ライフサイエンスコーパス: bronchodilator

1 ct that is typically not reversed by inhaled bronchodilator.

2 erity and resolved soon with inhalation of a bronchodilator.

3 ms are not adequately controlled by a single bronchodilator.

4 airway contraction after administration of a bronchodilator.

5 ), especially before the administration of a bronchodilator.

6 change from baseline in lung function after bronchodilator.

7 baseline spirometric indices, or response to bronchodilator.

8 al criteria for evaluating responsiveness to bronchodilators.

9 c medications, including corticosteroids and bronchodilators.

10 ncy, especially prescriptions of long-acting bronchodilators.

11 is not adequately controlled by long-acting bronchodilators.

12 e also less sensitive to glucocorticoids and bronchodilators.

13 e use of inhaled corticosteroids and inhaled bronchodilators.

14 their potential as inhaled ultralong-acting bronchodilators.

15 led corticosteroids and beta(2)-adrenoceptor bronchodilators.

16 in clinical trials assessing the efficacy of bronchodilators.

17 ideration when assessing the efficacy of new bronchodilators.

18 ion of the airway, and is a novel target for bronchodilators.

19 lung function improvement with short-acting bronchodilators.

20 long-acting anticholinergic and beta-agonist bronchodilators.

21 OCE may therefore form novel targets for new bronchodilators.

22 ht be more responsive to corticosteroids and bronchodilators.

23 6,607 (24%) were treated with methylxanthine bronchodilators, 10,051 (14%) had sputum testing, 8354 (

24 most asthma prescription refills, including bronchodilators (16.7%; 95% CI: 16.1%-17.3%; p<0.001), i

25 -75), both before and after treatment with a bronchodilator (180 microg of albuterol).

26 function tests before and after the use of a bronchodilator (400 mug of salbutamol).

27 d supplemental oxygen, 67 515 (97%) received bronchodilators, 59,240 (85%) received systemic steroids

28 tiotropium, a drug widely prescribed for its bronchodilator activity in patients with chronic obstruc

29 oncentrations measured at baseline, and post-bronchodilator-administered pulmonary function assessed

30 Bronchodilator administration by metered-dose inhaler is

31 increment of 200 ml or greater in FEV1 after bronchodilator administration.

32 d that GCs 'rapidly' enhanced the effects of bronchodilators, agents used in the treatment of allergi

33 dependent association between atopy and post-bronchodilator airflow limitation in the general populat

34 apparent association between atopy and post-bronchodilator airflow limitation in the general populat

35 and smoking-specific incidence trends of pre-bronchodilator airflow obstruction (AO) among adults wit

36 nce of atopy, ever diagnosed asthma and post-bronchodilator airflow obstruction was 44.8%, 19.3% and

37 enrolled subjects with mild to moderate post-bronchodilator airflow obstruction.

38 In addition to bronchodilator and anti-inflammatory activity, clinical

39 nhibitor, RPL554 for its ability to act as a bronchodilator and anti-inflammatory drug.

40 outinely receive a combination of an inhaled bronchodilator and anti-inflammatory glucocorticosteroid

41 ptomatic current or former smokers, 42% used bronchodilators and 23% used inhaled glucocorticoids.

42 acy of "triple therapy" with two long-acting bronchodilators and an inhaled corticosteroid in chronic

43 icacy of triple therapy with two long-acting bronchodilators and an inhaled corticosteroid in chronic

44 er to individualised medicine with available bronchodilators and anti-inflammatory drugs.

45 controller medications, such as long-acting bronchodilators and biologics, may be required in modera

46 ed most patients with asthma similarly, with bronchodilators and corticosteroids, but these therapies

47 thma have a long history, beginning with the bronchodilators and evolving into compounds that suppres

48 way hyperresponsiveness (AHR), improves with bronchodilators and inhaled corticosteroids (ICSs), and

49 While bronchodilators and inhaled corticosteroids are the main

50 tor (beta(2)-AR) agonists are very effective bronchodilators and play a major role in every stage of

51 (beta(2)AR) agonists are the most effective bronchodilators and relax airway smooth muscle cells thr

52 New long-acting bronchodilators and their combinations are currently und

53 forced vital capacity of 0.70 or less after bronchodilators (and an FEV(1) of 70% or less of predict

54 with asthma, (2) prescribed at least rescue bronchodilator, and (3) had the first visit to the respi

55 Tiotropium is a safe and effective bronchodilator, and an alternative to salmeterol in this

56 ivided into two groups, antiinflammatory and bronchodilator, and analyzed separately.

57 tics, inotropes, digoxin, anesthetic agents, bronchodilators, and drugs that cause electrolyte imbala

58 en, intravenous fluids, inhaled short-acting bronchodilators, and nebulized adrenaline.

59 beta2-agonists, oral corticosteroids, other bronchodilators, and no medications were measured on a m

60 n COPD such as inhaled steroids, long-acting bronchodilators, and their combinations.

61 nformation to estimate the incidence of post-bronchodilator AO (AO(post-BD)), which is the primary ch

62 Bronchodilators are a standard medicine for treating air

63 Anti-inflammatory steroids and bronchodilators are the gold-standard therapy for asthma

64 Aerosolised bronchodilators are useful in mechanically ventilated pa

65 Are glucocorticoids, alone or combined with bronchodilators, associated with reduced admission rates

66 t wheezers had persistent FEV1 deficit after bronchodilator at 18 years (reduced 198 ml; 46,350).

67 ation is a cornerstone of treatment, current bronchodilators become ineffective with worsening asthma

68 ed RPL554 is an effective and well tolerated bronchodilator, bronchoprotector, and anti-inflammatory

69 e 6MWD was not different between placebo and bronchodilators but increased after surgical lung volume

70 It was originally used as a bronchodilator, but the relatively high doses required a

71 ral studies have documented that long-acting bronchodilators can reduce exacerbation rate and/or seve

72 sponse in adults with asthma who underwent a bronchodilator challenge.

73 on exacerbations after accounting for use of bronchodilators, corticosteroids, benzodiazepines, and b

74 beta2 agonists, implying that new and better bronchodilators could be developed.

75 at provide a structural basis for many other bronchodilators currently in use.

76 ensate and airway resistance (pre- and post- bronchodilator) did not improve an asthma prediction.

77 mAChR ('M3 receptor', from rat) bound to the bronchodilator drug tiotropium and identify the binding

78 or response, which measures lung response to bronchodilator drugs.

79 beta2-Agonists are effective bronchodilators due primarily to their ability to relax

80 The extent of renarrowing following the bronchodilator effect of DI was used to assess the conti

81 The safety and bronchodilator effect of RPL554 (0.018 mg/kg) was assess

82 RB2) gene did not influence the differential bronchodilator effect of salmeterol versus montelukast a

83 s limited to supportive care; the 'value' of bronchodilators, epinephrine, or corticosteroids for tre

84 An acute response to a short-acting bronchodilator, especially albuterol, predicted a positi

85 Overuse of beta2-adrenoceptor agonist bronchodilators evokes receptor desensitization, decreas

86 he first discovery of dual pharmacology MABA bronchodilators, exemplified by 1.

87 Post-bronchodilator FEV (1) (% predicted) in the subjects wit

88 culture is associated with an impaired post-bronchodilator FEV (1) , which might be partly responsib

89 ed by sequencing (MZ; n = 74) had lower post-bronchodilator FEV(1) (P = 0.007), FEV(1)/FVC (P = 0.003

90 0.28 and 0.11 for rs7937 and rs2604894), pre-bronchodilator FEV(1) (P = 0.08 and 0.04) and severe (GO

91 regnancy was positively associated with post-bronchodilator FEV(1) at 5 yr, with a 7-ml (95% confiden

92 known airflow limitation (defined as a post-bronchodilator FEV(1)/forced vital capacity [FVC] ratio

93 -0.043L, 95% CI -0.086 to -0.0009) and post-bronchodilator FEV(1)/FVC ratio (adj.

94 e smoking as it relates to the ratio of post-bronchodilator FEV(1)/FVC, but only among those with ato

95 Spirometry testing was completed and the pre-bronchodilator FEV1 % value calculated.

96 a reduced median (interquartile range) post-bronchodilator FEV1 (% predicted) (92.0 [75.6-105.4] vs.

97 Benralizumab also significantly improved pre-bronchodilator FEV1 (Q4W and Q8W) and total asthma sympt

98 Adult patients with uncontrolled asthma, pre-bronchodilator FEV1 40-80% predicted, and stable backgro

99 Post bronchodilator FEV1 and FEV1/FVC ratio are considered th

100 associations with spirometric measures (post-bronchodilator FEV1 and FEV1/FVC).

101 Mean pre-bronchodilator FEV1 change from baseline to week 56 was

102 chrysogenum was associated with a lower post-bronchodilator FEV1 compared with those not sensitised t

103 n only the high-reversibility subgroup (post-bronchodilator FEV1 improvement >/= 20%; n = 112) was an

104 70% of the predicted value, a ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0.

105 rformed measuring prebronchodilator and post-bronchodilator FEV1, FVC, FEV1/FVC, and maximum mid-expi

106 ry endpoint was change from baseline in post-bronchodilator FEV1.

107 percentage change in prebronchodilator/post-bronchodilator FEV1.

108 rometric category (1-4) on the basis of post-bronchodilator FEV1.

109 COPD was defined as post-bronchodilator FEV1/FVC <0.7.

110 Airflow limitation was defined as post-bronchodilator FEV1/FVC less than 0.70.

111 , COPD was spirometrically defined as a post-bronchodilator FEV1/FVC less than the lower limit of nor

112 were quantitative variables of pre- and post-bronchodilator FEV1/FVC ratio, FEV1 (liters), FEV1 (% pr

113 ciated with lower prebronchodilator and post-bronchodilator FEV1/FVC ratios among subjects without as

114 Patients (post-bronchodilator FEV1: 94 +/- 10% predicted; mean +/- SD)

115 r (beta2AR) agonist that is widely used as a bronchodilator for the treatment of persistent asthma an

116 ta-AR) agonists are the most common clinical bronchodilators for asthma.

117 Over-reliance on SABA bronchodilators for rapid symptom relief is common in re

118 hibit potential as inhaled ultra-long-acting bronchodilators for the treatment of asthma and chronic

119 Given the need for efficacious bronchodilators for treating obstructive lung diseases,

120 nd-point was the change from baseline in pre-bronchodilator forced expiratory volume in 1 s (FEV(1) )

121 Key secondary endpoints were pre-bronchodilator forced expiratory volume in 1 s (FEV1) an

122 atients were aged 40-80 years and had a post-bronchodilator forced expiratory volume in 1 s (FEV1) be

123 Eligible patients with COPD had post-bronchodilator forced expiratory volume in 1 s (FEV1) of

124 8-75 years with symptomatic asthma and a pre-bronchodilator forced expiratory volume in 1 s (FEV1) of

125 lled trial, eligible patients had COPD, post-bronchodilator forced expiratory volume in 1 s (FEV1) of

126 sed with COPD within 1 year (defined as post-bronchodilator forced expiratory volume in 1 s [FEV1] to

127 inistered standardised format (CRQ-SAS), pre-bronchodilator forced expiratory volume in 1 second (FEV

128 ll the patients were symptomatic, had a post-bronchodilator forced expiratory volume in 1 second (FEV

129 The ratio of post-bronchodilator FVC and TLC(CT) from chest CT (FVC/TLC(CT

130 Post-bronchodilator FVC, FEV(1), peak expiratory flow (PEF),

131 ed with the single longacting antimuscarinic bronchodilator glycopyrronium, with concomitant improvem

132 TS, and ERS recommend treatment with inhaled bronchodilators (Grade: strong recommendation, moderate-

133 s, inhaled corticosteroids, and short-acting bronchodilators) had insufficient evidence, showing eith

134 FEV1) after administration of a short-acting bronchodilator has been widely used to identify patients

135 ucocorticoids in addition to two long-acting bronchodilators has not been fully explored.

136 (PGE2), which, in addition to its role as a bronchodilator, has anti-inflammatory actions.

137 the benefit of a long-acting anticholinergic bronchodilator in addition to beta(2)-agonists in patien

138 garding the potential for H(2) S to act as a bronchodilator in developing airways in the context of o

139 The mostly widely used bronchodilators in asthma therapy are beta2-adrenorecept

140 isms on the treatment response to longacting bronchodilators in chronic obstructive pulmonary disease

141 it might improve the delivery of aerosolised bronchodilators in obstructive lung disease in general.

142 st ICS as an additive therapy to long-acting bronchodilators in patients with COPD and blood eosinoph

143 are normal to near normal (before and after bronchodilator) in a person with suspected EIB, then fur

144 nflammation and might respond to long-acting bronchodilators, including long-acting muscarinic antago

145 Inhaled bronchodilators, including long-acting muscarinic recept

146 was more sensitive to changes in response to bronchodilator inhalation (58%) than spirometry (33%).

147 investigate regional ventilation response to bronchodilator inhalation in a cohort of patients with a

148 educed ventilation and a greater response to bronchodilator inhalation than the proximal lung.

149 and the ventilation increase in response to bronchodilator inhalation was greater in the peripheral

150 ation increased significantly in response to bronchodilator inhalation, globally and regionally, and

151 ine, and 1 image data set was acquired after bronchodilator inhalation.

152 rmal, and reversibility was determined after bronchodilator inhalation.

153 Appropriate use of long-acting maintenance bronchodilators, inhaled corticosteroids, and pulmonary

154 Prone positioning, bronchodilators, inhaled nitric oxide, tight glucose con

155 ilation.Methods: Participants underwent post-bronchodilator inspiratory CT, and prebronchodilator and

156 Recent data suggest that the response to bronchodilators is not enhanced in patients with COPD an

157 cocorticoids in combination with long-acting bronchodilators is recommended in patients with frequent

158 One of these structurally related bronchodilators is terbutaline; it is administered as a

159 ha5beta1 blockade enhanced the effect of the bronchodilator isoproterenol on airway relaxation.

160 These children had worse pre-bronchodilator lung function compared with asthmatics wi

161 Symptoms, pre-/post-bronchodilator lung function, atopy, and cleaning exposu

162 ygen, glucocorticosteroids, methylxanthines, bronchodilators, management plans, food labels, drug lab

163 and ERS suggest that treatment with inhaled bronchodilators may be used (Grade: weak recommendation,

164 comorbidities may be similarly challenging: bronchodilators may have cardiac side effects, and, vice

165 on pre-bronchodilator spirometry (using post-bronchodilator measurements from a subsample of subjects

166 dardized spirometry were performed with post-bronchodilator measures for those with airflow limitatio

167 lung function, including both pre- and post-bronchodilator measures of FEV1 (-77 +/- 19 mL; P = 5.8

168 ent might be more effective than long-acting bronchodilator monotherapy for the treatment of chronic

169 ased, including pulmonary rehabilitation and bronchodilators; n = 157) vs usual care plus bilateral c

170 In particular, DIs are potent bronchodilators of constricted airways in nonasthmatic s

171 ecommends the combination of two long-acting bronchodilators of different pharmacologic classes for t

172 ed by either asthma FEV1 reversibility after bronchodilator or a positive methacholine test (PC20 </=

173 3 (51%) of the players tested had a positive bronchodilator or bronchial provocation test.

174 Evidence suggests no benefit from bronchodilator or corticosteroid use in infants with a f

175 ater than or equal to 5 or asthma diagnosis, bronchodilator or inhaled steroids, or unscheduled clini

176 BA/LAMA combinations over single long-acting bronchodilators or LABA/inhaled corticosteroids in decre

177 mechanical ventilation, supplemental oxygen, bronchodilators or steroids at 28 days or discharge.

178 ardiovascular risk factors, long-term use of bronchodilators or steroids for lung disease, and type a

179 redictors of poor control were: short acting bronchodilator overuse [2.129 (2.091; 2.164)], days-off

180 ent could include steroids, analgesic drugs, bronchodilators, palliative radiotherapy [n=136]); to AS

181 a combination of anti-inflammatory drugs and bronchodilators, patients who remain symptomatic despite

182 ase in [Ca(2+)]i caused by effective tastant bronchodilators provides an efficient cell-based screeni

183 e questionnaire survey and had reliable post-bronchodilator pulmonary function test results and were

184 The dual bronchodilator QVA149 was superior in preventing moderat

185 Moreover, inhalation of an anticholinergic bronchodilator reduced apnea episodes in global and chol

186 s), allergic asthma (1,235-CpGs; 7-DMRs) and bronchodilator response (130-CpGs).

187 .17-0.97; >3 vs <=3 times/year), and reduced bronchodilator response (6% vs 9% mean FEV(1) -%-predict

188 Whether PTSD leads to clinically significant bronchodilator response (BDR) or new-onset asthma is unk

189 The bronchodilator response (BDR) reflects the reversibility

190 We performed a GWAS of acute bronchodilator response (BDR) to inhaled beta2-agonists.

191 ity in Puerto Ricans (PRs), who have reduced bronchodilator response (BDR).

192 for a genetic contribution to variability in bronchodilator response (BDR).

193 prebronchodilator FEV1 (P = 0.006), a higher bronchodilator response (P = 0.03), and higher exhaled n

194 Baseline bronchodilator response and fractional exhaled nitric ox

195 acculturation were associated with decreased bronchodilator response compared with low (Spanish prefe

196 Bronchodilator response has been noted in a significant

197 al lung index for comparison with metrics of bronchodilator response measured by using spirometry and

198 Study 2 examined the reproducibility of the bronchodilator response to a daily dose of nebulised RPL

199 in uncoupling of beta(2)ARs and a diminished bronchodilator response to beta(2)AR agonists (see the r

200 The bronchodilator response was inhibited by the E prostanoi

201 Lower baseline values for FEV1, smaller bronchodilator response, airway hyperresponsiveness at b

202 ses in 6 clinical phenotypes: lung function, bronchodilator response, airway responsiveness, symptoms

203 ACT score, percent predicted FEV1, degree of bronchodilator response, and ICS adherence were signific

204 res were change in prebronchodilator FEV(1), bronchodilator response, and PC(20) from enrollment to 8

205 sensitive measure of airway obstruction and bronchodilator response, which measures lung response to

206 re not associated with the FEV1/FVC ratio or bronchodilator response.

207 aternal atopy, early childhood wheezing, and bronchodilator response.

208 In contrast, bronchodilator responses to albuterol were similar in eo

209 -breathing mixed expired FENO (tidal-FENO ), bronchodilator responsiveness (BDR) and the Castro-Rodri

210 ciate with exacerbation frequency in SARP-3; bronchodilator responsiveness also discriminated exacerb

211 Those likely to respond had greater bronchodilator responsiveness and fractional exhaled nit

212 The roles of bronchoprovocation and bronchodilator responsiveness in asthma diagnosis were f

213 At baseline, FEV1 bronchodilator responsiveness was the most important cha

214 del, blood eosinophils, body mass index, and bronchodilator responsiveness were positively associated

215 Current asthma, bronchodilator responsiveness, and wheeze followed simil

216 e COPD were age, sex, pack-years of smoking, bronchodilator responsiveness, chronic bronchitis sympto

217 [FEV1] to forced vital capacity [FVC] <70%, bronchodilator reversibility >/=12%, fractional exhaled

218 , 6-minute-walk distance (1,424 ft [434 m]), bronchodilator reversibility (2.7%), % emphysema (0.9%),

219 P < 0.001) despite a higher proportion with bronchodilator reversibility (27% vs. 6%).

220 in HIV-infected subjects, the prevalence of bronchodilator reversibility (BDR) and asthma has not be

221 bronchial hyperresponsiveness (BHR), and low bronchodilator reversibility (BDR) but high rhinitis sym

222 ad male predominance, normal spirometry, low bronchodilator reversibility (BDR), intermediate bronchi

223 nnaire total score), 6-minute-walk distance, bronchodilator reversibility (FEV1 % change), computed t

224 erformance (6-minute-walk distance, <391 m), bronchodilator reversibility (FEV1 change, >12% and >/=2

225 03), blood eosinophil percentage (P = 0.03), bronchodilator reversibility (P = 0.01), and improvement

226 :fvc (p=0.0075) and FeNO (p<0.0001), but not bronchodilator reversibility (p=0.97), were independentl

227 cough, wheeze, or dyspnoea and less than 20% bronchodilator reversibility across 26 primary care cent

228 usting for age, sex, race, atopy, group, and bronchodilator reversibility and including an interactio

229 ts aged 12 to 56 years with greater than 12% bronchodilator reversibility and percent predicted FEV1

230 Bronchodilator reversibility and prebronchodilator and p

231 we will discuss the insight that studies of bronchodilator reversibility have provided into the natu

232 3 persistent phenotypes were associated with bronchodilator reversibility of 12% or greater (BDR) fro

233 and sensitivity of hyperpolarized gas MRI to bronchodilator reversibility suggests that it is suitabl

234 Bronchodilator reversibility testing does not reliably d

235 Bronchodilator reversibility was positive in 54 (9%) of

236 s only associated with acute care visits and bronchodilator reversibility when exposure was defined b

237 function tests are done, and the position of bronchodilator reversibility within the algorithm sequen

238 We also measured spirometry, bronchodilator reversibility, and FeNO at follow-up; dat

239 ive results for all three tests (spirometry, bronchodilator reversibility, and FeNO).

240 31), 1.58 (1.33-1.88), and 4.58 (3.42-6.12); bronchodilator reversibility-2.76 (2.24-3.40), 5.18 (4.2

241 fraction of exhaled nitric oxide levels, and bronchodilator reversibility.

242 ut not with FEV1 (% predicted), FEV1 /FVC or bronchodilator reversibility.

243 The endogenous bronchodilator, S-nitrosoglutathione (GSNO), increases e

244 ta2-agonists and has the potential to reduce bronchodilator sensitivity to them.

245 nstay of current drug therapy is long-acting bronchodilators; several longer acting inhaled beta(2)-a

246 nebulized epinephrine, hypertonic saline, or bronchodilators should be routinely trialled.

247 or agonists have been the most commonly used bronchodilators since their discovery.

248 Airflow limitation was defined as post-bronchodilator spirometric (FEV1 /FVC) ratio <lower limi

249 A single post-bronchodilator spirometric assessment may not be reliabl

250 rwent a further questionnaire, pre- and post-bronchodilator spirometry (n = 1,389), skin prick testin

251 lassification in the definition based on pre-bronchodilator spirometry (using post-bronchodilator mea

252 spiratory CT, and prebronchodilator and post-bronchodilator spirometry and hyperpolarized (3)He MRI.

253 Demographics, clinical, and post-bronchodilator spirometry data were collected at an in-p

254 BOLD study, who had provided acceptable post-bronchodilator spirometry measurements and information o

255 ted HIV testing, and performed pre- and post-bronchodilator spirometry on eligible participants.

256 Airflow obstruction assessed from post-bronchodilator spirometry was not associated with use of

257 t respiratory symptoms were invited for post-bronchodilator spirometry.

258 1,389) underwent prebronchodilator and post-bronchodilator spirometry.

259 ctivated during asthma, or by treatment with bronchodilators such as beta(2)-adrenergic receptor (bet

260 with abnormal resting spirometry performed a bronchodilator test.

261 Spirometry and bronchodilator testing were done at baseline, 12 months,

262 ildren was invited for spirometry, including bronchodilator tests and exhaled nitric oxide measuremen

263 s on PDE4D will guide further development of bronchodilators that are not subject to tachyphylaxis an

264 Bronchodilators that do not target beta2-adrenoceptors r

265 Metaproterenol and isoproterenol are bronchodilators that provide a structural basis for many

266 lation may result in improved dyspnea with a bronchodilator, the contribution of TGC reduction to imp

267 ; P = .002; I(2) = 0%), and combined ICS and bronchodilator therapy (RR, 1.57; 95% CI, 1.35-1.82; P <

268 oking cessation intervention with or without bronchodilator therapy in 5,887 smokers with mild to mod

269 h COPD with severe disease not controlled by bronchodilator therapy.

270 n with wheeze whose indrawing resolves after bronchodilator therapy.

271 de conflicting recommendations on how to use bronchodilators to manage childhood acute wheezing condi

272 herefore serve as a potential target for new bronchodilators to reduce airway hyper-responsiveness in

273 efficacy and safety of inhaled short-acting bronchodilators to treat asthma and wheeze exacerbations

274 0.28 for a 1-unit increase in NO2) and after bronchodilator treatment (-3.59%; 95% CI: -5.36, -1.83 a

275 The change in 6MWD after inhaled bronchodilator treatment and surgical lung volume reduct

276 Combination long-acting bronchodilator treatment might be more effective than lo

277 uated the effect of dual, longacting inhaled bronchodilator treatment on exacerbations in patients wi

278 tory volume in 1 sec (FEV1) before and after bronchodilator treatment.

279 Anti-inflammatory and bronchodilator treatments are the mainstay of asthma the

280 We compared the effects of a bronchodilator, two placebo interventions, and no interv

281 nt, compared with a non-ICS dual long-acting bronchodilator (umeclidinium-vilanterol n=2070).

282 as related to an average increase of 3.8% in bronchodilator usage at school (95% confidence interval

283 ulate are associated with early increases in bronchodilator use and urinary leukotriene E4 levels amo

284 old of 20 decreased from 42.7% to 28.8%, and bronchodilator use greater than 2 times per week decreas

285 Maternal bronchodilator use showed an elevated statistically sign

286 ve the lower limit of the normal range after bronchodilator use) and had symptoms (CAT score, >/=10)

287 association among ambient fine particulate, bronchodilator use, and urinary leukotriene E4 levels wa

288 Prognostic outcomes (wheeze, bronchodilator use, cough apart from colds) 5 years late

289 cancer malignancy, coexisting illnesses, and bronchodilator use, there was a dose-dependent decreased

290 ss than 0.70 as assessed by spirometry after bronchodilator use.

291 or previous episodes of wheezing or inhaled bronchodilator use.

292 ction or differences in antibiotic or rescue bronchodilator use.

293 t environment factors on asthma short-acting bronchodilator use.

294 E-COPD and TS-COPD, whereas reversibility to bronchodilator was a predictive factor for both groups w

295 e collected in triplicate before and after a bronchodilator was administered.

296 he mainstay of treatment for COPD is inhaled bronchodilators, whereas the role of inhaled corticoster

297 New bronchodilators with a longer duration of action are in

298 ations (FDCs) provide the convenience of two bronchodilators with different mechanism of action in a

299 Inhalational anesthetics are bronchodilators with immunomodulatory effects.

300 al care (n = 50) received rehabilitation and bronchodilators with or without inhaled corticosteroids