ライフサイエンスコーパス: ICS

1 ICS administration attenuated ACE2 expression in mice, a

2 ICS administration attenuated expression of ACE2 in airw

3 ICS technique was evaluated by using scales derived from

4 ICS therapies in COPD reduce expression of the SARS-CoV-

5 ICS treatment increased the risk of pneumonia in those p

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

7 ICS use was associated with reduced time in the hospital

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

9 S inhaler dose = 0.86, 0.77-0.93, p < 0.001; ICS mean daily = 0.80, 0.74-0.87, p < 0.001; LABA = 1.01

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

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

12 CS inhaler dose = 0.99, 0.98-1.00, p = 0.59; ICS mean daily = 0.78, 0.76-0.79, p < 0.001; LABA = 0.83

13 After ICS treatment of patients with asthma, the compositional

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

15 st year; 4) no recommendation for or against ICS as an additive therapy to long-acting bronchodilator

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

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

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

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

20 aints, and allowed households a choice among ICS.

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

22 er half of intervention households bought an ICS, although demand was highly price-sensitive.

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

24 Formoterol in combination with an ICS in a single inhaler (single maintenance and reliever

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

26 ly reveal intermediate cell states (ICS) and ICS-regulated transition trajectories, producing emergen

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

28 ol and budesonide as representative LABA and ICS, respectively.

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

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

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

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

33 onal circulating miRNAs predictive of asthma ICS treatment response over time.

34 rs were entered in a database implemented at ICS Maugeri in Pavia, Italy, and pooled for analysis.

35 Finally, baseline ICS was positively associated with incident "elevated de

36 The after/before ICS plus LABA treatment ratio of B2AR number was 1.0 for

37 high for electric stoves relative to biomass ICS.

38 ients for those who are poorly controlled by ICS alone.

39 ndividuals whose asthma is not controlled by ICS-formoterol therapy for step 5 (moderate-severe persi

40 This signature, decreased by ICS/LABA treatment was enriched for genes associated wit

41 es to corticosteroids relate to the clinical ICS response.

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

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

44 be less common than presumed in concomitant ICS plus LABA-treated asthmatic patients.

45 needed SABA therapy or as-needed concomitant ICS and SABA therapy are recommended.

46 magnitude of benefit of regimens containing ICS (fluticasone furoate-umeclidinium-vilanterol n=4151

47 Conventionally, ICS treatment is recommended for patients with symptoms

48 Improved cookstoves (ICS) can deliver "triple wins" by improving household he

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

50 aditional mud stoves or improved cookstoves (ICS).

51 icle formulations of inhaled corticosteroid (ICS) are associated with improved lung delivery.

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

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

54 Although inhaled corticosteroid (ICS) medication is considered the cornerstone treatment

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

56 on the microbiota of inhaled corticosteroid (ICS) treatment administered to ICS-naive subjects with a

57 following increased inhaled corticosteroid (ICS) treatment.

58 o understand whether inhaled corticosteroid (ICS) withdrawal affected IMPACT results, given direct tr

59 A-associated LOBP in inhaled corticosteroid (ICS)-treated patients.

60 ed to recommend that inhaled corticosteroid (ICS)/long-acting beta (2)-adrenoceptor agonist (LABA) co

61 combination drug of inhaled corticosteroid (ICS)/long-acting beta2 agonist is being used as a long-t

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

63 1 RCT of LABAs and inhaled corticosteroids (ICS) (n = 1097), 5 RCTs of the long-acting muscarinic an

64 erinflation and how inhaled corticosteroids (ICS) affect this important aspect of COPD pathophysiolog

65 herapies containing inhaled corticosteroids (ICS) and baseline blood eosinophil count in patients wit

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

67 Inhaled corticosteroids (ICS) are a mainstay of treatment in eosinophilic asthma.

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

69 Rationale: Inhaled corticosteroids (ICS) are key treatments for controlling asthma and preve

70 Inhaled corticosteroids (ICS) are the most widely prescribed and effective medica

71 thma who respond to inhaled corticosteroids (ICS) from refractory asthma is an important clinical cha

72 Daily dose of inhaled corticosteroids (ICS) inversely correlated with MUC1 expression in neutro

73 reasing the dose of inhaled corticosteroids (ICS) is commonly used at early signs of loss of asthma c

74 disease (COPD) with inhaled corticosteroids (ICS) is controversial, because it can reduce the risk of

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

76 and "high" doses of inhaled corticosteroids (ICS) to define daily maintenance doses of 100 to 250 mug

77 Use of inhaled corticosteroids (ICS) was associated with lower expression of ACE2 and TM

78 tients on high-dose inhaled corticosteroids (ICS) with type 2-high asthma (subgroups including baseli

79 aking high doses of inhaled corticosteroids (ICS).

80 triple therapy with inhaled corticosteroids (ICS)/LABA/LAMA over dual therapy with LABA/LAMA in patie

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

82 Inhaled corticosteroids (ICSs) are widely used in COPD, but the extent to which t

83 lity in response to inhaled corticosteroids (ICSs) can result in less than optimal asthma control.

84 ry maintenance with inhaled corticosteroids (ICSs) has been reserved for patients with more persisten

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

86 receiving high-dose inhaled corticosteroids (ICSs) is uncertain.

87 n: medium/high-dose inhaled corticosteroids (ICSs) or ICSs + add-on medication (long-acting beta2-ago

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

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

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

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

92 using immunological assays (flow cytometry, ICS, ELISPOT).

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

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

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

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

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

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

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

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

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

102 of Fe(NO) suppression testing to demonstrate ICS responsiveness and clinical benefit on electronicall

103 Despite ICS therapy, many asthmatic patients have persistent air

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

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

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

107 monitored treatment with standard high-dose ICS and long-acting beta(2)-agonist treatment.

108 atients with type 2-high asthma on high-dose ICS at baseline.

109 In high-dose ICS type 2-high subgroups, dupilumab 200/300 mg q2w vs p

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

111 ld persistent asthma), either daily low-dose ICS plus as-needed SABA therapy or as-needed concomitant

112 derate persistent asthma in step 3 (low-dose ICS-formoterol therapy) and step 4 (medium-dose ICS-form

113 entered a 1-month run-in period on low-dose ICS/LABA budesonide/formoterol (BUD/F) 200/6 one inhalat

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

115 -formoterol therapy) and step 4 (medium-dose ICS-formoterol therapy) for both daily and as-needed the

116 lso effective in patients taking medium-dose ICS.

117 Of those prescribed medium/high-dose ICSs as their first preventer, 13.0% already had documen

118 elines-based therapy and requiring high-dose ICSs had reduced in vitro responsiveness to corticostero

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

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

121 P subjects subsequently randomized to either ICS (budesonide) or placebo.

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

123 , reduced number of circulating eosinophils, ICS treatment, and the risk of pneumonia in patients wit

124 ent for patients with persistent asthma, few ICS pharmacogenomic studies have involved nonwhite popul

125 chains, and price discounts are critical for ICS diffusion.

126 st year; 3) a conditional recommendation for ICS withdrawal for patients with COPD receiving triple t

127 To minimize impact from ICS withdrawal, in an analysis excluding the first 30 da

128 This "functional" ICS signature was augmented in the presence of formotero

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

130 y, among men, lower serum albumin and higher ICS were linked with higher baseline "somatic complaints

131 The race-specific associations of hsCRP, ICS, IL-1beta and the sex-specific association of IL-12

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

133 ta showed greater deviation from baseline in ICS nonresponders than in ICS responders.

134 d the importance of the genetic component in ICS response.

135 ne induced a 28 percentage-point increase in ICS ownership.

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

137 n from baseline in ICS nonresponders than in ICS responders.

138 unscheduled physician visits, and increased ICS dose increased risk of non-serious adverse events.

139 C-allele appeared to particularly influence ICS treatment response in the presence of eosinophilic i

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

141 ren might benefit from daily or intermittent ICS therapy.

142 : 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

143 hen represent the doses at which maintenance ICS are prescribed at step 2 and within ICS/long-acting

144 SAPPHIRE) who underwent 6 weeks of monitored ICS therapy (n = 244).

145 After 3-month ICS/LABA treatment, residual volume (RV)/total lung capa

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

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

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

149 ior ICS users, 35% reduction; P < 0.001; non-ICS users, 35% reduction; P = 0.018), and overall when e

150 blood eosinophil count, compared with a non-ICS dual long-acting bronchodilator (umeclidinium-vilant

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

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

153 nitric oxide (Fe(NO)) with directly observed ICS therapy over 7 days can identify nonadherence to ICS

154 Associations of ICS response described in published GWAS were followed u

155 he maximum achievable therapeutic benefit of ICS is obtained in adult asthma across the spectrum of s

156 costs are lower than the social benefits of ICS promotion.

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

158 vation period while using the same dosage of ICS during a certain period of time.

159 o compare increased dose with stable dose of ICS among adults and children with asthma.

160 rate quality supports increasing the dose of ICS as part of a self-initiated action plan to reduce ri

161 However, increased dose of ICS increased the risk of non-serious adverse events (OR

162 Increased dose of ICS was associated with a significantly reduced risk of

163 dmission between increased or stable dose of ICS.

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

165 comparing increased doses vs stable doses of ICS for home management of asthma exacerbations in adult

166 he use of inappropriately excessive doses of ICS.

167 We evaluated the effect of ICS administration on pulmonary ACE2 expression in vitro

168 To investigate the effect of ICS/long-acting beta(2)-agonist (LABA) treatment on both

169 r lack thereof, of different formulations of ICS through direct and indirect bronchoprovocation testi

170 response effect of different formulations of ICS through direct or indirect bronchoprovocation testin

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

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

173 erve as biomarkers and biologic mediators of ICS clinical response over the 4-year clinical trial per

174 cell cultures and in vivo in mouse models of ICS administration.

175 OPD stratified according to use or nonuse of ICS.

176 ombined, these two miRNAs were predictive of ICS response over the course of the clinical trial, with

177 We sought to identify genetic predictors of ICS response in multiple population groups with asthma.

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

179 We propose a reclassification of ICS doses based on a "standard daily dose," which is def

180 vidence of the dose-response relationship of ICS in adult asthma.

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

182 r and embryogenesis, we uncover the roles of ICS on adaptation, noise attenuation, and transition eff

183 Uncontrolled Patients on Medium Strength of ICS + LABA [TRIMARAN] and Triple in Asthma High Strength

184 2 with ICS use warrants prospective study of ICS use as a predictor of decreased susceptibility to SA

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

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

187 re observed related to sex, race, and use of ICS.Conclusions: Higher expression of ACE2 and TMPRSS2 i

188 ed before randomization and after 8 weeks of ICS plus LABA treatment.

189 of this study was to evaluate the effect of ICSs following pulmonary expression of the SARS-CoV-2 vi

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

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

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

193 smoking status has the potential to optimise ICS use in clinical practice in patients with COPD and a

194 e important clinical benefits from optimized ICS/long-acting beta(2)-agonist treatment.

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

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

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

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

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

200 /high-dose inhaled corticosteroids (ICSs) or ICSs + add-on medication (long-acting beta2-agonist [LAB

201 Stepping down medication, either LABAs or ICSs, could save annually around pound 17,000,000 or pou

202 run-in with a constant dose of fine particle ICS (mean dose 710 ug), followed by switching to an equi

203 c switching from fine to extra-fine particle ICS at half the dose was associated with clinically rele

204 r switching from fine to extra-fine particle ICS in persistent asthma.

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

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

207 Of patients first prescribed ICSs + 1 add-on, 70.4% remained on the same medication d

208 y a numerical reduction was seen among prior ICS nonusers (12% reduction; P = 0.115).

209 Questionnaire results were analyzed by prior ICS use.

210 erbation rate compared with UMEC/VI in prior ICS users (29% reduction; P < 0.001), but only a numeric

211 vere exacerbation rates, regardless of prior ICS use (prior ICS users, 35% reduction; P < 0.001; non-

212 on rates, regardless of prior ICS use (prior ICS users, 35% reduction; P < 0.001; non-ICS users, 35%

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

214 ild to moderate, persistent asthma receiving ICS.

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

216 jects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma recei

217 and patients with nonsevere asthma receiving ICSs (n = 85).

218 lision point for inverse Compton scattering (ICS), a scheme where a laser is used to provide undulato

219 ein (hsCRP), z-inflammation composite score [ICS, combining elevated hsCRP and ESR with low serum alb

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

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

222 viruses by intracellular cytokine staining (ICS) using peripheral blood mononuclear cells (PBMCs) of

223 aboon using intracellular cytokine staining (ICS).

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

225 s naturally reveal intermediate cell states (ICS) and ICS-regulated transition trajectories, producin

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

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

228 nonusers, patients with COPD who were taking ICSs also had reduced sputum expression of ACE2.

229 Short-term ICS/LABA treatment improves RV/TLC% predicted in severe

230 (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

231 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

232 It is recommended that ICS treatment be started at these standard doses, which

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

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

235 A short-term increase in the ICS dose alone for worsening of asthma symptoms is not r

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

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

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

239 674 white subjects) and 298 subjects in the ICS- group (49 African American and 249 white subjects).

240 95% CI, 1.01-2.48; P = .046) but not in the ICS- group (P = .984).

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

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

243 Specifically, the ICS dose that achieves 80-90% of the maximum obtainable

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

245 rther, use of the IFEL acceleration with the ICS interaction produces a train of high intensity X-ray

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

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

248 LABAs or another add-on or by halving their ICS dose (halving their mean-daily dose or their inhaler

249 patients with COPD receiving triple therapy (ICS/LABA/LAMA) if the patient has had no exacerbations i

250 ristae edges, whereas trimeric OPA1 tightens ICS outlets.

251 with significant interaction (P <= 0.05) to ICS versus placebo treatments.

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

253 rticosteroid (ICS) treatment administered to ICS-naive subjects with asthma.

254 ns, and focus groups to diagnose barriers to ICS adoption.

255 fective means of identifying nonadherence to ICS in subjects with difficult-to-control asthma and the

256 apy over 7 days can identify nonadherence to ICS treatment in difficult-to-control asthma.

257 enrolling participants likely to respond to ICS therapy, and carefully selecting treatment durations

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

259 ed transrepression and predicted response to ICS through logistic regression models.Measurements and

260 27907, that appears to influence response to ICS treatment in multiple population groups and likely m

261 important modifiers of treatment response to ICS.

262 do not demonstrate reduced responsiveness to ICS therapy.

263 However, the responsiveness to ICS varies among individuals.

264 enetic markers determining responsiveness to ICS which could lead in the future the clinical identifi

265 Although clinically superior to ICS, mechanisms underlying the efficacy of this combinat

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

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

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

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

270 better than that of those continuing to use ICS.

271 97.1% used ICS (dose 2000 BDP), 93.6% LABA in association with ICS,

272 tinued their medication, and six (5.5%) used ICS periodically.

273 -specific CD8 T-cell responses ex-vivo using ICS may be variable, especially in humans with complex a

274 own (adjusted hazard ratio, 95% CI, p-value: ICS inhaler dose = 0.86, 0.77-0.93, p < 0.001; ICS mean

275 tions (adjusted odds ratio, 95% CI, p-value: ICS inhaler dose = 0.99, 0.98-1.00, p = 0.59; ICS mean d

276 N] and Triple in Asthma High Strength Versus ICS/LABA HS and Tiotropium [TRIGGER]) recruited patients

277 ndulator to generate up to 13 keV X-rays via ICS.

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

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

280 r oral steroids or hospitalization, for whom ICS is conditionally recommended as an additive therapy;

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

282 d a Fe(NO)-low population when adherent with ICS/long-acting beta(2)-agonist (median, 26 ppb [interqu

283 adherence were significantly associated with ICS response.

284 an American participants was associated with ICS responsiveness.

285 rs3827907, was significantly associated with ICS-mediated changes in asthma control in the discovery

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

287 Compared with ICS nonusers, patients with COPD who were taking ICSs al

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

289 he lower expression of ACE2 and TMPRSS2 with ICS use warrants prospective study of ICS use as a predi

290 formed in 1347 admixed children treated with ICS (Hispanics/Latinos and African Americans), analysing

291 sthma exacerbations in children treated with ICS and replicated previously identified genomic regions

292 acerbations in admixed children treated with ICS and to validate previous GWAS findings.

293 was 49%, 71.6% of patients were treated with ICS, 57.2% of them had bronchiectasis, and 20.9% had <10

294 pneumonia in patients with COPD treated with ICS.

295 change in lung function after treatment with ICS (P = 4.91 x 10(-3) ).

296 flammation persists in patients treated with ICSs and to evaluate the clinical features of patients w

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

298 ance ICS are prescribed at step 2 and within ICS/long-acting beta-agonist combination therapy at step

299 s available to prescribe higher doses within ICS/long-acting beta-agonist maintenance therapy in acco

300 d in this cohort of subjects with or without ICS-naive mild asthma.

301 ie, the combined effect of the SNP and SNP x ICS treatment interaction) with changes in asthma contro