ライフサイエンスコーパス: bronchodilation

1 e or Syk and p38 MAPK did not cause additive bronchodilation.

2 % [63.1-88.5] vs 82.9% [67.8-95.9], p=0.001) bronchodilation.

3 pressure fluctuations, can generate greater bronchodilation.

4 ransmural pressures can lead to only limited bronchodilation.

5 low limitation at day 0 was reversible after bronchodilation.

6 VC of 10% of predicted value or greater with bronchodilation.

7 ective airway reflexes, ciliary beating, and bronchodilation.

8 e exacerbation and provided modest sustained bronchodilation.

9 ay smooth muscle (ASM) relaxation leading to bronchodilation.

10 mportant than distal alveolar deposition for bronchodilation.

11 position for the larger particles, with less bronchodilation.

12 th a mean FEV(1) of 1.32+/-0.44 liters after bronchodilation (48% of predicted value), we randomly as

13 Therefore, the mechanism for reduced bronchodilation after DIs in subjects with mild asthma c

14 There was no bronchodilation after nine doses of the 5-lipoxygenase i

15 Bronchodilation after salbutamol was equal to or greater

16 ansient decreases in Pa(O(2)) levels despite bronchodilation, an effect that has been attributed to t

17 me in 1 second (FEV(1)) of 70% or less after bronchodilation and a ratio of FEV(1) to forced vital ca

18 not significantly different before and after bronchodilation and are different in patients with COPD

19 From these outcomes, bronchodilation and bronchoprotection indices were const

20 the trial (ranging from 87 to 103 ml before bronchodilation and from 47 to 65 ml after bronchodilati

21 omisation table for an assessment of safety, bronchodilation, and bronchoprotection.

22 fects of pathologic status, session, reader, bronchodilation, and CT examination were assessed by usi

23 s mediated by the EP2 receptor, unrelated to bronchodilation, and increased with time of exposure.

24 c inflammation in asthma may impede NO-based bronchodilation, and reveal that pharmacologic sGC agoni

25 ep inspiration-induced bronchoprotection and bronchodilation are impaired in asthma.

26 These results indicate the potential of dual bronchodilation as a treatment option for patients with

27 ) given twice daily cause the same degree of bronchodilation as tiotropium bromide given once daily.

28 e bronchodilation and from 47 to 65 ml after bronchodilation), as compared with the placebo group (P<

29 decline in the mean FEV(1) before and after bronchodilation beginning on day 30.

30 acholine responsiveness, deep-breath-induced bronchodilation (DeltaR(rs) ) and bronchoscopy with endo

31 th decreased and increased FENO levels after bronchodilation, depending on the site of airway obstruc

32 that pharmacologic sGC agonists can achieve bronchodilation despite this loss.

33 here were no significant session, reader, or bronchodilation effects on WT in third-generation airway

34 mucus production from submucosal glands and bronchodilation have been proposed.

35 onse to beta2 -agonists, as well as impaired bronchodilation in a mouse lung slices.

36 We recently described rapid TLR7-mediated bronchodilation in guinea pigs.

37 struction in all four groups, albeit percent bronchodilation in healthy subjects was somewhat stronge

38 nists BAY 41-2272 and BAY 60-2770, triggered bronchodilation in normal human lung slices and in mouse

39 RPL554 produced rapid bronchodilation in patients with asthma with an FEV1 inc

40 airway smooth muscle (ASM) causes a stronger bronchodilation in vitro and in vivo than beta2 agonists

41 n is associated with bronchoconstriction and bronchodilation in vivo.

42 Up to day 5 of hospital stay, FEV1 after bronchodilation increased by 90 mL daily (50.8-129.2) an

43 FEV1 after bronchodilation increased more rapidly and to a greater

44 on was equal to their ability to prevent it (bronchodilation index [BDI] versus bronchoprotection ind

45 Although bronchodilation is a cornerstone of treatment, current b

46 nsive characterization of salmeterol-induced bronchodilation, little is known about the molecular act

47 TLR7-mediated bronchodilation may be a new therapeutic strategy in ast

48 se (COPD) is a condition in which continuous bronchodilation may have clinical advantages.

49 already been induced by MCh, following a DI, bronchodilation occurred in the healthy subjects but fur

50 us to hypothesize that the maximum possible bronchodilation of an airway depends on its static compl

51 le blocking activated L-type VDCCs to induce bronchodilation of contracted ASM.

52 ls of peroxidases and H(2)O(2), NO-dependent bronchodilation of preconstricted tracheal rings was rev

53 potentially provide additive or synergistic bronchodilation over either inhaled antimuscarinic or be

54 bromide), in COPD is encouraging because the bronchodilation produced is of a magnitude greater than

55 eated group: percentage predicted FEV1 after bronchodilation rose from 25.7% (95% CI 21.0-30.4) to 32

56 e dissociation between bronchoprotection and bronchodilation suggests that the two effects involve di

57 rental interviews, clinical examinations and bronchodilation test of 138 of those children at 11-13 y

58 ) were more efficacious and achieved greater bronchodilation than 200 microg MDI albuterol (deltaFEV1

59 Alpha-adrenergic blockade may promote mild bronchodilation that offsets non-selective beta blockade

60 decline in the mean FEV(1) before and after bronchodilation were not significant.

61 (R)-enantiomer of racemic albuterol produces bronchodilation, whereas the (S)-enantiomer may increase

62 impaired subsequent beta(2)-agonist-induced bronchodilation, which occurred independently of changes

63 to understand the mechanisms underlying this bronchodilation, which remain ill-defined.

64 RPL554 produced bronchodilation with a mean maximum FEV1 increase of 17.

65 expiratory volume in 1 second (FEV1) before bronchodilation, with a difference of 0.10 liters (P=0.0