不同产地白肋烟腺毛分泌物GC-MS分析

目的:用气相色谱一质谱法分析4种不同产地的白肋烟腺毛分泌物化学成分.方法:采用二氯甲烷提取烟叶腺毛分泌物,毛细管柱进行分折,归一化法测定其百分含量,并用气相色谱一质谱法对化学成分进行鉴定.色谱条件:色谱柱为HP-5MS 5% Phenyl Methyl Siloxane (30m×0.25mm×0.25μm)弹性石英毛细管柱,柱温:80℃(8min)10℃/min200℃(10min)3℃/min280℃(10min);分流进样,分流比20:1;进样温度230℃,汽化室温度300℃.质谱条件:电离方式EI,电子能量70ev,离子源温度200℃,质量扫描范围30～500AMU.结果:对比各烟叶的总离子流图,进行了组分分析.不同产地白肋烟腺毛分泌物成分的总离子流图有较大共同点,但亦存在不同之处,各组分的相对百分含量不尽相同,共鉴定出52种化合物.结论:本方法稳定可靠,重现性好,适用于烟叶腺毛分泌物的化学成分分折.     

气相色谱-质谱法分析不同树龄肉桂挥发油成分

目的:用气相色谱-质谱法对不同树龄肉桂挥发油进行化学成分的分析。方法:采用水蒸气蒸馏法从肉桂中提取挥发油。毛细管柱进行分析,归一化法测定其百分含量,并用气相色谱-质谱法对化学成分进行鉴定。色谱条件:SE-30弹性石英毛细管柱(15 m×0.2 n.mm×0.33 mm),柱温:70℃(1 min)8℃·min~(-1)→250℃(5 min);分流进样,分流比30:1;进样温度250℃。质谱条件:电离方式EI,电子能量70 eV,接口温度280℃,离子源温度230℃,四级杆温度100℃,质量扫描范围29-450AMU,溶剂延迟2.0 min。结果:对比各药材的总离子流图,进行了组分差异分析。不同树龄肉桂的总离子流图有较大共同点,但亦存在不同之处,各组分的相对百分含量不尽相同。共鉴定出49个成分,占挥发油总组分的95%以上。结论:本方法稳定可靠,重现性好,适用于中药挥发油的化学成分分析。     

佩兰挥发油化学成分的研究

目的:用气相色谱-质谱法对山东平邑及河南南阳产佩兰挥发油进行化学成分的分析。方法:采用水蒸气蒸馏法从2种佩兰中提取挥发油。采用不同类型的毛细管柱进行分析,找出最佳分析条件,用归一化法测定其百分含量,并用气相色谱-质谱法对化学成分进行鉴定。色谱条件:SE-54毛细管柱(25m×0.25mm,0.25μm),柱温90℃(7min)5℃·min~(-1) 260℃(10 min);分流进样,分流比1:50;进样温度对270℃,FID检测器,温度为270℃。结果:山东平邑产佩兰共鉴定了38个成分,占挥发油总成分的82％以上;河南南阳产佩兰共鉴定了39个成分,占挥发油总成分的82％以上。结论:本方法稳定可靠,重现性好,适用于中药挥发油的化学成分分析。     

丁香挥发油化学成分的研究

目的:用气相色谱-质谱法对广东饶平及印度尼西亚产丁香挥发油进行化学成分的分析。方法:采用水蒸气蒸馏法从2种丁香中提取挥发油。采用不同类型的毛细管柱进行分析,找出最佳分析条件,用归一化法测定其百分含量,并用气相色谱-质谱法对化学成分进行鉴定。色谱条件:SE-54毛细管柱(25 m×0.25 mm,0.25μm),柱温90℃(5 min)11℃·min~(-1)170℃(3min)4℃·min~(-1) 230℃(30 min);分流进样,分流比1:50;进样温度280℃,FID检测器,温度为280℃。结果:广东饶平产丁香共鉴定了22个成分,占挥发油总成分的84％以上;印度尼西亚产丁香共鉴定了26个成分,占挥发油总成分的83％以上。结论:本方法稳定可靠,重现性好,适用于中药挥发油的化学成分分析。     

桂枝挥发油化学成分的GC／MS分析

目的 :用气相色谱 -质谱法对桂枝挥发油进行化学成分的分析。方法 :采用水蒸气蒸馏法从桂枝中提取挥发油。试用不同类型的毛细管柱进行分析 ,找出最佳分析条件 ,用归一化法测定其百分含量 ,并用气相色谱-质谱法对化学成分进行鉴定。色谱条件 :SE - 5 4毛细管柱 (2 5m× 0 2 5mm ,0 2 5 μm) ,柱温 90℃ (8min)4℃·min-12 30℃ (10min) ;分流进样 ,分流比 1∶5 0 ;进样温度 2 5 0℃ ,FID检测器 ,温度为 2 5 0℃。结果 :共鉴定了 37个成分 ,占挥发油总成分的 92 %以上。结论 :本方法稳定可靠 ,重现性好 ,适用于中药挥发油的化学成分分析     

不同方法提取的香椿子挥发油的气质联用成分分析

目的:采用超临界 CO_2流体萃取法及水蒸气蒸馏法从香椿籽中提取挥发油,用气相色谱-质谱联用技术对其化学成分进行分析。方法:采用超临界 CO_2流体萃取法与水蒸气蒸馏法从香椿籽中提取挥发油,用归一化法测定其百分含量。用气相色谱-质谱法对化学成分进行鉴定。色谱条件:DB-5毛细管柱(30 m×0.25 mm,0.25μm);程序升温:初始温度60℃,保持5 min,以4℃·min~(-1)升至180℃,保持10 min,再以15℃·min~(-1)升至260℃,保持50 min;分流进样,分流比50:1;进样口温度280℃。结果:超临界 CO_2流体萃取法提取的挥发油共鉴定了63种成分,占挥发油总成分的88%以上;水蒸气蒸馏法提取挥发油共鉴定了50种成分,占挥发油总成分的94%以上。结论:超临界 CO_2流体萃取法提取的挥发油能更真实、全面地反映药材中的化学成分。     

气相色谱-质谱法分析十八味珍宝香挥发油的化学成分

目的:采用气相色谱-质谱联用法对藏香十八味珍宝香的挥发油成分进行分析。方法:采用2010年版中国药典挥发油测定法对藏香十八味珍宝香挥发油进行提取,以毛细管柱进行分析,面积归一化法测定其百分含量,并用气相色谱-质谱法对化学成分进行鉴定。色谱柱为Rtx-5Sil MS弹性石英毛细管色谱柱(30 m×0.25 mm,0.25μm);升温程序:起始温度为60℃,以8℃.min-1升温至150℃,再以6℃.min-1升温至260℃,保持8 min;进样口温度为260℃;进样不分流。质谱条件:EI源,接口温度为280℃,电子能量70 eV,离子源温度230℃;扫描范围50~800 amu。结果:共分离鉴定出46个化学成分,相对含量超过5%的成分有异愈创木醇(18.29%)、愈创木醇(11.46%)、丁香酚(9.65%)、α-红没药烯(7.74%)、β-桉叶醇(7.70%)。结论:十八味珍宝香能够应用于卫生防御领域。     

草豆蔻挥发油化学成分的GC/MS研究

目的：用气相色谱-质谱法对草豆蔻挥发油进行化学成分的分析。方法：采用水蒸气蒸馏法从草豆蔻中提取挥发油，试用不同类型的毛细管柱进行分析。找出最佳分析条件。用归一化法测定各组分的相对百分含量。并用气相色谱-质谱法对其化学成分进行鉴定。结果：共鉴定了37个成分，占挥发油总成分的88%以上。结论：此方法稳定可靠，重现性好，适用于中药挥发油的化学成分分析。     

八角香兰果实挥发性成分的气相色谱／质谱分析

目的:利用气相色谱/质谱法对八角香兰果实挥发性成分进行分析研究。方法:采用水蒸气蒸馏法从八角香兰果实中提取总挥发油,然后经毛细管柱分离,用归一化法计算含量;色谱条件:DB-5MS 型石英毛细管柱(30 m×0.25 mm×0.25μm),起始柱温60℃维持3 min,以10℃·min~(-1)升至140℃,再以2℃·min~(-1)升至180℃;质谱条件:电离方式:EI,离子源温度:200℃,电子能量:70 eV。结果:分离和鉴定出22种化学成分,其中黄樟醚含量最高,占挥发油总量的92.81%,为挥发油的主要成分。结论:本法简便、快速、准确。     

广西莪术挥发油化学成分的分析

采用气相色谱-质谱联用仪(GC-MS)对广西莪术挥发油进行分离测定.色谱柱HP-5MS毛细管柱(30.0m×250μm×0.25μm), 进样温度250℃,不分流;程序升温:初始65℃:恒温2min,以5℃/min升至90℃恒温3 min,以20℃/min升至103℃恒温3 min,以8℃/min升至150℃恒温15 min,以20℃/min升至280℃.结合计算机检索对分离的化合物进行结构鉴定,用色谱峰面积归一化法测定各成分的相对百分含量.结果共分离得到52个气相色谱峰,鉴定出20种化学成分,其中β-榄香烯、莪术酮、莪术醇、莪术二酮4种主要抗肿瘤活性成分均能检测到.此方法可用于莪术原料药材和莪术挥发油制剂的检测和相对含量测定.     

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.