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1 13 are thought to be central to the allergic asthmatic response.
2 a key role in the activation of the allergic asthmatic response.
3 ory T cells into the BAL during the allergic asthmatic response.
4 cumulative component of the allergen-induced asthmatic response.
5 diator that is released in airways during an asthmatic response.
6 returned to baseline levels during the late asthmatic response.
7 e mechanism by which PGE(2) blocks the early asthmatic response.
8 nt effect on the allergen-induced dual-phase asthmatic response.
9 gnificantly reduce either the early- or late-asthmatic response.
10 s no effect on the fall in FEV1 during early asthmatic response.
11 after allergen challenge for early and late asthmatic responses.
12 measures of allergen-induced early and late asthmatic responses.
13 clinically attractive therapy for allergic, asthmatic responses.
14 ibutes to the development of severe allergic asthmatic responses.
15 nt for diminishing allergic and IgE-mediated asthmatic responses.
16 significantly attenuated both late and early asthmatic responses after allergen provocation in patien
17 lia and who also had biphasic early and late asthmatic responses after laboratory-based allergen prov
18 he role of eosinophils in mediating the late asthmatic response and causing airway hyper-responsivene
19 to increase during the immediate Ag-induced asthmatic response and continued to increase over 2-fold
20 s study introduce a novel participant in the asthmatic response and indicate that factor Xa functions
21 erged as a major contributor to allergic and asthmatic responses, and as such it represents an attrac
22 lammation in the lungs, inhibit allergic and asthmatic responses, and contribute to tolerance to inha
27 attenuated the fall in FEV1 during the late asthmatic response (both doses led to an 8.7% fall) vers
28 Inhaled prostaglandin (PG) E2 might inhibit asthmatic responses, but the mechanisms involved remain
29 t rich in IL-4, these CD8(+) T cells mediate asthmatic responses, but the mechanisms regulating the c
30 fter 28 days, SB010 attenuated the mean late asthmatic response by 34%, as compared with the baseline
33 tically significant attenuation of the early asthmatic response (EAR) by GSK2190915; treatment differ
34 ist (LABA) vilanterol (VI) on early and late asthmatic responses (EAR/LAR) and airway hyper-responsiv
36 ponse, whereas nitrosylation during the late asthmatic response generates SNO, safe reservoirs for re
38 combinant PAF-AH (rPAF-AH) on the dual phase asthmatic response in atopic subjects with mild asthma.
40 and placebo, for 7 days, on allergen-induced asthmatic responses in 18 non-smoking and 17 smoking ato
41 ach allergen (CRA), an allergen that induces asthmatic responses in both humans and mice, to further
45 btained at 4 h (n = 7), the time of the late asthmatic response (LAR) (n = 5), or 24 h (n = 4) after
47 stically significant attenuation of the late asthmatic response (LAR) by GSK2190915; the treatment di
50 rgen would seem to dictate the nature of the asthmatic response, little is known regarding how tolera
51 t of monoclonal antibody to IL-5 on the late asthmatic response or on airway hyper-responsiveness to
52 dose of allergen needed to provoke an early asthmatic response, reduced the mean maximal fall in FEV
53 malayi can result in development of a severe asthmatic response termed tropical pulmonary eosinophili
54 demonstrated a positive skin test and a dual asthmatic response to allergen inhalation challenge.
55 Th2 and mast cells are participants in the asthmatic response to allergens, and both cell types pro
56 Clinical experiments demonstrate that the asthmatic response to an aeroallergen can be enhanced by
58 HR1 have pharmacogenetic effects influencing asthmatic response to corticosteroids, provide a rationa
59 treatment greatly reduces the severity of an asthmatic response to several types of bronchoconstricto
61 tenuated the early (0-2 h) and late (4-10 h) asthmatic responses to inhaled allergen compared with pl
63 reactive oxygen species during the immediate asthmatic response, whereas nitrosylation during the lat
65 heep effectively antagonized antigen-induced asthmatic responses, with 70-75% blockade of the early r
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