱柱为Luna C₁₈柱(250 mm×4.6 mm,5 μm),流动相为乙腈 - 0.2mol.L_-1乙酸铵水溶液(58：42),检测波长为280nm,流速为1.0mL.min_-1。结果 长春西汀浓度在40.2～301.8μg.mL_-1范围内与峰面积呈现良好线性关系(r=0.99996),平均回收率为100.00%(RSD=0.04%),检出限为0.017μg.mL_-1,定量限为0.053μg.mL_-1。结论 该方法操作简便、灵敏、准确,适用于长春西汀注射液的含量测定。     

毛细管顶空气相色谱法测定左乙拉西坦中的残留溶剂

目的建立毛细管顶空气相色谱法测定左乙拉西坦有机残留溶剂。方法选用气相色谱配备顶空进样器法进行测定,DB-624毛细管柱作为分析柱,采用FID检测器;并对溶剂测定有影响的因素进行研究。结果甲醇在12~90μg·mL~(-1)、丙酮在20~150μg·mL~(-1)、二氯甲烷在1.44~10.8μg·mL~(-1)、乙酸乙酯在20~150μg·mL~(-1)与峰面积线性关系良好(r>0.999);各组分检测限分别为0.032、0.021、0.11、0.011μg·mL~(-1);4种溶剂回收率均在90%~110%以内,RSD<10.0%(n=5)。结论该方法简单、可靠、准确,可用于左乙拉西坦有机残留溶剂的测定。     

HPLC法测定浓维磷糖浆3种成分的含量

目的：建立同时测定浓维磷糖浆中咖啡因、维生素B₁和烟酸含量HPLC方法。方法：采用UltiMate XB-C18柱(250mm×4.6mm,5μm)色谱柱；以0.1%辛烷磺酸钠(含0.1%磷酸)为流动相A、乙腈为流动相B,梯度洗脱；流量1.0 mL.min_-1；柱温30℃；检测波长261nm。结果：咖啡因、维生素B₁和烟酸的线性范围分别为38.22μg/ml～382.25μg.mL_-1(r=1.0000)、7.28μg/ml～72.75μg.mL_-1(r=0.9995)和0.78μg/ml～7.84μg.mL_-1(r=1.0000)；平均回收率(n=9)分别为99.3%、99.8%、98.6%,RSD分别为0.66%、1.14%、1.30%。结论：所建方法快速、准确、可靠,可用于浓维磷糖浆的质量控制。     

顶空进样-毛细管气相色谱法测定伊潘立酮原料药中的溶剂残留

目的建立测定伊潘立酮原料药有机残留溶剂的顶空气相色谱法。方法采用顶空进样毛细管气相色谱法测定,色谱柱为DB-FFAP石英毛细管色谱柱(25m×320μm×3μm)。氮气为载气,测定伊潘立酮原料药中丙酮、乙醇与石油醚的残留量。结果 3种溶剂完全分离,在所考察的浓度范围内线性关系良好。伊潘立酮原料药中丙酮和石油醚的残留量的平均值分别为0.0371%、0.0291%,未检出乙醇。结论该方法简便、结果准确,适用于伊潘立酮原料药中有机残留溶剂的测定。     

HPLC测定奥格列汀中基因毒性杂质残留量

目的 建立奥格列汀原料药中基因毒性杂质的HPLC测定方法。方法 采用Zorbax SB-C₁₈色谱柱（250 mm×4.6 mm,5μm）,进样量：20 μl;流动相为0.1%乙酸水-乙腈（65：35）;流速为1mL·min^-1;紫外检测器,检测波长为220 nm;柱温为25℃,色谱乙腈为溶剂。结果 该方法专属性良好,测得苯磺酸异丙酯在4~60 μg·mL^-1内线性关系良好,平均回收率为98.56%（n=9,RSD=3.78%）,溶液在8 h内稳定。结论 该法操作简便,重复性好,结果准确可靠,可用于奥格列汀原料药中基因毒性杂质的测定。     

GC测定白芍总苷原料药中有机溶剂残留

目的 采用GC同时测定白芍总苷原料药中乙醇、乙酸乙酯和正丁醇3种残留溶剂。方法 检测器为氢火焰离子化检测器（FID）,色谱柱为Agilent DB-624石英毛细管柱（30 m×0.53 mm,3.0 μm）,溶剂为N,N-二甲基甲酰胺（DMF）,程序升温。结果 3种残留溶剂均能完全分离,乙醇、乙酸乙酯和正丁醇分别在24.60~491.98 μg·mL^-1（r=0.999 8）,21.01~420.25 μg·mL^-1（r=1.000 0）,23.37~467.48 μg·mL^-1（r=0.999 8）内与峰面积呈良好的线性关系,检测限分别为0.002 37%,0.000 08%和0.000 63%。结论 该方法简单可靠,灵敏度高,可用于白芍总苷原料中的残留溶剂控制。     

顶空毛细管气相色谱法测定本芴醇中多种残留溶剂

目的 建立测定本芴醇原料药中残留溶剂的顶空毛细管气相色谱法。方法 以DB-624毛细管柱(0.53 mm×30 m,3.0 μm)为色谱柱,氮气为载气,用FID检测器,测定本芴醇原料药中甲醇、乙醇、乙酸乙酯、甲苯、异丙醇和丙酮的残留量(外标法计算)。结果 6种有机溶剂完全分离,浓度在考察范围内与峰面积具有良好的线性关系,r为0.999 9~1.000 0,平均回收率为99.3%~101.5%,精密度RSD均<10%,最低检出限为0.173~0.396 μg·mL^-1。结论 本法快速、灵敏、准确,能较好地检测本芴醇原料药中有机溶剂残留量,控制产品质量。     

HPLC-PAD法测定硫酸依替米星注射液有关物质及含量

目的：建立硫酸依替米星注射液有关物质及含量的反相高效液相色谱-脉冲安培电化学(HPLC-PAD)法。方法：采用十八烷基硅烷键合硅胶为填充剂(4.6mm×250mm,5μm或效能相当的色谱柱),柱温35℃。以0.2mol.L_^-1三氟乙酸溶液(含0.05%五氟丙酸,1.5g.L_^-1无水硫酸钠,0.8%(V/V)的50%氢氧化钠溶液,用50%氢氧化钠溶液调节pH值至3.5)-乙腈(95：5)为流动相,流速为每分钟1.0ml。柱后加碱(50%氢氧化钠溶液1→25,流速每分钟0.5ml)。用积分脉冲安培电化学检测器检测。结果：依替米星在0.075~50μg.mL_^-1(r =0.9996)内线性关系良好;单个最大杂质的重复性试验的RSD(n =6)为1.4%,总杂质的重复性试验的RSD(n =6)为1.7%,含量测定的重复性试验的RSD(n =6)为0. 8%;方法的检测限(S/N =3)为75ng.mL_^-1,定量限(S/N =10)为250ng.mL_^-1;供试品溶液在12 h内稳定性良好。结论：经方法学验证,该方法可以用于硫酸依替米星注射液有关物质及含量的测定。     

顶空气相色谱法测定左卡尼汀原料药中三甲胺的含量

目的 建立了气相色谱法准确测定左卡尼汀原料药中三甲胺的检测方法。方法 采用程序升温法,FID检测器,色谱柱为Pora PLOT Amines毛细管柱(25 m×0.32 mm×10 μm)进行测定。结果 在选定的测定条件下,三甲胺在0.081 6~4.079 7 μg﹒mL^-1范围内与峰面积呈良好的线性关系,相关系数为0.999 1,平均回收率为99.6%（RSD=1.9%）,检测限为0.025 0 μg﹒mL^-1。结论 该气相色谱方法准确,灵敏度高,可用于左卡尼汀原料药中三甲胺的质量控制。     

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.