克林霉素-过氧苯甲酰凝胶对皮肤刺激和过敏反应试验

目的:观察克林霉素-过氧苯甲酰凝胶对豚鼠皮肤的刺激性和过敏反应。方法:用克林霉素-过氧苯甲酰凝胶多次接触豚鼠完整皮肤及破损皮肤,观察皮肤刺激性;对豚鼠皮肤重复接触,观察过敏反应。结果:克林霉素-过氧苯甲酰凝胶对豚鼠完整皮肤及破损皮肤无刺激性,对豚鼠无皮肤局部过敏反应和全身过敏反应。结论:克林霉素-过氧苯甲酰凝胶对皮肤无刺激性和过敏性作用,具有良好的皮肤用药安全性。     

甲磺酸帕珠沙星搽剂皮肤用药安全性实验

目的：对甲磺酸帕珠沙星搽剂进行皮肤急性毒性试验、皮肤刺激性试验及皮肤过敏性试验,以考察其皮肤用药安全性。方法：将甲磺酸帕珠沙星搽剂涂抹于家兔背部完整或破损区脱毛皮肤,观察给药后动物局部皮肤红斑及水肿等急性毒性和刺激性情况。采用致敏与激发接触甲磺酸帕珠沙星搽剂,观察豚鼠过敏反应。结果：甲磺酸帕珠沙星搽剂对家兔完整或破损皮肤无明显局部毒性或局部刺激性。对豚鼠皮肤无过敏反应。结论：甲磺酸帕珠沙星搽剂短期皮肤用药是安全的。     

咳喘凝胶贴膏皮肤安全性考察

摘要：目的:制备咳喘凝胶贴膏,并进行皮肤安全性评价。方法:将处方药材经水煎煮提取、浓缩制成一定比例的药液加入凝胶贴膏基质并快速涂抹,制成凝胶贴膏;分别进行大鼠皮肤急性毒性、家兔皮肤刺激性、豚鼠皮肤过敏性试验,观察咳喘凝胶贴膏对动物经皮给药的急毒性、刺激性和过敏性。结果:皮肤急性毒性试验中,大鼠完整皮肤及破损皮肤均未出现红斑及水肿;皮肤刺激性试验中,家兔完整及破损皮肤组未出现异常情况;豚鼠皮肤过敏性试验中,咳喘凝胶贴膏低剂量及高剂量组均无过敏反应。结论:咳喘凝胶贴膏临床剂量用于大鼠、家兔及豚鼠皮肤安全、可靠。     

紫苏油乳剂的皮肤刺激和过敏反应研究

目的：对紫苏油乳剂进行皮肤急性毒性试验、皮肤刺激性试验及皮肤过敏性试验,以了解其安全性。方法：将紫苏油乳剂用于家兔背部完整或破损去毛区皮肤,观察其产生急性毒性和皮肤刺激性情况;采用致敏与激发接触紫苏油,观察豚鼠过敏情况。结果：紫苏油乳剂未产生明显皮肤刺激性;反复致敏后使用,也无皮肤与全身过敏反应。结论：紫苏油乳剂皮肤用药是安全的。     

糖足洗液皮肤安全性的动物实验

目的：观察糖足洗液对动物皮肤的毒性作用。方法皮肤急性毒性试验采用最大给药量法,观察大鼠完整皮肤及破损皮肤接触糖足洗液后所产生的急性毒性反应和死亡情况;皮肤刺激性试验观察实验兔完整皮肤皮肤和破损皮肤多次接触糖足洗液后所产生的刺激反应情况和恢复情况;皮肤过敏性试验观察豚鼠经皮肤重复接触糖足洗液后所产生的皮肤过敏反应及过敏强度。结果糖足洗液对大鼠完整皮肤及破损皮肤未见急性毒性反应、对实验兔完整皮肤皮肤和破损皮肤无刺激性、对豚鼠皮肤无致敏作用。结论糖足洗液皮肤急性毒性、皮肤刺激以及皮肤过敏试验结果未见明显毒性反应,用于糖尿病足的治疗是较安全的。     

盐酸特比萘芬乳膏的皮肤安全性评价

目的对盐酸特比萘芬乳膏进行皮肤过敏和刺激试验,为其应用提供临床前安全性评价依据。方法将1%盐酸特比萘芬乳膏涂敷于豚鼠背部皮肤,三次致敏接触,隔14天后,再涂药激发接触,观察过敏反应;用1%盐酸特比萘芬乳膏多次重复涂敷于家兔完整及破损皮肤（1次/天,共21天）,采用同体左右侧自身对比,涂药期间每日观察局部皮肤红斑及水肿情况。结果皮肤过敏性试验中盐酸特比萘芬乳膏组豚鼠给药部位皮肤均无出现红斑及水肿等过敏反应。皮肤刺激性试验对家兔皮肤无刺激性。结论盐酸特比萘芬乳膏对家兔皮肤无刺激性,对豚鼠皮肤未出现过敏症状。     

复方利多卡因乳膏外用安全性试验

目的:对复方利多卡因乳膏进行了动物实验研究,包括皮肤急性毒性试验,皮肤过敏性试验和皮肤刺激性试验,以了解其安全性。方法:将不同剂量的复方利多卡因乳膏用于白色豚鼠背部正常和破损去毛区皮肤,观察其产生急性毒性情况;采用致敏与激发接触复方利多卡因乳膏,观察动物过敏情况;以一次给药和多次给药方法,将复方利多卡因乳膏外涂于白色豚鼠背部正常和破损去毛区皮肤,观察其产生豚鼠皮肤刺激性反应。结果:复方利多卡因乳膏未产生急性毒性反应,反复致敏后使用也无皮肤与全身过敏反应,一次或多次给药的刺激性强度对豚鼠正常皮肤平均反应分值均低于0.5分,对破损皮肤平均反应分值在给药后24 h和48h高于0.5分,但低于2.99分,48 h或72 h后平均反应分值均低于0.5分。结论:外用复方利多卡因乳膏未产生急性毒性和过敏反应,对豚鼠正常皮肤无刺激性,对破损皮肤有轻度刺激性,但给药后48 h或72 h,这种刺激性消失。     

复方环磷腺苷乳膏毒性研究

目的:考察复方环磷腺苷乳膏经皮肤给药的安全性.方法:将不同剂量的复方环磷腺苷乳膏和基质用于白色豚鼠背部正常或破损去毛区皮肤,观察皮肤急性毒性、刺激性反应和动物的过敏情况.结果:复方环磷腺苷乳膏未产生急性毒性反应;反复致敏后使用,也无皮肤与全身过敏反应;一次或多次给药对豚鼠正常皮肤无刺激性.对破损皮肤有轻度刺激性,但给药后 48 h 或 72 h,这种刺激性消失.结论:复方环磷腺苷乳膏未产生急性毒性和过敏反应,也无明显刺激性反应.     

舒阴洗液皮肤毒性及黏膜刺激性实验研究

目的对舒阴洗液进行了部分动物实验研究,包括皮肤急性毒性实验、皮肤刺激性实验、皮肤过敏性实验及黏膜刺激性实验,以了解其安全性。方法将不同剂量的舒阴洗液用于大耳白兔背部完整或破损去毛区皮肤,观察其产生急性毒性和皮肤刺激性情况;采用致敏与激发接触舒阴洗液,观察豚鼠过敏情况;将舒阴洗液注入大耳白兔的阴道中,观察大耳白兔阴道黏膜的情况。结果舒阴洗液未产生皮肤急性毒性和刺激性;也未产生阴道黏膜刺激性;反复致敏后无皮肤与全身过敏反应。结论舒阴洗液是安全的新型外用洗剂。     

氯倍霜毒理学研究

目的对氯倍霜进行动物实验研究,包括皮肤急性毒性试验、皮肤过敏性试验和皮肤刺激性试验,以了解其安全性。方法将不同剂量的氯倍霜用于白色豚鼠背部正常或破损去毛区皮肤,观察其产生急性毒性情况;采用致敏与激发接触氯倍霜,观察动物过敏情况;以1次给药和多次给药方法,将氯倍霜外涂于白色豚鼠背部正常或破损去毛区皮肤,观察其产生豚鼠皮肤刺激性反应。结果氯倍霜未产生急性毒性反应,反复致敏后使用,也无皮肤与全身过敏反应,1次或多次给药的刺激性强度为对豚鼠正常皮肤平均反应分值均〈0．5分,对破损皮肤平均反应分值在给药后24h和48h〉0．5分,但〈2．99分,48h或72h后平均反应分值均〈0．5分。结论外用氯倍霜未产生急性毒性和过敏反应,对豚鼠正常皮肤无刺激性,对破损皮肤有轻度刺激性,但给药后48h或72h这种刺激性消失。     

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.