ライフサイエンスコーパス: beta2 agonist

1 with inhaled corticosteroids and long-acting beta2 agonists.

2 ose inhaled corticosteroids plus long-acting beta2 agonists.

3 shown to affect responses to regular use of beta2-agonists.

4 There are some differences between beta2-agonists.

5 eive inhaled corticosteroids plus longacting beta2-agonists.

6 sm for the mast cell "stabilizing" effect of beta2-agonists.

7 n (i.e., HR*G yields HR* + G*) for different beta2-agonists.

8 t lead to increased binding affinity for the beta2-agonists.

9 s, beta-blockers, prostaglandin analogs, and beta2-agonists.

10 r HD inhaled corticosteroids and long-acting beta2-agonists.

11 pairment was induced experimentally by using beta2-agonists.

12 ute bronchodilator response (BDR) to inhaled beta2-agonists.

13 ng (salbutamol) and long-acting (formoterol) beta2 -agonists.

14 o severely curtail the beneficial actions of beta2 -agonists.

15 FENO behaviors were observed in response to beta2-agonists: a decrease likely caused by relief of an

16 seen in heart failure may be related to the beta2-agonist actions of these compounds.

17 timization of both muscarinic antagonist and beta2 agonist activities, through modification of the li

18 FEV1 in response to treatment and subsequent beta2-agonist administration, the provocative concentrat

19 selective beta-blocker and administration of beta2-agonist after the study drug.

20 cultured in the presence of the short-acting beta2-agonist albuterol, and the long-acting beta2-agoni

21 Traditional inhaled short-acting beta2-agonists albuterol, fenoterol, and terbutaline pro

22 to 0.94]) but not compared with long-acting beta2-agonists alone (relative risk, 0.82 [CI, 0.52 to 1

23 The use of inhaled long-acting beta2-agonists alone is not appropriate.

24 asthma treatment (including so-called rescue beta2-agonists alone) at a stable dose for more than 8 w

25 ated at least twice a week with short-acting beta2-agonist, alone or in combination with inhaled ster

26 Because inhaled long-acting beta2 agonists and corticosteroid combination treatment

27 benefit less from treatment with longacting beta2 agonists and inhaled corticosteroids than do those

28 ed nitric oxide is rarely indicated and both beta2 agonists and late corticosteroids should be avoide

29 4% received prescriptions for a short-acting beta2-agonist and 41.2% for inhaled corticosteroids; 76.

30 beta2-Agonists and corticosteroids inhibited neutrophil

31 ce tolerance to bronchoprotective effects of beta2-agonists and has the potential to reduce bronchodi

32 corticosteroids with or without long-acting beta2-agonists and in patients with COPD with severe dis

33 d exposure to the combination of long-acting beta2-agonists and inhaled corticosteroids (OR, 3.95; 95

34 splasia associated with combined long-acting beta2-agonists and inhaled corticosteroids.

35 muscle protector, acts synergistically with beta2-agonists and potentiates their positive effects on

36 with an inhaled corticosteroid, long-acting beta2-agonist, and long-acting muscarinic antagonist, se

37 ed on inhaled corticosteroids and longacting beta2 agonists are effective in controlling asthma in mo

38 All beta2-agonists are canonical orthosteric ligands that bi

39 beta2-Agonists are effective bronchodilators due primari

40 Traditional beta2-agonists are seen as first-line therapies for mode

41 beta2-Agonists are the most common form of treatment of

42 beta2-Agonists are the treatment of choice for exercise-

43 tropium bromide (IB), when administered with beta2-agonists, are effective in reducing hospital admis

44 SMART) or inhaled corticosteroid-long-acting beta2-agonist as maintenance plus short-acting beta2-ago

45 ta2-agonist as maintenance plus short-acting beta2-agonist as reliever.

46 i-inflammatory molecule MKP-1 in response to beta2 -agonists, as well as impaired bronchodilation in

47 side effects, so its use declined as inhaled beta2-agonists became more widely used.

48 he bronchodilator response to a short-acting beta2-agonist before and after chronic therapy with salm

49 Use of long-acting beta2-agonists before achieving a reduction in FeNO may

50 beta2ARs, Cmpd-6 allosterically potentiated beta2-agonist binding to guinea pig beta2ARs and downstr

51 relative roles of the conserved alpha4(+)/(-)beta2 agonist-binding sites in and between the isoforms

52 Both isoforms contain a pair of alpha4(+)/(-)beta2 agonist-binding sites.

53 ed that the long-term regular use of inhaled beta2-agonist bronchodilators might lead to a deteriorat

54 Treatment with long-acting beta2 agonists can reduce but not eliminate the plasma o

55 Long-acting beta2-agonists can also increase steroid responsiveness

56 Here we describe for the first time that beta2-agonists can inhibit cytokine-induced eotaxin rele

57 e sleep-wake effects of microinfusion of the beta2 agonist, clenbuterol, into the MS and MPOA were ex

58 fixed inhaled corticosteroid and longacting beta2 agonist combination.

59 D from an inhaled corticosteroid/long-acting beta2-agonist combination treatment to triple therapy us

60 ess to an inhaled corticosteroid/long-acting beta2-agonist combination versus a long-acting beta2-ago

61 Inhaled corticosteroids and long-acting beta2-agonist combinations are more effective than inhal

62 f exposure to first-trimester use of inhaled beta2-agonists compared with nonchromosomal control regi

63 s, suggesting that the beneficial effects of beta2-agonists could be blunted in patients with type 2

64 We evaluated beta2-agonist drugs, which increased CI-MPR expression i

65 iated any inhaled corticosteroid-long-acting beta2-agonist during that period.

66 he unmeasured inotropic, oxygen-wasting, and beta2-agonist effects of the drug.

67 atening bronchospasm and reduced efficacy of beta2-agonist emergency rescue therapy.

68 Because beta2-agonists enhance the function of slow- and fast-tw

69 -relief treatment for asthma, and use of any beta2-agonist except the study treatment was prohibited.

70 ids (ICS) or low-dosage ICS plus long-acting beta2 agonist fixed-combination therapy at screening, ha

71 14) days inhaled corticosteroid/long-acting beta2-agonist fluticasone furoate/vilanterol 100/25 mug

72 atients continued to use their usual inhaled beta2-agonist for symptomatic relief.

73 odds of first-trimester exposure to inhaled beta2-agonists for cleft palate and gastroschisis and fo

74 g environmental factors, use of short-acting beta2-agonists for rapid relief of symptoms, and daily u

75 beta2-agonist albuterol, and the long-acting beta2-agonists formoterol and olodaterol.

76 The twice-daily beta2-agonists formoterol and salmeterol represent impor

77 CRE-gene transcription responses to beta2-agonists, forskolin, and cAMP-analogs were sensiti

78 ef of the symptoms of asthma, yet the use of beta2 agonists has been known to induce bronchial hyperr

79 In general, beta2-agonists have an acceptable safety profile, althou

80 formoterol, a member of a new generation of beta2-agonists, histologically and functionally rescued

81 mbination inhaled corticosteroid long-acting beta2-agonist (ICS-LABA) medications (change, 0.06 [95%

82 ed corticosteroids combined with long-acting beta2-agonist (ICS/LABA) are standard treatments for ast

83 sage inhaled corticosteroids and long-acting beta2-agonists (ICS plus LABA) in the previous year.

84 er bronchodilation in vitro and in vivo than beta2 agonists, implying that new and better bronchodila

85 Inhaled long-acting beta2 agonists improve lung function and health status i

86 ific response to treatment with a longacting beta2 agonist in combination with inhaled corticosteroid

87 polymorphisms affect response to longacting beta2-agonists in combination with inhaled corticosteroi

88 rs on FEV1, symptoms, and the use of inhaled beta2-agonists in patients with reactive airway disease

89 ), a fixed-dose combination of a long-acting beta2-agonist (indacaterol) and a long-acting muscarinic

90 More recently, a newer beta2-agonist (indacaterol) with a longer pharmacodynami

91 nium 110/50 mug with twice-daily long-acting beta2-agonist/inhaled corticosteroid salmeterol/fluticas

92 beta2-Agonists inhibit cytokine production in splenocyte

93 residues involved in polar interactions with beta2-agonists into the neurokinin-1 receptor did not le

94 e inhaled corticosteroids plus a long-acting beta2 agonist, irrespective of baseline eosinophil count

95 of inhaled corticosteroid (ICS)/long-acting beta2 agonist is being used as a long-term control medic

96 ns of inhaled corticosteroids and longacting beta2 agonists is unknown.

97 Although desensitization to repeated use of beta2-agonists is well studied, type 2 inflammation coul

98 ding inhaled corticosteroids and long-acting beta2-agonists, is effective in patients for whom inhale

99 ual inhaled corticosteroid (ICS)/long-acting beta2-agonist (LABA) therapy in patients with chronic ob

100 Long-acting beta2-agonists (LABA) and leukotriene receptor antagonis

101 Long-acting beta2-agonists (LABA) in combination with inhaled cortic

102 Long-acting beta2-agonists (LABA) were shown to inhibit LPS-induced

103 Ss) or ICSs + add-on medication (long-acting beta2-agonist [LABA], leukotriene receptor antagonist [L

104 Combination inhaled therapy with long-acting beta2 agonists (LABAs) and corticosteroids is beneficial

105 Safety concerns associated with long-acting beta2-agonists (LABAs) have led to many US Food and Drug

106 Dual bronchodilators (long-acting beta2-agonists /long-acting muscarinic antagonist, LABA/

107 ted with inhaled corticosteroid, long-acting beta2 agonist, long-acting muscarinic antagonist, and le

108 ta2-agonist combination versus a long-acting beta2-agonist/long-acting muscarinic antagonist combinat

109 study, which compared once-daily long-acting beta2-agonist/long-acting muscarinic antagonist indacate

110 to step 4 inhaled corticosteroid-long-acting beta2-agonist maintenance plus short-acting beta2-agonis

111 otriene receptor antagonists and long-acting beta2-agonists may allow for reduction of inhaled steroi

112 The regular administration of beta2-agonists may be associated with the development of

113 still controversy as to whether long-acting beta2-agonists may increase the risk of asthma mortality

114 Moreover, Cmpd-6 robustly potentiated beta2 agonist-mediated bronchoprotection against allerge

115 Cmpd-6 similarly enhanced beta2 agonist-mediated bronchoprotection against methach

116 Importantly, Cmpd-6 enhanced beta2 agonist-mediated bronchoprotection against methach

117 We sought to investigate whether beta2-agonists might induce divergent effects on FENO va

118 lation over either inhaled antimuscarinic or beta2-agonist monotherapy.

119 steroids (n = 14), dual D2 dopamine receptor-beta2-agonist (n = 3), or short-acting beta2-agonist plu

120 cting anticholinergics (n = 10), long-acting beta2-agonists (n = 22), corticosteroids (n = 14), dual

121 Some novel once-daily beta2-agonists (olodaterol, vilanterol, abediterol) are

122 s of inhaled corticosteroids plus longacting beta2-agonists on asthma exacerbations.

123 ve beta1-agonist) and terbutaline (selective beta2-agonist) on glycerol release (lipolytic index) in

124 ) reversed neutrophil dysfunction induced by beta2-agonists or corticosteroids but did not increase R

125 dose inhaled corticosteroids and long-acting beta2-agonists or medium- to high-dose inhaled corticost

126 (ICSs), leukotriene modifiers, short-acting beta2-agonists, oral corticosteroids, other bronchodilat

127 offspring ASD, and (b) prenatal exposures to beta2-agonists, other asthma medications and offspring A

128 se results suggest that the combination of a beta2-agonist, PDE inhibitor, and a corticosteroid may h

129 hould continue to be treated with longacting beta2 agonists plus moderate-dose inhaled corticosteroid

130 s of tiotropium monotherapy or a long-acting beta2-agonist plus inhaled corticosteroid (LABA-ICS) who

131 eptor-beta2-agonist (n = 3), or short-acting beta2-agonist plus ipratropium (n = 3).

132 intenance inhaled corticosteroid-long-acting beta2-agonist plus short-acting beta2-agonist reliever t

133 intenance inhaled corticosteroid-long-acting beta2-agonist plus short-acting beta2-agonist reliever.

134 intenance inhaled corticosteroid-long-acting beta2-agonist plus short-acting beta2-agonist reliever.

135 bserved when stratifying by time since first beta2-agonist prescription and by duration of follow-up.

136 P = 0.9; L-glutamate, P = 0.4), nor did the beta2 agonist procaterol (SSS, P = 0.6; L-glutamate, P =

137 on of beta2-adrenoceptors with the selective beta2 agonist procaterol caused a biphasic decrease in c

138 eta2-adrenergic receptor (beta2AR) agonists (beta2-agonists) promote - with limited efficacy - bronch

139 Inhaled short-acting beta2-agonists provide rapid relief of acute symptoms, b

140 (COPD) and, in combination with long-acting beta2 agonists, reduce exacerbations and improve lung fu

141 Inhaled corticosteroids plus long-acting beta2-agonists reduced deaths in relative terms compared

142 A-kinase-anchoring protein (AKAP79/150) for beta2 agonist regulation.

143 beta2-agonist maintenance plus short-acting beta2-agonist reliever (hazard ratio, 0.71; 95% CI, 0.52

144 -long-acting beta2-agonist plus short-acting beta2-agonist reliever therapy.

145 -long-acting beta2-agonist plus short-acting beta2-agonist reliever.

146 -long-acting beta2-agonist plus short-acting beta2-agonist reliever.

147 e inhaled corticosteroids plus a long-acting beta2 agonist require additional treatment options as ad

148 beta2-Agonists rescue wild-type mice from established po

149 The combined use of beta2-agonists, rolipram, and steroids abolished TNF-alp

150 the previous year were inhaled short-acting beta2 agonists (SABA; range across age groups, 29.3-85.3

151 tent asthma) therapy (as-needed short-acting beta2-agonists [SABAs] for rescue therapy).

152 Similarly, the beta2 agonist salbutamol also could induce Ca(2+) shuttl

153 82]) in addition to ICS and the short-acting beta2-agonist salbutamol.

154 fecting the affinity or selectivity of other beta2-agonists (salbutamol, formoterol, fenoterol, clenb

155 ssociated with the beta2 adrenergic agonist (beta2-agonist) salbutamol.

156 eroid fluticasone propionate and long-acting beta2-agonist salmeterol xinafoate, which are widely use

157 ation sequence to receive inhaled longacting beta2 agonist (salmeterol 50 microg twice a day) or plac

158 hypothesis that inhaled combined long-acting beta2-agonist (salmeterol) and corticosteroid (fluticaso

159 r doses of inhaled steroids with long-acting beta2 agonists should be used for total control of sympt

160 The hydrophilic aromatic groups of all five beta2 agonists show maximum distribution in the lipid/wa

161 boring the otherwise equivalent alpha4(+)/(-)beta2 agonist sites modifies their contributions to nACh

162 espite inhaled corticosteroid and longacting beta2 agonist therapy, even in combination with tiotropi

163 to inhaled corticosteroids plus long-acting beta2-agonist therapy could improve the lives of patient

164 ixed-dose inhaled corticosteroid/long-acting beta2-agonist therapy was analyzed.

165 leukotriene receptor antagonist; long-acting beta2-agonist therapy was not permitted during the study

166 or (ADRB2) might not benefit from longacting beta2-agonist therapy.

167 Regional targeting of inhaled beta2-agonist to the proximal airways is more important

168 nflammatory potential of the vagus nerve and beta2-agonists to control inflammation in both beta2-kno

169 establish the anti-inflammatory potential of beta2-agonists to control systemic inflammation, organ d

170 n with inhaled corticosteroid and longacting beta2 agonist treatment.

171 In summary, beta2-agonist treatment enhanced CI-MPR-mediated uptake

172 In summary, adjunctive beta2-agonist treatment increased CI-MPR expression and

173 during the first few days of regular use of beta2-agonist treatment may account for the commonly obs

174 t 1 for at least 2 days, rescue short-acting beta2 agonist use for at least 2 days, or night-time awa

175 Regular beta2-agonist use for at least 1 week in patients with a

176 The LOB that occurs with chronic long-acting beta2-agonists use is not affected by ADRB2 Arg16Gly pol

177 f tolerance to the bronchodilator effects of beta2-agonists used in asthma therapy has been the subje

178 Ever-use of beta2-agonists was associated with a 17% decreased rate

179 Impairment of neutrophil phagocytosis by beta2-agonists was associated with significantly reduced

180 epsilonRI-dependent HLMC mediator release by beta2-agonists was greatly reduced in HLMC-HASMC cocultu

181 The effect of beta2-agonists was mimicked by forskolin and 8-bromo-cAM

182 ed corticosteroids alone or with long-acting beta2 agonists) was high in all age groups, and was sign

183 e inhaled corticosteroids plus a long-acting beta2 agonist were eligible for participation.

184 nce rate ratios of PD associated with use of beta2-agonists were estimated using conditional logistic

185 Nonsignificant ORs of exposure to inhaled beta2-agonists were found for spina bifida, cleft lip, a

186 ed with oral corticosteroids and long-acting beta2-agonists) were extracted from 65 Dutch pharmacy da

187 Salmeterol is a long-acting beta2-agonist, widely used as an inhaled treatment of as

188 igated the location and distribution of five beta2 agonists with distinct clinical durations and onse

189 receiving inhaled corticosteroid/long-acting beta2-agonist with or without LAMA daily for 3 or more m

190 The apparent association of beta2-agonists with a decreased risk of PD is likely the

191 respiratory symptoms, and the use of inhaled beta2-agonists with active treatment compared with place