Titlebook: Asthma Treatment; A Multidisciplinary D. Olivieri,P. J. Barnes,G. C. Folco Book 1992 Springer Science+Business Media New York 1992 Atmen.P

侧面上下

书目名称Asthma Treatment影响因子(影响力)




书目名称Asthma Treatment影响因子(影响力)学科排名




书目名称Asthma Treatment网络公开度




书目名称Asthma Treatment网络公开度学科排名




书目名称Asthma Treatment被引频次




书目名称Asthma Treatment被引频次学科排名




书目名称Asthma Treatment年度引用




书目名称Asthma Treatment年度引用学科排名




书目名称Asthma Treatment读者反馈




书目名称Asthma Treatment读者反馈学科排名

HALO

勉励

Injury and Repair of the Airway Epithelium in Asthma,rized by a marked accumulation of acute inflammatory cells including eosinophils and neutrophils (5-11). Both of these cell types possess a considerable armamentarium of proteases, oxidants and toxic molecules. There are, therefore, a number of mechanisms by which airway epithelial cell damage could

使隔离

tariff

Allergen Inhalation Increases Cough Sensitivity in Subjects with Allergic Asthma, heterogeneity of the populations studied, which included non-allergic and allergic asthmatics. Furthermore, subjects with allergic asthma were sensitized to allergens with different seasonal distribution. Therefore, we hypothesized that allergen exposure increases airway sensitivity to cough stimul

宠爱

https://doi.org/10.1007/978-3-642-57865-6thma, it is not a feature of mild stable disease as evidenced by studies of the numbers of tryptase positive mast cells and by morphometry of cells examined by electron microscopy. Release of cytokines, particularly IL-5, by lymphocytes, favour selective eosinophil adhesion to endothelium and their

Endometrium

不满分子

,Spannung, Verzerrung, Elastizitätsgesetz,rized by a marked accumulation of acute inflammatory cells including eosinophils and neutrophils (5-11). Both of these cell types possess a considerable armamentarium of proteases, oxidants and toxic molecules. There are, therefore, a number of mechanisms by which airway epithelial cell damage could

割公牛膨胀

https://doi.org/10.1007/978-3-662-07290-5clinical findings. Indeed, these and other studies have indirectly (by using variables derived from the classical three-compartment lung model, such as the venous admixture ratio or the physiologic dead space) recognised ventilation-perfusion (V./ Q) mismatching as the principal mechanism underlying

surrogate