ライフサイエンスコーパス: hyperreactivity

1 ine production, serum IgE levels, and airway hyperreactivity.

2 es of the allergic response including airway hyperreactivity.

3 ted in resolution of airway inflammation and hyperreactivity.

4 tion of neurons that are required for airway hyperreactivity.

5 ities and efficiently dampen allergic airway hyperreactivity.

6 ing pregnancy results in offspring bronchial hyperreactivity.

7 strated reversal of hypoxia-induced platelet hyperreactivity.

8 ole in influenza-induced and allergic airway hyperreactivity.

9 owth factors, thereby predisposing to airway hyperreactivity.

10 nia, bronchiolitis, bronchitis, or bronchial hyperreactivity.

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

12 atitis resulted in increased allergic airway hyperreactivity.

13 potential link between neural and endocrine hyperreactivity.

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

15 n CLE, which related significantly to airway hyperreactivity.

16 eosinophil infiltration and increased airway hyperreactivity.

17 concentrations of CXC chemokines, and airway hyperreactivity.

18 retion, Th2 cytokine production, and airways hyperreactivity.

19 stnatally, but develop emphysema and airways hyperreactivity.

20 tion and prevented the development of airway hyperreactivity.

21 histology, lung cytokine levels, and airway hyperreactivity.

22 ctivities influence functions such as airway hyperreactivity.

23 ype 2 cytokine responses and allergic airway hyperreactivity.

24 sinophilia, mucus hypersecretion, and airway hyperreactivity.

25 eased mucus production/secretion, and airway hyperreactivity.

26 ignificantly reduces inflammation and airway hyperreactivity.

27 rm expulsion, tissue inflammation, or airway hyperreactivity.

28 d mucus production, inflammation, and airway hyperreactivity.

29 way are correlated to airflow limitation and hyperreactivity.

30 nd may contribute to airway inflammation and hyperreactivity.

31 quent development of allergen-induced airway hyperreactivity.

32 flammatory cytokine responsible for platelet hyperreactivity.

33 DCs suppressed lung inflammation and airway hyperreactivity.

34 y a significant role in determining platelet hyperreactivity.

35 ulmonary eosinophil accumulation, and airway hyperreactivity.

36 o allergic pulmonary inflammation and airway hyperreactivity.

37 d ORMDL3 overexpression are linked to airway hyperreactivity.

38 gic airway inflammation and had no bronchial hyperreactivity.

39 ukin-13 and interleukin-5 levels, and airway hyperreactivity.

40 cient mice did not experience AAI and airway hyperreactivity.

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

42 induces neutrophilic airway inflammation and hyperreactivity.

43 hich largely stems from airway smooth muscle hyperreactivity.

44 , subepithelial fibrosis and enhanced airway hyperreactivity.

45 zation to environmental allergens and airway hyperreactivity.

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

47 n of allergic airway inflammation and airway hyperreactivity.

48 ernatively activated macrophages, and airway hyperreactivity.

49 naling and its genetic knockdown resulted in hyperreactivity.

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

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

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

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

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

55 rrant parasympathetic innervation and airway hyperreactivity after postnatal reinfection.

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

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

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

59 ory effects of CpG A in IL-33-induced airway hyperreactivity (AHR) and airway inflammation.

60 nflammatory disorder characterized by airway hyperreactivity (AHR) and driven by T(H)2 cytokine produ

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

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

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

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

65 he influence of regulatory B cells on airway hyperreactivity (AHR) and remodeling in asthma is poorly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 examined for airway inflammation and airway hyperreactivity (AHR), a cardinal feature of asthma.

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

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

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

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

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

92 cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia rem

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

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

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

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

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

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

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

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

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

102 ce as adults against allergen-induced airway hyperreactivity (AHR).

103 ading chronic disease associated with airway hyperreactivity (AHR).

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

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

106 Bronchial hyperreactivity, airway inflammation, and sensitization

107 Platelet hyperreactivity and accelerated thrombosis, specifically

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

109 epresents the confluence of bronchial airway hyperreactivity and chronic airflow limitation and has b

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

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

112 he ability of induced Treg to control airway hyperreactivity and effector functions of lung T cells w

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

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

115 tterite homes significantly inhibited airway hyperreactivity and eosinophilia.

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

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

118 Preterm infants can develop airway hyperreactivity and impaired bronchodilation following s

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

120 mmation promotes the development of platelet hyperreactivity and increases thrombotic risk during agi

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

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

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

124 cheally before Ag challenge mitigated airway hyperreactivity and inflammation.

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

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

127 Induction of airway hyperreactivity and lung inflammation increased lung CD1

128 hallenged with IL-33 and assessed for airway hyperreactivity and lung inflammation.

129 s 13-15) followed by determination of airway hyperreactivity and lung T cell effector functions.

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

131 enged Apoe(-/-) mice display enhanced airway hyperreactivity and mucous cell metaplasia.

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

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

134 ith imatinib significantly attenuated airway hyperreactivity and peribronchial eosinophil accumulatio

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

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

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

138 Further, this subset dampens airway hyperreactivity and significantly reduces lung inflammat

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

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

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

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

143 e marrow niche and aging-associated platelet hyperreactivity and thrombosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 transfer to mice, and measurement of airway hyperreactivity by Flexivent.

173 Emotional hyperreactivity can inhibit maternal responsiveness in f

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

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

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

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

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

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

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

181 This hyperreactivity correlated with decreased frequency of a

182 This hyperreactivity corresponds to dramatically elevated num

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

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

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

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

187 the development of ovalbumin-induced airway hyperreactivity, eosinophilia, and goblet cell metaplasi

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

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

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

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

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

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

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

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

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

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

198 ed neurotrophic factor contributes to airway hyperreactivity in a mouse model of allergic asthma.

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

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

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

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

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

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

205 ng of IFN-gamma activity, exacerbates airway hyperreactivity in allergen-challenged mice, providing e

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

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

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

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

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

211 antibody and reduces allergen-induced airway hyperreactivity in mice.

212 stablished a causative link between platelet hyperreactivity in old mice and increased systemic level

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

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

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

216 bjects, patients with AUD showed significant hyperreactivity in the ventromedial prefrontal cortex (v

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

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

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

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

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

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

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

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

225 We further showed that platelet hyperreactivity is neutralized by abrogating signaling t

226 Platelet hyperreactivity leading to thrombosis is the main reason

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

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

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

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

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

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

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

234 nelrhodopsin dramatically exacerbates airway hyperreactivity of inflamed airways.

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

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

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

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

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

240 nergic activation pattern and cardiac stress hyperreactivity only in black participants.

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

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

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

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

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

246 Airway hyperreactivity, recruitment of infiltrating cells, and

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

248 4/IL-13 for allergic inflammation and airway hyperreactivity remains unclear.

249 ge and monitored by mini endoscopy or airway hyperreactivity, respectively.

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

251 hat allergen sensitization and severe airway hyperreactivity subsequently occurred.

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

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

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

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

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

257 11-19 weeks' gestation had greater bronchial hyperreactivity than those with more rapid abdominal gro

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

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

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

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

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

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

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

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

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

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

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

269 Airway hyperreactivity to methacholine observed on Day 73 in OV

270 Unexpectedly, airway hyperreactivity to methacholine was essentially ablated

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

272 nophils, and MCTR3 potently decreased airway hyperreactivity to methacholine, bronchoalveolar lavage

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

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

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

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

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

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

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

280 Vascular hyperreactivity was blunted in the presence of a nitric

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

282 CF platelet hyperreactivity was incompletely inhibited by prostaglan

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

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

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

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

287 gen-induced IgE-dependent colitis and airway hyperreactivity were also enhanced in ATI-fed mice.

288 synthesis, airway remodeling, and bronchial hyperreactivity were measured.

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

290 ns expressed type 2 genes and induced airway hyperreactivity when adoptively transferred to mice.

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

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

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

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

295 -CoV-2 infection is associated with platelet hyperreactivity, which may contribute to COVID-19 pathop

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