ライフサイエンスコーパス: beta-agonist

1 such as beta2-adrenergic receptor agonists (beta-agonists).

2 rect prodrug of MB07344, a liver-targeted TR-beta agonist.

3 reating LXRalpha-/- mice with a pan-LXRalpha/beta agonist.

4 per day; 80% were also taking a long-acting beta-agonist.

5 and rapidly reconstituted responsiveness to beta-agonist.

6 owing can be reversed by the inhalation of a beta-agonist.

7 se inhaled corticosteroid plus a long-acting beta-agonist.

8 increasing responsiveness to bronchodilating beta-agonist.

9 of the receptor but reduces the efficacy of beta-agonists.

10 e of inhaled glucocorticoids and long-acting beta-agonists.

11 hallenge testing or test of reversibility to beta-agonists.

12 ls allowed the use of as-needed short-acting beta-agonists.

13 c receptor may not benefit from short-acting beta-agonists.

14 wer requirement for both corticosteroids and beta-agonists.

15 cts of small- and large-particle long-acting beta-agonists.

16 apacity ratios) and greater reversibility to beta-agonists.

17 myocardial infarction and the use of inhaled beta-agonists.

18 d by inhaled corticosteroids and long-acting beta-agonists.

19 led corticosteroids and frequent long-acting beta-agonists.

20 Benzopyran selective estrogen receptor beta agonist-1 (SERBA-1) shows potent, selective binding

21 ces (51.7%, 511/988) and use of short-acting beta-agonists (55.2%, 545/988) was high.

22 ipants with at least one high-use episode of beta agonist (84 [56%] vs 68 [45%], respectively, relati

23 of beta-adrenergic stimulation although the beta-agonist accelerated the kinetics of the twitch and

24 eroids (ICSs), with or without a long-acting beta-agonist, achieved the MID.

25 In asthma, the response to beta-agonists acting at beta2-adrenergic receptors (beta

26 E are mediated at least in part by their TGF-beta agonist activities.

27 nhibitory activity and confers a partial TGF-beta agonist activity (growth inhibition but not transcr

28 After DSS activation, Tg possessed TGF-beta agonist activity and inhibited DNA synthesis of min

29 Tg also exerted a small but significant TGF-beta agonist activity in transcriptional activation of p

30 with cardiovascular disease, to new users of beta-agonists (adjusted OR: 7.32 [95% CI, 2.34 to 22.8])

31 ormal betaAR responsiveness that occurs with beta-agonist administration.

32 Pretreatment of ASM cultures with beta-agonists albuterol, isoproterenol, or salmeterol (1

33 aseline airway responsiveness to the inhaled beta-agonist, albuterol, using changes in maximal expira

34 th muscle cells, the physiological target of beta-agonists, alendronate treatment functionally revers

35 We found that several beta blockers and a beta agonist all traverse the same well-defined, dominan

36 beta-agonists alone (n=346, 7%) were the most frequently

37 espiratory symptoms should be managed with a beta agonist and short-term treatment of oral steroids,

38 osteroids, >5 prescriptions for short acting beta agonists and more than four visits to a physician f

39 ( approximately 30-90%) increase in maximal beta-agonist and histamine [phosphoinositide (PI) hydrol

40 beta-agonist and PGE2 also inhibited phorbol myristate a

41 3 + CD28-stimulated IL-13 production by both beta-agonist and PGE2 was reversed at low agonist concen

42 cal analysis of urine samples confirmed both beta-agonist and SARM treatment.

43 oncomitant medications included short-acting beta-agonists and a systemic corticosteroid burst for as

44 phil infiltration of the airways, actions of beta-agonists and corticosteroids that alter eosinophil

45 We propose that beta-agonists and endothelin-1 regulate cardiac twitch d

46 ated with montelukast tended to receive less beta-agonists and have fewer treatment failures than pat

47 Once-daily longacting beta-agonists and inhaled corticosteroids are being deve

48 Long-acting beta-agonists and inhaled corticosteroids are used to tr

49 ontrolled despite treatment with long-acting beta-agonists and medium-to-high doses of inhaled glucoc

50 Among patients treated with long-acting beta-agonists and medium-to-high doses of inhaled glucoc

51 Early initiation of inhaled beta-agonists and oral or parenteral steroids remain the

52 h COPD or asthma who were concurrently using beta-agonists and patients with evidence of severe disea

53 r when patients are treated with long-acting beta-agonists and whether such effects are modified by c

54 for atypical infections, fluids, aerosolized beta agonists, and adequate pain control are necessary t

55 ium, 0.92 (CI, 0.88 to 0.96) for long-acting beta-agonists, and 1.05 (CI, 0.99 to 1.10) for theophyll

56 led therapies (anticholinergics, long-acting beta-agonists, and corticosteroids), pulmonary rehabilit

57 urrently accepted therapy, including oxygen, beta-agonists, and corticosteroids.

58 et for improving the therapeutic efficacy of beta-agonists, and demonstrate the utility of the unique

59 0.6 (37 degrees C), increased to 16 +/- 1 by beta-agonists, and inhibited to less than 2.0 by amilori

60 tory to inhaled corticosteroids, long-acting beta-agonists, and leukotriene receptor antagonists.

61 ed corticosteroids, ipratropium, long-acting beta-agonists, and theophylline in the 6 months precedin

62 Three classes of bronchodilators-beta agonists, anticholinergics, and theophylline-are av

63 esponsiveness of these phenotypes to inhaled beta-agonist, antimuscarinic, and corticosteroid therapy

64 azoles as highly selective estrogen receptor-beta agonists are reported.

65 Inhaled beta-agonists are effective airway smooth muscle (ASM)-r

66 Inhaled beta-agonists are effective at reversing bronchoconstric

67 a therapeutic target in asthma when chronic beta-agonists are required.

68 beta-Agonists are used for relief and control of asthma

69 R, 0.74 [95% CI, 0.35-1.57]) or short-acting beta-agonists (ARR, 0.95 [95% CI, 0.68-1.33]).

70 f treatment with the addition of long-acting beta agonists as the next step if symptoms continue.

71 d corticosteroids (ICSs) with a short-acting beta-agonist as a separate inhaler used when needed for

72 ospitalizations, and (3) use of short-acting beta-agonists as quick-relief (sometimes referred to as

73 rimary target of both short- and long-acting beta-agonist asthma medications.

74 in lung function included responsiveness to beta-agonist, baseline FEV(1), methacholine reactivity,

75 This study evaluated salmeterol, a beta-agonist bronchodilator with a duration of action su

76 modified fused receptor was not activated by beta-agonists but rather by a nonbiogenic amine agonist

77 cells may increase therapeutic responses to beta-agonist by increasing beta(2)AR expression or minim

78 Chronic use of inhaled beta-agonists by asthmatics is associated with a loss of

79 nization (HMO) was used to assess the use of beta-agonists by metered dose inhaler (MDI).

80 Thus, in vitro beta-agonists can independently increase inflammatory me

81 LQTS3 on ECG phenotypes before and following beta-agonist challenge, and upon fibrotic change.

82 xpressing polyglutamine-expanded AR with the beta-agonist clenbuterol increases their size.

83 nist was decreased by approximately 50% with beta-agonist co-treatment.

84 2.47% to 6.78%) increase in FEV1 response to beta-agonist compared with placebo, with no increase in

85 bstantially longer than that of short-acting beta-agonists, compared with ipratropium, an anticholine

86 This strategy will only work if the beta-agonist component has a rapid onset of action for s

87 Beta-agonists continue to be used frequently despite evi

88 In contrast, beta-agonists decreased expression of regulator of G pro

89 simpler, cheaper, and practical methods for beta-agonist delivery using indigenous spacers.

90 In beta-arrestin-deficient COS-7 cells, beta-agonist-dependent co-precipitation of c-Src with th

91 17-beta-Estradiol or estrogen receptor beta agonists dipropylnitrile and beta-LGND2 comparably

92 Infusion of the beta-agonist dobutamine resulted in accelerated rates of

93 ic function before and after infusion of the beta-agonist dobutamine.

94 this approach is to titrate both the ICS and beta-agonist dose according to need and enhance ICS use

95 The ER-beta agonist DPN did not mimic the effect of estradiol o

96 stradiol, and the specific estrogen receptor-beta agonist DPN, decreased current amplitude measured i

97 less likely to require rescue therapy with a beta-agonist during or after exercise challenge.

98 t change in PEF, symptoms, and use of rescue beta-agonists during the 425 severe exacerbations that o

99 n whole-cell cAMP accumulation stimulated by beta-agonist (EC(50) and B(max)) concentrations, but sig

100 considered a candidate locus for predicting beta-agonist efficacy in the absence and presence of cor

101 Activation with beta-agonist enables stimulation of only a single Frizzl

102 elucidate the molecular mechanisms by which beta-agonists exert anti-inflammatory effects in allerge

103 siologically relevant effector through which beta-agonists exert their relaxant effects.

104 beta-Agonists exhibit PKA-dependent antimitogenic effect

105 With prolonged beta-agonist exposure, TAS2R14 internalized, consistent

106 ide generation, which is observed with acute beta-agonist exposure.

107 the efficacy of inhaled corticosteroids and beta agonists for prevention of acute respiratory distre

108 reatment with corticosteroids and longacting beta-agonists for symptomatic asthma.

109 aled anticholinergics or long-acting inhaled beta-agonists for symptomatic patients with COPD and FEV

110 d the safety and efficacy of the long-acting beta-agonist formoterol compared with terbutaline, each

111 We identified 61,712 members who received a beta-agonist from January 1, 1993 to August 31, 1995, in

112 Functional gains in response to beta-agonist from the selective loss of these mechanisms

113 Compared with recipients of other beta-agonists, future salmeterol recipients had higher r

114 Long-acting beta-agonists have been shown to increase severe and lif

115 with inhaled corticosteroid and long-acting beta-agonist (ICS/LABA).

116 by assessing the bronchodilator response to beta agonist in asthmatics.

117 We studied pan-LXRalpha/beta agonists in LXRalpha knockout mice to assess the co

118 PGE2 was more efficacious than beta-agonist in activating PKA and inhibiting cytokine p

119 ine airway tone and the airway response to a beta-agonist in this subject population.

120 e of inhaled corticosteroids and long-acting beta-agonists in asthma, the lack of efficacy of oral co

121 Beta-adrenoceptor agonists (beta-agonists), in widespread clinical use for obstructi

122 whether the high doses of corticosteroid and beta agonist increase the risk of adverse effects with b

123 the highly selective estrogen receptor (ER) beta agonist indazole chloride (Ind-Cl) on functional re

124 ose-dependent manner, whereas isoproterenol (beta agonist) induced a dose-dependent decline in prolac

125 improved contraction and protection against beta-agonist-induced apoptosis.

126 t Ser16 may provide cardioprotection against beta-agonist-induced apoptosis.

127 ken together, our findings indicate that (1) beta-agonist-induced cardiac injury is associated with a

128 fold) of Hsp20 may protect the heart against beta-agonist-induced cardiac remodeling, associated with

129 responses that were associated with impaired beta-agonist-induced denitrosylation of cardiac ryanodin

130 rors the central role of protein kinase A in beta-agonist-induced desensitization.

131 terenol, which resulted in the inhibition of beta-agonist-induced parotid gland hypertrophy and hyper

132 ot PDE4A or PDE4B, had a major effect on the beta-agonist-induced PDE activation, with only a minimal

133 , obstruction, hyperreactivity, and impaired beta-agonist-induced relaxation.

134 SYK inhibition in vivo represses beta-agonist-induced thermogenesis and oxygen consumptio

135 eezing disorders in baseline as well as post-beta agonist inhalation, and it is significantly reduced

136 Despite pharmacologic therapy with inhaled beta-agonists, inhaled anticholinergics, systemic cortic

137 short-acting beta-agonist or ICS/long-acting beta-agonist inhaler as a reliever rather than regular m

138 ials investigating different combination ICS/beta-agonist inhaler products prescribed according to th

139 Concomitant rescue beta-agonist inhaler use and the need for corticosteroid

140 rent patients who overrely on their reliever beta-agonist inhaler.

141 s hospitalization and ED visits, six or more beta-agonist inhalers (units) during the prior 6 mo, and

142 er conditions of GRK2 C-terminal expression, beta-agonist inhibition of methacholine-stimulated PI hy

143 an estrogen receptor (ER)-alpha (but not ER-beta) agonist into the dorsal hippocampus rapidly improv

144 dividual or combined infusion of alpha1- and beta-agonists into these regions.

145 recently reported that prolonged exposure to beta-agonists is associated with transient increases in

146 Activation of beta2AR by beta-agonists is attenuated by receptor down-regulation,

147 beta2AR desensitization to beta-agonists is primarily mediated by G protein-coupled

148 olite and a selective estrogen receptor (ER) beta agonist, is approximately 400x more potent than 17-

149 during systemic infusion of the nonselective beta-agonist isoprenaline (ISO) and compared this with c

150 This inhibition was mimicked by the beta agonist isoproterenol and blocked by the beta antag

151 bnormal automaticity) in the presence of the beta-agonist isoproterenol (0.1 mum; ISO), from 0% to 64

152 ated cells were increased in response to the beta-agonist isoproterenol (contraction: 57.5+/-6.6% ver

153 pon challenge with high glucose (HG) and the beta-agonist isoproterenol (ISO).

154 reductions in cell stiffness induced by the beta-agonist isoproterenol (ISO).

155 In wild-type myocytes, the beta-agonist isoproterenol decreased twitch duration and

156 s to graded brachial artery infusions of the beta-agonist isoproterenol in 41 healthy normotensive Ca

157 Stimulation of wild-type EPCs with beta-agonist isoproterenol induced a significant increas

158 y and showed increased responsiveness to the beta-agonist isoproterenol.

159 ith wild-type controls when treated with the beta-agonist isoproterenol.

160 bone loss and osteoclast hyperfunction while beta-agonist (isoproterenol) exacerbated those responses

161 Varying doses of NE, the beta-agonist, isoproterenol, or the alpha1-agonist, phen

162 ither TR alpha 1-/- mice or the selective TR beta agonist KB-141 in mice, rats, and monkeys.

163 hreatening events associated with longacting beta agonist (LABA) use have caused the US Food and Drug

164 rs1042713 (Arg16 amino acid) and long-acting beta-agonist (LABA) exposure for asthma exacerbations in

165 st guidelines recommend either a long-acting beta-agonist (LABA) plus an inhaled glucocorticoid or a

166 Long-acting beta-agonist (LABA) therapy improves symptoms in patient

167 se [<600 vs >/=600 mug/day], and long-acting beta-agonist [LABA] use [yes/no]).

168 derate COPD included 2 trials of long-acting beta-agonists (LABAs) (n = 3174), 1 RCT of LABAs and inh

169 The safe and appropriate use of long-acting beta-agonists (LABAs) for the treatment of asthma has be

170 ety concerns surround the use of long-acting beta-agonists (LABAs) for the treatment of asthma, even

171 The efficacy and safety of long-acting beta-agonists (LABAs) have been questioned.

172 Long-acting beta-agonists (LABAs) have been shown to increase the ri

173 able benefits to the addition of long-acting beta-agonists (LABAs) to ICSs.

174 with inhaled glucocorticoids and long-acting beta-agonists (LABAs).

175 ticosteroid therapy with/without long-acting beta-agonists (LABAs).

176 e effect on treatment response to longacting beta-agonists (LABAs).

177 ose inhaled glucocorticoids plus long-acting beta-agonists (LABAs).

178 nic administration of sympathomimetic drugs (beta-agonists) leads to anabolic adaptations in skeletal

179 less than 60% predicted: long-acting inhaled beta-agonists, long-acting inhaled anticholinergics, or

180 y treatment with inhaled corticosteroids and beta agonists may reduce progression to acute respirator

181 Long-acting beta-agonists may increase the risk for fatal and nonfat

182 st prescription, subjects who had filled one beta-agonist MDI prescription in the 3 mo prior to their

183 that beta-arrestin-2 gene ablation augments beta-agonist-mediated airway smooth muscle relaxation, w

184 PKI and RevAB peptides results in increased beta-agonist-mediated cAMP release, abolishes the inhibi

185 -ARs and the hamster beta(2)-AR mRNA undergo beta-agonist-mediated destabilization.

186 enhanced cAMP production and led to greater beta-agonist-mediated inhibition of basal and TGFbeta-st

187 PKA inhibition eliminates most, if not all, beta-agonist-mediated relaxation of contracted smooth mu

188 ild-type mice resulted in a profound loss of beta-agonist-mediated relaxation of methacholine-contrac

189 ine ASM enabled approximately 30-50% greater beta-agonist-mediated relaxation of methacholine-induced

190 iveness by mitigating both agonist-specific (beta-agonist-mediated) desensitization and cytokine (IL-

191 ids alone or in combination with long-acting beta-agonists might result in improved long-term asthma

192 Isoproterenol (a beta-agonist) mimicked NE's effect on ET-1-induced [Ca2+

193 ipants with at least one high-use episode of beta agonist (more than eight actuations per day of bude

194 In agreement with these findings, the beta-agonists noradrenaline and isoproterenol stimulate

195 did not augment the inhibitory effect of the beta-agonist on mitogen-stimulated increases in ASM grow

196 he role of PKA in the prorelaxant effects of beta-agonists on ASM.

197 tein-coupled receptor (GPCR), the effects of beta-agonists on T-cell subtype function remain poorly u

198 Effects of small-particle long-acting beta-agonists on the small airways have been poorly docu

199 decline) or "steroids" (2.7%) as opposed to beta agonists or xanthines (0.8%) or cromolyn without st

200 "prn") use of a combination ICS/short-acting beta-agonist or ICS/long-acting beta-agonist inhaler as

201 Here, we show that beta-agonists or catecholamines released during intense

202 not found among patients concurrently using beta-agonists or with severe COPD or asthma.

203 eceptor are shown to be enhanced by insulin, beta-agonist, or both.

204 Finally, cold, beta-agonists, or forced expression of PGC-1alpha are un

205 nhaled anticholinergics, long-acting inhaled beta-agonists, or inhaled corticosteroids) for symptomat

206 Beta-agonist overuse is associated with adverse outcomes

207 These results establish a mechanism of the beta-agonist paradox and identify a potential asthma mod

208 ll surface expression, but when activated by beta-agonist, partially offsetting the expression phenot

209 ients with COPD or asthma who were not using beta-agonists, patients with COPD or asthma who were con

210 ER alpha and ER beta agonists PPT and DPN inhibited and 4-OHT increased

211 In comparison to subjects who did not fill a beta-agonist prescription, subjects who had filled one b

212 Indeed, with beta-agonist pretreatment, the TG mice displayed no resp

213 Beta-agonist-promoted desensitization of airway smooth m

214 The estrogen receptor-beta agonist provided a comparable level of protection i

215 drolone phenylpropionate (Nandrosol) and the beta-agonist ractopamine administration in veal calves,

216 regimen would reduce the risk of overuse of beta agonist, reduce the likelihood of patients to seek

217 I/ARDS, sustained treatment with intravenous beta-agonists reduces extravascular lung water.

218 (p=0.069) and fewer adverse events requiring beta-agonist rescue (p=0.031) after subcutaneous adminis

219 This mechanism may contribute to beta-agonist resistance found in asthma.

220 hyperreactivity, but a mechanism that evokes beta-agonist resistance.

221 lar volume (reverse remodeling) and restored beta-agonist response in cardiac muscle from patients wi

222 The attenuated beta-agonist response was associated with decreased (50%

223 d an 8.74% (CI, 1.96% to 15.52%) increase in beta-agonist response.

224 may be important in delineating variation in beta-agonist responses, especially in African Americans.

225 beta(2)AR function and maximally upregulates beta-agonist-responsive active Na(+) transport by improv

226 ar volume using isolated perfused hearts and beta-agonist responsiveness using muscle strips from pat

227 Cells stimulated with different beta-agonists revealed time courses of beta2AR-GFP redis

228 lts demonstrate the efficacy of short-acting beta-agonist (SABA) delivered by metered-dose inhaler as

229 uidelines recommend that long-acting inhaled beta-agonists should be used as maintenance therapy for

230 modalities such as magnesium and intravenous beta-agonists show some benefit.

231 isplayed a phenotypic switch, with decreased beta-agonist signaling to adenylyl cyclase and decreased

232 are chronically treated with bronchodilating beta-agonists sometimes experience a worsening of their

233 a-aminobutyric acid inhibited both basal and beta agonist-stimulated alveolar fluid clearance.

234 y smooth muscle relaxation, while augmenting beta-agonist-stimulated cyclic adenosine monophosphate p

235 ediated knockdown of arrestins also augments beta-agonist-stimulated cyclic adenosine monophosphate p

236 GRK2ct, or siRNA-mediated knockdown restored beta-agonist-stimulated inhibition of collagen synthesis

237 PKC alpha in transgenic mice led to impaired beta-agonist-stimulated ventricular function, blunted cy

238 vated in failing CF and was not inhibited by beta-agonist stimulation in contrast to normal controls.

239 Here we investigated the effect of beta-agonist stimulation in SBMA myotube cells derived f

240 tor of the contractile response to increased beta-agonist stimulation in vivo.

241 These results indicate that beta-agonist stimulation is a novel therapeutic strategy

242 intracellular cAMP accumulation mediated via beta-agonist stimulation of the beta-2-adrenergic recept

243 mals, the ability of the heart to respond to beta-agonist stimulation, as measured in the intact anim

244 le in regulating the contractile response to beta-agonist stimulation.

245 l inhibition of collagen synthesis following beta-agonist stimulation.

246 ischemia/reperfusion injury or by prolonged beta-agonist stimulation.

247 confirmed phosphorylation of Ser16 in p20 on beta-agonist stimulation.

248 )-calmodulin-dependent protein kinase during beta-agonist stimulation.

249 r(17) phosphorylation and attenuation of the beta-agonist stimulatory effects in perfused mouse heart

250 rine formation results in attenuation of the beta-agonist stimulatory responses in the mammalian hear

251 R sensorfor rapid screening and detection of beta-agonists such as RAC.

252 ine in lung function and increases in use of beta-agonists, systemic corticosteroids, and health care

253 heart and lung and is the primary target of beta-agonists, the mainstay asthma drugs.

254 corticosteroids with or without long-acting beta agonists, theophyllines, or leukotriene-receptor an

255 patients with COPD or asthma who were not on beta-agonist therapy (relative risk [RR] = 0.85, 95% con

256 cts of such polymorphisms on the response to beta-agonist therapy have produced inconsistent results.

257 ment to reduce inflammation is combined with beta-agonist therapy in current asthma guidelines.

258 atopic asthma (receiving inhaled placebo and beta-agonist therapy only).

259 s the gene coding for the receptor target of beta-agonist therapy, the beta2-adrenergic receptor (ADR

260 thma pathogenesis and diminished efficacy of beta-agonist therapy.

261 costeroids in combination with a long-acting beta-agonist, there remains a significant subset of pati

262 nd less than 2 puffs per day of short-acting beta-agonist; they also experienced a lower rate of resp

263 Those requiring an inhaled beta-agonist three to eight times a day during the study

264 NF-kappaB explained the capacity of PGE2 and beta-agonist to inhibit IFN-gamma but not IL-13 producti

265 isturbances are likely mediated by decreased beta-agonist transduction, increased circulating inflamm

266 s a surrogate biomarker of responsiveness to beta-agonist treatment and childhood asthma severity.

267 the immune system associated with stress or beta-agonist treatment and pave the way for the developm

268 smooth muscle and bronchodilate, but chronic beta-agonist treatment in asthma causes increased sensit

269 declined rapidly following the initiation of beta-agonist treatment in vivo, while laminin B1 and B2

270 djunct therapy or biased ligands may improve beta-agonist treatment of obstructive lung disease.

271 nfluence airway responses to regular inhaled beta-agonist treatment.

272 of airway smooth muscle (ASM) observed with beta-agonist treatment.

273 Additionally, periodic ER-beta agonist treatments every 48 hr improved post-ischem

274 fluticasone plus 50 microg of a long-acting beta-agonist twice daily (LABA step-up), or 100 microg o

275 < 0.0001], nocturnal symptoms [P < 0.0001], beta-agonist use [P < 0.0001]).

276 Greater shortness of breath and beta-agonist use appears to be partially mediated via es

277 iratory flow diurnal variability, and rescue beta-agonist use diurnal variability.

278 Rescue beta-agonist use independently predicted HRQL in subject

279 2 to 3 d; an increase in symptoms and rescue beta-agonist use occurred in parallel, and both the seve

280 te disease with controller treatment, rescue beta-agonist use predicted HRQL.

281 FEV(1), symptom scores, rescue short-acting beta-agonist use, and exacerbations.

282 reduced asthma symptoms, decreased as-needed beta-agonist use, and improved pulmonary function withou

283 rates in the morning and evening, as-needed beta-agonist use, nocturnal awakenings, asthma-specific

284 of Life Questionnaire-Symptom domain, rescue beta-agonist use, nocturnal awakenings, peak expiratory

285 re was no dose-response relationship between beta-agonists use and risk of myocardial infarction.

286 ic stimulation of the beta2AR by long acting beta-agonists used in the treatment of asthma can promot

287 beta-Agonists used to combat hypercontractility in airwa

288 one or greater with or without a long-acting beta-agonist versus 100 mug or less assigned on at least

289 id, fluticasone furoate, and the long-acting beta agonist, vilanterol could improve survival compared

290 rtmentalized cAMP accumulation stimulated by beta-agonist was assessed by radioimmunoassay and membra

291 unction was depressed, but responsiveness to beta-agonist was not impaired.

292 ility/relaxation) as a result of infusion of beta-agonist was significantly decreased in all of the m

293 In this study, new use of beta-agonists was associated with an increased risk of m

294 , a nonsteroidal selective estrogen receptor-beta agonist, was tested in the murine listeriosis model

295 inhaled albuterol were assessed after a 2-wk beta-agonist washout period, before administering study

296 Long-acting beta-agonists were not allowed during the treatment peri

297 -dose inhaled corticosteroids and longacting beta agonists, with two to six exacerbations in the past

298 d an enhanced responsiveness (relaxation) to beta-agonist, with a 60-fold decrease in the ED(50), ind

299 d lymphocytes (PBLs) can respond directly to beta-agonist, with effects including induction of protei

300 ispensing of three or more prescriptions for beta-agonists within the year before enrollment in the s