ライフサイエンスコーパス: methacholine

1 nor airway responsiveness to allergen or to methacholine.

2 irway resistance, and hyperresponsiveness to methacholine.

3 AHR was assessed on day 22 using methacholine.

4 y less airway hyperresponsiveness induced by methacholine.

5 ibers and enhance the contraction induced by methacholine.

6 apid resolution of airway hyperreactivity to methacholine.

7 ype-specific difference in responsiveness to methacholine.

8 o induce airway hyperresponsiveness (AHR) to methacholine.

9 ling, or increased airway hyperreactivity to methacholine.

10 nt decrease in airway hyperresponsiveness to methacholine.

11 ), and airway hyperresponsiveness to inhaled methacholine.

12 prevented the bronchoconstrictor response to methacholine.

13 improvement in airway hyperresponsiveness to methacholine.

14 -5 TG mice showed lower airway reactivity to methacholine.

15 ial cells, and airway hyperresponsiveness to methacholine.

16 at or HOE 140 on the FBF or t-PA response to methacholine.

17 emonstrated severe airway hyperreactivity to methacholine.

18 nd induced airway hyperreactivity to inhaled methacholine.

19 ay resistance, and compliance in response to methacholine.

20 response, and airway hyperresponsiveness to methacholine.

21 flammation and airway hyperresponsiveness to methacholine.

22 lammation, and airway hyperresponsiveness to methacholine.

23 tly attenuated airway hyperresponsiveness to methacholine.

24 ry cells, and decreased the sRaw response to methacholine.

25 annitol responders (n = 76) were negative to methacholine.

26 in dyspnea during bronchial provocation with methacholine.

27 rreactivity, measured at age six years using methacholine.

28 Methacholine (10 micromol/L) enhanced Ca(2+) channel cur

29 challenge increased airway responsiveness to methacholine 24 h postchallenge; the geometric mean (95%

30 nfusion of bradykinin (25 to 400 ng/min) and methacholine (3.2 to 12.8 microg/min) in 24 smokers pret

31 e animals, airway hyperreactivity to inhaled methacholine (40 micro g/ml) was diminished 38% in mice

32 12A TRPC3 mutant-mediated Ca(2+) entry after methacholine activation was significantly greater than t

33 0337), increased bronchial responsiveness to methacholine (adjusted beta-coefficient log-mumol, -0.80

34 umin exhibited airway hyperresponsiveness to methacholine aerosol and increased airway inflammatory c

35 ic mothers) showed AHR (enhanced pause after methacholine aerosol, 50 mg/ml, 3.7 +/- 0.7, 4.2 +/- 0.5

36 7 and 24 hours after allergen challenge, and methacholine airway responsiveness was measured before a

37 lization of airway responsiveness to inhaled methacholine, an effect that was neutralized by the rece

38 al, but not postnatal, SS strongly increased methacholine and allergen (Aspergillus)-induced airway r

39 reatment, the two bronchoscopies and inhaled methacholine and allergen challenges were repeated.

40 nflammation, and bronchial responsiveness to methacholine and allergen in atopic asthmatics in vivo.

41 of bronchoscopy and bronchoprovocation with methacholine and antigen to be acceptable for volunteer

42 ibited indomethacin-resistant relaxations to methacholine and arachidonic acid and indomethacin-resis

43 nfidence interval (CI), 0.92-0.96] per mumol methacholine and beta = 1.10 [95% CI, 1.06-1.15] per %,

44 assess the predictive value of BHR tested by methacholine and exercise challenge at age 10 years for

45 ndividuals with mild atopic asthma underwent methacholine and inhaled allergen challenges, and endobr

46 significantly lower airway responsiveness to methacholine and less airway inflammation.

47 antly lower airway responsiveness to inhaled methacholine and lung eosinophilia, and exhibited decrea

48 ollowing tests were carried out: spirometry, methacholine and mannitol challenge, exhaled nitric oxid

49 emonstrated clear translocation responses to methacholine and noradrenaline.

50 y decreased bronchoconstrictive responses to methacholine and other Gq-coupled receptor agonists.

51 ve enhanced airway responsiveness to inhaled methacholine and serotonin under basal conditions.

52 , patients underwent inhaled challenges with methacholine and specific allergen.

53 d no effect on airway hyperresponsiveness to methacholine and the reactivity to specific allergen.

54 r single-dose bronchial challenges, two with methacholine and two with allergen, on 10 subjects with

55 how significant differences in reactivity to methacholine and unloaded tissue shortening velocity (Vm

56 as to evaluate the potential role of direct (methacholine) and indirect (mannitol) challenge testing

57 with moderate/severe hyperresponsiveness to methacholine, and 12 with mild/borderline hyperresponsiv

58 us production, airway hyperresponsiveness to methacholine, and parenchymal tissue inflammation were a

59 pecific airway resistance (sRaw) response to methacholine; and upregulation of MMP-12 and PAR2 expres

60 n and enhanced airway hyperresponsiveness to methacholine as compared with wild-type mice, which were

61 responsiveness to the direct-acting stimuli methacholine at 3 and 24 h after exposure.

62 p < 0.001) and hyperreactivity (p < 0.05) to methacholine, BAL (p < 0.05) and peribronchial (p < 0.01

63 concentrations of the mACh receptor agonist methacholine before (R1) and after (R2) a short (60 sec)

64 sion increased airway hyperresponsiveness to methacholine both in naive mice as well as in response t

65 airway hyperresponsiveness (AHR) to inhaled methacholine, bronchoalveolar lavage (BAL) cytokine leve

66 potently decreased airway hyperreactivity to methacholine, bronchoalveolar lavage fluid albumin, and

67 Airway responsiveness to inhaled methacholine, bronchoalveolar lavage fluid cell composit

68 chanically ventilated sheep before and after methacholine bronchoconstriction (n = 3) and pulmonary e

69 yl acetate improved airway responsiveness to methacholine but did not alter airway reactivity to spec

70 had increased baseline airway reactivity to methacholine but markedly reduced experimental chronic o

71 pendently associated with more severe BHR to methacholine, but not FEV1 or R20 values.

72 ion while improving airway responsiveness to methacholine by 41%.

73 found that treatment with both histamine and methacholine caused strong increases in tracheal perfusi

74 al capacity [FEF50], and provocative dose of methacholine causing a 15% decrease in lung function [PD

75 years (FEV1, FEF50, and provocative dose of methacholine causing a 20% decrease in lung function [PD

76 responsiveness (provocative concentration of methacholine causing a 20% drop in FEV1: r = -0.740, P <

77 log PC(20) (the provocative concentration of methacholine causing a 20% fall in FEV(1); higher log PC

78 1 s (FEV1) and provocative concentration of methacholine causing a 20% fall in FEV1 (PC20MCh) in par

79 nique, and airway reactivity was assessed by methacholine challenge (0.015-10 mg/ml), which was stopp

80 rformed on day 6 (2 h postdose), followed by methacholine challenge (day 7), and induced sputum colle

81 plethysmography (sRaw; n = 567), and AHR by methacholine challenge (n = 498).

82 rway hyperresponsiveness as indicated by the methacholine challenge (p=0.031), confirming our earlier

83 had increased airway hyperresponsiveness to methacholine challenge and eosinophilia compared with na

84 rwegian birth cohort, 530 children underwent methacholine challenge and exercise-induced bronchoconst

85 Methacholine challenge and sputum induction were perform

86 nsiveness than females following aerosolized methacholine challenge as evidenced by increased respira

87 Participants underwent methacholine challenge at baseline (January 2010 to Apri

88 When considering all subjects tested by a methacholine challenge at least once while at work (479)

89 edictor of active asthma 6 years later, with methacholine challenge being superior to exercise test.

90 receiving asthma medication who had positive methacholine challenge compared with children without an

91 ed an enhanced airway hyperresponsiveness to methacholine challenge compared with littermates and C57

92 n and enhanced airway hyperresponsiveness to methacholine challenge from 11 years throughout young ad

93 ulmonary function and responses to bronchial methacholine challenge from childhood up to age 32 years

94 However, the predictive value of the methacholine challenge has never been addressed specific

95 A negative methacholine challenge in a patient still exposed to the

96 ncreases airway hyperresponsiveness (AHR) to methacholine challenge in C57BL/6J mice in association w

97 sitive and negative predictive values of the methacholine challenge in OA.

98 At baseline, the methacholine challenge showed an overall sensitivity of

99 The methacholine challenge test (MCT) is commonly used to as

100 thm on the basis of spirometry testing and a methacholine challenge test against the current standard

101 hial hyperresponsiveness was measured with a methacholine challenge test and bronchial inflammation w

102 A lung function test and a methacholine challenge test were performed at EGEA1 and

103 Diagnosis of asthma was confirmed by either methacholine challenge testing or test of reversibility

104 Methacholine challenge testing was performed before trea

105 n testing, high-resolution chest tomography, methacholine challenge testing, and fiberoptic bronchosc

106 d 3851 subjects who underwent spirometry and methacholine challenge tests both at baseline (1991-1993

107 o assessed whether nonspecific AHR caused by methacholine challenge was elicited by gVPLA2 secreted f

108 AHR to methacholine challenge was measured by whole-body plethy

109 on technique and bronchial responsiveness to methacholine challenge were assessed in 411 high-risk ne

110 cked pulmonary hyperresponsiveness following methacholine challenge while the 250-IU/g diet exacerbat

111 responsiveness (BHR) (dose-response slope of methacholine challenge) were measured.

112 pirometry) and airway hyper-reactivity (AHR; methacholine challenge).

113 althy control subjects underwent spirometry, methacholine challenge, and bronchoscopy, and their airw

114 5)/Ile(105) mild atopic asthmatics underwent methacholine challenge, inhaled allergen challenge and e

115 On Day 1 and 4 they had a methacholine challenge, on Day 3 they had an inhaled all

116 Airway hyperresponsiveness after methacholine challenge, peribronchovascular inflammation

117 ptoms, underwent pulmonary function testing, methacholine challenge, specific inhalation challenge to

118 For methacholine challenge, the doubling dilution difference

119 ncreased airway hyperresponsiveness (AHR) to methacholine challenge, total IgE, OVA-specific IgE and

120 ested improved lung mechanics in response to methacholine challenge.

121 Primary outcome was methacholine challenge.

122 way reactivity was assessed using an inhaled methacholine challenge.

123 cumented by increased airway resistance upon methacholine challenge.

124 terms of airway resistance and compliance to methacholine challenge.

125 1 over time, and the greatest sensitivity to methacholine challenge.

126 production and bronchial hyperreactivity to methacholine challenge.

127 Bronchial responsiveness was assessed by methacholine challenge.

128 Salmeterol-protected methacholine challenges (SPMChs) and PBMC B2AR numbers (

129 d positive and negative predictive values of methacholine challenges at baseline of the specific inha

130 ned efficacy, safety and pharmacokinetics of Methacholine Chloride (name of study drug: SK-1211) in o

131 In abroad, Methacholine Chloride (Provocholine(R)) is used to meet

132 easured by thermodilution) after exposure to methacholine chloride.

133 obese mice showed higher AHR at 30 mg/ml of methacholine compared to CD and food restricted groups,

134 taneously increased airway responsiveness to methacholine compared to wild-type mice.

135 ficient mice had reduced airway responses to methacholine compared with C57BL/6 mice.

136 to model the relationship between PC20 (the methacholine concentration causing a 20% fall in FEV1) w

137 7) caused rapid dose-dependent relaxation of methacholine-contracted human airways in vitro.

138 loss of beta-agonist-mediated relaxation of methacholine-contracted rings, whereas rings from EP2 re

139 n in this model (enhanced pause at 100 mg/ml methacholine: CpG, 0.9 +/- 0.1; ODN control, 3.8 +/- 0.6

140 ps, significantly reduced OVA-induced AHR to methacholine; decreased numbers of eosinophils and level

141 Responsiveness to methacholine did not differ between salmeterol and place

142 ore than 30% decline in FEF(75) at any given methacholine dose (hazard ratio = 0.4, p = 0.001).

143 The methacholine dose causing 20% reduction in FEV(1) (PD(20

144 way responsiveness, such as the slope of the methacholine dose-response curve, in clinical practice a

145 nderwent a series of protocols to assess its methacholine dose-response relationship, shortening velo

146 y of collagen I and III were correlated with methacholine dose-response slope and DeltaR(rs) , respec

147 rway responsiveness was defined based on the methacholine dose-response slope on both occasions.

148 tment) 15 min before methacholine, increased methacholine-elicited peak Raw values by 33.7% and 67.7%

149 nd IL-17 production correlated with PC20 for methacholine, eosinophil counts, and FEV1.

150 ion, airway pathology, and responsiveness to methacholine, even after animals were presensitized and

151 by increased airway responsiveness following methacholine exposure.

152 ter, the mice were rechallenged with OVA and methacholine, followed by bronchoalveolar lavage (BAL) a

153 serum IgE, bronchial hyperresponsiveness to methacholine, forced expiratory volume in 1s (FEV1 ) and

154 ial hyper-responsiveness (PC(20) ) to either methacholine/histamine or adenosine 5'-monophosphate (AM

155 a, decreased tissue inflammation, and absent methacholine hyper-responsiveness.

156 y disease, including airway eosinophilia and methacholine hyper-responsiveness.

157 The reduction in methacholine hyperresponsiveness after FP was greater in

158 airway collapsibility, and a high degree of methacholine hyperresponsiveness.

159 Bronchoconstriction was induced by inhaled methacholine in 15 subjects with mild asthma (FEV(1)/FVC

160 ally linked to airway hyperresponsiveness to methacholine in mild to moderate asthma.

161 cell metaplasia, and hyperresponsiveness to methacholine in the mGX-sPLA(2)-deficient mice.

162 Bronchial responsiveness to methacholine in the neonates was associated with the dev

163 t was used to determine airway resistance to methacholine in these mice.

164 ay smooth muscle strips were contracted with methacholine in vitro, and responses to TLR7 and TLR8 ag

165 ion did not alter airway hyper-reactivity to methacholine in vivo.

166 Incubation of lung parenchyma with methacholine increased the activation of NF-kappaB, whic

167 v. injection (acute treatment) 15 min before methacholine, increased methacholine-elicited peak Raw v

168 d airway hyper-responsiveness in response to methacholine indistinguishable from eosinophilic wild-ty

169 MCL-3G1 also blocked methacholine-induced airway bronchoconstriction in aller

170 K7975A and GSK5498A were able to fully relax methacholine-induced airway contraction by abolishing th

171 Furthermore, methacholine-induced airway contraction ex vivo increase

172 5 mug/g) during the challenge period reduced methacholine-induced airway hyperreactivity (AHR) in OVA

173 baseline lung resistance and also increased methacholine-induced airway hyperresponsiveness (AHR) as

174 antly, gamma-tocotrienol markedly suppressed methacholine-induced airway hyperresponsiveness in exper

175 viously reported that RSV infection prolongs methacholine-induced airway hyperresponsiveness in ovalb

176 monia with eosinophilia, Ym1 deposition, and methacholine-induced airway hyperresponsiveness, as well

177 iological changes exemplified by exacerbated methacholine-induced airway hyperresponsiveness.

178 antly affect hexosaminidase release, IgG, or methacholine-induced airway resistance, it significantly

179 ositron emission tomography (PET) imaging of methacholine-induced bronchoconstriction in sheep.

180 washout kinetics of (13)NN before and during methacholine-induced bronchoconstriction were analyzed.

181 During methacholine-induced bronchoconstriction, perfusion to v

182 ion in ASMCs and attenuated IL-17A-enhanced, methacholine-induced contraction of airway smooth muscle

183 greater beta-agonist-mediated relaxation of methacholine-induced contraction.

184 endogenous currents in smooth muscle cells, methacholine-induced currents were transient, and sponta

185 Our findings show that ET-1 attenuates methacholine-induced cutaneous vasodilatation through a

186 ung levels of some Th2 cytokines, and higher methacholine-induced increases in central airway resista

187 Without deep inspirations, the methacholine-induced reduction in FEV1 from baseline was

188 We show that ET-1 does not modulate methacholine-induced sweating at any of the administered

189 smooth muscle cell-dependent mechanism, and methacholine-induced sweating is not altered by ET-1.

190 same lung locations as depicted at baseline methacholine-induced ventilation.

191 duced relaxations, (2) the EDHF component of methacholine-induced, bradykinin-induced, and arachidoni

192 +/- 2.0 when five deep inspirations preceded methacholine inhalation (p = 0.0001).

193 gitudinal change in airway responsiveness to methacholine (LnPC20) on ICS.

194 ween the effects of deep inspiration and the methacholine log PC(20) that did not exist at baseline.

195 antly lower airway responsiveness to inhaled methacholine, lower goblet cell hyperplasia in the airwa

196 developed significantly lower AHR to inhaled methacholine, lower goblet cell metaplasia, and eosinoph

197 f Syk in airway contractility in response to methacholine (MCh) and particulate matter (PM) air pollu

198 Respiratory mechanics and methacholine (MCh) responsiveness were assessed by using

199 Methacholine (MCh) was co-administered in a dose-depende

200 required for airway hyperreactivity (AHR) to methacholine (MCh).

201 tion (n=402) and bronchial responsiveness to methacholine (n=363) using the raised-volume rapid thora

202 Airway hyperreactivity to methacholine observed on Day 73 in OVA-treated mice was

203 vere BHR was defined as a cumulative dose of methacholine of less than 0.3 mg causing an FEV1 decreas

204 veloped exaggerated airway responsiveness to methacholine on airway infection, an effect that require

205 igher concentration and were then exposed to methacholine, only wild-type mice developed a substantia

206 way mast cells, enhanced airway responses to methacholine or antigen, chronic inflammation including

207 ed nitric oxide nor airway responsiveness to methacholine or eucapnic voluntary hyperpnea challenge c

208 propranolol compared with placebo on either methacholine or histamine airway hyperresponsiveness and

209 No significant difference was observed in methacholine or histamine challenge after exposure to pr

210 At baseline, FEV(1) , PC(20) methacholine or histamine, and PC(20) AMP values were co

211 In random order, methacholine or mannitol challenges were performed 24 h

212 response to the muscarinic receptor agonist methacholine or the synthetic diacylglycerol, 1-oleoyl-2

213 y, and airway inflammation (FEV1, sRaw, PD20 methacholine, or eNO).

214 There was no effect on methacholine PC(20) post allergen.

215 variants were also associated with AHR (log-methacholine PC(20), p = 0.02-0.04).

216 ce of nonspecific bronchial hyperreactivity (methacholine PC20 < or =8 mg/mL) in a representative sam

217 In Gly/Gly participants, methacholine PC20 (20% reduction in forced expiratory vo

218 h postchallenge; the geometric mean (95% CI) methacholine PC20 decreased from 5.9 mg/ml (1.8-19.4) to

219 At 6 months, the methacholine PC20 increased by a mean (+/-SD) of 1.73+/-

220 (n = 19) with an FEV1 of 70% or greater and methacholine PC20 of 16 mg/mL or less were recruited.

221 Seventy percent had either a positive methacholine (PC20 < 8 mg/mL) or mannitol challenge (PD1

222 production correlated significantly with the methacholine PD (r = 0.50, p = 0.03), and the ratio of R

223 se in FEV1 at the cumulative dose of 1 mg of methacholine (PD20 >1 mg).

224 develop airway hyperresponsiveness (AHR) to methacholine, peribronchial eosinophilic and lymphocytic

225 d be: positive airway hyperresponsiveness to methacholine, positive reversibility (a change in FEV(1)

226 Urocortin III caused relaxation of methacholine-precontracted mouse tracheal segments.

227 iveness to methacholine (provocative dose of methacholine producing a 15% decrease in transcutaneous

228 or the primary analysis, we defined AHR by a methacholine provocation concentration of 4 mg/mL or les

229 Borg dyspnea scores at baseline and during a methacholine provocation test in 15 subjects with asympt

230 increase in small airway dysfunction during methacholine provocation was associated with a higher in

231 The increase in dyspnea during the methacholine provocation was strongly and independently

232 During methacholine provocation, small airway dysfunction was m

233 ar and bronchial exhaled nitric oxide, and a methacholine provocation.

234 s had a 2.5-fold increased responsiveness to methacholine (provocative dose of methacholine producing

235 Methacholine reactivity was more strongly related to rat

236 with mild/borderline hyperresponsiveness to methacholine, received inhaled fluticasone (880 microg d

237 q/11)-coupled M(3)-muscarinic receptors with methacholine, reduced current amplitudes at all potentia

238 onsiveness, measured as the concentration of methacholine required to decrease the forced expiratory

239 resistance upon challenge with 25 and 100 mg methacholine, respectively), and they developed a lung p

240 Fourteen percent of methacholine responders (n = 74) were negative to mannit

241 attenuated RV-induced mucous metaplasia and methacholine responses, and IL-4R null mice failed to sh

242 e examined associations of lung function and methacholine responsiveness (PC20) with ozone, carbon mo

243 ide (30.0 vs 62.6 ppb; P = .037) and reduced methacholine responsiveness (PC20FEV1 1.87 vs 0.45 mg/mL

244 There was no effect on methacholine responsiveness or FeNO.

245 The lack of effect of omalizumab on methacholine responsiveness suggests that IgE or eosinop

246 Spirometry, methacholine responsiveness, deep-breath-induced broncho

247 derably, reducing eosinophil recruitment and methacholine responsiveness, while increasing neutrophil

248 n induced sputum and bronchial biopsies, and methacholine responsiveness.

249 fluorescence microscopy, flow cytometry, and methacholine responsiveness.

250 sputum eosinophils, basal lung function, or methacholine responsiveness.

251 Mechanical stretch and/or treatment with methacholine resulted in an increased activation of ERK1

252 volume in one second (FEV(1)); (ii) dose of methacholine resulting in 20% fall in FEV(1) from baseli

253 low concentrations of the muscarinic agonist methacholine results in the activation of complex and re

254 trated airway hyperresponsiveness to inhaled methacholine significantly greater than in WT BALB/c mic

255 (K215R)GRK6 expression inhibited methacholine-stimulated M(3) mACh receptor phosphorylati

256 minal expression, beta-agonist inhibition of methacholine-stimulated PI hydrolysis was greater.

257 weight) attenuated airway responsiveness to methacholine stimulation by up to 42%, concomitantly red

258 tacept on FEV1, provocative concentration of methacholine sufficient to induce a 20% decline in FEV1,

259 8 healthy controls (HC) were subjected to a methacholine test (MT) before (Visit 1) and 24 hours aft

260 rsibility after bronchodilator or a positive methacholine test (PC20 </= 4 mg/mL).

261 Airway hyper-responsiveness (AHR) using a methacholine test, airway inflammation in bronchoalveola

262 All had exhaled nitric oxide measurement, methacholine test, eucapnic voluntary hyperpnea challeng

263 old PC(20) (the provocative concentration of methacholine that results in a 20% drop in FEV(1)) of 8

264 minal expression did not affect signaling by methacholine, thrombin, or LTD4.

265 ction was produced in five dogs by injecting methacholine through a central venous catheter.

266 six of 11 participants; the concentration of methacholine to decrease FEV(1) by 20% (PC(20)) was grea

267 dose inhalation challenges with allergen or methacholine to determine PD20 FEV1 during a control stu

268 ations in response to a low concentration of methacholine to the level seen in the absence of externa

269 actor) and plethysmography, before and after methacholine, to assess airway obstruction (AO) and airw

270 , and plethysmography, both before and after methacholine treatment.

271 e also showed significant AHR in response to methacholine up to 154 days.

272 of ventilatory timing in response to inhaled methacholine was also seen in IL-17F-transduced, Ag-sens

273 In addition, the airway reactivity to methacholine was elevated moderately in DQ6/CD4(null) mi

274 Unexpectedly, airway hyperreactivity to methacholine was essentially ablated in M pneumoniae-inf

275 nsitized and challenged with OVA, and AHR to methacholine was established.

276 deep inspirations on the airway response to methacholine was evaluated on the basis of inspiratory v

277 The response to methacholine was insensitive to intracellular BAPTA, but

278 pm for 3 hours, and airway responsiveness to methacholine was measured 8 hours after O3 exposure.

279 Lung hyperresponsiveness to methacholine was measured by use of a Buxco unrestrained

280 l spirometry and bronchial responsiveness to methacholine was measured during sedation by forced flow

281 Airway hyperresponsiveness in response to methacholine was measured.

282 Airway hyperresponsiveness to aerosolized methacholine was measured.

283 he airways; airway responsiveness to inhaled methacholine was monitored.

284 Airway function in response to inhaled methacholine was monitored; bronchoalveolar lavage fluid

285 nt airway hyperresponsiveness to intravenous methacholine was observed at day 3 in CCR4-/- mice, wher

286 ype-specific difference in responsiveness to methacholine was significant (1.32 doubling dose differe

287 he forearm blood flow dose-response curve to methacholine was significantly attenuated by hyperglycem

288 gen deposition and airway hyperreactivity to methacholine were all clearly sensitive to IL-13-PE.

289 hole-cell currents activated by ionomycin or methacholine were anion-selective and showed minimal rec

290 Lung mechanics and airway responsiveness to methacholine were assessed by using the flexiVent.

291 ed sputum cell counts, and responsiveness to methacholine were assessed the following day.

292 Pulmonary functions and AHR to methacholine were examined after rechallenge with OVA.

293 ce responses (Raw) to the muscarinic agonist methacholine were measured by using the forced oscillati

294 tric oxide and airway hyperresponsiveness to methacholine were not affected by either SB010 or placeb

295 the lung, and airway hyperresponsiveness to methacholine were significantly reduced in LTC(4)S(null)

296 luding airway hyperresponsiveness to inhaled methacholine, were assessed.

297 osinophilia and heightened responsiveness to methacholine when compared with nonsensitized animals.

298 equency that depends on the concentration of methacholine, whereas the magnitude of the [Ca(2+)](i) s

299 ge also caused airway hyperresponsiveness to methacholine, which was dose dependently blocked by trea

300 2) overexpression decreased contractility to methacholine, while G(alphai2) inhibition enhanced contr