孙丽平教授从肺脾论治气虚质小儿反复呼吸道感染经验

小儿反复呼吸道感染是儿科临床常见病及多发病,严重影响儿童的生长发育和身心健康。孙丽平教授从小儿体质特点出发,指出气虚质是反复呼吸道感染患儿的常见体质,其本质为元气虚弱,气的功能长期低下导致脏腑气血阴阳失衡,故疾病反复发作。孙教授以五行学说为指导,提出气虚质小儿反复呼吸道感染当从肺脾论治,祛邪以治标,扶正以固本。同时注重"治未病"思想在临床中的应用,通过调节患儿体质,从根本上降低了小儿反复呼吸道感染的发生率。附案例1则,以资验证。     

王烈教授运用泻肺方治疗小儿咳嗽变异性哮喘风热袭肺证经验

王烈教授认为小儿咳嗽变异性哮喘风热袭肺证发作与先天不足、后天失养,肺脾肾虚以及风、气、痰、瘀有关。外因为风,病机关键为气逆、痰阻和血瘀。当以哮论治,明确提出"久咳痰瘀终成哮"的观点,以疏风清肺、解痉止咳为主要治法,创立泻肺方治疗小儿咳嗽变异性哮喘发作期风热袭肺证,临床随证加减,疗效满意。同时重视药后调护,强调预防上呼吸道感染、避免接触过敏源、进行适量的体育锻炼等。附典型案例1则,以资验证。     

孙思邈治疗小儿咳嗽学术特色探析

为了提高中医治疗小儿咳嗽的临床疗效,研读《备急千金要方》小儿咳嗽篇,并结合临床体会,探析孙思邈治疗小儿咳嗽的学术思想及临床经验。发现孙思邈治疗小儿咳嗽的学术特色鲜明,有很多方面与现今不同,主要包括:病机上"风冷入肺""膈中有癖""乳食"导致小儿咳嗽;病位仅言"肺脾";治法上善于辛温解表、宣肺通腑、温化痰浊,酌用攻逐。     

开瑞坦联合顺尔宁治疗小儿咳嗽变异性哮喘的临床研究

目的探讨开瑞坦联合顺尔宁治疗小儿咳嗽变异性哮喘的临床疗效。方法选择2010年3月至2011年6月我院收治的小儿咳嗽变异性哮喘患儿86例,随机将患儿分成研究组和对照组。两组患儿均给予硫酸特布他林和盐酸赛庚啶,而研究组则在此基础上加用开瑞坦与顺尔宁的联合用药,并对两组患儿的临床治疗效果进行比较分析。结果与对照组相比,研究组的显效率、总有效率均显著提高,而无效率则显著降低,差别均呈现出统计学意义(P<0.05);研究组的症状消失时间明显缩短,同时复发比率亦明显减少,差别均具有统计学意义(P<0.05)。讨论采用开瑞坦联合顺尔宁治疗小儿咳嗽变异性哮喘,其临床治疗效果较为显著,是小儿咳嗽变异性哮喘患者较为理想的联合用药方案。     

陈竹教授从脾治肺法辨治小儿咳嗽经验

总结陈竹教授从脾治肺法辨治小儿咳嗽的临床经验。陈教授认为小儿咳嗽的病因主要为外因"风",内因"虚",病理因素"痰",把小儿咳嗽分为初、中、后3期,指出小儿"脾常不足、肺常虚"因素应该贯穿治疗的始终,故以从脾治肺为总治则,初期以外感风邪为主,治以运脾宣肺祛风,予止嗽散加减;中期以脾虚生痰为主,治以运脾泻肺化痰,予自拟运脾泻肺化痰方;后期以肺脾两虚为主,治以运脾补肺补虚,予六君子汤加减。同时结合小儿推拿、穴位贴敷、拔罐、超声波穴位治疗等多种疗法,达到标本兼治、治病求本的目的。特别强调家长应培养小儿正确的喂养观,合理健康的饮食,良好的饮食习惯。附案例1则,以资验证。     

李家凤主任医师治疗小儿咳嗽经验总结

对李家凤主任医师治疗小儿咳嗽的经验进行总结提炼。李老师认为,小儿由于肺常不足,又属娇脏,故临床咳嗽多见。又因发病原因及年龄、体质等因素的不同,其临床证候各异。故外感咳嗽应以宣散为主;燥热咳嗽宣润并举;痰热咳嗽应清热豁痰;阴虚咳嗽则肺肾同治。     

布地奈德混悬液联合肺力咳糖浆治疗小儿咳嗽性变异哮喘的效果及安全性

目的 分析布地奈德混悬液联合肺力咳糖浆治疗小儿咳嗽性变异哮喘的效果及安全性.方法 前瞻性选取2015年5月至2016年5月于本院医治的134例小儿咳嗽性变异哮喘,依据给药方式的不同,分别设为研究组(67例)与对照组(67例).对照组布地奈德混悬液治疗,研究组肺力咳糖浆复合布地奈德混悬液治疗,比对两组肺功能指标改善情况、相关临床指标以及不良反应情况.结果 研究组肺功能相关指标改善情况优于对照组,差异有统计学意义(P＜0.05);研究组咳嗽消失时间、发作次数、医治时间等指标优于对照组,差异有统计学意义(P＜0.05);两组不良反应情况对比,差异无统计学意义(P＞0.05).结论 肺力咳糖浆复合布地奈德混悬液治疗小儿咳嗽性变异哮喘可改善肺功能指标,缩短医治时间与咳嗽消失时间,且无明显不良反应,具有一定临床应用与研究价值.     

一例慢性阻塞性肺疾病患者的药历及用药讨论

笔者通过撰写一例慢性阻塞性肺疾病患者药历,对其治疗方案、病程及用药情况进行分析,从而讨论临床药师在参与临床用药过程中,在药物使用方面的作用和优势,保证临床安全、合理、有效地使用药物。     

汪受传教授运用“肺主皮毛”理论治疗儿科疾病经验举隅

介绍了汪受传教授运用"肺主皮毛"理论治疗儿科疾病的经验。汪教授认为,肺、卫、皮毛之间关系密切,肺强则卫合而皮毛健,"肺主皮毛"功能失司,常导致肺、皮肤等多种病变。治疗上分别运用宣肺、清肺、补肺法治疗小儿咳嗽等肺系疾病、急性荨麻疹等皮肤病、小儿体虚汗证,临证效佳,颇有心得。附典型病案3则,以资说明。     

基于气机升降理论辨治小儿咳嗽变异性哮喘探析

基于气机升降理论,对小儿咳嗽变异性哮喘的发病脏腑特性、基本病机、治疗法则以及遣方用药等进行探讨,对小儿咳嗽变异性哮喘的临床治疗具有一定的指导价值。     

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.