ライフサイエンスコーパス: salmeterol

1 fected the efficacy or duration of action of salmeterol.

2 on outcomes in response to tiotropium versus salmeterol.

3 e not associated with the LOB in response to salmeterol.

4 steric binding site for larger drugs such as salmeterol.

5 eta-adrenoceptor agonists, isoproterenol and salmeterol.

6 be equivalent to those with the addition of salmeterol.

7 cells, which was enhanced by fluticasone and salmeterol.

8 thma treatment failure in patients receiving salmeterol.

9 se was partially inhibited by salbutamol and salmeterol.

10 choprotection at weeks 4 and 8 was seen with salmeterol.

11 gonist before and after chronic therapy with salmeterol.

12 ontributes to the long duration of action of salmeterol.

13 chronic dosing with formoterol compared with salmeterol.

14 roduct (0.48 L) than with placebo (-0.11 L), salmeterol (0.05 L), or FP (0.25 L).

15 Intra-alveolar salmeterol 10 (-6) M attenuated the degree of pulmonary

16 Racemic albuterol 10(-5) M, salmeterol 10(-6) M, and isoproterenol 10(-6) M each sti

17 Salmeterol (10 muM), a beta-2-adrenergic receptor agonis

18 numbered treatment packs containing inhaled salmeterol (100 mug twice daily) or a matching placebo.

19 h beta-agonists albuterol, isoproterenol, or salmeterol (100 nM to 10 muM) caused a significant ( app

20 L/min) as compared with placebo (-14 L/min), salmeterol (-11.6 L/min), or FP (15.2 L/min).

21 of the selective beta2-adrenoceptor agonist salmeterol (15 microM) facilitated the excitatory field

22 reatment with a single inhalation of 100 mug salmeterol 30 min before bronchial segmental challenge.

23 and five patients with COPD received either salmeterol 42 microg twice daily, ipratropium bromide 36

24 0 microg twice per day; n = 54) or switch to salmeterol (42 microg twice per day; n = 54) or to place

25 Combination treatment with salmeterol 50 microg and FP 250 microg given twice daily

26 -in period were randomized to treatment with salmeterol 50 microg combined with fluticasone propionat

27 to receive inhaled longacting beta2 agonist (salmeterol 50 microg twice a day) or placebo given in a

28 with fluticasone propionate (FP) 250 microg, salmeterol 50 microg, FP 250 microg, or placebo, each gi

29 ily tiotropium 5 mug or 2.5 mug, twice-daily salmeterol 50 mug, or placebo, while maintaining inhaled

30 h montelukast (10 mg once in the evening) or salmeterol (50 microg [2 puffs] twice daily).

31 patients), or fluticasone (100 microg) plus salmeterol (50 microg) each night (165 patients).

32 50 mug twice a day) was compared with adding salmeterol (50 mug twice a day) and doubling the flutica

33 tiotropium (at a dose of 18 mug once daily), salmeterol (50 mug twice daily), and the inhaled glucoco

34 ycopyrronium (50 mug) once daily or the LABA salmeterol (50 mug) plus the inhaled glucocorticoid flut

35 Subjects were administered salmeterol, 50 mug twice a day for 2 weeks, and underwen

36 She is on fluticasone/salmeterol 500/50 mug one inhalation twice daily and mon

37 n cluster had best response with fluticasone/salmeterol (64% vs 23% 2.5x fluticasone and 13% fluticas

38 ifference 133 mL, 95% CI 105-161, p<0.0001), salmeterol (73 mL, 46-101, p<0.0001), or fluticasone alo

39 This study evaluated salmeterol, a beta-agonist bronchodilator with a duratio

40 se asthma symptoms improve after addition of salmeterol, a substantial reduction (50%) in triamcinolo

41 ospectively evaluated the safety of the LABA salmeterol, added to fluticasone propionate, in a fixed-

42 ler monitors recorded fluticasone propionate/salmeterol adherence (covertly for non-IRF groups) and,

43 during the period examined: (1) fluticasone/salmeterol (Advair), (2) mometasone furoate (Asmanex), (

44 lso had a major effect (18-fold reduction in salmeterol affinity).

45 primary end point of trough FEV1 compared to salmeterol after 4 weeks of dosing in patients with mode

46 tyryl cyclic adenosine monophosphate (cAMP), salmeterol, albuterol, and isoproterenol in normal rat l

47 15d-PGJ(2), fluticasone, and salmeterol all inhibited TNFalpha-induced histone H4 ace

48 The mortality rate for salmeterol alone or fluticasone propionate alone did not

49 istered with a single inhaler, with placebo, salmeterol alone, or fluticasone propionate alone for a

50 of FP, and to a lesser extent with 50 microg salmeterol alone.

51 the contribution of inhaled fluticasone and salmeterol, alone or combined, to the reversal of bronch

52 Salmeterol also attenuated activation of NF-kappaB via i

53 tive agonist site, it has been proposed that salmeterol also binds with very high affinity at a secon

54 Salmeterol also directly activated immunoprecipitated PP

55 A total of 179 patients were randomized to salmeterol and 183 to placebo.

56 g fluticasone twice daily (n=374), 50 microg salmeterol and 500 microg fluticasone twice daily (n=358

57 ble, were found after administration of both salmeterol and albuterol.

58 ticipants received high-dose fluticasone and salmeterol and continued other pre-study controller drug

59 Combined activity of salmeterol and fluticasone at equimolar concentrations h

60 Fluticasone/salmeterol and fluticasone monotherapy decreased periphe

61 Fluticasone/salmeterol and fluticasone monotherapy equally reverse p

62 Subsequently, we determined the effects of salmeterol and fluticasone propionate (FP) in seven ster

63 The combination of salmeterol and fluticasone propionate has a broad spectr

64 s, such as the beta(2)-adrenoceptor agonists salmeterol and formeterol, and the new anticholinergic t

65 terol has a 24 h duration of action, whereas salmeterol and formoterol require twice-daily administra

66 ion (indacaterol, two indacaterol analogues, salmeterol and formoterol) in monounsaturated model memb

67 ond cohort, B16Arg/Arg subjects treated with salmeterol and ICS concurrently (n = 8) had a lower A.M.

68 ly/Gly genotypes, combination treatment with salmeterol and inhaled corticosteroid improved airway fu

69 eness to methacholine did not differ between salmeterol and placebo in Arg/Arg participants (p=0.87).

70 Salmeterol and salbutamol enhanced rhinovirus- and IL-1b

71 fluticasone propionate and beta(2) agonists salmeterol and salbutamol on IL-6 production in BEAS-2B

72 dual and differential treatment responses to salmeterol and tiotropium and predictors of a positive r

73 f patients showed a differential response to salmeterol and tiotropium in terms of morning PEF (n = 9

74 ferential responses of asthmatic patients to salmeterol and tiotropium when added to an inhaled corti

75 roup) was randomly assigned to continue both salmeterol and triamcinolone for the remaining 16 weeks

76 riod, no significant differences between the salmeterol and triamcinolone groups were observed for co

77 inhaled combined long-acting beta2-agonist (salmeterol) and corticosteroid (fluticasone propionate)

78 /- 0.89 mm Hg (mean +/- SEM) at 30 min after salmeterol, and -3.45 +/- 0.92 mm Hg at 20 min after alb

79 patients received 18 mug tiotropium, 100 mug salmeterol, and 1000 mug fluticasone propionate daily fo

80 th tiotropium doses were similar to those of salmeterol, and all active compounds had good safety and

81 On both assessment days for salmeterol, and during placebo administration periods, s

82 with no awakenings as compared with placebo, salmeterol, and FP (p </= 0.016).

83 for simulation vs. trial in the in placebo, salmeterol, and triamcinolone arms, respectively.

84 ts that the high affinity and selectivity of salmeterol are due to specific amino acids within the re

85 ior to the combination of beclomethasone and salmeterol as judged by protection against asthma treatm

86 d a randomized, double-blind trial comparing salmeterol at a dose of 50 microg plus fluticasone propi

87 , combination therapy with 100 microg FP and salmeterol augmented the action of FP on GR nuclear loca

88 l relaxation assays, IAS and the parent drug salmeterol behave essentially the same.

89 biochemical evidence demonstrates that when salmeterol binds to the receptor, its hydrophobic arylox

90 Salmeterol, but not dexamethasone, increased PP2A activi

91 Salmeterol can significantly inhibit activation of macro

92 Salmeterol caused an augmentation of rhinovirus-induced

93 onclusion, this study shows that fluticasone/salmeterol combination decreases extracellular matrix re

94 valents, was reduced to 64 +/- 9 microL with salmeterol compared with 119 +/- 51 microL in saline-tre

95 on of primary microglial-enriched cells with salmeterol could inhibit the inflammatory response induc

96 ination of the LTRA montelukast and the LABA salmeterol could provide an effective therapeutic strate

97 Only fluticasone/salmeterol decreased bronchoalveolar neutrophilia (p = 0

98 time points, the bronchoprotective effect of salmeterol decreased significantly.

99 In addition to genotype, FEV1, response to salmeterol, degree of EIB, and exhaled nitric oxide (FE(

100 PEF, l/min) after 16 weeks of treatment with salmeterol (DeltaPEFsal) versus montelukast (DeltaPEFmon

101 -selective, G protein-biased partial agonist salmeterol depends on specific hydrogen bonding between

102 r for both agonists demonstrated significant salmeterol desensitization, although it was reduced rela

103 nflammation and therapeutically administered salmeterol, dexamethasone, or the PP2A-activating drug (

104 Treatment with salmeterol did not prevent early lung injury (32 [19.2%]

105 rticosteroid treatment, chronic therapy with salmeterol does not result in tolerance to the bronchodi

106 +/- 4.1% bronchoprotection) after the first salmeterol dose, and 22.8 +/- 3.2% (18.9 +/- 11.5% bronc

107 Salmeterol downregulated PgLPS-mediated phosphorylation

108 moterol solution or 50 mug of large-particle salmeterol dry powder twice daily plus inhaled corticost

109 ction on guinea pig trachea, and longer than salmeterol duration of action in vivo, suitable for once

110 Second, to assess salmeterol efficacy for functional desensitization, we e

111 In vitro, salmeterol enhanced FP effects on GR nuclear translocati

112 Results showed salmeterol exerted potent neuroprotection against both L

113 Salmeterol exerts anti-inflammatory effects by increasin

114 hat administration of extremely low doses of salmeterol exhibit potent neuroprotective effects by inh

115 icasone (F), (2) once daily fluticasone plus salmeterol (F + S), or (3) once daily oral montelukast (

116 Rather, salmeterol failed to induce microglial cAMP production,

117 horses/group) were treated with fluticasone, salmeterol, fluticasone/salmeterol, or with antigen avoi

118 indacaterol-glycopyrronium group than in the salmeterol-fluticasone group (0.98 vs. 1.19; rate ratio,

119 indacaterol-glycopyrronium group than in the salmeterol-fluticasone group (3.59 vs. 4.03; rate ratio,

120 time to the first exacerbation than did the salmeterol-fluticasone group (71 days [95% CI, 60 to 82]

121 indacaterol-glycopyrronium group than in the salmeterol-fluticasone group (hazard ratio, 0.78; 95% CI

122 caterol-glycopyrronium group and 4.8% in the salmeterol-fluticasone group (P=0.02).

123 aterol-glycopyrronium group, and 1682 to the salmeterol-fluticasone group.

124 terol-glycopyrronium was more effective than salmeterol-fluticasone in preventing COPD exacerbations

125 only noninferiority but also superiority to salmeterol-fluticasone in reducing the annual rate of al

126 effect of indacaterol-glycopyrronium versus salmeterol-fluticasone on the rate of COPD exacerbations

127 erved with indacaterol/glycopyrronium versus salmeterol/fluticasone (hazard ratio, 0.76; 95% CI, 0.56

128 -acting beta2-agonist/inhaled corticosteroid salmeterol/fluticasone combination 50/500 mug in patient

129 glycopyrronium was significantly superior to salmeterol/fluticasone for the prevention of exacerbatio

130 ischarge from hospital patients were given a salmeterol/fluticasone inhaler with an INCA device attac

131 wk double-blind study to placebo (n = 73) or salmeterol/fluticasone propionate 50/500 microg (n = 67)

132 m provides superior or similar benefits over salmeterol/fluticasone regardless of blood eosinophil le

133 50 cells/mul subgroups, and at no cutoff was salmeterol/fluticasone superior to indacaterol/glycopyrr

134 f pneumonia was higher in patients receiving salmeterol/fluticasone than indacaterol/glycopyrronium i

135 The cells were then treated with 10 muM salmeterol followed by Western blot analysis or ELISA.

136 AW264.7 and THP-1 cells were pretreated with salmeterol, followed by PgLPS, and monitored for product

137 nute pretreatment with TNF-alpha followed by salmeterol for 6 hours.

138 s formoterol, or fixed-dose fluticasone plus salmeterol for 6 months.

139 s formoterol and fixed-dose fluticasone plus salmeterol for 7 months.

140 eive alendronate or placebo while initiating salmeterol for 8 weeks.

141 pium was also noninferior to the addition of salmeterol for all assessed outcomes and increased the p

142 to induce AAD while receiving treatment with salmeterol, formoterol, or salbutamol.

143 n patients with asthma receiving fluticasone/salmeterol (FP/SM) combination and FP alone.

144 significantly (p </= 0.001) greater with the salmeterol/FP combination product (0.48 L) than with pla

145 g of fluticasone propionate and 50 microg of salmeterol [FSC]) administered twice daily through the D

146 g (1.33, 1.03-1.72; p=0.031) groups, and the salmeterol group (1.46, 1.13-1.89; p=0.0039), than in th

147 Adverse events were less frequent in the salmeterol group (55 vs. 70; OR, 0.63; 95% CI, 0.39-0.99

148 m 2.5 mug group, and 196 mL (158-234) in the salmeterol group (all p<0.0001); difference in trough FE

149 ), the tiotropium 2.5 mug group (n=520), the salmeterol group (n=541), or the placebo group (n=523);

150 2% in the montelukast group and 33.0% in the salmeterol group (P = 0.002).

151 ebo-minus group was assigned and half of the salmeterol group (salmeterol-minus group) was randomly a

152 The other half of the salmeterol group (salmeterol-plus group) was randomly as

153 208 patients, 27 patients in the fluticasone-salmeterol group and 21 in the fluticasone-alone group h

154 al of 265 patients (8.5%) in the fluticasone-salmeterol group and 309 (10.0%) in the fluticasone-alon

155 36 events in 34 patients in the fluticasone-salmeterol group and 38 events in 33 patients in the flu

156 However, the salmeterol group had more treatment failures than the tr

157 xacerbation was 21% lower in the fluticasone-salmeterol group than in the fluticasone-only group (haz

158 ious asthma-related event in the fluticasone-salmeterol group was 1.03 (95% confidence interval [CI],

159 up, 15.2% in the placebo group, 13.5% in the salmeterol group, and 16.0% in the fluticasone group.

160 480 of 5834 patients (8%) in the fluticasone-salmeterol group, as compared with 597 of 5845 patients

161 In the salmeterol group, patients with Arg16Arg genotype had a

162 onger in the triamcinolone group than in the salmeterol group.

163 terol > terbutaline = zinterol = albuterol > salmeterol > dobutamine > or = ephedrine.

164 ng montelukast and 46% of patients receiving salmeterol had a maximal percentage decrease in FEV1 of

165 is study, the authors sought to determine if salmeterol had a similar inhibitory effect on the inflam

166 Patients receiving fluticasone-salmeterol had fewer severe asthma exacerbations than di

167 switched to treatment with fluticasone plus salmeterol had treatment failure, as compared with 30.3%

168 onstriction) with fluticasone propionate and salmeterol in a combination product was a more effective

169 n this trial involving children with asthma, salmeterol in a fixed-dose combination with fluticasone

170 Patients who received salmeterol in a fixed-dose combination with fluticasone

171 Salmeterol in a rat model of acid-induced lung injury.

172 greater improvements with formoterol versus salmeterol in all IOS outcomes and FEF25-75, but not FEV

173 evaluate the risk of administering the LABA salmeterol in combination with an inhaled glucocorticoid

174 In addition, salmeterol in combination with FP enhanced glucocorticoi

175 may have an impaired therapeutic response to salmeterol in either the absence or presence of concurre

176 t with the combination of beclomethasone and salmeterol in moderate asthma.

177 ects of long-acting beta2AR agonists such as salmeterol in rodent models of Parkinson's disease.

178 yl ring of the aralkyloxyalkyl side chain of salmeterol in the beta 2AR binding site, we designed and

179 ective bronchodilator, and an alternative to salmeterol in this patient population.

180 ference at 60 minutes between formoterol and salmeterol in total airway resistance at 5 Hz, 7.50% (95

181 treated with the selective beta2-AR agonist, salmeterol, in the presence of osteogenic medium showed

182 cting beta (2)-adrenoceptor agonists (LABAs) salmeterol, indacaterol, and formoterol.

183 desensitization, we examined the kinetics of salmeterol-induced cAMP accumulation (0-30 minutes) in h

184 roid, two during double-blind treatment with salmeterol/inhaled corticosteroid, and one during double

185 Salmeterol is a long-acting beta2-adrenergic receptor (b

186 Salmeterol is a long-acting beta2-adrenergic receptor (b

187 Salmeterol is a long-acting beta2-adrenergic receptor ag

188 Salmeterol is a long-acting beta2-agonist, widely used a

189 terminal right-hand-side phenyl ring of (R)-salmeterol is presented.

190 Sulfone 10b had salmeterol-like potency and selectivity profile, long du

191 lmeterol than to an increase in fluticasone (salmeterol-low-dose fluticasone vs. medium-dose fluticas

192 nflammation by PgLPS, suggesting that use of salmeterol may be an effective treatment in inhibiting o

193 ptor kinase/arrestin and protein kinase A in salmeterol-mediated desensitization through bioluminesce

194 Further studies demonstrated that salmeterol-mediated neuroprotection is not a direct effe

195 m-dose fluticasone, 49% vs. 28% [P = 0.003]; salmeterol-medium-dose fluticasone vs. high-dose flutica

196 e occurred in 46.3% (95% CI, 34%-59%) of the salmeterol-minus group 8 weeks after triamcinolone thera

197 95% confidence interval [CI], 2%-15%) of the salmeterol-minus group 8 weeks after triamcinolone treat

198 f the triamcinolone elimination phase in the salmeterol-minus group was 4.3 (2.0-9.2) compared with t

199 s assigned and half of the salmeterol group (salmeterol-minus group) was randomly assigned to reduce

200 during the first half of the SLIC study and salmeterol monotherapy during the second half.

201 doses of triamcinolone cannot be switched to salmeterol monotherapy without risk of clinically signif

202 asthma-related deaths was obtained from the Salmeterol Multi-center Asthma Research Trial (SMART).

203 tropium 5 mug n=11, tiotropium 2.5 mug n=12, salmeterol n=11, placebo n=14).

204 sponse to tiotropium for FEV1 (n = 104) than salmeterol (n = 62).

205 flow (PEF; p = 0.005) in B16Arg/Arg subjects(salmeterol, n = 12; placebo, n = 5) as compared with B16

206 n = 5) as compared with B16Gly/Gly subjects (salmeterol, n = 13; placebo, n = 13).

207 Seven Arg/Arg participants (placebo, n=5; salmeterol, n=2) and six Gly/Gly participants (placebo,

208 and six Gly/Gly participants (placebo, n=3; salmeterol, n=3) had an asthma exacerbation.

209 The long duration of action of salmeterol offers the advantage of twice daily dosing co

210 he effect of the long-acting beta(2)-agonist salmeterol on airway inflammation induced by segmental a

211 f Indacaterol Glycopyrronium vs. Fluticasone Salmeterol on COPD Exacerbations) study used the Exacerb

212 of Indacaterol Glycopyronium vs Fluticasone Salmeterol on COPD Exacerbations) study, which compared

213 the effects of treatment with tiotropium or salmeterol on exacerbations in 7376 patients with COPD.

214 sess airway inflammation, and the effects of salmeterol on this process.

215 assigned to receive either fluticasone with salmeterol or fluticasone alone for 26 weeks.

216 year to receive fluticasone propionate plus salmeterol or fluticasone alone for 26 weeks.

217 ticosteroid arms (fluticasone propionate and salmeterol or fluticasone furoate and vilanterol); a con

218 ces in the albuterol dose response following salmeterol or placebo.

219 e statistically significantly increased with salmeterol (OR, 1.7 [CI, 1.1 to 2.7]) and formoterol (OR

220 relative to baseline over that with placebo, salmeterol, or FP at Day 1, Week 1, and Week 12 (p </= 0

221 ing asthma than did patients in the placebo, salmeterol, or FP groups (p </= 0.002).

222 ed with fluticasone, salmeterol, fluticasone/salmeterol, or with antigen avoidance for 12 weeks.

223 It had lower than salmeterol oral absorption in rat, lower bioavailability

224 s) or once-daily fluticasone propionate plus salmeterol (our secondary hypothesis) has not yet been d

225 /- 11.5% bronchoprotection) after 2 weeks of salmeterol (P = 0.0001).

226 ren with doubling the fluticasone and adding salmeterol (P = 0.99).

227 ich showed the noninferiority of fluticasone-salmeterol (P=0.006).

228 us group was 4.3 (2.0-9.2) compared with the salmeterol-plus group (P<.001).

229 ed compared with 2.8% (95% CI, 0%-7%) of the salmeterol-plus group during the same period.

230 The other half of the salmeterol group (salmeterol-plus group) was randomly assigned to continue

231 compared with 13.7% (95% CI, 5%-22%) of the salmeterol-plus group.

232 m (10 minutes) or long-term (2 and 14 hours) salmeterol pretreatments, we found that salmeterol progr

233 urs) salmeterol pretreatments, we found that salmeterol progressively depressed isoproterenol stimula

234 s (epinephrine, terbutaline, metaproterenol, salmeterol, propranolol, alprenolol, bisoprolol, ICI 118

235 Systemic or intranasal administration of salmeterol protected against the development of allergen

236 Salmeterol-protected methacholine challenges (SPMChs) an

237 Salmeterol provided similar maximal bronchodilatation to

238 RET demonstrated a much reduced efficacy for salmeterol recruitment of arrestin to beta2AR relative t

239 Salmeterol reduced some biomarkers of alveolar inflammat

240 he twice-daily beta2-agonists formoterol and salmeterol represent important advances.

241 The anti-inflammatory effects of salmeterol required beta2AR expression in microglia but

242 synergistically enhanced by fluticasone and salmeterol, respectively.

243 We compared salmeterol response in patients with asthma homozygous f

244 In central airways, fluticasone/salmeterol reversed extracellular matrix remodelling aft

245 with an inhaled long-acting beta(2)-agonist, salmeterol (S), to treat the inflammatory and bronchocon

246 the double mutant beta2-H296K-K305D, reduced salmeterol's affinity by 275-fold, to within 4-fold of t

247 5) had the largest single effect by reducing salmeterol's affinity for the beta2-adrenoceptor by 31-f

248 rity comparison) or the addition of the LABA salmeterol (secondary noninferiority comparison).

249 Previous studies demonstrated that salmeterol showed weak efficacy for activation of adenyl

250 desensitization, demonstrating that although salmeterol shows weak efficacy for adenylyl cyclase acti

251 Salmeterol significantly inhibited LPS-induced productio

252 Pretreatment with salmeterol significantly inhibited production of proinfl

253 Both TNF-alpha shRNA and salmeterol significantly reduced death of the retinal Mu

254 r treatment with fluticasone propionate (FP)/salmeterol (SM) (50/500, 4 wk).

255 ffects of fluticasone propionate (FP) and of salmeterol (SM), on the response of well-differentiated

256 ntermediate strengths, such as albuterol and salmeterol, stimulate GRK site phosphorylations that are

257 better exacerbation outcomes in response to salmeterol than Gly16Gly and Arg16Gly genotypes, suggest

258 and adults had a superior response to added salmeterol than to an increase in fluticasone (salmetero

259 es higher when participants were assigned to salmeterol than when assigned to placebo (p<0.0001).

260 r when participants were assigned to receive salmeterol than when assigned to receive placebo (p<0.00

261 r when participants were assigned to receive salmeterol than when assigned to receive placebo (p<0.00

262 re significantly greater with tiotropium and salmeterol than with placebo and were similar in both st

263 s with severe COPD receiving tiotropium plus salmeterol, the risk of moderate or severe exacerbations

264 We conclude that salmeterol therapy alone does not meaningfully reduce ai

265 Salmeterol therapy improved FEV(1), but had no significa

266 ces of airway inflammation were unchanged by salmeterol therapy.

267 1(Ser307), which was further decreased after salmeterol+TNF-alpha shRNA.

268 Noninferiority of fluticasone-salmeterol to fluticasone alone was defined as an upper

269 eeks with the combination of montelukast and salmeterol to that with the combination of beclomethason

270 rapy, which included the addition of a LABA (salmeterol) to an inhaled glucocorticoid (fluticasone pr

271 of alveolar fluid clearance at 4 hrs in the salmeterol-treated group.

272 ter increased to only 180 +/- 30 microL with salmeterol treatment, compared with 296 +/- 65 microL in

273 ne Modifier Corticosteroid or Corticosteroid-Salmeterol) trial of the American Lung Association Airwa

274 erformed less well for patients treated with salmeterol/triamcinolone during the entire study duratio

275 07], respectively, for patients treated with salmeterol/triamcinolone during the first half of the SL

276 acebo-controlled study with either 50 microg salmeterol twice daily (n=372), 500 microg fluticasone t

277 established that the sensitivity of genes to salmeterol varied by ~7.5-fold.

278 izations); the hazard ratio with fluticasone-salmeterol versus fluticasone alone was 1.28 (95% confid

279 ce the differential bronchodilator effect of salmeterol versus montelukast as an add-on therapy to IC

280 in determining the differential response to salmeterol versus montelukast in patients with chronic a

281 GER4 could explain differential responses to salmeterol versus montelukast using the participants of

282 Salmeterol was an effective bronchodilator with a consis

283 hort, compared with placebo, the addition of salmeterol was associated with a 51.4 L/min lower A.M. p

284 The anti-inflammatory effect of salmeterol was blocked by targeting the catalytic subuni

285 g16Gly polymorphism on treatment response to salmeterol was dependent on the use of inhaled corticost

286 The induction of IL-6 by salmeterol was dependent upon the beta(2) receptor and c

287 The combination of montelukast and salmeterol was inferior to the combination of beclometha

288 efit compared with B16Gly/Gly subjects after salmeterol was initiated.

289 The decline in PaO2 after salmeterol was of lesser magnitude but was more prolonge

290 Perioperative treatment with inhaled salmeterol was well tolerated but did not prevent ALI.

291 orticoid fluticasone and the beta(2)-agonist salmeterol, whereas MCP-1 inhibition was post-transcript

292 ects were randomized to regular therapy with salmeterol while continuing concomitant ICS.

293 ects were randomized to regular therapy with salmeterol while simultaneously discontinuing ICS therap

294 ompared the acute effects on gas exchange of salmeterol with those of albuterol and the anticholinerg

295 sed the prebronchodilator FEV1 more than did salmeterol, with a difference of 0.11 liters (P=0.003).

296 n be switched to once-daily fluticasone plus salmeterol without increased rates of treatment failure.

297 icasone propionate (FP) 100 mug, FP 500 mug, salmeterol xinafoate (SLM) 50 mug, and combination FP 10

298 e propionate at 1743, 1661, and 1700 cm(-1), salmeterol xinafoate at 1580 cm(-1), and lactose at 1030

299 her placebo (placebo-minus group, n = 21) or salmeterol xinafoate, 42 microg twice per day (n = 154)

300 one propionate and long-acting beta2-agonist salmeterol xinafoate, which are widely used to treat ast