复方酮康唑霜的二阶导数分光光度测定

采用二阶导数分光光度法测定复方酮康唑霜中酮康唑的含量，可以消除制剂中氯霉素和空白基质等的干扰，方法简便、准确。平均回收率为９９．３９％，ＲＳＤ为０．５５％。     

用二阶导数紫外法快速检测酮康唑软膏有效成分

目的：建立酮康唑软膏主成分快速检测方法。方法：采用二阶导数紫外分光光度法直接测定酮康唑的含量。检测波长为277nm。结果：相关系数r=0．9959，回收率为99．87％，RSD=0．70％。结论：方法简便快速，结果准确。     

用 HPLC 法测定复方酮康唑霜中酮康唑含量

复方酮康唑霜是我院应用多年的外用抗真菌药（主要由酮康唑、特美肤等成分组成），疗效确切。为保证制剂质量和疗效均衡性，采用高效液相色谱（HPLC）法对处方中主药酮康哇进行了含量测定。1试药与仪器1．1试药：二氯甲烷、乙醚均为分析纯，酮康唑对照品系英国进口（符合BP标准）。复方酮康唑霜，由我院制剂室提供。1．1．1酮康唑对照品溶液制备：精密称取80℃减压干燥至恒重的酮康唑对照品适量，加甲醇溶解，使之成为01mg／ml。1．1．2供试品溶液的制备：复方酮康唑霜约1g，精密称量置分液漏斗中，加二氯甲烷-乙醚（2：1）混合液40ml，…     

一阶导数光谱法测定复方酮康唑霜的含量

一阶导数光谱法测定复方酮康唑霜中酮康唑的含量，可消除基质的干扰．在４～１２ｍｇ／Ｌ范围内线性关系良好，回收率为９９．９１％，ＲＳＤ＝０．７９％。     

强灭霜的研制与质量控制

报道强灭霜的处方及制备方法，建立了用一阶导数光谱法测定其主药甲硝唑含量的方法，以290nm为测定波长，平均回收率为99．75％（RSD为0．67％）.     

差示分光光度法测定复方酮康唑霜中酮康唑的含量

差示分光光度法测定复方酮康唑霜中酮康唑的含量解放军广州医学高等专科学校５１０３１５夏志祥，兰树敏，詹重明复方酮康唑霜为医院内部制剂，主要成分有：酮康唑、丙酸倍氯米松、硫酸新霉素等。组成和功效与多效癣炎霜［１］相似。含量测定方法主要是高效液相色谱法［２...     

高效液相色谱法测定复方酮康唑霜中酮康唑含量

为测定复方酮康唑霜中酮康唑含量，采用高效液相色谱法，于239nm检测，结果表明，酮康唑量在0.5～2.5μg范围内峰面积与浓度线性关系良好，平均回收率为97．56%(RSD=0.43%)，结论：本方法准确、稳定，重现性好，可作为样品的测定方法。     

紫外分光光度法测定复方酮康唑软膏中酮康唑和氧氟沙星的含量

目的：建立复方酮康唑软膏的含量测定方法。方法：用双波长分光光度法测定酮康唑的含量，用单波长法测定氧氟沙星的含量。结果：两被测组分的平均回收率和相对标准偏差分别为酮康唑１００．３３％和０．３２％；氧氟沙星１００．８５％和０．２７％。结论：方法简便、准确，可用于复方酮康唑软膏的质量控制。     

双波长分光光度法测定复方萘替芬霜的含量

用双波长等吸收点法测定复方萘替芬霜中萘替芬和酮康唑的含量。方法：萘替芬测定在２８３ｎｍ和３０１ｎｍ进行。酮康唑测定在２４２ｎｍ的２６５ｎｍ进行。结果：该法线性良好,精密度高。结论：该法可用于复方萘替芬霜的含量测定。     

高效液相色谱法测定酮康唑乳膏中酮康唑含量

目的建立测定酮康唑乳膏中酮康唑含量的方法。方法采用反相高效液相色谱法,固定相为十八烷基硅烷键舍硅胶柱（150mm×4．6mm,5um）,流动相为0．5％醋酸铵溶液-0．2％二异丙铵的甲醇溶液（23：77）,流速为1．0mL／min,检测波长为240nm。结果酮康唑质量浓度在0．1—2．0mg／mL范围内与峰面积呈良好的线性关系（r=0．9999）,最低检测限为0．2ug／mL。平均加样回收率为100．39％,RSD为0．58％（n=9）。结论该方法专属性好,准确、灵敏,可用于酮康唑乳膏中酮康唑的含量测定。     

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.     

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.