ライフサイエンスコーパス: ICS

1 ICS improved FEV1 and hyperresponsiveness in the IL-25-h

2 ICS technique was evaluated by using scales derived from

3 ICS treatment reduced the expression of CLC, CPA3, and D

4 ICS use was associated with 91% reduced use of firewood

5 ICS use was associated with reduced time in the hospital

6 ICS was more sensitive than ELISpot.

7 ICS with Indacaterol and Tiotropium (IND/TIO) vs ICS wit

8 ICS/LABAs were switched to FP/FM-pMDI and slow and deep

9 harmacogenetic investigation to date in 2672 ICS-treated patients with asthma.

10 phenotype: ICS+ group: 19% vs 16%, P = .28; ICS- group: 39% vs 35%, P = .65; respectively).

11 deployed SUMs in an effectiveness study of 6 ICSs in 45 Kenyan rural homes.

12 els during the steroid-naive phase and after ICS therapy.

13 the 2296 patients receiving treatment after ICS withdrawal, moderate or severe exacerbation rate was

14 corticosteroid and long-acting beta-agonist (ICS/LABA).

15 ids combined with long-acting beta2-agonist (ICS/LABA) are standard treatments for asthma.

16 osteroids plus long-acting beta(2)-agonists (ICS plus LABA) and a history of two or more exacerbation

17 ticosteroids and long-acting beta2-agonists (ICS plus LABA) in the previous year.

18 Stacking, defined as using both a TCS and an ICS in the same day, occurred on 40% of the study days,

19 These studies identify an ICS recycling pathway for C3(H2O).

20 % vs 36.3%; OR, 0.12; 95% CI, 0.02-0.64) and ICS boost (2.0% vs 27.8%; OR, 0.05; 95% CI, 0.002-0.98).

21 at Week 24 for triple therapy (n = 911) and ICS/LABA therapy (n = 899), mean changes from baseline i

22 similar with a LABA plus ICS combination and ICS monotherapy at higher doses, suggesting that both th

23 with inhaled corticosteroids (ICSs; ICS+ and ICS-, respectively).

24 fferences from placebo exceeded the MID, and ICS-based treatments provided the greatest improvements.

25 ignificant difference between omalizumab and ICS boost (8.4% vs 11.1%; OR, 0.73; 95% CI, 0.33-1.64).

26 We show that, unlike in Arabidopsis, PAL and ICS pathways are equally important for pathogen-induced

27 igated the relative contributions of PAL and ICS to defense-related SA accumulation in soybean (Glyci

28 These results show that PAL- and ICS-catalyzed reactions function cooperatively in soybea

29 FEV1, degree of bronchodilator response, and ICS adherence were significantly associated with ICS res

30 tions between candidate genetic variants and ICS response (DeltaFEV1) in patients with asthma.

31 asthma that is not adequately controlled by ICS alone.

32 llergy-related asthma not well controlled by ICS or combination products, and with HDM allergy-relate

33 llergy-related asthma not well controlled by ICS, the addition of HDM SLIT to maintenance medications

34 (as-required or "prn") use of a combination ICS/short-acting beta-agonist or ICS/long-acting beta-ag

35 d trials investigating different combination ICS/beta-agonist inhaler products prescribed according t

36 edictors of differential responses comparing ICS with LTRA step-up therapy were not apparent, probabl

37 ll in FEV1 /cumulative dose), when comparing ICS/IND/TIO to ICS/IND.

38 We did a post-hoc analysis after complete ICS withdrawal (months 3-12) to compare rate of exacerba

39 ated to the exacerbation rate after complete ICS withdrawal in patients with severe to very severe CO

40 Electron microscopy confirmed ICS expansion (maximum in glycolytic cells), which was a

41 localization microscopy with Eos-conjugated, ICS-located lactamase-beta indicated hypoxic ICS expansi

42 Conventionally, ICS treatment is recommended for patients with symptoms

43 ent interventions using improved cookstoves (ICS) to reduce HAP have incorporated temperature sensors

44 aditional mud stoves or improved cookstoves (ICS).

45 igher NAV2 score was associated with correct ICS technique (rho = 0.24, P = .0002), knowledge of ICSs

46 to a higher dose of inhaled corticosteroid (ICS step-up therapy) or addition of leukotriene receptor

47 led asthma; negative inhaled corticosteroid (ICS) beliefs and complementary and alternative medicine

48 ) omalizumab with an inhaled corticosteroid (ICS) boost with regard to fall exacerbation rates when i

49 on that early use of inhaled corticosteroid (ICS) could change the natural history of asthma if start

50 s during the 16-week inhaled corticosteroid (ICS) dose-stable phase were evaluated with respect to ba

51 atment when added to inhaled corticosteroid (ICS) maintenance therapy.

52 s) and prediction of inhaled corticosteroid (ICS) response (n = 71 asthmatic patients).

53 se asthma and poorer inhaled corticosteroid (ICS) response in older children and adults.

54 Inhaled corticosteroid (ICS) therapy is a mainstay of treatment for asthma, but

55 respond less well to inhaled corticosteroid (ICS) therapy than asthmatics who do not smoke.

56 asthma attacks with inhaled corticosteroid (ICS) treatment.

57 following increased inhaled corticosteroid (ICS) treatment.

58 by smoking status or inhaled corticosteroid (ICS) use.

59 Their use of inhaled corticosteroid (ICS) was standardized and adjusted at baseline and the e

60 nical superiority of inhaled corticosteroid (ICS)/LABA combinations in asthma and chronic obstructive

61 le therapy with dual inhaled corticosteroid (ICS)/long-acting beta2-agonist (LABA) therapy in patient

62 1 RCT of LABAs and inhaled corticosteroids (ICS) (n = 1097), 5 RCTs of the long-acting muscarinic an

63 BACKGROUND AND Inhaled corticosteroids (ICS) and inhaled corticosteroids combined with long-acti

64 pede adherence with inhaled corticosteroids (ICS) and often underlie poor asthma control.

65 Low-dose inhaled corticosteroids (ICS) are highly effective for reducing asthma exacerbati

66 hat can be added to inhaled corticosteroids (ICS) for patients with asthma that is not adequately con

67 Report 3 recommends inhaled corticosteroids (ICS) for patients with moderate to severe persistent ast

68 predict response to inhaled corticosteroids (ICS) in patients with chronic obstructive pulmonary dise

69 Inhaled corticosteroids (ICS) increase community-acquired pneumonia (CAP) inciden

70 linical response to inhaled corticosteroids (ICS) is associated with single nucleotide polymorphisms

71 w- to medium-dosage inhaled corticosteroids (ICS) or low-dosage ICS plus long-acting beta2 agonist fi

72 Inhaled corticosteroids (ICS) target gene transcription through their interaction

73 ance treatment with inhaled corticosteroids (ICS).

74 ndent on the use of inhaled corticosteroids (ICS).

75 controller therapy, inhaled corticosteroids (ICS).

76 Inhaled corticosteroids (ICSs) are considered the most effective anti-inflammator

77 nancy when low-dose inhaled corticosteroids (ICSs) are insufficient include adding a long-acting beta

78 Inhaled corticosteroids (ICSs) are the preferred treatment for achieving asthma c

79 Inhaled corticosteroids (ICSs) are widely used as first-line treatment for variou

80 systemic effect of inhaled corticosteroids (ICSs) is often done by measuring 24-hour urine free cort

81 ildren treated with inhaled corticosteroids (ICSs) plus LABAs but not for treatment with ICSs alone (

82 treatment), (2) use inhaled corticosteroids (ICSs) properly, and (3) understand ICS function.

83 regular maintenance inhaled corticosteroids (ICSs) with a short-acting beta-agonist as a separate inh

84 n add-on therapy to inhaled corticosteroids (ICSs) with or without other maintenance therapies in pat

85 periods with daily inhaled corticosteroids (ICSs), daily leukotriene receptor antagonists, and as-ne

86 ontaining products, inhaled corticosteroids (ICSs), leukotriene modifiers, short-acting beta2-agonist

87 with placebo, only inhaled corticosteroids (ICSs), with or without a long-acting beta-agonist, achie

88 treated or not with inhaled corticosteroids (ICSs; ICS+ and ICS-, respectively).

89 ity of best response was highest for a daily ICS and was predicted by aeroallergen sensitization but

90 probability for whom treatment with a daily ICS is beneficial despite possible risks of growth suppr

91 In these children daily ICS use was associated with more asthma control days and

92 ldren had similar asthma symptom days (daily ICS: 47.2 vs 44.0 days, P = .44; short-term ICS: 61.8 vs

93 , P = .53), and similar exacerbations (daily ICS: 0.6 vs 0.8, P = .10; short-term ICS: 1.1 vs 0.8 day

94 SQ-HDM and placebo in the reduction in daily ICS dose of 81 mug (P = .004).

95 Compared with placebo, daily ICS in OW led to fewer annualized asthma symptom days (9

96 ACQ score 0.79 +/- SD 0.83) prescribed daily ICS [BDP-equivalent median dose 1000 mug (IQR: 500, 1000

97 The probability of best response to daily ICS was further increased in children with both aeroalle

98 Participants had been randomized to daily ICS, intermittent ICS, or daily placebo.

99 ug/25 mug; ELLIPTA inhaler) with twice-daily ICS/LABA therapy (budesonide/formoterol 400 mug/12 mug;

100 lth-related quality of life with twice-daily ICS/LABA therapy in patients with COPD.

101 urrent guidelines which recommend decreasing ICS by 50% after a period of asthma stability.

102 s placebo for patients receiving high-dosage ICS plus LABA with baseline blood eosinophils 300 cells

103 phils, which are uncontrolled by high-dosage ICS plus LABA, and provide support for benralizumab to b

104 inhaled corticosteroids (ICS) or low-dosage ICS plus long-acting beta2 agonist fixed-combination the

105 gnificant decreases in the use of fixed-dose ICS-LABA agents in children (-0.98 percentage points) an

106 tropium Respimat add-on therapy to high-dose ICS with 1 or more controller medications, or medium-dos

107 -dose ICS was used compared with a high-dose ICS.

108 dose ICS combination or users of a high-dose ICS.

109 medium-dose ICS and 156 users of a high-dose ICS.

110 were 643 women who used a LABA plus low-dose ICS and 305 who used a medium-dose ICS; the other subcoh

111 s follows: (1) users of a LABA plus low-dose ICS combination or users of a medium-dose ICS and (2) us

112 uppression of allergic markers with low-dose ICS treatment.

113 (95% CI, 0.6-1.9) when a LABA plus low-dose ICS was used compared with a medium-dose ICS and 1.2 (95

114 se ICS combination or users of a medium-dose ICS and (2) users of a LABA plus medium-dose ICS combina

115 ose ICS was used compared with a medium-dose ICS and 1.2 (95% CI, 0.5-2.7) when a LABA plus medium-do

116 ncluded 198 users of a LABA plus medium-dose ICS and 156 users of a high-dose ICS.

117 ICS and (2) users of a LABA plus medium-dose ICS combination or users of a high-dose ICS.

118 5% CI, 0.5-2.7) when a LABA plus medium-dose ICS was used compared with a high-dose ICS.

119 more controller medications, or medium-dose ICS with 2 or more controller medications, in the first

120 low-dose ICS and 305 who used a medium-dose ICS; the other subcohort included 198 users of a LABA pl

121 rbation rate with triple therapy versus dual ICS/LABA therapy (35% reduction; 95% CI, 14-51; P = 0.00

122 oderate or severe asthma exacerbation during ICS reduction, with an estimated absolute reduction at 6

123 tion to interpret HAP levels measured during ICS intervention studies.

124 hronic compared to single dosing with either ICS/IND (P<.005) or ICS/IND/TIO (P<.05).

125 oefficient = 0.77 for CAM items and 0.79 for ICS items).

126 tested using IFN-gamma-ELISPOT and IFN-gamma-ICS on CD8(+) T cells from DENV-infected mice, and five

127 Inhaled glucocorticosteroids (ICS) are the mainstay of treatment in asthma.

128 ICS-located lactamase-beta indicated hypoxic ICS expansion with an unchanged OMM (visualized by Eos-m

129 d or not with inhaled corticosteroids (ICSs; ICS+ and ICS-, respectively).

130 ould be more likely to have exacerbations if ICS treatment was withdrawn.

131 e use persists, although pollution levels in ICS households still remained above WHO guidelines.

132 The primary end point was a reduction in ICS dose from the individual subject's baseline dose aft

133 may be needed when initiating or increasing ICSs.

134 arch studies with intranasal or inhalational ICS.

135 d been randomized to daily ICS, intermittent ICS, or daily placebo.

136 ren might benefit from daily or intermittent ICS therapy.

137 There was no difference between LABA + ICS vs tiotropium + ICS in time to first exacerbation (m

138 nge in FEV1 at 12 months (0.003 L for LABA + ICS vs -0.018 L for tiotropium + ICS; between-group diff

139 nge in score from baseline, -0.68 for LABA + ICS vs -0.72 for tiotropium + ICS; between-group differe

140 ngs do not support the superiority of LABA + ICS compared with tiotropium + ICS for black patients wi

141 : OR 3.76 [2.14-6.61]), and drug use (LABA + ICS: 1.86 [1.27-2.74], antileukotrienes 4.83 [1.63-14.34

142 in the effects of tiotropium + ICS vs LABA + ICS (hazard ratio for time to first exacerbation, 0.84 [

143 t on Exacerbations in Patients on Dual [LABA/ICS] Therapy) trial (NCT01443845), participants aged 40

144 , sensitize, and prolong the effects of LABA/ICS combination therapies.

145 fe and well tolerated when added to at least ICS maintenance therapy in adolescent patients with mode

146 validity, which may be useful for monitoring ICS side-effects in clinical practice.

147 kotriene receptor antagonists, and as-needed ICS treatment coadministered with albuterol.

148 erm ICS: 1.1 vs 0.8 days, P = .25; as-needed ICS: 1.0 vs 1.1, P = .72).

149 m ICS: 61.8 vs 52.9 days, P = .46; as-needed ICS: 53.3 vs 47.3 days, P = .53), and similar exacerbati

150 Negative ICS beliefs and CAM endorsement were common and associat

151 igh rates of CAM endorsement (93%), negative ICS beliefs (68%), and uncontrolled asthma (69%).

152 th low literacy demands to identify negative ICS beliefs and CAM endorsement and (2) evaluated the cl

153 tions were observed in never smokers and non-ICS users.

154 tions were stronger in never smokers and non-ICS users.

155 ients (aged >/=12 years; uncontrolled by non-ICS therapy) were randomized to treatment (1 : 1 : 1) wi

156 In non-ICS users, low 25(OH)D levels were associated with more

157 he LAR observed in smokers in the absence of ICS treatment is a novel observation.

158 ation for the epidemiological association of ICS therapy of COPD patients with increased risk for CAP

159 to prove useful as predictive biomarkers of ICS response in patients with asthma.

160 quencies were reduced in peripheral blood of ICS-treated subjects with COPD (median 0.38%; interquart

161 t discomfort with the middle or high dose of ICS/LABA combination agents under well technique (32 of

162 more might identify a deleterious effect of ICS withdrawal, an effect not seen in most patients with

163 non-smoking atopic asthmatics at the end of ICS treatment, but attenuation of the LAR in smokers was

164 ment's clinical utility in that knowledge of ICS beliefs and CAM endorsement prompted providers to in

165 uctions in national guidelines; knowledge of ICS function was evaluated by using a validated 10-item

166 We sought to identify genetic markers of ICS response by conducting the largest pharmacogenetic i

167 The primary measure of ICS response was a change in Asthma Control Test (ACT) s

168 agonist tiotropium (n = 4592), and 6 RCTs of ICS (n = 3983).

169 Despite this expectation, the role of ICS therapy in altering the natural course of disease in

170 ection is associated with the suppression of ICS gene expression.

171 haler technique and limited understanding of ICS function, as well as limited numeracy and print lite

172 Here we discuss the potential use of ICS therapy to alter the natural disease course in child

173 of cooking events, days of exclusive use of ICS, and how stove use patterns affect HAP.

174 However, as delivery of ICSs to the lungs improves, the systemic absorption incr

175 most in patients taking the highest doses of ICSs but is reported with moderate or even low doses as

176 a review of the endocrine adverse effects of ICSs in children and offer recommendations relating to t

177 armacodynamic measure of systemic effects of ICSs than 24-hour UFC excretion and that a parametric de

178 hnique (rho = 0.24, P = .0002), knowledge of ICSs (rho = 0.35, P < .001), better print literacy (rho

179 steroid-naive phase 1 and a 28-day trial of ICSs (phase 2) during which Feno values, sputum eosinoph

180 cipating in a randomized controlled trial of ICSs with longitudinal concomitant assessments of LLGR a

181 After 28-day trial of ICSs, Feno values decreased in 82% of asthmatic patients

182 Increased use of ICSs and leukotriene modifiers was observed just after t

183 y responsiveness to methacholine (LnPC20) on ICS.

184 d 39.2% in Gly16Gly), whereas in patients on ICS at baseline, only the Arg16Arg genotype was associat

185 ingle dosing with either ICS/IND (P<.005) or ICS/IND/TIO (P<.05).

186 combination ICS/short-acting beta-agonist or ICS/long-acting beta-agonist inhaler as a reliever rathe

187 or A was defined as poor adherence to ICS or ICS/LABA inhaler of 75% or less.

188 -controlled asthma patients receiving ICS or ICS/LABA were assessed for physical and psychiatric prob

189 step-up responses from responses to LTRA or ICS step-up therapy.

190 for treatment with ICSs alone (n = 1758) or ICSs plus leukotriene receptor antagonist (LTRAs; n = 35

191 iene receptor antagonist (LTRAs; n = 354) or ICSs plus LABAs plus LTRAs (n = 569).

192 ferential FEV(1) response favoring LABA over ICS step-up therapy, whereas higher urinary leukotriene

193 ic obstructive pulmonary disease (COPD) over ICSs alone.

194 with the Individualized Care Scale-Patient (ICS-Patient), the Oncology Patients' Perceptions of Qual

195 We converted patients' ICS treatments to 180 mug or 200 mug budesonide dry powd

196 oup (percentage with eosinophilic phenotype: ICS+ group: 19% vs 16%, P = .28; ICS- group: 39% vs 35%,

197 r malformations was similar with a LABA plus ICS combination and ICS monotherapy at higher doses, sug

198 ns in asthmatic women exposed to a LABA plus ICS combination and those exposed to ICS monotherapy at

199 ted with longer duration of use, more potent ICS compounds, and higher doses.

200 res and self-reported asthma control predict ICS response, whereas self-reported race-ethnicity and g

201 The 6-gene signature predicted ICS response (>12% change in FEV1; AUC, 91.5%).

202 flammatory phenotypes of asthma and predicts ICS treatment response.

203 Part 2: Patients prescribed ICS for asthma completed the ICQ at baseline (BL), ICQ-S

204 When researchers were not present, ICS use declined, which can have implications for long-t

205 st year (stable condition under the previous ICS/LABA).

206 vs 0.6, P = .006), while similar protective ICS effects were less apparent among NW.

207 ng, and Blood Institute guidelines, received ICS plus either once-daily tiotropium (n = 532) or twice

208 ild to moderate, persistent asthma receiving ICS.

209 Eleven subjects with COPD receiving ICS, 8 steroid-naive subjects with COPD, and 21 healthy

210 wo well-controlled asthma patients receiving ICS or ICS/LABA were assessed for physical and psychiatr

211 f 4 weeks or more, an intervention to reduce ICS, and a follow-up period of at least 3 months.

212 cally to receive either continued or reduced ICS over 12 weeks.

213 thma exacerbation in individuals who reduced ICS compared to those who maintained the same ICS dose w

214 no more likely among individuals who reduced ICS compared to those who maintained their ICS dose, sup

215 Individuals who reduced ICS had a decreased% predicted FEV1 of 0.87% (95% CI -1.

216 However, the benefits of regular ICS use in actual clinical practice are limited by poor

217 hat this regimen has advantages over regular ICS therapy and might represent an effective, safe, and

218 CS compared to those who maintained the same ICS dose was 1.25 (95% CI 0.96, 1.62; P = 0.10; I(2) = 0

219 viability of isotope-controlled selectivity (ICS), a novel control element of chemical reactivity whe

220 Isotropic chemical shifts, ICS(gamma), were determined for sp, sp(x), and sp(2) N-h

221 M) cristae structure and intracristal space (ICS) to oxidative phosphorylation (oxphos) is not well u

222 to those individuals who maintained a stable ICS dose.

223 Intracellular cytokine staining (ICS) assays were also used to examine phenotypes of thes

224 LISpot) and intracellular cytokine staining (ICS) assays, ex vivo and after in vitro stimulation with

225 ta sets: an intracellular cytokine staining (ICS) data set from a published HIV vaccine trial focused

226 LISPOT) and intracellular cytokine staining (ICS) in ZIKV-infected IFN-alpha/beta receptor-deficient

227 aboon using intracellular cytokine staining (ICS).

228 e previous symptom-based cutoff for starting ICS by establishing whether there was a differential res

229 a lyase (PAL) or the isochorismate synthase (ICS) catalyzed steps.

230 An intracellular complement system (ICS) has recently been described in immune and nonimmune

231 The ICQ-S consists of fifteen local/systemic ICS side-effects of similar range to the full ICQ.

232 (daily ICS: 0.6 vs 0.8, P = .10; short-term ICS: 1.1 vs 0.8 days, P = .25; as-needed ICS: 1.0 vs 1.1

233 ICS: 47.2 vs 44.0 days, P = .44; short-term ICS: 61.8 vs 52.9 days, P = .46; as-needed ICS: 53.3 vs

234 Having shown that ICS significantly increase AMo efferocytosis, we hypothe

235 The ICS pathway is thought to be the primary contributor of

236 ate or severe asthma exacerbation during the ICS reduction period.

237 an LLGR was significantly reduced during the ICS versus placebo run-in periods: 0.18 mm/wk (SD, 0.55

238 e statistically significant reduction in the ICS dose required to maintain asthma control.

239 the placebo run-in period with values in the ICS treatment period by using paired t tests.

240 There were 922 subjects in the ICS+ group (248 African American and 674 white subjects)

241 rway inflammation than white subjects in the ICS+ group (odds ratio, 1.58; 95% CI, 1.01-2.48; P = .04

242 674 white subjects) and 298 subjects in the ICS- group (49 African American and 249 white subjects).

243 95% CI, 1.01-2.48; P = .046) but not in the ICS- group (P = .984).

244 r severe exacerbation rate was higher in the ICS-withdrawal group versus the ICS-continuation group i

245 ing beta(2)-agonist (LABA) or increasing the ICS dose.

246 of the study days, and exclusive use of the ICS occurred on 25% of study days.

247 igher in the ICS-withdrawal group versus the ICS-continuation group in patients with eosinophil count

248 Within the ICS-treated groups, OW and NW children had similar asthm

249 We placed SUMs on the ICSs and traditional cookstoves (TCS), and the continuou

250 atic children and young adults despite their ICS use.

251 d ICS compared to those who maintained their ICS dose, supporting current guidelines which recommend

252 ristae edges, whereas trimeric OPA1 tightens ICS outlets.

253 for LABA + ICS vs -0.018 L for tiotropium + ICS; between-group difference, 0.020 [95% CI, -0.021 to

254 .68 for LABA + ICS vs -0.72 for tiotropium + ICS; between-group difference, 0.04 [95% CI, -0.18 to 0.

255 h differences in the effects of tiotropium + ICS vs LABA + ICS (hazard ratio for time to first exacer

256 ifference between LABA + ICS vs tiotropium + ICS in time to first exacerbation (mean No. of exacerbat

257 ity of LABA + ICS compared with tiotropium + ICS for black patients with asthma.

258 al studies in which controllers are added to ICS treatment.

259 275] or 12 SQ-HDM [n = 282]) in addition to ICS and the short-acting beta2-agonist salbutamol.

260 Factor A was defined as poor adherence to ICS or ICS/LABA inhaler of 75% or less.

261 BA plus ICS combination and those exposed to ICS monotherapy at higher doses during the first trimest

262 odemographic, and genetic factors related to ICS response among African American and European America

263 tween OW and asthma severity and response to ICS in preschool children.

264 ted to the magnitude of clinical response to ICS therapy.

265 P < .01) to predict a favorable response to ICS therapy.

266 dividual variability in clinical response to ICS treatment in children and young adults.

267 ay eosinophilia, and beneficial responses to ICS treatment.

268 asthma phenotypes and different responses to ICS.

269 patients predicts clinical responsiveness to ICS therapy.

270 do not demonstrate reduced responsiveness to ICS therapy.

271 and was well tolerated as add-on therapy to ICS with other maintenance therapies in children with se

272 l versus montelukast as an add-on therapy to ICS within 16 weeks of follow-up (the J-Blossom study).

273 ulative dose), when comparing ICS/IND/TIO to ICS/IND.

274 e every evening, each as add-on treatment to ICS background therapy, with or without a leukotriene re

275 y of once-daily tiotropium Respimat added to ICSs with or without a leukotriene receptor antagonist i

276 ohort of asthmatic pregnant women exposed to ICSs during the first trimester who delivered between Ja

277 xcretion for evaluating systemic exposure to ICSs in prepubertal children with asthma.

278 ent for asthma, but the clinical response to ICSs is variable.

279 The response to ICSs was based on clinical improvements, including a 12%

280 plants silenced for five PAL isoforms or two ICS isoforms were analyzed for SA concentrations and SA-

281 beliefs and behaviors that likely undermine ICS adherence might be a leveraging tool to change the c

282 steroids (ICSs) properly, and (3) understand ICS function.

283 97.1% used ICS (dose 2000 BDP), 93.6% LABA in association with ICS,

284 ed risk of exacerbations in asthmatics using ICS in the three cohorts studied.

285 with Indacaterol and Tiotropium (IND/TIO) vs ICS with Indacaterol (IND) over 4 weeks with challenge p

286 In the 16-week ICS dose-stable phase, rates of exacerbations requiring

287 d during the last 6 months of the trial when ICS was reduced by 50% for 3 months and then completely

288 p cristae edges and expanding cristae width (ICS) by partial mitofilin/Mic60 down-regulation.

289 adherence were significantly associated with ICS response.

290 an American participants was associated with ICS responsiveness.

291 R in smokers was only partly associated with ICS treatment.

292 se 2000 BDP), 93.6% LABA in association with ICS, 53.3% LTRAs, 64.1% anti-IgE, 10.7% theophylline, an

293 s, might explain the association of CAP with ICS therapy in COPD.

294 single-inhaler triple therapy compared with ICS/LABA therapy in patients with advanced COPD.

295 significant dose-response relationship with ICS adherence.

296 Among black adults with asthma treated with ICS, adding a LABA did not improve time to asthma exacer

297 ns in children and young adults treated with ICS.

298 despite being on maintenance treatment with ICS.

299 In patients untreated with ICS at baseline, Arg16Gly and Arg16Arg genotypes were as

300 (ICSs) plus LABAs but not for treatment with ICSs alone (n = 1758) or ICSs plus leukotriene receptor