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1  of pneumonia, bronchiolitis, bronchitis, or bronchial hyperreactivity.
2 have allergic airway inflammation and had no bronchial hyperreactivity.
3  T cells had no effect on the development of bronchial hyperreactivity.
4  bronchodilator and 24 percent (9 of 37) had bronchial hyperreactivity.
5 cus occlusion of the airways, and results in bronchial hyperreactivity.
6 lated with disease chronicity, severity, and bronchial hyperreactivity.
7 ucus occlusion of the airways and results in bronchial hyperreactivity.
8 ; and provocation with histamine to test for bronchial hyperreactivity.
9 rition during pregnancy results in offspring bronchial hyperreactivity.
10                                              Bronchial hyperreactivity, airway inflammation, and sens
11 nd lung function impairment and increases in bronchial hyperreactivity and eosinophilic lower airway
12 ic bronchial inflammation, post-AAI mice had bronchial hyperreactivity and increased inflammatory cel
13  IL-33 and eotaxin production, eosinophilia, bronchial hyperreactivity, and goblet cell hyperplasia i
14 similar baseline pulmonary function, without bronchial hyperreactivity, and had not participated in a
15 ressed allergen-induced airway eosinophilia, bronchial hyperreactivity, and in vitro allergen-recall
16 antly related to lower respiratory symptoms, bronchial hyperreactivity, and reductions in blood total
17 f eosinophils into the airways and increased bronchial hyperreactivity as are observed in human asthm
18 atal variables and the prevalence of asthma, bronchial hyperreactivity (BHR), flexural eczema (FE), a
19 llergic inflammation of the airways and with bronchial hyperreactivity (BHR).
20 ord: a compensatory event mitigating against bronchial hyperreactivity, but a mechanism that evokes b
21 ecretion, airway goblet cell metaplasia, and bronchial hyperreactivity compared to controls.
22 flammation of airways, mucus production, and bronchial hyperreactivity in a mouse model.
23 en with ACE inhibitors and may contribute to bronchial hyperreactivity in asthma.
24 ns were associated with an increased risk of bronchial hyperreactivity in children (risk ratio, 1.41;
25 Helminth infections may increase the risk of bronchial hyperreactivity in children and atopy in adult
26  exposure and the prevalence and severity of bronchial hyperreactivity in firefighters without severe
27 nophilic inflammation, mucus production, and bronchial hyperreactivity in response to HDM inhalation
28 he influence of developmental programming on bronchial hyperreactivity is investigated in an animal m
29 ode cytokine production, lung histology, and bronchial hyperreactivity measured.
30 measurements of fetal growth were related to bronchial hyperreactivity, measured at age six years usi
31 t new data on the persistence of nonspecific bronchial hyperreactivity (methacholine PC20 < or =8 mg/
32 promoting asthmatic phenotypes, establishing bronchial hyperreactivity, or influencing the response t
33  demonstrated that complement contributes to bronchial hyperreactivity, recruitment of airway eosinop
34          eNO, sputum induction combined with bronchial hyperreactivity testing, and exhaled breath co
35 th during 11-19 weeks' gestation had greater bronchial hyperreactivity than those with more rapid abd
36  exhibited much weaker responses in terms of bronchial hyperreactivity to aerosolized methacholine, l
37  for the proasthmatic phenotypes of enhanced bronchial hyperreactivity to contraction mediated by M(3
38 duces airway epithelial mucin production and bronchial hyperreactivity to methacholine challenge.
39 luid that was predominantly eosinophils, and bronchial hyperreactivity to methacholine.
40       Among the cohort without severe cough, bronchial hyperreactivity was present in 77 firefighters
41  longitudinal study were to (1) determine if bronchial hyperreactivity was present, persistent, and i
42 ssed by using multicolor flow cytometry, and bronchial hyperreactivity was studied.
43 noglobulin synthesis, airway remodeling, and bronchial hyperreactivity were measured.
44  Th2 cytokine induction, IgE production, and bronchial hyperreactivity were prevented by coadministra
45        Likewise, T-cell cytokine content and bronchial hyperreactivity were reduced.
46 and neutrophil influx in the lung along with bronchial hyperreactivity, which were reversed by IL-17