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 essentially abolished, resulting in improved airway responsiveness.

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

5 o lung size is significantly associated with airway responsiveness.

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

7 eosinophils, concomitant with an increase in airway responsiveness.

8 predominantly from tests dominated by large airway responsiveness.

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

10 ow obstruction and the level of methacholine airway responsiveness.

11 urse of sensitization developed increases in airway responsiveness.

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

13 sensitization and the development of altered airway responsiveness.

14 nces, T cells enhance genetically determined airway responsiveness.

15 hypersensitivity and development of altered airway responsiveness.

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

17 els are associated with asthma and decreased airway responsiveness.

18 gnaling does not contribute significantly to airway responsiveness.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 5 ppm, 3 h) caused a significant increase in airway responsiveness as indicated by a 1.2 log leftward

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 Airway responsiveness is known to be partly explained by

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

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

111 Because airway responsiveness is moderated by the use of inhaled

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Airway responsiveness predicted new-onset asthma, COPD,

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

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

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

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

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

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

133 Airway responsiveness, serum IgE and IgG levels were ass

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

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

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

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

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

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

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

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

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

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

144 Airway responsiveness to allergen in patients with aller

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

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

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

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

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

150 Airway responsiveness to indirect stimuli correlates pos

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

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

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

154 Airway responsiveness to inhaled MCh was assessed and nu

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

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

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

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

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

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

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

162 Airway responsiveness to inhaled methacholine, bronchoal

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

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

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

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

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

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

169 Allergen challenge increased airway responsiveness to methacholine 24 h postchallenge

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

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

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

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

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

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

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

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

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

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

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

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

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

183 Significantly increased airway responsiveness to methacholine was noted, infecte

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

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

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

187 85, for FEV1; D16S412, for FVC; D19S433, for airway responsiveness to MTCH; D1S518, for TIgE; and D4S

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

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

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

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

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

193 Airway responsiveness was assessed, bronchoalveolar lava

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

195 Airway responsiveness was defined based on the methachol

196 Airway responsiveness was estimated before, and 2 h afte

197 Airway responsiveness was expressed as the cumulative pr

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

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

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

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

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

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

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

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

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

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

208 Cytokine levels and airway responsiveness were determined.

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

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

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

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

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

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

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

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

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

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