ライフサイエンスコーパス: hyperresponsiveness

1 distress in response to allergen and airway hyperresponsiveness.

2 terized by airway inflammation and bronchial hyperresponsiveness.

3 y targeted to mitigate the effects of airway hyperresponsiveness.

4 anced development of allergen-induced airway hyperresponsiveness.

5 tivity, increased ASM contraction and airway hyperresponsiveness.

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

7 ameliorated allergic airway inflammation and hyperresponsiveness.

8 associated with airway remodeling and airway hyperresponsiveness.

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

10 creased aeroantigen sensitization and airway hyperresponsiveness.

11 nflammation, cellular infiltrate, and airway hyperresponsiveness.

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

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

14 to uncontrolled cytokine release and immune hyperresponsiveness.

15 gene ORMDL3 leads to airway remodelling and hyperresponsiveness.

16 and MMP-1 protein associated with bronchial hyperresponsiveness.

17 s in PTSD is associated with locus coeruleus hyperresponsiveness.

18 tentially promoting sensitization and airway hyperresponsiveness.

19 sistant neutrophilic inflammation and airway hyperresponsiveness.

20 flammation, mucus hypersecretion, and airway hyperresponsiveness.

21 eosinophilia, high level of FENO, bronchial hyperresponsiveness.

22 useful in the diagnosis of bronchial airway hyperresponsiveness.

23 ibrotic mediators and contributes to airways hyperresponsiveness.

24 on, mucus metaplasia, airway remodeling, and hyperresponsiveness.

25 nflammation, tissue remodeling and bronchial hyperresponsiveness.

26 inflammation, mucous metaplasia, and airways hyperresponsiveness.

27 ich leads to mucus hypersecretion and airway hyperresponsiveness.

28 th asthma and with the severity of bronchial hyperresponsiveness.

29 rway mucus production, and attenuated airway hyperresponsiveness.

30 te-induced airway inflammation and bronchial hyperresponsiveness.

31 e binding affinity and contributes to T cell hyperresponsiveness.

32 in parasympathetic-mediated asthmatic airway hyperresponsiveness.

33 s production together with pronounced airway hyperresponsiveness.

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

35 of ORMDLs, influencing airway remodeling and hyperresponsiveness.

36 ophageal infiltration, and suppressed airway hyperresponsiveness.

37 mucus production, and development of airways hyperresponsiveness.

38 ses persistent mucous metaplasia and airways hyperresponsiveness.

39 aining neutrophil quiescence and suppressing hyperresponsiveness.

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

41 endothelial vasorelaxation capacity, but not hyperresponsiveness.

42 ergen-induced airway inflammation and airway hyperresponsiveness.

43 tion and, if appropriate, negative bronchial hyperresponsiveness.

44 ILC2 expansion, mucus metaplasia, and airway hyperresponsiveness.

45 tter lung mechanics, but unaltered bronchial hyperresponsiveness.

46 tokine production, IgE secretion, and airway hyperresponsiveness.

47 utrophilic pulmonary inflammation and airway hyperresponsiveness.

48 and exaggerated mucus metaplasia and airway hyperresponsiveness.

49 inished eosinophilic inflammation and airway hyperresponsiveness.

50 patient-related outcome measures and airways hyperresponsiveness.

51 hilia without affecting IgE levels or airway hyperresponsiveness.

52 tion of neutrophilic inflammation and airway hyperresponsiveness.

53 epithelial injury, inflammation, and airway hyperresponsiveness.

54 observation has been the increase in airway hyperresponsiveness, a characteristic of asthma, on expo

55 ed in murine asthma models attenuated airway hyperresponsiveness, a hallmark of asthma.

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

57 2-related inflammation and change in airway hyperresponsiveness after 6 weeks of fluticasone treatme

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

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

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

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

62 rgen coexposure resulted in increased airway hyperresponsiveness (AHR) and accumulation of pathogenic

63 emic application of ApoA-IV prevented airway hyperresponsiveness (AHR) and airway eosinophilia in mic

64 Airway hyperresponsiveness (AHR) and bronchial inflammation wer

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

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

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

68 We assessed airways hyperresponsiveness (AHR) and lung inflammation in germl

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

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

71 We determined airway hyperresponsiveness (AHR) and pulmonary inflammation by

72 g the 4-wk allergen challenge blunted airway hyperresponsiveness (AHR) and reduced fibronectin mRNA e

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

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

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

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

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

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

79 cholinergic neurons are mediators of airway hyperresponsiveness (AHR) in asthma, however, mechanisms

80 rrelates with airway neutrophilia and airway hyperresponsiveness (AHR) in COPD patients.

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

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

83 to inhaled allergens, which leads to airway hyperresponsiveness (AHR) to contractile stimuli and air

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

85 fat diet (HFD) for 2 weeks increases airway hyperresponsiveness (AHR) to methacholine challenge in C

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

87 mation, mRNA levels in the lungs, and airway hyperresponsiveness (AHR) were examined.

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

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

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

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

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

93 c manifestation of asthma is indirect airway hyperresponsiveness (AHR), and a prominent molecular end

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 cigarette smoke-induced inflammation, airway hyperresponsiveness, airspace enlargements, and loss of

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

112 response in the lung with features of airway hyperresponsiveness and Ag-specific type 2 airway inflam

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

114 IL-33 enhanced airway hyperresponsiveness and airway inflammation by suppressi

115 IT ameliorated airway hyperresponsiveness and airway inflammation in a chronic

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

117 ovide evidence that processes evoking airway hyperresponsiveness and airway smooth muscle thickening

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

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

120 ocyte driven disease characterized by airway hyperresponsiveness and eosinophilia.

121 kout mice, the IL-33- and OVA-induced airway hyperresponsiveness and eosinophilic airway inflammation

122 pe mice, IL-33 or OVA induced similar airway hyperresponsiveness and eosinophilic airway inflammation

123 knockout mice, IL-33 and OVA induced airway hyperresponsiveness and eosinophilic airway inflammation

124 with reduced airway mucus production, airway hyperresponsiveness and eosinophils.

125 and bronchoalveolar lavage as well as airway hyperresponsiveness and goblet cell metaplasia were eval

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

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

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

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

130 enhances CD8(+) T(C)2 cell-dependent airway hyperresponsiveness and inflammation through HIF-1alpha

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

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

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

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

135 increased disease severity including airway hyperresponsiveness and lung eosinophilia.

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

137 ase characterized by inflammation, bronchial hyperresponsiveness and narrowing of the airways.

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

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

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

141 isease characterized by airway inflammation, hyperresponsiveness and remodelling, affects over 300 mi

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

143 Airway hyperresponsiveness and serum IgE levels were compared i

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

145 airways and induced mucus metaplasia, airway hyperresponsiveness, and airway eosinophil activation.

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

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

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

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

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

151 line, particularly in those without baseline hyperresponsiveness, and exhibited immunomodulatory effe

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

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

154 h airway eosinophilia, development of airway hyperresponsiveness, and goblet cell metaplasia, without

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

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

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

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

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

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

161 er viral load, worse airway symptoms, airway hyperresponsiveness, and reductions in lung function dur

162 s were related to greater viral load, airway hyperresponsiveness, and reductions in lung function.

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

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

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

166 hanisms by which airway inflammation, airway hyperresponsiveness, and variable airflow obstruction ca

167 an indicator of airway infection and airway hyperresponsiveness as an indicator of smooth muscle dys

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

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

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

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

175 osinophilia, mucus overproduction, bronchial hyperresponsiveness (BHR), and immunogloubulin E (IgE) s

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

179 Be2 cells were essential in airway hyperresponsiveness, but not in other parameters.

180 suppression of lung inflammation and airway hyperresponsiveness, but SCIT was associated with higher

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

182 We measured airway hyperresponsiveness by using flexiVent; inflammatory ind

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

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

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

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

187 roid-unresponsive inflammation and bronchial hyperresponsiveness driven by IL-13.

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

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

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

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

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

193 24 hours, Darc(E2) mice had increased airway hyperresponsiveness; however, at 7 days airway hyperresp

194 lood, lungs, and airways and prevents airway hyperresponsiveness in a mouse eosinophilic asthma model

195 ta inhibitors prevented ILC2-mediated airway hyperresponsiveness in a mouse model of acute Alternaria

196 inhibits leucocyte diapedesis and bronchial hyperresponsiveness in a murine model of allergic lung i

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

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

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

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

201 s a new strategy for the treatment of airway hyperresponsiveness in asthma.

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

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

204 examethasone had no effects on IL-13-induced hyperresponsiveness in human bronchi, the increased Ca(2

205 2 cytokines, airway eosinophilia, and airway hyperresponsiveness in juvenile Scnn1b-Tg mice.

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

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

208 vels in bronchial fluid, and improved airway hyperresponsiveness in mice.

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

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

211 system may underlie behavioral and autonomic hyperresponsiveness in PTSD.

212 Airway hyperresponsiveness in response to methacholine was meas

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

214 4 as a novel therapeutic target for neuronal hyperresponsiveness in the airways and symptoms, such as

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

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

217 response, mucus cell hyperplasia, and airway hyperresponsiveness in vivo.

218 nflammation and the asthma surrogate, airway hyperresponsiveness, in a murine acute model of asthma.

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

220 Profoundly enhanced airway hyperresponsiveness, inflammation, and fibrosis were exc

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

222 )-X gene (Pla2g10) display attenuated airway hyperresponsiveness, innate and adaptive immune response

223 locus coeruleus system hyperactivity to PTSD hyperresponsiveness is sparse.

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

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

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

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

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

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

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

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

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

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

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

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

236 ch of the type 2 and type 17 cytokines cause hyperresponsiveness of airway smooth muscle.

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

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

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

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

241 (p < 0.001 for all) but did not alter airway hyperresponsiveness or airway remodeling.

242 1.37-3.85; P = 0.002), but not for bronchial hyperresponsiveness or atopy.

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

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

245 BP exposure in participants without baseline hyperresponsiveness (P = 0.01).

246 (p = 0.045) and increased peripheral airway hyperresponsiveness (p = 0.02), nicotine-free Banana Pud

247 We conclude that obesity leads to the airway hyperresponsiveness preventable by caloric restriction a

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

249 ual involvement in the development of airway hyperresponsiveness remains unexplored.

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

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

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

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

254 lls that can mediate airway inflammation and hyperresponsiveness through production of IL-5, IL-13 an

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

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

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

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

259 Airway hyperresponsiveness to aerosolized methacholine was meas

260 s in response to allergen and reduces airway hyperresponsiveness to bradykinin.

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

262 ve mutant HNF-1beta in mIMCD3 cells produces hyperresponsiveness to exogenous Wnt ligands, which is i

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

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

265 nd lung allergic responses, including airway hyperresponsiveness to inhaled methacholine, were assess

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

267 eficits in lung function and enhanced airway hyperresponsiveness to methacholine as compared with wil

268 s in their lung function and enhanced airway hyperresponsiveness to methacholine challenge from 11 ye

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

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

271 ast 5 years, which could be: positive airway hyperresponsiveness to methacholine, positive reversibil

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

273 aneous eosinophilic inflammation, and airway hyperresponsiveness to methacholine.

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

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

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

277 Chromatin decondensation and hyperresponsiveness to TCR stimulation persisted followi

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

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

280 Neutrophil hyperresponsiveness to type I IFNs promoted enhanced res

281 ta in mIMCD3 renal epithelial cells produces hyperresponsiveness to Wnt ligands and increases express

282 ergen-sensitized participants (9 with airway hyperresponsiveness) underwent inhaled allergen challeng

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

284 Improved airway hyperresponsiveness was also observed in mice that recei

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

286 tilated with a flexiVent setup and bronchial hyperresponsiveness was determined using acetylcholine.

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

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

289 Airway hyperresponsiveness was increased in allergen-treated ST

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

291 C2 responses, airway inflammation and airway hyperresponsiveness were examined in Balb/c mice challen

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

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

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

295 ure mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the expansi

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

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

298 to assess incremental improvement in airway hyperresponsiveness while reducing the likelihood of a c

299 ed asthma phenotype (inflammation and airway hyperresponsiveness), with increased development of T(H)

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