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流行病学研究表明,空气细颗粒污染物(PM_(2.5))的暴露与过敏性疾病有一定的联系;然而,PM_(2.5)暴露与过敏性疾病之间的关系尚未完全阐明,特别是室内环境中PM_(2.5)涉及到过敏或非过敏的作用不详.为了比较研究过敏与非过敏儿童室内PM_(2.5)的细胞毒性,在武汉市洪山区10户家庭室内进行了为期3个月的采样,分别收集过敏与非过敏儿童的室内PM_(2.5).采用有机/元素碳测定仪对二者PM_(2.5)成分中的含碳组分进行了分析,并通过检测昆明小鼠巨噬细胞的形态及吞噬功能影响、细胞活力、乳酸脱氢酶(LDH)漏出率等指标,来检测PM_(2.5)暴露所致的细胞毒性.结果表明,高剂量(200μg·mL~(-1))PM_(2.5)暴露对小鼠巨噬细胞的形态及吞噬功能会产生不利的影响;与非过敏儿童的室内PM_(2.5)暴露组相比,过敏儿童的室内PM_(2.5)暴露组诱导巨噬细胞产生的毒性作用更明显.细胞体外测试结果提示:在相同PM_(2.5)暴露剂量下,引起儿童过敏症的室内PM_(2.5)成分具有重要影响.  相似文献   
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DINP皮肤暴露对小鼠过敏性皮肤炎症的佐剂作用   总被引:1,自引:0,他引:1  
为了探究新型增塑剂邻苯二甲酸二异壬醋(DINP)对小鼠过敏性皮肤炎症的影响,采用皮肤染毒的暴露方式,56只SPF级雄性Balb/C小鼠随机平均分为7组处理40d用0、1.4、14和140mg/kg DINP对小鼠进行皮肤染毒,并用抗氧化剂褪黑素设置2组来探究氧化应激的介导作用,以及1组生理盐水对照组染毒结束后取耳组织测定耳肿指数和双耳重量差,并制作耳组织病理学切片,最后检测氧化应激指标.实验结果显示,14和140mg/kg DINP皮肤暴露组的皮肤炎症有明显加剧(p0.01),氧化应激指标也有明显变化(p0.01).这表明,一定浓度的DINP,经较长时间的暴露,对小鼠过敏性皮肤炎症具有明显的佐剂作用、并且,随着DINP浓度升高,小鼠机体氧化应激过度活化,造成机体组织或细胞的氧化损伤,并加剧了炎症反应.  相似文献   
3.
为了研究增塑剂邻苯二甲酸二异壬酯(diisononyl phthalate,DINP)致Allergic March的作用机制,以雄性BALB/c小鼠为受试动物,随机分为5组,包括空白对照组(生理盐水)、20 mg·kg-1 DINP组、OVA组、20 mg·kg-1 DINP+OVA组和4-苯基丁酸(4-PBA)拮抗组(20 mg·kg-1 DINP+OVA+4-PBA),染毒周期为47 d.以肺组织匀浆测定活性氧(reactive oxygen species,ROS)、还原型谷胱甘肽(glutathione,GSH)、丙二醛(malondialdehyde,MDA)和一氧化氮(nitric oxide,NO).采用ELISA试剂盒检测血清中总免疫球蛋白E(T-IgE)、OVA特异性免疫球蛋白E(OVA-IgE)和白细胞介素-33(IL-33)评价机体的炎症因子,并同时观察肺组织的病理变化结果.与生理盐水组比较,OVA组的肺功能、Th2免疫系统功能亢进的分子、氧化应激指标和肺组织病理学损伤都有所加重.与OVA组比较,20 mg·kg-1 DINP+OVA组的肺功能、Th2免疫系统功能亢进的分子、氧化应激指标和肺组织病理学损伤同样也有所加重.而4-PBA拮抗组(20 mg·kg-1 DINP+OVA+4-PBA)与20 mg·kg-1 DINP+OVA组相比较,其各项指标都有了明显的减轻.实验结果表明,20 mg·kg-1的DINP能加重小鼠的Allergic March,内质网应激拮抗剂4-PBA可使Allergic March症状减轻,对小鼠肺组织起保护作用,说明内质网应激通路可能通过调节氧化应激介导了DINP所致的Allergic March.  相似文献   
4.
Air pollution poses a serious threat to human health in Asia. This study analyzes the association of air pollutants and greenness with incidence rates of allergic rhinitis in Seoul at the administrative district level to gain insight into district-level urban policies to improve public health. A spatial regression model is constructed to investigate the correlation between allergic rhinitis incidence rates and five air pollutants measured at 128 air pollution monitoring stations around Seoul: sulfur dioxide (SO2), particulate matter less than 10 μm (PM10), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO). The allergic rhinitis incidence data are derived from the National Health Insurance Service’s database that includes the number of allergic rhinitis-related clinic visits by the patients over 20 years of age and living in Seoul. A kriging geostatistical interpolation was used to estimate average air pollution level of 423 administrative districts. To assess pollen concentrations that can affect allergic rhinitis, the average normalized difference vegetation index (NDVI) is measured based on the urban greenness. The model, controlling for built environment and socio-economic attributes, identifies the possibility of a weak association between allergic rhinitis incidence rates and carbon monoxide levels. The NDVI value is negatively correlated with allergic rhinitis incidence rates, implying a complicated aspect in relation to the effect of urban greenness.  相似文献   
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Epidemiological studies have shown that there is a link between asthma and brain damage,but toxicological studies have not fully confirmed yet,especially the effects of asthma on the brain. In this study,at first,we explore the effects of asthma on the brain through the establishment of an allergic asthma model. Then PM_(2.5),a typical outdoor air pollutant and formaldehyde,a typical indoor air pollutant were selected to be closer to the true environment and find whether there is any synergism between them. In this study,an ovalbumin( OVA)-sensitized mice asthma model was established. 30 male Balb/c mice were randomly divided into 5 groups:( 1) saline control group,( 2) OVA-sensitized group,( 3) OVA-combined with formaldehyde exposure group,( 4) OVA-combined with PM_(2.5) exposure group,( 5) Combination of OVA,formaldehyde and PM_(2.5) exposure group. The mice were inhaled with formaldehyde or/and instilled with PM_(2.5) from day 1 to 18. The mice asthma model was developed by OVA sensitization and challenge. The mice were sensitized with OVA+Al( OH)3( 5 mg OVA and 175 mg Al( OH)3 in 30 m L saline each time) or saline( 30 m L saline each time) by intraperitoneal injection on day 1,7 and 14.This was then followed by an aerosol challenge in 1% OVA( 30 min·d~(-1)) from day 19 to 25( 7 times) using an ultrasonic nebulizer. On the 26 th day,the organ coefficient of mice brain was counted,then the contents of oxidative stress of mice brain were measured,including reactive oxygen species( ROS),glutathione( GSH) and malondialdehyde( MDA),and the concentrations of NF-κB and interleukin-1β( IL-1β) were detected by using ELISA kits.Detection of interleukin-6( IL-6) was made with immunohistochemical method. Histological assay for brain was also conducted. In our results,all the OVA treated groups showed a significant increase of ROS and a significant decrease of GSH contents when compared with the control group. Except OVA-sensitized group,other OVA treated groups also showed a significant increase of MDA contents when compared with the control group,and MDA contents of OVA-sensitized group showed significant change when compared to the combined exposure group. In ROS and GSH,combined exposure showed some joint effect compared with single exposure. When OVA was applied in combination with formaldehyde and PM_(2.5),NF-κB was activated. And all the OVA treated groups showed increased levels of IL-1β and IL-6 compared with the control group. And the combined exposure showed an aggravated effect when compared with OVA-sensitized group. Histopathological observation of the hippocampus in mice brain clearly showed the difference of eosin( EO) stained neurons in the combined exposure group compared with the control group and OVA-sensitized group. The pyramidal neurons of the mice with allergic asthma exposed to formaldehyde and/or PM_(2.5) had been reduced in number,the cells were swollen and the dendrites had disappeared. Allergic asthma can cause damage to the brain through oxidative stress. Exposure to formaldehyde and PM_(2.5) will increase the damage caused by allergic asthma to the brain,which may be mediated by oxidative stress and NF-κB activation.This promotes the release of the inflammatory factors,resulting in increased inflammation.  相似文献   
6.
为了考察大气细颗粒物水溶性成分与过敏性疾病的相关性,对北京市石景山区PM2.5中水溶性离子分布特征进行分析,对文献中报道的有机酸浓度进行总结,选取其中9种典型水溶性无机盐(硝酸铵、硫酸铵、氯化铵、硝酸钠、无水硫酸钠、硝酸钾、硫酸钾、硝酸钙、硫酸钙)及3种水溶性有机酸(丙二酸、丁二酸、乙二酸)进行肥大细胞激活实验,观察上述成分经IgE及非IgE途径对肥大细胞β-Hex释放率的影响.结果表明:铵离子、硝酸离子和硫酸离子是研究区PM2.5中占比最大的3种离子,丙二酸、丁二酸、乙二酸是北京市PM2.5中3种浓度较高的水溶性有机酸.非IgE途径下,100μg·mL-1的9种水溶性无机盐和80μg·mL(-1(的3种水溶性有机酸均无法提高肥大细胞β-Hex释放率.IgE途径下,仅观察到80μg·mL-1丙二酸能使肥大细胞β-Hex释放率提高约3%,其增敏作用还需进一步研究证实.本研究将为进一步研究PM2.5水溶性成分诱发或加重过敏性疾病的潜在机制...  相似文献   
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