川渝产山银花中绿原酸和总绿原酸的测定

目的 采用HPLC法和uV法测定川渝产山银花中的绿原酸和总绿原酸.方法 色谱柱为Dikma Kromasil C18柱(250mm ×4.6 mm,5 μm);流动相为乙腈-0.4%磷酸溶液(12:88);流速0.8 ml·min-1;检测波长326 nm;柱温30℃;进样量10μ1.结果 绿原酸0.8-8.0 μg具有良好的线性关系(r=0.9998),平均回收率为98.75%,RSD=0.29%.结论 方法操作简便、快速、具有良好的重复性和回收率,可作为川渝产山银花中绿原酸和总绿原酸的含量测定方法.     

HPLC法测定忍冬藤中绿原酸及咖啡酸含量

本文以绿原酸、咖啡酸为含量测定指标,采用HPLC法测定了不同产地忍冬藤中绿原酸、咖啡酸含量.色谱柱为DiamonsilTMC18,4.6mm×250mm,10μm柱,流动相为乙腈-0.2%磷酸溶液(11:89),检测波长为324nm.线性范围:绿原酸为0.08～0.40μg,r=0.9995,咖啡酸为0.03～0.15μg,r=0.9996;加样回收率:绿原酸为100.79%,RSD=2.17%,咖啡酸为98.05%,RSD=2.44%.本法快速、简便,重现性好,可用于控制忍冬藤的内在质量.     

高效液相色谱法测定感愈胶囊中绿原酸的含量

目的建立测定感愈胶囊中绿原酸含量。方法色谱柱为Kromasil C18柱（4.6 mm×250 mm,5μm）;流动相：乙腈-0.4%磷酸（10∶90）;流速1.0 ml.min-1;柱温：40℃;检测波长326 nm。结果绿原酸进样量在0.0414-0.828μg范围内线性关系良好（r=1.0000,n=7）,平均加样回收率为99.01%,RSD为1.40%（n=9）。结论该方法简便快速,结果准确,可用于感愈胶囊中绿原酸含量的测定。     

RP-HPLC法测定消银颗粒中绿原酸的含量

目的建立反相高效液相色谱法测定消银颗粒中绿原酸含量的方法。方法色谱柱:Zorbax SB-C18柱,流动相:乙腈-0.4%磷酸(12∶88),检测波长:327 nm,柱温:30℃。结果绿原酸进样量在0.094 7~0.568 0μg(r=0.999 9)范围内线性关系良好,平均回收率为99.79%,RSD值为1.86%(n=6)。结论该方法简便,快速,准确,适用于消银颗粒中绿原酸的含量测定。     

HPLC法测定速克感冒片中阿司匹林、绿原酸的含量

目的建立速克感冒片中绿原酸和阿司匹林的含量测定方法。方法采用高效液相色谱法,色谱柱C18柱(250 mm×4.6mm,5μm),测定阿司匹林的流动相为甲醇-水-冰醋酸(26∶23∶1)、检测波长为280 nm。测定绿原酸的流动相为甲醇-水-冰醋酸(13∶87∶1)、检测波长为327nm。结果线性范围:阿司匹林30.65~490.4 mg.L-1(r2=0.999 6)、绿原酸5.4~108 mg.L-1(r2=0.999 9)。加样回收率:阿司匹林为99.55%,RSD为0.38%(n=6);绿原酸为98.78%,RSD为0.56%(n=6)。结论本方法操作简单、结果准确,可作为控制本品质量的方法。     

HPLC测定细叶亚菊中的绿原酸

目的 采用HPLC测定细叶亚菊中的绿原酸含量.方法 采用Hypersil ODS-2柱(250 mm×4.6 mm,5 μm),流动相为甲醇-含0.04%磷酸的水溶液(19:81),流速1 mL·min~(-1),检测波长328 nm,柱温30℃.结果 绿原酸进样量的线性范围为0.0306～1.530 μg,与峰面积呈良好的线性关系(r=0.9999),平均回收率为99.7%,RSD=2.6%(n=5),细叶亚菊中绿原酸的含量为9.457 mg·g~(-1).结论 所建方法快速、简便、准确、重复性好,绿原酸可作为细叶亚菊的质量控制指标.     

HPLC测定炒苍耳子配方颗粒中绿原酸及咖啡酸的含量

目的建立同时测定炒苍耳子配方颗粒中绿原酸和咖啡酸的高效液相色谱法。方法采用Shim-packVP-ODS柱（250mm×4.6mm,5μm）;流动相为乙腈-0.1%磷酸水溶液（10：90）;检测波长为327nm;柱温为35℃。结果绿原酸在0.2152～1.7216μg内线性关系良好（r=0.9999）,咖啡酸在0.02296～0.1148μg内线性关系良好（r=0.9999）;绿原酸、咖啡酸平均加样回收率分别为96.39%（RSD=1.48%）、100.02%（RSD=1.81%）。结论所建立的方法简便、准确,可同时测定炒苍耳子配方颗粒中绿原酸和咖啡酸的含量。     

HPCL法测定忍冬藤中绿原酸含量

本文以绿原酸（Chlorogenic acid）为含量测定指标，采用HPLC法测定了不同产地忍冬藤中绿原酸含量。色谱柱为C18柱，流动相为甲醇-水-冰醋酸（20：80：1），检测波长为324nm，线性范围为0.049-0.441цg，r=0.9999；加样回收率为99.2%，RSD=1.4%。本法快速、简便，重现性好，可用于控制忍冬藤的内在质量。     

HPLC法测定银黄颗粒中绿原酸的含量

目的建立银黄颗粒中绿原酸的含量测定方法。方法采用高效液相色谱法,色谱柱VP-ODS柱(150 mm×4.6 mm,5μm);流动相:乙腈-0.4%磷酸溶液(13∶87),检测波长327 nm,流速1.0 ml.min-1,柱温室温。结果回归方程Y=-1.440×102 1.245×106X(r=0.999 9,n=5),绿原酸在0.88~13.2μg范围内线性良好,加样回收率99.39%,RSD=0.53%。结论本法灵敏度高,操作简便,重复性好,准确可靠,可作为银黄颗粒中绿原酸的含量测定方法。     

高效液相色谱法测定麻杏口服液中绿原酸和黄芩苷的含量

目的建立麻杏口服液中绿原酸和黄芩苷含量的测定方法。方法色谱柱为Smmetry Shield RP C18,绿原酸、黄芩苷的流动相分别为乙腈-0.4%磷酸溶液（13∶8）、甲醇-水-冰醋酸（50∶50∶1）,检测波长分别为327、274nm,流速为1.0mL·min^-1,进样量为20μL,柱温为25℃。结果绿原酸、黄芩苷进样量分别在0.1040mg（r=0.9998）、0.6240mg-6.240mg（r=0.9997）范围内与峰面积积分值呈良好的线性关系,平均回收率分别为96.4%（RSD=1.4%）、98.0%（RSD=1.1%）。结论本方法简便、准确,重现性、专属性好,可用于麻杏口服液的质量控制。     

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.     

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.     

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.     

Gender-related symptoms and correlates of alcohol dependence among men and women with a lifetime diagnosis of alcohol use disorders

This study explored gender-related symptoms and correlates of alcohol dependence in a crosssectional study of 150 men and 150 women with a lifetime diagnosis of alcohol use disorders (AUD). Participants were recruited in equal numbers from treatment settings, correctional centres and the general community. Standardized measures were used to determine participants' use of substances, history of psychiatric disorders and psychosocial stress, their sensation seeking and family history of substance use and mental health disorders. Multivariate analyses were used to detect patterns of variables associated with gender and the lifetime severity of AUD. Men had a longer history of severe AUD than women. Women had similar levels of alcohol dependence and medical and psychological sequelae as men, despite 6 fewer years of AUD. More women than men had a history of severe psychosocial stress, severe dependence on other substances and antecedent mental health problems, especially mood and anxiety disorders. There were differences in family history of alcohol-related problems approximating same-gender aggregation. The severity of a lifetime AUD was predicted by its earlier age at onset and the occurrence of other disorders, especially anxiety, among both men and women. The limitations in the generalizability of these findings due to sample idiosyncrasies are discussed.     

Biochemical and molecular characterisation of cubozoan protein toxins

Class Cubozoa includes several species of box jellyfish that are harmful to humans. The venoms of box jellyfish are stored and discharged by nematocysts and contain a variety of bioactive proteins that are cytolytic, cytotoxic, inflammatory or lethal. Although cubozoan venoms generally share similar biological activities, the diverse range and severity of effects caused by different species indicate that their venoms vary in protein composition, activity and potency. To date, few individual venom proteins have been thoroughly characterised, however, accumulating evidence suggests that cubozoan jellyfish produce at least one group of homologous bioactive proteins that are labile, basic, haemolytic and similar in molecular mass (42-46 kDa). The novel box jellyfish toxins are also potentially lethal and the cause of cutaneous pain, inflammation and necrosis, similar to that observed in envenomed humans. Secondary structure analysis and remote protein homology predictions suggest that the box jellyfish toxins may act as α-pore-forming toxins. However, more research is required to elucidate their structures and investigate their mechanism(s) of action. The biological, biochemical and molecular characteristics of cubozoan venoms and their bioactive protein components are reviewed, with particular focus on cubozoan cytolysins and the newly emerging family of box jellyfish toxins.     

Dose tolerability of chronically inhaled voriconazole solution in rodents

Invasive pulmonary aspergillosis (IPA) is a fungal disease of the lung associated with high mortality rates in immunosuppressed patients despite treatment. Targeted drug delivery of aqueous voriconazole solutions has been shown in previous studies to produce high tissue and plasma drug concentrations as well as improved survival in a murine model of IPA. In the present study, rats were exposed to 20 min nebulizations of normal saline (control group) or aerosolized aqueous solutions of voriconazole at 15.625 mg (low dose group) or 31.25 mg (high dose group). Peak voriconazole concentrations in rat lung tissue and plasma after 3 days of twice daily dosing in the high dose group were 0.85 ± 0.63 μg/g wet lung weight and 0.58 ± 0.30 μg/mL, with low dose group lung and plasma concentrations of 0.38 ± 0.01 μg/g wet lung weight and 0.09 ± 0.06 μg/mL, respectively. Trough plasma concentrations were low but demonstrated some drug accumulation over 21 days of inhaled voriconazole administered twice daily. Following multiple inhaled doses, statistically significant but clinically irrelevant abnormalities in laboratory values were observed. Histopathology also revealed an increase in the number of alveolar macrophages but without inflammation or ulceration of the airway, interstitial changes, or edema. Inhaled voriconazole was well tolerated in a rat model of drug inhalation.