ライフサイエンスコーパス: salmeterol

1 eta-adrenoceptor agonists, isoproterenol and salmeterol.

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

3 steric binding site for larger drugs such as salmeterol.

4 be equivalent to those with the addition of salmeterol.

5 cells, which was enhanced by fluticasone and salmeterol.

6 thma treatment failure in patients receiving salmeterol.

7 se was partially inhibited by salbutamol and salmeterol.

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

9 gonist before and after chronic therapy with salmeterol.

10 ontributes to the long duration of action of salmeterol.

11 cations during the year before they received salmeterol.

12 ust 31, 1995, including 2, 708 recipients of salmeterol.

13 chronic dosing with formoterol compared with salmeterol.

14 fected the efficacy or duration of action of salmeterol.

15 on outcomes in response to tiotropium versus salmeterol.

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

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

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

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

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

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

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

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

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

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

26 0 microg twice per day; n = 54) or switch to salmeterol (42 microg twice per day; n = 54) or to place

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 We examined the effect of salmeterol, a long-acting beta2-adrenergic receptor agon

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

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

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

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

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

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

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

49 15d-PGJ(2), fluticasone, and salmeterol all inhibited TNFalpha-induced histone H4 ace

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

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

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

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

54 Salmeterol also attenuated activation of NF-kappaB via i

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

56 Salmeterol also directly activated immunoprecipitated PP

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

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

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

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

61 Combined activity of salmeterol and fluticasone at equimolar concentrations h

62 Fluticasone/salmeterol and fluticasone monotherapy decreased periphe

63 Fluticasone/salmeterol and fluticasone monotherapy equally reverse p

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

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

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

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

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

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

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

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

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

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

74 gland insurer to assess the relation between salmeterol and severe nonfatal asthma.

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

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

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

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

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

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

81 /- 0.89 mm Hg (mean +/- SEM) at 30 min after salmeterol, and -3.45 +/- 0.92 mm Hg at 20 min after alb

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

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

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

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

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

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

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

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

90 The morning dose of salmeterol attenuated the degree of bronchoconstriction

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

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

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

94 Salmeterol, but not dexamethasone, increased PP2A activi

95 maintained with long-term administration of salmeterol, but the length of time that the drug remains

96 Salmeterol can significantly inhibit activation of macro

97 Salmeterol caused an augmentation of rhinovirus-induced

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

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

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

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

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

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

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

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

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

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

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

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

110 +/- 4.1% bronchoprotection) after the first salmeterol dose, and 22.8 +/- 3.2% (18.9 +/- 11.5% bronc

111 Salmeterol downregulated PgLPS-mediated phosphorylation

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

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

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

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

116 Results showed salmeterol exerted potent neuroprotection against both L

117 Salmeterol exerts anti-inflammatory effects by increasin

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

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

120 Rather, salmeterol failed to induce microglial cAMP production,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 50 cells/mul subgroups, and at no cutoff was salmeterol/fluticasone superior to indacaterol/glycopyrr

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

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

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

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

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

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

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

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

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

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

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

148 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

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

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

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

152 2% in the montelukast group and 33.0% in the salmeterol group (P = 0.002).

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

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

155 208 patients, 27 patients in the fluticasone-salmeterol group and 21 in the fluticasone-alone group h

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

157 36 events in 34 patients in the fluticasone-salmeterol group and 38 events in 33 patients in the flu

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

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

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

161 ors, incidence rates of severe asthma in the salmeterol group were not elevated for emergency care (r

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

163 480 of 5834 patients (8%) in the fluticasone-salmeterol group, as compared with 597 of 5845 patients

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

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

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

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

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

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

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

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

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

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

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

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

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

177 In addition, salmeterol in combination with FP enhanced glucocorticoi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Combination therapy with theophylline or salmeterol may allow clinicians to minimize the dose of

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

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

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

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

198 95% confidence interval [CI], 2%-15%) of the salmeterol-minus group 8 weeks after triamcinolone treat

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Each patient received inhaled salmeterol or placebo twice daily for a month, with a on

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

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

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

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

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

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

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

226 /- 11.5% bronchoprotection) after 2 weeks of salmeterol (P = 0.0001).

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 Similarly, salmeterol pretreatment (0.05 to 5 mg/ml for 10 min) red

233 We conclude that salmeterol pretreatment can reduce the plasma leakage an

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

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

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

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

238 Salmeterol provided similar maximal bronchodilatation to

239 ents and, after adjusting for baseline risk, salmeterol recipients did not have a greater risk than t

240 th recipients of other beta-agonists, future salmeterol recipients had higher rates of asthma hospita

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

242 Salmeterol reduced some biomarkers of alveolar inflammat

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

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

245 synergistically enhanced by fluticasone and salmeterol, respectively.

246 We compared salmeterol response in patients with asthma homozygous f

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

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

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

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

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

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

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

254 Salmeterol significantly inhibited LPS-induced productio

255 Pretreatment with salmeterol significantly inhibited production of proinfl

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

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

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

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

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

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

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

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

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

265 With long-term administration of salmeterol, the extent of protection afforded by the dru

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

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

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

269 ces of airway inflammation were unchanged by salmeterol therapy.

270 1(Ser307), which was further decreased after salmeterol+TNF-alpha shRNA.

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

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

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

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

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

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

277 07], respectively, for patients treated with salmeterol/triamcinolone during the first half of the SL

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

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

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

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

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

283 Salmeterol was an effective bronchodilator with a consis

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

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

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

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

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

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

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

291 We conclude that salmeterol was prescribed preferentially to high-risk pa

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

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

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

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

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

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

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

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

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