ライフサイエンスコーパス: beta2 agonist

1 ose inhaled corticosteroids plus long-acting beta2 agonists.

2 eive inhaled corticosteroids plus longacting beta2-agonists.

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

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

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

6 pairment was induced experimentally by using beta2-agonists.

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

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

9 There are some differences between beta2-agonists.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 4% received prescriptions for a short-acting beta2-agonist and 41.2% for inhaled corticosteroids; 76.

26 beta2-Agonists and corticosteroids inhibited neutrophil

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

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

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

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

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

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

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

34 beta2-Agonists are effective bronchodilators due primari

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 fixed inhaled corticosteroid and longacting beta2 agonist combination.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 beta2-Agonists inhibit cytokine production in splenocyte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 82]) in addition to ICS and the short-acting beta2-agonist salbutamol.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 n with inhaled corticosteroid and longacting beta2 agonist treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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