ライフサイエンスコーパス: hyperresponsiveness

1 ibrotic mediators and contributes to airways hyperresponsiveness.

2 nflammation, tissue remodeling and bronchial hyperresponsiveness.

3 inflammation, mucous metaplasia, and airways hyperresponsiveness.

4 ich leads to mucus hypersecretion and airway hyperresponsiveness.

5 th asthma and with the severity of bronchial hyperresponsiveness.

6 rway mucus production, and attenuated airway hyperresponsiveness.

7 te-induced airway inflammation and bronchial hyperresponsiveness.

8 e binding affinity and contributes to T cell hyperresponsiveness.

9 s production together with pronounced airway hyperresponsiveness.

10 ung function, and a greater degree of airway hyperresponsiveness.

11 of ORMDLs, influencing airway remodeling and hyperresponsiveness.

12 ophageal infiltration, and suppressed airway hyperresponsiveness.

13 mucus production, and development of airways hyperresponsiveness.

14 ses persistent mucous metaplasia and airways hyperresponsiveness.

15 aining neutrophil quiescence and suppressing hyperresponsiveness.

16 rway inflammation, IgE Ab levels, and airway hyperresponsiveness.

17 endothelial vasorelaxation capacity, but not hyperresponsiveness.

18 attenuated allergic airway inflammation and hyperresponsiveness.

19 is a prototypical feature of indirect airway hyperresponsiveness.

20 ensitization, airway inflammation and airway hyperresponsiveness.

21 ir, blood and sputum eosinophils, and airway hyperresponsiveness.

22 prevented DEP-induced exacerbation of airway hyperresponsiveness.

23 stimuli, which is suggestive of cough-reflex hyperresponsiveness.

24 6% (p </= 0.001) and fully normalized airway hyperresponsiveness.

25 mediated lysosome degradation suppressed LPS hyperresponsiveness.

26 ed by chronic airway inflammation and airway hyperresponsiveness.

27 nary inflammation, and development of airway hyperresponsiveness.

28 ted with behavioral inhibition and/or airway hyperresponsiveness.

29 erapeutic benefit of MSC treatment on airway hyperresponsiveness.

30 lar infiltration in BALF and allergic airway hyperresponsiveness.

31 trophilic inflammation, but very mild airway hyperresponsiveness.

32 ts on systemic allergic responses and airway hyperresponsiveness.

33 y targeted to mitigate the effects of airway hyperresponsiveness.

34 CSF) and a partial protection against airway hyperresponsiveness.

35 some evidence of associations with bronchial hyperresponsiveness.

36 anced development of allergen-induced airway hyperresponsiveness.

37 tivity, increased ASM contraction and airway hyperresponsiveness.

38 ppb, 25 of 38 subjects (65.7%) had bronchial hyperresponsiveness.

39 ameliorated allergic airway inflammation and hyperresponsiveness.

40 ppb, 29 of 43 subjects (67.4%) had bronchial hyperresponsiveness.

41 creased aeroantigen sensitization and airway hyperresponsiveness.

42 ed IL-1beta-induced steroid-resistant airway hyperresponsiveness.

43 e levels, goblet cell metaplasia, and airway hyperresponsiveness.

44 gene ORMDL3 leads to airway remodelling and hyperresponsiveness.

45 and MMP-1 protein associated with bronchial hyperresponsiveness.

46 s in PTSD is associated with locus coeruleus hyperresponsiveness.

47 tentially promoting sensitization and airway hyperresponsiveness.

48 sistant neutrophilic inflammation and airway hyperresponsiveness.

49 flammation, mucus hypersecretion, and airway hyperresponsiveness.

50 eosinophilia, high level of FENO, bronchial hyperresponsiveness.

51 useful in the diagnosis of bronchial airway hyperresponsiveness.

52 fect of imatinib, a KIT inhibitor, on airway hyperresponsiveness, a physiological marker of severe as

53 2-related inflammation and change in airway hyperresponsiveness after 6 weeks of fluticasone treatme

54 The reduction in methacholine hyperresponsiveness after FP was greater in non-smokers

55 reversible airflow obstruction, or bronchial hyperresponsiveness after having all asthma medications

56 TGF-beta1, 5-lipoxygenase (5-LO)] and airway-hyperresponsiveness (AHR) (5-LO).

57 Airway hyperresponsiveness (AHR) affects 55%-77% of children wi

58 S1P and SphK1 to mast cell-dependent airway hyperresponsiveness (AHR) and airway inflammation in mic

59 Airway hyperresponsiveness (AHR) and bronchial inflammation wer

60 ice induced Treg cells and attenuated airway hyperresponsiveness (AHR) and inflammation comparably wi

61 evelopment of ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) and inflammation in an experim

62 el compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experiment

63 monstrated that IVIg protects against airway hyperresponsiveness (AHR) and inflammation in mouse mode

64 Airway hyperresponsiveness (AHR) and inflammation were assessed

65 role of H2S against allergen-induced airway hyperresponsiveness (AHR) and inflammation.

66 irway function, bacterial LPS-induced airway hyperresponsiveness (AHR) and lung inflammation, and ble

67 e resulted in significantly increased airway hyperresponsiveness (AHR) and macrophage and neutrophil

68 contractility and the development of airway hyperresponsiveness (AHR) are cardinal features of asthm

69 d also increased methacholine-induced airway hyperresponsiveness (AHR) as measured by lung resistance

70 MCs) contraction and proliferation in airway hyperresponsiveness (AHR) associated with asthma are sti

71 ooth muscle (ASM) plays a key role in airway hyperresponsiveness (AHR) but it is unclear whether its

72 ILC) and TH2 cell numbers but similar airway hyperresponsiveness (AHR) compared with those after hous

73 neutrophilic airway inflammation and airway hyperresponsiveness (AHR) following allergen challenge,

74 elopment of allergic inflammation and airway hyperresponsiveness (AHR) in acute murine models.

75 ment of eosinophilic inflammation and airway hyperresponsiveness (AHR) in sensitized individuals is n

76 Although airway hyperresponsiveness (AHR) is a defining feature of asthm

77 Indirect airway hyperresponsiveness (AHR) is a fundamental feature of as

78 Airway inflammation, airway hyperresponsiveness (AHR) to inhaled methacholine, bronc

79 objective evidence of athlete asthma/airway hyperresponsiveness (AHR) were collected for all aquatic

80 echanism may result in a reduction of airway hyperresponsiveness (AHR) when using triple therapy.

81 IL-21R-deficiency reduces HDM-driven airway hyperresponsiveness (AHR) with only partial effects on a

82 cted to this SA model failed to mount airway hyperresponsiveness (AHR) without appreciable effect on

83 ma phenotype that is characterized by airway hyperresponsiveness (AHR) without eosinophilic inflammat

84 gillus fumigatus (AF) extract-induced airway hyperresponsiveness (AHR), airway inflammation, immunogl

85 for preservation of allergen-induced airway hyperresponsiveness (AHR), airway resistance, and compli

86 characterized by airflow obstruction, airway hyperresponsiveness (AHR), and airway inflammation.

87 e inflammation, NF-kappaB activation, airway hyperresponsiveness (AHR), and airway remodeling.

88 osed to ozone, and lung inflammation, airway hyperresponsiveness (AHR), and mitochondrial function we

89 (MSCs) decrease airway eosinophilia, airway hyperresponsiveness (AHR), and remodelling in murine mod

90 hours after the final OVA challenge, airway hyperresponsiveness (AHR), bronchoalveolar fluid (BALF)

91 r features of allergic asthma include airway hyperresponsiveness (AHR), eosinophilic inflammation, an

92 an aerosolized antagonist attenuates airway hyperresponsiveness (AHR), eosinophilic inflammation, an

93 ditional treatment with sGARP reduced airway hyperresponsiveness (AHR), influx of neutrophils and mac

94 role of IL-13 and IL-17A in mediating airway hyperresponsiveness (AHR), lung inflammation, and mucus

95 d wild type mice displayed a striking airway hyperresponsiveness (AHR), mMCP-6(-/-) mice had less AHR

96 trast to the anticipated reduction in airway hyperresponsiveness (AHR), OVA allergen-challenged Ormdl

97 nflammatory disease characterized by airways hyperresponsiveness (AHR), reversible airflow obstructio

98 lavage fluid (BALF), airway inflammation and hyperresponsiveness (AHR), serum immunoglobulin and sple

99 asthma, it is not a prerequisite for airway hyperresponsiveness (AHR), suggesting that underlying ab

100 of O3-induced airway inflammation and airway hyperresponsiveness (AHR), we sought to investigate the

101 s ozone, exacerbates airway inflammation and hyperresponsiveness (AHR).

102 homeostasis and in obesity-associated airway hyperresponsiveness (AHR).

103 has been linked to steroid-resistant airway hyperresponsiveness (AHR).

104 ed by chronic airway inflammation and airway hyperresponsiveness (AHR).

105 production, airway inflammation, and airway hyperresponsiveness (AHR).

106 rgic sensitization, inflammation, and airway hyperresponsiveness (AHR).

107 nflammation, mucus secretion, remodeling and hyperresponsiveness (AHR).

108 was determined by the measurement of airway hyperresponsiveness, airway inflammation, and cytokine p

109 n, excessive Th2 polarization, marked airway hyperresponsiveness, alveolar simplification, decreased

110 some inhibition using CRID3 prevented airway hyperresponsiveness and airway inflammation (both neutro

111 IT ameliorated airway hyperresponsiveness and airway inflammation in a chronic

112 pressed RSV-induced steroid-resistant airway hyperresponsiveness and airway inflammation.

113 e inflammatory response leading to bronchial hyperresponsiveness and asthma.

114 enetics and Environment of Asthma, bronchial hyperresponsiveness and atopy) (170 with and 170 without

115 Conversely, airway hyperresponsiveness and contractile tissue underwent a l

116 ad an increased propensity to develop airway hyperresponsiveness and displayed significantly elevated

117 ocyte driven disease characterized by airway hyperresponsiveness and eosinophilia.

118 a single exposure to HDM resulted in airway hyperresponsiveness and increased TH2 cytokine levels in

119 e, periostin is required for maximal airways hyperresponsiveness and inflammation after HDM sensitiza

120 ure to respiratory allergens triggers airway hyperresponsiveness and inflammation characterized by th

121 Anti-ST2 reduced ozone-induced airway hyperresponsiveness and inflammation in obese mice but h

122 of anti-IFN-gamma antibodies induced airway hyperresponsiveness and inflammation in wild-type but no

123 ivotal in the development of allergic airway hyperresponsiveness and inflammation, and yet remains me

124 oughing occurs as a consequence of bronchial hyperresponsiveness and inflammation, but the possibilit

125 wild-type (WT) recipients exacerbates airway hyperresponsiveness and inflammation, whereas transfer o

126 eficient recipients failed to restore airway hyperresponsiveness and inflammation.

127 in vivo, such as bronchoconstriction, airway hyperresponsiveness and inflammatory cell influx suggest

128 tently induce bronchial constriction, airway hyperresponsiveness and inflammatory cell influx to the

129 to Neu5Gc in mice resulted in reduced airway hyperresponsiveness and inflammatory cell recruitment to

130 hma and atopy at 7(1/2) years, and bronchial hyperresponsiveness and lung function at 8(1/2) years in

131 PARP activity reduced the severity of airway hyperresponsiveness and lung inflammation.

132 ith it in a model of AAD dependent on airway hyperresponsiveness and lung inflammation.

133 ce were resistant to the induction of airway hyperresponsiveness and manifested improved lung mechani

134 OCK2(+/-) vs. wild-type mice, as were airway hyperresponsiveness and mucous hypersecretion.

135 n patients with moderate to severe bronchial hyperresponsiveness and nasal polyposis, the chance of r

136 analysis, only moderate to severe bronchial hyperresponsiveness and nasal polyps were independent pr

137 ally, older Ndrg1-deficient mice show T-cell hyperresponsiveness and Ndrg1-deficient T cells aggravat

138 o on either methacholine or histamine airway hyperresponsiveness and no change in ACQ or AQLQ.

139 ation and airway dysfunction, manifesting as hyperresponsiveness and obstruction.

140 hat NQO1-null mice are protected from airway hyperresponsiveness and pulmonary inflammation following

141 This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to

142 Airway hyperresponsiveness and serum IgE levels were compared i

143 mice with low doses of IFN-gamma rescued TLR hyperresponsiveness and the capacity to control heterolo

144 t microbiota and TMAO in modulating platelet hyperresponsiveness and thrombosis potential and identif

145 rized by variable airway obstruction, airway hyperresponsiveness, and airway inflammation.

146 inhibition on allergic airway inflammation, hyperresponsiveness, and airway remodeling were analyzed

147 ory effects on allergic airway inflammation, hyperresponsiveness, and airway remodeling.

148 Asthma is defined by airway inflammation and hyperresponsiveness, and contributes to morbidity and mo

149 ed mucous metaplasia, ILC2 expansion, airway hyperresponsiveness, and epithelial cell IL-25 expressio

150 ers, TH2 cell numbers and activation, airway hyperresponsiveness, and expression of the transcription

151 hood is associated with asthma and bronchial hyperresponsiveness, and faster weight growth across chi

152 allergen-induced tissue inflammation, airway hyperresponsiveness, and goblet cell metaplasia in 2 ast

153 , MMP-1 levels are associated with bronchial hyperresponsiveness, and MMP-1 activation are associated

154 which promoted chronic inflammation, airway hyperresponsiveness, and mucus production during house d

155 otype, including airway inflammation, airway hyperresponsiveness, and mucus production.

156 pic sensitization, a lesser degree of airway hyperresponsiveness, and no concomitant allergic disease

157 inflammation, mucous cell metaplasia, airway hyperresponsiveness, and OVA-specific IgE compared with

158 y eosinophilia, mucus hypersecretion, airway hyperresponsiveness, and OVA-specific IgE production in

159 reduced allergic airway inflammation, airway hyperresponsiveness, and pulmonary collagen deposition.

160 rways and its effect on airway inflammation, hyperresponsiveness, and remodeling as pathological feat

161 ion with respiratory syncytial virus, airway hyperresponsiveness, and severe bronchopulmonary dysplas

162 ted to both behavioral inhibition and airway hyperresponsiveness, and so could not mediate their rela

163 lung, IgE production, development of airway hyperresponsiveness, and Th2 T cell priming.

164 by increased goblet cell metaplasia, airway hyperresponsiveness, and Th2-mediated inflammation.

165 is a critical determinant of indirect airway hyperresponsiveness, and the airway epithelium might ser

166 hip between behavioral inhibition and airway hyperresponsiveness, and whether hormonal and immune mea

167 Behaviorally inhibited monkeys had airway hyperresponsiveness as indicated by the methacholine cha

168 Airway hyperresponsiveness, as well as inflammation, and intrac

169 ificantly attenuated allergen-induced airway hyperresponsiveness at 24 hours after allergen challenge

170 EV1, smaller bronchodilator response, airway hyperresponsiveness at baseline, and male sex were assoc

171 Bronchial hyperresponsiveness (BHR) can be present in subjects wit

172 The severity of bronchial hyperresponsiveness (BHR) is a fundamental feature of as

173 Bronchial hyperresponsiveness (BHR) is a phenotypic hallmark of as

174 The bronchial hyperresponsiveness (BHR) test is useful to diagnose or

175 unts in relation to lung function, bronchial hyperresponsiveness (BHR), and asthma control in a cohor

176 f exhaled nitric oxide (Feno), low bronchial hyperresponsiveness (BHR), and low bronchodilator revers

177 tions of parental asthma severity, bronchial hyperresponsiveness (BHR), and total and specific IgEs,

178 n with H. pylori extract prevents the airway hyperresponsiveness, bronchoalveolar eosinophilia, pulmo

179 stic features of asthma, including bronchial hyperresponsiveness, bronchoconstriction, airway inflamm

180 ity during ontogeny exhibit a cell-intrinsic hyperresponsiveness but a diminished capacity to survive

181 IL-33 induces airway hyperresponsiveness, but its role in airway remodeling a

182 n rhesus monkeys (Macaca mulatta) and airway hyperresponsiveness, but not atopy, and the suggestion w

183 uisite for the suppression of AAI and airway hyperresponsiveness by GCs.

184 We measured airway hyperresponsiveness by using flexiVent; inflammatory ind

185 and HDM coexposure markedly enhanced airway hyperresponsiveness compared with HDM exposure alone and

186 ells, type 2 cytokine production, and airway hyperresponsiveness compared with sole DEPs or HDM.

187 um allergen-specific antibody levels, airway hyperresponsiveness, cytokine levels in spleen cells and

188 Development of airway hyperresponsiveness, cytokine levels, and airway inflamm

189 nificantly decreased allergen-induced airway hyperresponsiveness, decreased the number of inflammator

190 orly controlled severe asthma who had airway hyperresponsiveness despite receiving maximal medical th

191 ta6-deficient mice are protected from airway hyperresponsiveness, due in part to increased expression

192 Live C cladosporioides induced robust airway hyperresponsiveness, eosinophilia, and a predominately T

193 various time points for evaluation of airway hyperresponsiveness, eosinophilia, mucus production, inf

194 allmark features of asthma, including airway hyperresponsiveness, eosinophilic accumulation, and Th2

195 e of nocturnal asthma, more severe bronchial hyperresponsiveness, exercise-induced asthma, and the la

196 resses Th2 pulmonary inflammation and airway hyperresponsiveness following aeroallergen exposure, imp

197 The effect of IL-17A on IL-13-induced airway hyperresponsiveness, gene expression, mucus hypersecreti

198 perresponsiveness; however, at 7 days airway hyperresponsiveness had completely resolved in Darc(E2)

199 C-w/o-c-Myc) in allergic diseases and airway hyperresponsiveness has not been investigated.

200 24 hours, Darc(E2) mice had increased airway hyperresponsiveness; however, at 7 days airway hyperresp

201 Targeting Axl also inhibited airway hyperresponsiveness, IL-4 and IL-13 production, and gobl

202 uction, type 2 cytokine response, and airway hyperresponsiveness in 4 wk, followed by airway remodeli

203 y roles of FENO and FOT to predict bronchial hyperresponsiveness in adult stable asthmatic patients t

204 and FENO can predict the level of bronchial hyperresponsiveness in adult stable asthmatics.

205 g inflammation, mucus production, and airway hyperresponsiveness in an experimental model of OVA-indu

206 ective in preventing airway inflammation and hyperresponsiveness in animal models of asthma.

207 owing association with severity of bronchial hyperresponsiveness in asthma patients.

208 amics, smooth muscle contraction, and airway hyperresponsiveness in asthma.

209 Ca(2+) Turning down the gain of sympathetic hyperresponsiveness in cardiovascular disease associated

210 d the sGC signaling and attenuated bronchial hyperresponsiveness in CS-exposed mice.

211 kedly suppressed methacholine-induced airway hyperresponsiveness in experimental asthma.

212 or 8 (Mfge8(-/-)) develop exaggerated airway hyperresponsiveness in experimental models of asthma.

213 2 cytokines, airway eosinophilia, and airway hyperresponsiveness in juvenile Scnn1b-Tg mice.

214 BAY 41-2272 and BAY 60-2770 reversed airway hyperresponsiveness in mice with allergic asthma and res

215 y attenuated allergen/IgE-mediated mast cell hyperresponsiveness in mice.

216 E and TH2 cytokine production but not airway hyperresponsiveness in OVA-challenged DNA-PKcs(+/-) mice

217 Behavioral and autonomic hyperresponsiveness in PTSD may arise from a hyperactive

218 system may underlie behavioral and autonomic hyperresponsiveness in PTSD.

219 Airway hyperresponsiveness in response to methacholine was meas

220 of Cardif(-/-) NK cells can result in their hyperresponsiveness in some settings and support recent

221 e that JAK2V617I induces sufficient cytokine hyperresponsiveness in the absence of other molecular ev

222 4 as a novel therapeutic target for neuronal hyperresponsiveness in the airways and symptoms, such as

223 ICS improved FEV1 and hyperresponsiveness in the IL-25-high but not the IL-25-

224 epigenetic pathways that underlie endotoxin hyperresponsiveness in the setting of preceding unilater

225 hibition of GSNO reductase attenuated airway hyperresponsiveness in vivo among juvenile and adult mic

226 OVA, as indicated by airway inflammation and hyperresponsiveness, increased serum OVA-specific IgE le

227 ated mice produced significantly less airway hyperresponsiveness induced by methacholine.

228 An anti-TSLP antibody abrogated airway hyperresponsiveness, inflammation, and mucus production

229 n for 8 consecutive days, after which airway hyperresponsiveness, inflammatory cell influx into the l

230 Airway hyperresponsiveness is common to atopic and non-atopic a

231 locus coeruleus system hyperactivity to PTSD hyperresponsiveness is sparse.

232 This LPS hyperresponsiveness is transcriptionally mediated.

233 pared with WT mice, had diminished bronchial hyperresponsiveness (lung airway resistance); numbers of

234 results in a dramatic upregulation of airway hyperresponsiveness, lung resistance, and TH2 responses

235 s were noted between the 2 sexes with airway hyperresponsiveness (mannitol provocation testing) or in

236 ith severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell counts, and tryptase rele

237 e primary end point was the change in airway hyperresponsiveness, measured as the concentration of me

238 mitation, bronchial reversibility, or airway hyperresponsiveness (misdiagnosed asthma).

239 The IL-25-high subset had greater airway hyperresponsiveness, more airway and blood eosinophils,

240 aled corticosteroids, had more severe airway hyperresponsiveness, more often nasal polyps, and higher

241 nduced asthma-like features including airway hyperresponsiveness, mucus hyperplasia, airway eosinophi

242 lts in increased lung granulocytosis, airway hyperresponsiveness, mucus overproduction, collagen depo

243 sed to IL-13 and IL-17A had augmented airway hyperresponsiveness, mucus production, airway inflammati

244 PTX3 deficiency results in augmented airway hyperresponsiveness, mucus production, and IL-17A-domina

245 ough the assessment of nonspecific bronchial hyperresponsiveness (NSBH) is a key step in the diagnosi

246 in long-term airway inflammation and airway hyperresponsiveness occurred at least partially via modu

247 ted populations, both hyporesponsiveness and hyperresponsiveness of brain regions (e.g., ventral stri

248 of fetal immunity (including the functional hyperresponsiveness of CD4(+) and CD8(+) T cells and the

249 s structural changes in the bronchial SM and hyperresponsiveness of the airway without evidence of in

250 Cocaine users showed hyperresponsiveness of the amygdala and insula during fe

251 1.37-3.85; P = 0.002), but not for bronchial hyperresponsiveness or atopy.

252 TH2 immune responses and OVA-induced airway hyperresponsiveness or goblet cell hyperplasia, irrespec

253 ipients by </= 23% but did not affect airway hyperresponsiveness or IgE levels, whereas equal numbers

254 cantly associated with more severe bronchial hyperresponsiveness (P < .0001) and with current asthma

255 nly OVA Ag were sufficient to trigger airway hyperresponsiveness, prominent eosinophilic inflammation

256 FAM129A, SYNPO2) were associated with airway hyperresponsiveness (provocative concentration of methac

257 deep inspirations (DI) in modulating airway hyperresponsiveness remains poorly understood.

258 211) in order to get approved for the airway hyperresponsiveness test in Japan.

259 The airway hyperresponsiveness test with SK-1211 was conducted in a

260 The airway hyperresponsiveness test with SK-1211 was no specific co

261 re mice, causes mucous metaplasia and airway hyperresponsiveness that are associated with the expansi

262 omization, imatinib treatment reduced airway hyperresponsiveness to a greater extent than did placebo

263 ed these patients before and after bronchial hyperresponsiveness to acetylcholine (ACh) or histamine

264 ations in patients with normalized bronchial hyperresponsiveness to ACh or Hist.

265 ents with asthma having normalized bronchial hyperresponsiveness to ACh or Hist.

266 Airway hyperresponsiveness to aerosolized methacholine was meas

267 amine neuron population activity, behavioral hyperresponsiveness to amphetamine, and impairments in h

268 and cellular immunological profiles, airway hyperresponsiveness to bronchospastic stimuli, and lung

269 eased IL-21 receptor (IL-21R) expression and hyperresponsiveness to IL-21 signalling as Grail promote

270 that were exposed to Cl2 demonstrated airway hyperresponsiveness to inhaled methacholine significantl

271 aintaining normal airway tone and preventing hyperresponsiveness to innocuous allergen.

272 Induced sputum was obtained, and airway hyperresponsiveness to mannitol and fraction of exhaled

273 The GSTP1 genotype had no effect on airway hyperresponsiveness to methacholine and the reactivity t

274 f fractional exhaled nitric oxide and airway hyperresponsiveness to methacholine were not affected by

275 l and allergen-specific serum IgE, bronchial hyperresponsiveness to methacholine, forced expiratory v

276 d HDM-induced airway inflammation and airway hyperresponsiveness to methacholine.

277 aneous eosinophilic inflammation, and airway hyperresponsiveness to methacholine.

278 s in BAL and significantly attenuated airway hyperresponsiveness to methacholine.

279 ance, increased basal airway resistance, and hyperresponsiveness to methacholine.

280 c vascular tone (endothelial dysfunction and hyperresponsiveness to methoxamine) by means of an in si

281 impact on BAK1-regulated processes, such as hyperresponsiveness to pathogen-associated molecular pat

282 (-/-) mice exposed to CS exhibited bronchial hyperresponsiveness to serotonin.

283 o determine whether behavioral and autonomic hyperresponsiveness to sudden sounds in PTSD is associat

284 Chromatin decondensation and hyperresponsiveness to TCR stimulation persisted followi

285 l organs into the blood was due to selective hyperresponsiveness to the blood localizing chemokine S1

286 nus kinase 1/2 inhibitor ruxolitinib reduced hyperresponsiveness to type I and II interferons, normal

287 leading to increased inflammation and airway hyperresponsiveness upon RV infection.

288 Airway hyperresponsiveness was also associated with lower lymph

289 were higher in CysLTr1(-/-) mice and airway hyperresponsiveness was ameliorated using a granulocyte

290 challenged with aerosols to HDM, and airway hyperresponsiveness was evaluated by using plethysmograp

291 e in OVA-challenged WT mice, although airway hyperresponsiveness was greater in Stard7(+/-) recipient

292 Airway hyperresponsiveness was increased in allergen-treated ST

293 ot reduce remodeling or IL-33 levels; airway hyperresponsiveness was only partially reduced.

294 ly, chronic allergic inflammation and airway hyperresponsiveness were dependent on IL-4Ralpha-respons

295 wild-type levels, whereas eotaxin and airway hyperresponsiveness were not affected.

296 lic and eosinophilic airway inflammation and hyperresponsiveness were reduced in TLR2(-/-) and anti-T

297 hyperplasia, collagen deposition, and airway hyperresponsiveness were significantly diminished on Sem

298 infection drives parasite Ag-specific T cell hyperresponsiveness, which is characterized largely by a

299 Finally, asthma is characterized by airway hyperresponsiveness, which largely stems from airway smo

300 SLE) is marked by a Th cell-dependent B cell hyperresponsiveness, with frequent germinal center react