ライフサイエンスコーパス: hyperreactivity

1 cient mice did not experience AAI and airway hyperreactivity.

2 owth factors, thereby predisposing to airway hyperreactivity.

3 hallenged with IL-33 and assessed for airway hyperreactivity.

4 ol, demographics, and pre-treatment platelet hyperreactivity.

5 atitis resulted in increased allergic airway hyperreactivity.

6 potential link between neural and endocrine hyperreactivity.

7 ith AGE-CD36-mediated platelet signaling and hyperreactivity.

8 n CLE, which related significantly to airway hyperreactivity.

9 concentrations of CXC chemokines, and airway hyperreactivity.

10 retion, Th2 cytokine production, and airways hyperreactivity.

11 stnatally, but develop emphysema and airways hyperreactivity.

12 tion and prevented the development of airway hyperreactivity.

13 ctivities influence functions such as airway hyperreactivity.

14 sinophilia, mucus hypersecretion, and airway hyperreactivity.

15 eased mucus production/secretion, and airway hyperreactivity.

16 ignificantly reduces inflammation and airway hyperreactivity.

17 induces neutrophilic airway inflammation and hyperreactivity.

18 rm expulsion, tissue inflammation, or airway hyperreactivity.

19 hich largely stems from airway smooth muscle hyperreactivity.

20 d mucus production, inflammation, and airway hyperreactivity.

21 way are correlated to airflow limitation and hyperreactivity.

22 , subepithelial fibrosis and enhanced airway hyperreactivity.

23 nd may contribute to airway inflammation and hyperreactivity.

24 quent development of allergen-induced airway hyperreactivity.

25 DCs suppressed lung inflammation and airway hyperreactivity.

26 ulmonary eosinophil accumulation, and airway hyperreactivity.

27 o allergic pulmonary inflammation and airway hyperreactivity.

28 nduced peribronchial inflammation and airway hyperreactivity.

29 ad no effect on the development of bronchial hyperreactivity.

30 ed pulmonary B and T lymphocytes, and airway hyperreactivity.

31 which were associated with increased airway hyperreactivity.

32 nduced peribronchial inflammation and airway hyperreactivity.

33 zation to environmental allergens and airway hyperreactivity.

34 ght have a role in the development of airway hyperreactivity.

35 n of allergic airway inflammation and airway hyperreactivity.

36 ernatively activated macrophages, and airway hyperreactivity.

37 naling and its genetic knockdown resulted in hyperreactivity.

38 es of the allergic response including airway hyperreactivity.

39 ted in resolution of airway inflammation and hyperreactivity.

40 tion of neurons that are required for airway hyperreactivity.

41 ities and efficiently dampen allergic airway hyperreactivity.

42 ing pregnancy results in offspring bronchial hyperreactivity.

43 strated reversal of hypoxia-induced platelet hyperreactivity.

44 ole in influenza-induced and allergic airway hyperreactivity.

45 In highly exposed subjects, hyperreactivity 1 or 3 months post-collapse was the sole

46 deal PFT should: 1) detect baseline platelet hyperreactivity; 2) allow individualization of antiplate

47 acity to induce lung inflammation and airway hyperreactivity, a cardinal asthma feature.

48 KT cells and unexpectedly resulted in airway hyperreactivity, a cardinal feature of asthma, in an NKT

49 ations of sickle cell disease include airway hyperreactivity, acute chest syndrome, chronic sickle lu

50 persistent mucous cell metaplasia and airway hyperreactivity after clearance of replicating virus, we

51 rrant parasympathetic innervation and airway hyperreactivity after postnatal reinfection.

52 sed inflammation, a high incidence of airway hyperreactivity (AH), and increased circulating leukotri

53 esized that hyaluronan contributes to airway hyperreactivity (AHR) after exposure to ambient ozone.

54 , T-bet(-/-) mice develop spontaneous airway hyperreactivity (AHR) and airway inflammation.

55 tory disorder that is associated with airway hyperreactivity (AHR) and driven by Th2 cytokine secreti

56 antly attenuated airway inflammation, airway hyperreactivity (AHR) and goblet cell hyperplasia.

57 ating ILC2 function and ILC2-mediated airway hyperreactivity (AHR) and lung inflammation.

58 mice showed significant decreases in airway hyperreactivity (AHR) and peribronchial eosinophils comp

59 rtness of breath, and coughing due to airway hyperreactivity (AHR) and reversible airway obstruction.

60 develop in vivo in a model of chronic airway hyperreactivity (AHR) and what factors control this deve

61 n, MOL 294 on airway inflammation and airway hyperreactivity (AHR) in a mouse model of asthma.

62 y a critical role in the induction of airway hyperreactivity (AHR) in animal models and are associate

63 n induced significant dose-responsive airway hyperreactivity (AHR) in BALB/c mice at days 6 and 9 aft

64 e (ASM) axis that underlies prolonged airway hyperreactivity (AHR) in mice.

65 ppaB p65 and p50 subunits, as well as airway hyperreactivity (AHR) in nonallergic mice.

66 e period reduced methacholine-induced airway hyperreactivity (AHR) in OVA- and HDM-sensitized mice (4

67 Airway hyperreactivity (AHR) is a key feature of bronchial asth

68 The impact of airway hyperreactivity (AHR) on respiratory mortality and syste

69 s in a failure of mice to generate an airway hyperreactivity (AHR) response on both the BALB/c and C5

70 gic inflammation that is required for airway hyperreactivity (AHR) to methacholine (MCh).

71 ratios, airway obstruction (AO), and airway hyperreactivity (AHR) were significantly increased in mi

72 m of nonallergic asthma that leads to airway hyperreactivity (AHR), a cardinal feature of asthma inde

73 lls are required for the induction of airway hyperreactivity (AHR), a cardinal feature of asthma, but

74 e, we show here that allergen-induced airway hyperreactivity (AHR), a cardinal feature of asthma, doe

75 is sufficient for the development of airway hyperreactivity (AHR), a cardinal feature of asthma, in

76 The development of airway hyperreactivity (AHR), a cardinal feature of asthma, req

77 pendent conditions that might lead to airway hyperreactivity (AHR), a cardinal feature of asthma.

78 ce as adults against allergen-induced airway hyperreactivity (AHR), a cardinal feature of asthma.

79 d IL-13, which cause eosinophilia and airway hyperreactivity (AHR), a cardinal feature of asthma.

80 ted in obesity and the development of airway hyperreactivity (AHR), a cardinal feature of asthma.

81 f asthma, including mucus metaplasia, airway hyperreactivity (AHR), and airway inflammation.

82 ne exposure for air pollution-induced airway hyperreactivity (AHR), and ovalbumin (OVA)-induced aller

83 ation and by a central feature called airway hyperreactivity (AHR), development of which requires the

84 Airway hyperreactivity (AHR), IgE, inflammatory cells, cytokine

85 asthma, including IgE, goblet cells, airway hyperreactivity (AHR), inflammatory cells, cytokines/che

86 Airway hyperreactivity (AHR), lung inflammation, and atopy are

87 -driven inflammation but also reduced airway hyperreactivity (AHR), mucus hypersecretion, and fibrosi

88 cells to OVA-sensitized mice reduced airway hyperreactivity (AHR), recruitment of eosinophils, and T

89 a, it is nevertheless associated with airway hyperreactivity (AHR), which is a cardinal feature of as

90 g cells to investigate their role in airways hyperreactivity (AHR).

91 ecruitment of inflammatory cells, and airway hyperreactivity (AHR).

92 to assess airway obstruction (AO) and airway hyperreactivity (AHR).

93 esponses, pulmonary inflammation, and airway hyperreactivity (AHR).

94 ) innervation (P<0.05) and persistent airway hyperreactivity (AHR).

95 This disease is characterized by airway hyperreactivity (AHR, defined by exaggerated airflow obs

96 gen challenge significantly increased airway hyperreactivity, airway eosinophil accumulation, and IL-

97 gen-specific IgG1 and IgE antibodies, airway hyperreactivity, airway inflammation and airway remodell

98 Bronchial hyperreactivity, airway inflammation, and sensitization

99 ic pulmonary disease characterized by airway hyperreactivity, airway obstruction, and histologic infl

100 r the collapse that would predict persistent hyperreactivity and a diagnosis of reactive airways dysf

101 Platelet hyperreactivity and accelerated thrombosis, specifically

102 otides can attenuate the magnitude of airway hyperreactivity and airways remodeling produced in nonhu

103 viruses cause both acute airway inflammation/hyperreactivity and chronic airway remodeling/hyperreact

104 n but not alone, resulting in reduced airway hyperreactivity and collagen deposition.

105 t of allergen- and rhinovirus-induced airway hyperreactivity and decreased eosinophil recruitment to

106 verall inflammation, and their relation with hyperreactivity and emphysema type in COPD.

107 xide (TMAO), directly contribute to platelet hyperreactivity and enhanced thrombosis potential.

108 tterite homes significantly inhibited airway hyperreactivity and eosinophilia.

109 nction impairment and increases in bronchial hyperreactivity and eosinophilic lower airway inflammati

110 tive when tested orally in LPS-evoked airway hyperreactivity and fully confirmed the working hypothes

111 also triggers a chronic response with airway hyperreactivity and goblet cell hyperplasia lasting at l

112 al inflammation, post-AAI mice had bronchial hyperreactivity and increased inflammatory cell influx w

113 uch reversal was established in which airway hyperreactivity and inflammation in ovalbumin-sensitized

114 ggesting that reductions in allergen-induced hyperreactivity and inflammation in pendrin-deficient mi

115 icient mice had less allergen-induced airway hyperreactivity and inflammation than did control mice,

116 cheally before Ag challenge mitigated airway hyperreactivity and inflammation.

117 the increased susceptibility to RSV-induced hyperreactivity and inflammation.

118 h IPEX and also in scurfy mice, T cells show hyperreactivity and levels of Th1- and Th2-associated cy

119 Induction of airway hyperreactivity and lung inflammation increased lung CD1

120 T cells are not necessary for virus-induced hyperreactivity and M2R dysfunction in nonsensitized gui

121 Thus, CD8+ T cells play a role in airway hyperreactivity and M2R dysfunction of sensitized virus-

122 novel innate pathway that results in airway hyperreactivity and may help to explain how TIM-1 and NK

123 a1 was essential for allergen-induced airway hyperreactivity and mucus hypersecretion but not for fib

124 levels and mitigated airway inflammation and hyperreactivity and mucus hypersecretion in house dust m

125 ith imatinib significantly attenuated airway hyperreactivity and peribronchial eosinophil accumulatio

126 gnificantly reducing allergen-induced airway hyperreactivity and peribronchial eosinophilic inflammat

127 n conclusion, development and persistence of hyperreactivity and reactive airways dysfunction were st

128 a, they were redundant in maintaining airway hyperreactivity and remodeling.

129 athway, causes unprovoked spontaneous airway hyperreactivity and severe neutrophilic lung inflammatio

130 strong association between asthma and airway hyperreactivity and sickle cell disease, as well as a li

131 ptide, which together contribute to platelet hyperreactivity and stroke complications.

132 cient for CCR1, we observed decreased airway hyperreactivity and Th2 cytokine production from CD4(+)

133 and cigarette smoke (SS) exacerbates airways hyperreactivity and Th2 responses in the lung.

134 tion and that this contributes to the airway hyperreactivity and Th2-type inflammation seen in this m

135 eveal that TLR2 plays a key role in platelet hyperreactivity and the prothrombotic state in the setti

136 of these tests can reliably detect platelet hyperreactivity and thus identify a prothrombotic state.

137 ow variability (dPFV, an indicator of airway hyperreactivity) and indoor particulate matter (PM) PM2.

138 ncreased sensitivity to airway constriction (hyperreactivity) and is associated with exacerbations.

139 t IL-6 mediates the thrombocytosis, platelet hyperreactivity, and accelerated thrombus development as

140 athophysiology: airway epithelial damage and hyperreactivity, and airway remodeling including smooth

141 th objective outcomes (lung function, airway hyperreactivity, and atopy), asthma medication, and seve

142 mmation, epithelial cell hyperplasia, airway hyperreactivity, and diminished blood oxygen saturation.

143 s promote IgE-mediated sensitization, airway hyperreactivity, and eosinophilia.

144 eotaxin production, eosinophilia, bronchial hyperreactivity, and goblet cell hyperplasia in the airw

145 ergen-induced airway eosinophilia, bronchial hyperreactivity, and in vitro allergen-recall Th2 respon

146 chronic symptoms were predicted by amygdala hyperreactivity, and poor recovery was predicted by a fa

147 ted to lower respiratory symptoms, bronchial hyperreactivity, and reductions in blood total and CD8(+

148 eduction of pulmonary arterial inflammation, hyperreactivity, and remodeling.

149 liferation and migration, pulmonary arterial hyperreactivity, and secretion of proinflammatory cytoki

150 tion, Prdx1(-/-) platelets showed no sign of hyperreactivity, and their aggregation both in vitro and

151 The hyperreactivity appeared to be a feature of mature T cel

152 Because AC and airway hyperreactivity are allergic diseases of mucosal tissues

153 The mechanisms leading to platelet hyperreactivity are complex and not yet fully understood

154 Thrombocytosis and platelet hyperreactivity are known to be associated with malignan

155 Allergic airway inflammation and hyperreactivity are modulated by gammadelta T cells, but

156 y inflammation, mucus production, and airway hyperreactivity are the major contributors to the freque

157 h as reduced hippocampal volume and amygdala hyperreactivity, are more consistently observed in maltr

158 the mechanism underlying the reversal of the hyperreactivity as active suppression, but did not affec

159 time of allergen challenge increased airway hyperreactivity as well as airway eosinophil accumulatio

160 fe, and airway inflammation, remodeling, and hyperreactivity assessed.

161 In FDNY rescue workers, we found persistent hyperreactivity associated with exposure intensity, inde

162 Hyperreactivity at 1, 3, and 6 months post-collapse was

163 bles and the prevalence of asthma, bronchial hyperreactivity (BHR), flexural eczema (FE), allergic rh

164 tion phase was sufficient to suppress airway hyperreactivity, bronchiolar inflammatory infiltrate and

165 pensatory event mitigating against bronchial hyperreactivity, but a mechanism that evokes beta-agonis

166 l peanut sensitization prime mice for airway hyperreactivity, but the initial mucosal route of sensit

167 Emotional hyperreactivity can inhibit maternal responsiveness in f

168 On-treatment platelet hyperreactivity cannot be considered as a risk factor re

169 s of GM-CSF and TNF-alpha, as well as airway hyperreactivity, cellular inflammation, smooth muscle th

170 lp transgene induced airway inflammation and hyperreactivity characterized by T helper type 2 cytokin

171 Asthma is characterized by airway hyperreactivity, chronic inflammation, and airway wall r

172 As adults, these mice showed enhanced airway hyperreactivity, chronic pulmonary inflammation, and dif

173 ety disorder is thought to involve emotional hyperreactivity, cognitive distortions, and ineffective

174 also had the greatest airway obstruction and hyperreactivity compared with the TH2(predominant) and T

175 This hyperreactivity correlated with decreased frequency of a

176 inflammation, and the severity of the airway hyperreactivity correlates with the degree of inflammati

177 This hyperreactivity corresponds to dramatically elevated num

178 OVA-immunized and OVA-challenged OVA airway hyperreactivity-diseased littermates 24 h after intraper

179 bitofrontal volume, amygdala and hippocampus hyperreactivity during aversive recall, and impaired cin

180 d markedly decreased allergen-induced airway hyperreactivity, eosinophil infiltration, and production

181 h AAL(S) abolished rhinovirus-induced airway hyperreactivity, eosinophil influx, and CCL11, CCL20, an

182 perimental allergic asthma, including airway hyperreactivity, eosinophilic airway inflammation, mucus

183 Allergic conjunctivitis (AC) and airway hyperreactivity exacerbate corneal allograft rejection.

184 ice in Southwest Asia should focus on airway hyperreactivity from exposures to higher levels of ambie

185 te, eosinophilia, serum anti-OVA IgE, airway hyperreactivity, goblet cell hyperplasia, and phosphoryl

186 rgen-specific IgE, lung inflammation, airway hyperreactivity, goblet cell metaplasia, Th2/Th17 cytoki

187 elated variables that contribute to platelet hyperreactivity-high blood glucose, oxidative stress, an

188 xposure to ozone resulted in enhanced airway hyperreactivity, higher concentrations of both total pro

189 l mice showed normal allergen-induced airway hyperreactivity, immunoglobulin E production, mucus meta

190 ing of 5-HTTLPR short allele-driven amygdala hyperreactivity in a large independent cohort of healthy

191 irway smooth muscle alterations, and airways hyperreactivity in a memory CD4(+) T cell-dependent mann

192 ach allergen-induced inflammation and airway hyperreactivity in a mouse model of asthma.

193 ceptor M3 prevents the progression of airway hyperreactivity in a mouse model of childhood asthma.

194 of airways, mucus production, and bronchial hyperreactivity in a mouse model.

195 d airway resistance and airway smooth muscle hyperreactivity in a murine model of asthma.

196 onstrated to prevent inflammation and airway hyperreactivity in a murine model of asthma.

197 reduced airway resistance and smooth muscle hyperreactivity in a murine model of asthma.

198 peribronchial fibrosis, resulting in airway hyperreactivity in adult mice.

199 response that drives airway inflammation and hyperreactivity in allergic asthma.

200 m patients with OSA induced ex vivo vascular hyperreactivity in aortas with functional endothelium bu

201 attenuated pulmonary inflammation and airway hyperreactivity in BALB/c recipient mice in response to

202 MCs, and their contributions to the vascular hyperreactivity in CHPH.

203 f mucous cell metaplasia and possibly airway hyperreactivity in experimental models and in humans.

204 and the prevalence and severity of bronchial hyperreactivity in firefighters without severe cough cla

205 t contributes to mucus production and airway hyperreactivity in our model of RSV infection.

206 xploited to investigate the role of platelet hyperreactivity in plaque development.

207 cations of the diagnosis of bronchial airway hyperreactivity in subjects who do not have clinically a

208 usly been found to exhibit hyperactivity and hyperreactivity in terms of ROS production in chronic pe

209 were unable to mount airway inflammation and hyperreactivity in two different models of asthma, acute

210 Thus, these procedures model emotional hyperreactivity, including enhanced contextual fear and

211 Having airway hyperreactivity increased the risk of rapid decline in F

212 Previous studies using OVA-induced airway hyperreactivity indicated that P-selectin, a member of t

213 id not impact systemic T-cell activation and hyperreactivity, indicating that autoantibody production

214 ther hand, was associated with resistance to hyperreactivity induced by increased platelet cholestero

215 oxide dismutase mimetic reduced the vascular hyperreactivity induced by MPs from patients with OSA bu

216 thma has multiple features, including airway hyperreactivity, inflammation and remodelling.

217 ce of developmental programming on bronchial hyperreactivity is investigated in an animal model and e

218 Platelet hyperreactivity leading to thrombosis is the main reason

219 Thus, AGE-CD36-mediated platelet hyperreactivity may play an important role in the increa

220 ts of fetal growth were related to bronchial hyperreactivity, measured at age six years using methach

221 on the persistence of nonspecific bronchial hyperreactivity (methacholine PC20 < or =8 mg/mL) in a r

222 gand (Dll)-4, significantly decreased airway hyperreactivity, mucus production, and Th2 cytokines.

223 and lung, and prevented eosinophilia, airway hyperreactivity, mucus secretion, and Th2 cyto-kine prod

224 e association between the reduction in nasal hyperreactivity (NHR) and response to capsaicin treatmen

225 ells demonstrated that NT4 was necessary for hyperreactivity of ASM induced by early-life OVA exposur

226 The sensory hyperreactivity of fragile X can be reproduced in fmr-1

227 nelrhodopsin dramatically exacerbates airway hyperreactivity of inflamed airways.

228 rons, contributing to chronic stress-induced hyperreactivity of stress effector systems in the brain.

229 resents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis, suggesting an ex

230 Although early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS)

231 The hyperreactivity of Twf2a(-/-) platelets was attributed t

232 d nasally sensitized mice experienced airway hyperreactivity on nasal peanut challenge.

233 nflammation, and, importantly, marked airway hyperreactivity only when allergen exposure occurred dur

234 lution of airway inflammation but not airway hyperreactivity or remodeling.

235 n the development of allergen-induced airway hyperreactivity, our results strongly suggest that CD4+

236 02), airway hypersensitivity (p < 0.001) and hyperreactivity (p < 0.05) to methacholine, BAL (p < 0.0

237 nfidence interval, 1.8-25.2; p = 0.004), and hyperreactivity persisted in 55% of those hyperreactive

238 Our results show that the airway hyperreactivity phenotype can be physiologically dissoci

239 yperreactivity and chronic airway remodeling/hyperreactivity phenotypes (the latter by a hit-and-run

240 ysfunction seems to be associated with vagal hyperreactivity rather than vagal hypofunction.

241 ted that complement contributes to bronchial hyperreactivity, recruitment of airway eosinophils, IL-4

242 Airway hyperreactivity, recruitment of infiltrating cells, and

243 zation of CXCR2 resulted in decreased airway hyperreactivity relative to the RSV-infected controls.

244 4/IL-13 for allergic inflammation and airway hyperreactivity remains unclear.

245 al activities including regulation of airway hyperreactivity, resistance to nematode parasites, and t

246 emodeling changes did not resolve and airway hyperreactivity resolved only partly.

247 Thus, we propose that later airway hyperreactivity results from selective retention of alle

248 Hyperreactivity shortly post-collapse predicted reactive

249 hat allergen sensitization and severe airway hyperreactivity subsequently occurred.

250 erated from a mouse model of allergic airway hyperreactivity suggests that disordered coagulation and

251 Conversely, airway hyperreactivity, suppressed as a result of long-term all

252 umin-induced allergic airway disease, airway hyperreactivity, T(H)2 responses, mucus hypersecretion,

253 NO, sputum induction combined with bronchial hyperreactivity testing, and exhaled breath condensate c

254 ays a more important in vivo role in airways hyperreactivity than IL-25.

255 11-19 weeks' gestation had greater bronchial hyperreactivity than those with more rapid abdominal gro

256 hanisms of postviral airway inflammation and hyperreactivity that have been proposed to explain the e

257 ipidemia associated with it lead to platelet hyperreactivity that was mechanistically linked to incre

258 A (6 weeks) produced airway inflammation and hyperreactivity that were similar to acute (10 days) res

259 than being associated with general emotional hyperreactivity, this disorder may be due to dysfunction

260 xposure causes detrimental effects on airway hyperreactivity through microRNA-342-3p-mediated upregul

261 Sephadex instillation also induced airway hyperreactivity to acetylcholine and bradykinin.

262 s lung inflammation, airway obstruction, and hyperreactivity to allergen in a mouse model of allergic

263 Vessels from the HL group demonstrated hyperreactivity to angiotensin II that could not be corr

264 lls could, in part, account for their unique hyperreactivity to antigen, which contributes to acceler

265 tion, and almost completely abolished airway hyperreactivity to contractile stimuli.

266 roasthmatic phenotypes of enhanced bronchial hyperreactivity to contraction mediated by M(3)-muscarin

267 atory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often t

268 atients demonstrated some evidence of airway hyperreactivity to include eight who met asthma criteria

269 to bronchoalveolar lavage and induced airway hyperreactivity to inhaled methacholine.

270 ay epithelial mucin production and bronchial hyperreactivity to methacholine challenge.

271 Airway hyperreactivity to methacholine observed on Day 73 in OV

272 as increased collagen deposition and airway hyperreactivity to methacholine were all clearly sensiti

273 diators, and more rapid resolution of airway hyperreactivity to methacholine.

274 tion, airway remodeling, or increased airway hyperreactivity to methacholine.

275 HDM-exposed mice demonstrated severe airway hyperreactivity to methacholine.

276 can attenuate inflammation and revert airway hyperreactivity to normal responsiveness.

277 e susceptible El mice exhibit a multifaceted hyperreactivity to noxious environmental stimuli.

278 oups, administration of Y-27632 reverted the hyperreactivity to vasopressin.

279 late to the tear dysfunction and nonspecific hyperreactivity typical of these patients.

280 ic pathways predisposing to postnatal airway hyperreactivity upon reinfection with the virus.

281 o that in MpP mice (P = 0.048), while airway hyperreactivity was also elevated in MpIL12 mice but did

282 Vascular hyperreactivity was blunted in the presence of a nitric

283 peutic response evaluation scores, and nasal hyperreactivity was evaluated by means of cold dry air p

284 CF platelet hyperreactivity was incompletely inhibited by prostaglan

285 nal study were to (1) determine if bronchial hyperreactivity was present, persistent, and independent

286 Interestingly, airway hyperreactivity was significantly decreased at early tim

287 ing multicolor flow cytometry, and bronchial hyperreactivity was studied.

288 r the development of allergen-induced airway hyperreactivity, we hypothesized that natural killer T c

289 cells during experimental OVA-induced airway hyperreactivity, we injected 10(7 64)Cu-OVA-Th1 cells in

290 elial fibrosis, mucus metaplasia, and airway-hyperreactivity were also attenuated by VE-cadherin bloc

291 ewise, T-cell cytokine content and bronchial hyperreactivity were reduced.

292 layer, increased mucus, and increased airway hyperreactivity which was significantly enhanced by coex

293 l tobacco smoking was associated with airway hyperreactivity, which could contribute to lower airway

294 In vivo, asperamide B rapidly induced airway hyperreactivity, which is a cardinal feature of asthma,

295 RATIONALE: Platelet hyperreactivity, which is common in many pathological co

296 s mellitus has been associated with platelet hyperreactivity, which plays a central role in the hyper

297 phil influx in the lung along with bronchial hyperreactivity, which were reversed by IL-17 blockade.

298 Allergic asthma is a T(H)2-promoted hyperreactivity with an immediate, IgE, and mast cell-de

299 om patients with OSA induce ex vivo vascular hyperreactivity with the obligatory role of the endothel

300 irway challenge significantly reduced airway hyperreactivity, with a concomitant decrease in eosinoph