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1 T cells had no effect on the development of bronchial hyperreactivity.
2 bronchodilator and 24 percent (9 of 37) had bronchial hyperreactivity.
3 cus occlusion of the airways, and results in bronchial hyperreactivity.
4 lated with disease chronicity, severity, and bronchial hyperreactivity.
5 ucus occlusion of the airways and results in bronchial hyperreactivity.
6 ; and provocation with histamine to test for bronchial hyperreactivity.
7 rition during pregnancy results in offspring bronchial hyperreactivity.
9 nd lung function impairment and increases in bronchial hyperreactivity and eosinophilic lower airway
10 ic bronchial inflammation, post-AAI mice had bronchial hyperreactivity and increased inflammatory cel
11 IL-33 and eotaxin production, eosinophilia, bronchial hyperreactivity, and goblet cell hyperplasia i
12 similar baseline pulmonary function, without bronchial hyperreactivity, and had not participated in a
13 ressed allergen-induced airway eosinophilia, bronchial hyperreactivity, and in vitro allergen-recall
14 antly related to lower respiratory symptoms, bronchial hyperreactivity, and reductions in blood total
15 f eosinophils into the airways and increased bronchial hyperreactivity as are observed in human asthm
16 atal variables and the prevalence of asthma, bronchial hyperreactivity (BHR), flexural eczema (FE), a
18 ord: a compensatory event mitigating against bronchial hyperreactivity, but a mechanism that evokes b
21 exposure and the prevalence and severity of bronchial hyperreactivity in firefighters without severe
22 he influence of developmental programming on bronchial hyperreactivity is investigated in an animal m
23 measurements of fetal growth were related to bronchial hyperreactivity, measured at age six years usi
24 t new data on the persistence of nonspecific bronchial hyperreactivity (methacholine PC20 < or =8 mg/
25 promoting asthmatic phenotypes, establishing bronchial hyperreactivity, or influencing the response t
26 demonstrated that complement contributes to bronchial hyperreactivity, recruitment of airway eosinop
28 th during 11-19 weeks' gestation had greater bronchial hyperreactivity than those with more rapid abd
29 exhibited much weaker responses in terms of bronchial hyperreactivity to aerosolized methacholine, l
30 for the proasthmatic phenotypes of enhanced bronchial hyperreactivity to contraction mediated by M(3
31 duces airway epithelial mucin production and bronchial hyperreactivity to methacholine challenge.
34 longitudinal study were to (1) determine if bronchial hyperreactivity was present, persistent, and i
36 Th2 cytokine induction, IgE production, and bronchial hyperreactivity were prevented by coadministra
38 and neutrophil influx in the lung along with bronchial hyperreactivity, which were reversed by IL-17
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