ライフサイエンスコーパス: bronchodilator

1 ms are not adequately controlled by a single bronchodilator.

2 airway contraction after administration of a bronchodilator.

3 change from baseline in lung function after bronchodilator.

4 ), especially before the administration of a bronchodilator.

5 was trough FEV(1) before and after use of a bronchodilator.

6 baseline spirometric indices, or response to bronchodilator.

7 ct that is typically not reversed by inhaled bronchodilator.

8 erity and resolved soon with inhalation of a bronchodilator.

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 usual care, except for other anticholinergic bronchodilators.

19 lso improve airflow and can be combined with bronchodilators.

20 rbation frequency and severity as might some bronchodilators.

21 ht be more responsive to corticosteroids and bronchodilators.

22 al criteria for evaluating responsiveness to bronchodilators.

23 OCE may therefore form novel targets for new bronchodilators.

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

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

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

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

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

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

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

36 irefighters (149 of 237) had a response to a bronchodilator and 24 percent (9 of 37) had bronchial hy

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

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

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

40 th asthma results in tolerance to the drug's bronchodilator and nonbronchodilator effects and may be

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

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

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

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

51 ontline therapies used to treat asthma (i.e. bronchodilators and steroids) inadequately control mast

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

53 Treatment with long-acting inhaled bronchodilators and, in more severe disease, inhaled cor

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

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

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

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

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

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

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

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

62 Bronchodilators are a standard medicine for treating air

63 Bronchodilators are the mainstay of therapy for patients

64 Aerosolised bronchodilators are useful in mechanically ventilated pa

65 t at risk, use of necessary therapies (i.e., bronchodilators) as early as feasible, and treatment tit

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

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

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

69 Three classes of bronchodilators-beta agonists, anticholinergics, and the

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

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

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

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

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

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

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

77 aerosol particle size could optimize inhaled bronchodilator delivery.

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

79 ction between genotype, asthma severity, and bronchodilator drug responsiveness.

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

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

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

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

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

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

86 Bronchodilators, epinephrine, and corticosteroids have a

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

88 The routine and repetitive use of bronchodilators, epinephrine, or corticosteroids to trea

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

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

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

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

93 0.28 and 0.11 for rs7937 and rs2604894), pre-bronchodilator FEV(1) (P = 0.08 and 0.04) and severe (GO

94 e phenotypes including BDR measures and post-bronchodilator FEV(1) and FEV(1)/FVC.

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

96 Post-bronchodilator FEV(1) was linked to multiple regions, mo

97 -0.043L, 95% CI -0.086 to -0.0009) and post-bronchodilator FEV(1)/FVC ratio (adj.

98 Post-bronchodilator FEV(1)/FVC was also linked to multiple re

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

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

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

102 therapy produced greater improvements in pre-bronchodilator FEV1 (P=0.005), bronchial reactivity (P<0

103 symptom-free days (P=0.03), but not in post-bronchodilator FEV1 (P=0.29) or in the quality of life (

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

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

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

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

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

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

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

111 70% of the predicted value, a ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0.

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

113 percentage change in prebronchodilator/post-bronchodilator FEV1.

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

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

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

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

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

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

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

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

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

123 t' and after patients had abstained from all bronchodilators for at least 6h and from study medicatio

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

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

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

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

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

129 8-75 years with symptomatic asthma and a pre-bronchodilator forced expiratory volume in 1 s (FEV1) of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Inhaled bronchodilators, including long-acting muscarinic recept

147 rmal, and reversibility was determined after bronchodilator inhalation.

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

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

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

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

152 S-nitrosoglutathione (GSNO), an endogenous bronchodilator, is depleted from asthmatic airways, sugg

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

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

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

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

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

158 ovement in spirometric measures with inhaled bronchodilator medications, and bronchodilator responsiv

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

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

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

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

163 However, the effect of bronchodilators on maximal expiratory flow may be confou

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

165 3 (51%) of the players tested had a positive bronchodilator or bronchial provocation test.

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

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

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

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

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

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

172 in FEV(1) from baseline (PC(20)); (iii) post-bronchodilator percent change in FEV(1) (BDPR); (iv) ser

173 ce of linkage between chromosome 19q and pre-bronchodilator (pre-BD) FEV(1) (LOD=3.30) and suggestive

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

175 The dual bronchodilator QVA149 was superior in preventing moderat

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

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

178 The bronchodilator response (BDR) reflects the reversibility

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

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

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

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

183 Baseline bronchodilator response and fractional exhaled nitric ox

184 Bronchodilator response has been noted in a significant

185 AC9 is associated with an improved albuterol bronchodilator response in asthmatics was investigated i

186 een Arg16Gly genotypes, asthma severity, and bronchodilator response in Puerto Ricans and Mexicans wi

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

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

189 beta(2)AR genotypes with asthma severity and bronchodilator response to albuterol in Puerto Ricans an

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

191 (Arg) 16 allele was associated with greater bronchodilator response using both family-based and cros

192 The bronchodilator response was inhibited by the E prostanoi

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

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

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

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

197 ciation of single SNPs with asthma severity, bronchodilator response, or IgE levels in Mexicans or in

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

199 rg16Glycine (Gly) polymorphism in predicting bronchodilator response.

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

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

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

203 with inhaled bronchodilator medications, and bronchodilator responsiveness (BDR) has been associated

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

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

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

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

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

209 3 gene variants and asthma, asthma severity, bronchodilator responsiveness, and total IgE levels usin

210 Current asthma, bronchodilator responsiveness, and wheeze followed simil

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

212 Bronchodilator responsiveness, measured as percentage ch

213 ation between the Arg16 genotype and greater bronchodilator responsiveness.

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

215 , 6-minute-walk distance (1,424 ft [434 m]), bronchodilator reversibility (2.7%), % emphysema (0.9%),

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

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

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

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

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

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

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

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

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

225 Bronchodilator reversibility and prebronchodilator and p

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

227 interval [CI], 4.6 to 9.9; p < 0.001) lower bronchodilator reversibility in FEV1, higher risk of an

228 3 persistent phenotypes were associated with bronchodilator reversibility of 12% or greater (BDR) fro

229 Bronchodilator reversibility testing does not reliably d

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

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

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

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

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

235 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

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

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

238 5.9 months), with decreased sGaw but without bronchodilator reversibility; and Group C: 15 infants wi

239 eased specific airway conductance (sGaw) and bronchodilator reversibility; Group B: 22 infants with a

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

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

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

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

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

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

246 When compared with pre-bronchodilator spirometric indices, the post-bronchodila

247 mes 2q and 8p, and further suggest that post-bronchodilator spirometric measures are optimal phenotyp

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

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

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

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

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

253 1,389) underwent prebronchodilator and post-bronchodilator spirometry.

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

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

256 with abnormal resting spirometry performed a bronchodilator test.

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

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

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

260 ms a very stable structure when bound to the bronchodilator theophylline, but the theophylline bindin

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

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

263 Bronchodilator therapy is key in improvement of lung fun

264 low limitation were recorded after nebulized bronchodilator therapy on the first 3 d after admission,

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

266 n with wheeze whose indrawing resolves after bronchodilator therapy.

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

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

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

270 t bronchodilatory effect with no evidence of bronchodilator tolerance.

271 0.28 for a 1-unit increase in NO2) and after bronchodilator treatment (-3.59%; 95% CI: -5.36, -1.83 a

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

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

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

275 volume in one second (FEV1) before and after bronchodilator treatment, the frequency of exacerbations

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

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

278 Bronchodilator treatments avoiding albuterol may be appr

279 intermittent positive-pressure breathing or bronchodilator treatments, sighs, and chest physiotherap

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

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

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

283 Maternal bronchodilator use showed an elevated statistically sign

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

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

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

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

288 or previous episodes of wheezing or inhaled bronchodilator use.

289 ction or differences in antibiotic or rescue bronchodilator use.

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

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

292 bronchodilator spirometric indices, the post-bronchodilator values demonstrated increased evidence of

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

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

295 ants we evaluated the response to an inhaled bronchodilator was greatest in the youngest infants and

296 A positive response to bronchodilators was associated with more severe airflow

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