ライフサイエンスコーパス: airway responsiveness

1 activation, airway smooth muscle growth, and airway responsiveness.

2 with measurements of airflow obstruction and airway responsiveness.

3 ryptase beta I-treated mice exhibited normal airway responsiveness.

4 o lung size is significantly associated with airway responsiveness.

5 eosinophils, concomitant with an increase in airway responsiveness.

6 predominantly from tests dominated by large airway responsiveness.

7 of a DI) tended to have greater methacholine airway responsiveness.

8 ow obstruction and the level of methacholine airway responsiveness.

9 urse of sensitization developed increases in airway responsiveness.

10 d to ultimately identify gene(s) that modify airway responsiveness.

11 sensitization and the development of altered airway responsiveness.

12 nces, T cells enhance genetically determined airway responsiveness.

13 essentially abolished, resulting in improved airway responsiveness.

14 hypersensitivity and development of altered airway responsiveness.

15 ing is lacking, especially as concerns small-airway responsiveness.

16 ry cells, inflammation index in the lung and airway responsiveness.

17 ion and challenge, Iqgap1-/- mice had higher airway responsiveness.

18 els are associated with asthma and decreased airway responsiveness.

19 gnaling does not contribute significantly to airway responsiveness.

20 es not modulate baseline or allergen-induced airway responsiveness.

21 d ILC2 expansion, mucous hypersecretion, and airways responsiveness.

22 The strict definition also included normal airways responsiveness.

23 Participants with increased airways responsiveness (1281 observations) were more lik

24 ml [males], -53 ml [females]), and increased airway responsiveness (-225 ml [males], -213 ml [females

25 ge in IL-13 expression, mucus production, or airways responsiveness 28 d postinfection.

26 ere more likely than those without increased airways responsiveness (5801 observations) to develop th

27 Knockout mice showed decreased airway responsiveness (60% reduced P(enh) and 58% reduce

28 ction of IL-5 and the development of altered airway responsiveness after antigen sensitization throug

29 a chronic disease characterized by increased airway responsiveness and airway inflammation.

30 atment with inhaled corticosteroids improves airway responsiveness and asthma control.

31 The relationship between increased airway responsiveness and asthma severity in children is

32 th muscle mass are correlated with increased airway responsiveness and asthma severity.

33 ns were each associated with increased FeNO, airway responsiveness and B-Eos in asthmatics.

34 tion profile in asthmatics and examine FeNO, airway responsiveness and blood eosinophilia in relation

35 id not play a role in the reversal to normal airway responsiveness and gammadelta T cells did not pla

36 airway function and is required for maximal airway responsiveness and healthy lung function.

37 y allergen airway challenges and analysis of airway responsiveness and inflammation.

38 ody specific for Amb a I (A-IgA) to modulate airway responsiveness and lung eosinophilia after airway

39 there was a significant reduction in overall airway responsiveness and lung inflammation in response

40 isoform appears to be involved in modulating airway responsiveness and only the inducible NOS isoform

41 challenge and was characterized by increased airway responsiveness and significant lung eosinophilia.

42 in allergic mice can reverse the changes in airway responsiveness and suggest that CGRP may have pot

43 cence and to examine the association between airways responsiveness and active asthma symptoms, child

44 d increases in baseline pulmonary mechanics, airway responsiveness, and cellular inflammation were gr

45 DE and allergen coexposure on lung function, airway responsiveness, and circulating leukocytes, and d

46 -dependent differences in ORMDL3 expression, airway responsiveness, and remodeling.

47 ate that the IL-8r modulates IgE production, airway responsiveness, and the composition of the cells

48 onary disease, normal spirometry, and normal airways responsiveness, and had smoked for a maximum of

49 The combination of normal FEV(1)/FVC ratio, airways responsiveness, and serum eosinophil count at ba

50 tics underlying the development of increased airway responsiveness (AR) after allergic sensitization,

51 Immunoglobulin E (IgE) levels and increased airway responsiveness (AR) are correlated traits that ar

52 Studies of airway responsiveness (AR) have typically used similar d

53 At 11 years of age, airway responsiveness (AR) to inhaled histamine and atop

54 ous reactivity to the peptide, and increased airway responsiveness (AR).

55 flammation in the airways leading to altered airway responsiveness (AR).

56 5 ppm, 3 h) caused a significant increase in airway responsiveness as indicated by a 1.2 log leftward

57 in 1 s (FEV1), forced vital capacity (FVC), airway responsiveness as indicated by methacholine (MTCH

58 cantly related to the degree of methacholine airway responsiveness as measured by Log10 dose response

59 Small airway responsiveness as represented by SRC slope was ca

60 In addition to baseline differences, small-airway responsiveness (as represented by the change in M

61 To test this hypothesis, airway responsiveness, as determined by calculating the

62 o cigarette smoke exposure of Balb/c mice on airway responsiveness, as determined by Penh measurement

63 of this study was therefore to compare small-airway responsiveness, as represented by the change in e

64 Keywords: airway responsiveness; asthma; tobacco smoke; infant pul

65 n the analysis of recurrent asthma episodes, airways responsiveness at a given visit was associated w

66 FeNO, airway responsiveness, blood eosinophil count (B-Eos) an

67 ed A/J mice develop significant increases in airway responsiveness, bronchoalveolar lavage eosinophil

68 secondary anti-OVA IgE responses and altered airway responsiveness but did not induce a secondary ris

69 F-beta by the alphavbeta6 integrin regulates airway responsiveness by modulating mast cell protease e

70 (in particular smooth muscle thickness) and airway responsiveness by up-regulating expression of che

71 For subjects presenting multiple airways responsiveness challenge studies, two successive

72 icate that TNF-alpha can negatively modulate airway responsiveness, controlling airway function in al

73 cigarette smoke did not significantly alter airway responsiveness, cyclic adenosine monophosphate le

74 The alteration of airway responsiveness did not depend on the timing of RS

75 pulmonary chemokine levels, inflammation, or airway responsiveness during allergen-induced airway dis

76 In the analysis of wheeze incidence, airways responsiveness (elicited via eucapnic hyperventi

77 into hyperreactive mice also restored normal airway responsiveness, establishing the mechanism underl

78 s significantly correlated with methacholine airway responsiveness, even after adjustment for age and

79 f studies have shed light on the genetics of airway responsiveness; even fewer have sought to identif

80 the development of allergen-induced altered airway responsiveness following airway challenge, even w

81 cantly higher serum IgE levels and increased airway responsiveness following intranasal aspergillus s

82 ith airway dysfunction assessed by increased airway responsiveness following methacholine exposure.

83 The induction of increased airway responsiveness following transfer of CD8+ T(EFF)

84 d mice reduced eosinophilic inflammation and airways responsiveness following RV infection.

85 cells, but their effects on allergen-induced airway responsiveness have not been well defined.

86 and furry animals (P = 0.02) was related to airway responsiveness in a similar model.

87 suggest that T-bet variation contributes to airway responsiveness in asthma.

88 hronic exposure to SO2 resulted in increased airway responsiveness in both groups of rats, but the ef

89 understanding of the primary pathobiology of airway responsiveness in both the absence and the presen

90 econdary RSV infection persistently enhances airway responsiveness in Df-sensitized mice, with a conc

91 cells also contributes to adenosine-induced airway responsiveness in mice.

92 ate that Egr-1 modulates TNF-alpha, IgE, and airway responsiveness in mice.

93 ifically in the genetic modulation of native airway responsiveness in mice.

94 Collectively, these data indicate that airway responsiveness in naive mice is influenced by gen

95 ased AHR in these mice, but had no effect on airway responsiveness in normal, nonchallenged mice.

96 lergen and PDDE plus allergen each increased airway responsiveness in normally responsive participant

97 ter increases in BAL IL-33, neutrophils, and airway responsiveness in obese than lean mice.

98 ter increases in BAL IL-33, neutrophils, and airway responsiveness in obese than lean mice.

99 The ROCK inhibitor, fasudil, also reduced airway responsiveness in OVA-challenged mice, without af

100 Airway responsiveness in OVA/OVA neuronal (NOS1)-deficie

101 evels of eosinophilic airway inflammation or airway responsiveness in Smad 3-deficient compared with

102 alter inflammatory end points but did reduce airway responsiveness in spite of increased serum IgE le

103 ubset of gammadelta T cells regulates innate airway responsiveness in the absence of alphabeta T cell

104 hanism of Th2-dependent mediation of altered airway responsiveness in the atopic asthmatic state, the

105 IgE-dependent mechanisms in inducing altered airway responsiveness in the atopic asthmatic state, the

106 The role of IL-1beta in regulating altered airway responsiveness in the atopic/asthmatic sensitized

107 fic viral respiratory infections and altered airway responsiveness in the development and exacerbatio

108 crosses are but some of the reasons to study airway responsiveness in the mouse.

109 igated the serial distribution of individual airway responsiveness in vivo following stimulation with

110 n alpha9beta1 in smooth muscle had increased airway responsiveness in vivo, and loss or inhibition of

111 HDM increased airways responsiveness in Postn(+/+) but not Postn(-/-)

112 To describe the role of airways responsiveness in predicting incidence of wheeze

113 results confirm the predictive importance of airways responsiveness in the natural history of the dev

114 Allergen challenge resulted in increases in airway responsiveness, in numbers of lung eosinophils, a

115 In naive mice, Syk inhibition diminished airway responsiveness independently of mast cells, or PK

116 demonstrated improvements in lung function, airway responsiveness, inflammation, and importantly, a

117 In vivo measures of airway responsiveness, inflammation, and remodelling wer

118 Lung function, early allergic response, airway responsiveness, inflammation, immune mediators, a

119 One of these, focused on airway responsiveness, involves active suppression and r

120 Airway responsiveness is known to be partly explained by

121 ese data provide evidence that the degree of airway responsiveness is linked to disease severity in c

122 now demonstrate that negative regulation of airway responsiveness is mediated by a small subpopulati

123 Because airway responsiveness is moderated by the use of inhaled

124 ese prospective analyses show that increased airways responsiveness is positively associated with the

125 mpaired airway constriction and thus reduced airway responsiveness; long-term lung pathology develops

126 d with ovalbumin (OVA), A-IgA did not affect airway responsiveness, lung eosinophilia, cytokine produ

127 h the other hsp failed to prevent changes in airway responsiveness, lung eosinophilia, or cytokine pr

128 these toxins were evaluated by the extent of airway responsiveness, neutrophil recruitment to the low

129 f chromosomal loci linked to the variance in airway responsiveness observed in the absence of any man

130 muscle mass and contribute to the increased airway responsiveness observed in these animals.

131 Basal airway responsiveness of AT2CC(-/-) mice was decreased c

132 cant improvement in the PC(20) (a measure of airway responsiveness) of asthmatic children in a large

133 mbination of respiratory symptoms, increased airway responsiveness or bronchodilator response, and a

134 utamine to glutamate) affect an individual's airway responsiveness, or response to acute or chronic b

135 min(-1); P < 0.05), but did not alter upper airway responsiveness (P = 0.7).

136 nkage: asthma at 68 cM (exact P-value=0.05), airways responsiveness (PC(20)) at 147 cM (P=0.01), and

137 y pups of recipient mothers showed increased airway responsiveness (Penh), allergic airway inflammati

138 Airway responsiveness predicted new-onset asthma, COPD,

139 e investigated the hypothesis that increased airways responsiveness predicts the development and remi

140 ed A/J mice develop significant increases in airway responsiveness, pulmonary eosinophilia, and pulmo

141 lts suggest that, in the general population, airway responsiveness relates in part to airway smooth m

142 s challenge studies, two successive positive airways responsiveness results were independently associ

143 tically reduced mucoid cell hyperplasia, and airway responsiveness returned to normal.

144 ve measurements of atopy, lung function, and airway responsiveness (school age).

145 Airway responsiveness, serum IgE and IgG levels were ass

146 eater), subjects with the greatest degree of airway responsiveness (slope less than the first quintil

147 use of a continuous noncensored indicator of airway responsiveness, such as the slope of the methacho

148 ytokine production, airway inflammation, and airway responsiveness, suggesting that the reduced aller

149 pes: lung function, bronchodilator response, airway responsiveness, symptoms, need for oral steroids

150 ion of a standard questionnaire, spirometry, airway-responsiveness testing, and chest imaging.

151 but males demonstrated significantly greater airway responsiveness than females following aerosolized

152 d C57BL/6 mice injected with OC-20 had lower airways responsiveness than HDM-treated mice injected wi

153 RMDL3 as an estrogen-responsive regulator of airway responsiveness that may contribute to sex-related

154 we found that TNF-alpha negatively regulates airway responsiveness through the activation of gammadel

155 h increased allergen-induced IgE production, airway responsiveness, tissue eosinophilia, and mucus pr

156 of mast cells to this process, we quantified airway responsiveness to aerosolized adenosine in wild-t

157 Airway responsiveness to allergen in patients with aller

158 b did not change baseline lung function, nor airway responsiveness to allergen or to methacholine.

159 sms has been suggested in causing changes in airway responsiveness to bronchoconstrictors.

160 ergen challenge is a paradoxical increase in airway responsiveness to cholinergic stimulation.

161 Allergen-induced changes in airway responsiveness to direct and indirect stimuli are

162 ral blood eosinophil counts, and testing for airway responsiveness to histamine.

163 Airway responsiveness to indirect stimuli correlates pos

164 The effect(s) of allergen exposure on airway responsiveness to indirect-acting stimuli require

165 tance (R(L)), dynamic compliance (Cdyn), and airway responsiveness to inhaled aerosolized methacholin

166 veness in mice, underlies the variability in airway responsiveness to inhaled LPS in humans.

167 Airway responsiveness to inhaled MCh was assessed and nu

168 CD8(-/-) mice developed significantly lower airway responsiveness to inhaled methacholine and lung e

169 t acute viral infection results in increased airway responsiveness to inhaled methacholine and pulmon

170 ung function abnormalities and have enhanced airway responsiveness to inhaled methacholine and seroto

171 Six days postinfection, airway responsiveness to inhaled methacholine was assess

172 fectious RSV intranasally, and 6 days later, airway responsiveness to inhaled methacholine was assess

173 quently challenged with OVA via the airways; airway responsiveness to inhaled methacholine was monito

174 lenged mice resulted in the normalization of airway responsiveness to inhaled methacholine, an effect

175 Airway responsiveness to inhaled methacholine, bronchoal

176 BLT1 -/- mice developed significantly lower airway responsiveness to inhaled methacholine, lower gob

177 Following sensitization, airway responsiveness to inhaled methacholine, numbers o

178 Conversely, allergen challenge decreased airway responsiveness to mannitol; geometric mean (95% C

179 There was a slightly greater individual airway responsiveness to Mch throughout the airway tree,

180 ciations of eQTL with longitudinal change in airway responsiveness to methacholine (LnPC20) on ICS.

181 onchial regions of the lungs), and increased airway responsiveness to methacholine (MCh).

182 Allergen challenge increased airway responsiveness to methacholine 24 h postchallenge

183 revented the significant 11-fold increase in airway responsiveness to methacholine after multiple Ag

184 fB-/- mice demonstrated significantly lower airway responsiveness to methacholine and less airway in

185 ways after RSV infection developed increased airway responsiveness to methacholine and pulmonary eosi

186 a combination of physician-diagnosed asthma, airway responsiveness to methacholine at < or = 25 mg/ml

187 a attacks ("asthma"); or as a combination of airway responsiveness to methacholine at < or = 8 mg/ml

188 l-source d-alpha-tocopheryl acetate improved airway responsiveness to methacholine but did not alter

189 tion in mucus overproduction while improving airway responsiveness to methacholine by 41%.

190 L3(zp3-Cre) mice had spontaneously increased airway responsiveness to methacholine compared to wild-t

191 sed the expression of endothelial VCAM-1 and airway responsiveness to methacholine in these animals.

192 rus-specific IgE, mice developed exaggerated airway responsiveness to methacholine on airway infectio

193 Neither exhaled nitric oxide nor airway responsiveness to methacholine or eucapnic volunt

194 at BK-1361 (25 mug/g body weight) attenuated airway responsiveness to methacholine stimulation by up

195 were exposed to O3 at 2 ppm for 3 hours, and airway responsiveness to methacholine was measured 8 hou

196 Significantly increased airway responsiveness to methacholine was noted, infecte

197 Lung mechanics and airway responsiveness to methacholine were assessed by u

198 ize relative to lung size is associated with airway responsiveness to methacholine.

199 a symptoms, asthma quality-of-life score, or airway responsiveness to methacholine.

200 Our study showed significant linkage between airway responsiveness to MTCH and D2S1780 on chromosome

201 85, for FEV1; D16S412, for FVC; D19S433, for airway responsiveness to MTCH; D1S518, for TIgE; and D4S

202 ammation is independent of smoking status or airway responsiveness to ozone.

203 TNFR1(-/-) animals displayed reduced airway responsiveness to RV1B, even when exogenous MIP-2

204 y was to evaluate in normal infants baseline airway responsiveness to the inhaled beta-agonist, albut

205 onic obstructive lung disease show increased airways responsiveness to histamine.

206 Airways responsiveness to LTD(4)in vivo was measured in

207 Airway responsiveness was assessed, bronchoalveolar lava

208 Upper airway responsiveness was defined as the ratio of the in

209 Airway responsiveness was defined based on the methachol

210 Airway responsiveness was estimated before, and 2 h afte

211 Airway responsiveness was evaluated at 24 hours.Measurem

212 Airway responsiveness was expressed as the cumulative pr

213 Airway responsiveness was increased by 48.1% after DBP e

214 Airway responsiveness was lower in IL-10(-/-) mice and w

215 s after allergen challenge, and methacholine airway responsiveness was measured before and 24 hours a

216 Airway responsiveness was measured by spirometry during

217 rty-eight hours after the last nebulization, airway responsiveness was monitored by the contractile r

218 le in similarly treated NOS2-deficient mice, airway responsiveness was not significantly different be

219 Decreased airways responsiveness was also a predictor for both rem

220 Increased airways responsiveness was defined as a PC10 value (conc

221 However, the peripheral airways responsiveness was significantly enhanced in ast

222 PR, characterized by a transient increase in airway responsiveness, was observed 5-30 minutes after a

223 ific proinflammatory cytokines in regulating airway responsiveness, we examined the effects and mecha

224 infiltrates, airway mucus goblet cells, and airway responsiveness were analyzed and compared with th

225 ssion, histology, dendritic cells (DCs), and airway responsiveness were assessed 1-12 d postinfection

226 Cytokine levels and airway responsiveness were determined.

227 s serum levels of ovalbumin-specific IgE and airway responsiveness were not altered.

228 monary eosinophilia, mucus goblet cells, and airway responsiveness were significantly lower than thos

229 Participants with increased airways responsiveness were less likely than those witho

230 erosolized ovalbumin (OVA) develop increased airway responsiveness when deficient in gammadelta T cel

231 eases in both the number of goblet cells and airway responsiveness, which are also features of reacti

232 in Df-sensitized mice transiently increases airway responsiveness, which is accompanied by increases

233 Incidence rate ratios for the association of airway responsiveness with disease occurrence were compu

234 Evidence on the longitudinal association of airway responsiveness with respiratory diseases is scarc

235 We investigated the association of airway responsiveness with the incidence of asthma, chro

236 rogen receptor-alpha also leads to increased airway responsiveness without increased inflammation aft