ライフサイエンスコーパス: airway disease

1 that specific IgE contributes to the 'united airways disease'.

2 n-induced severe, steroid-resistant allergic airway disease.

3 implicated as a modifier of cystic fibrosis airway disease.

4 thma is a widespread, multifactorial chronic airway disease.

5 s TH2-mediated allergic responses and linked airway disease.

6 and restored steroid sensitivity to allergic airway disease.

7 y to prevent development of postviral atopic airway disease.

8 sential role in neutrophil-dominant allergic airway disease.

9 he lungs and development of postviral atopic airway disease.

10 abolite for potential prevention of allergic airway disease.

11 ations, activity limitation, and evidence of airway disease.

12 gs-related lung disease, a potentially fatal airway disease.

13 t and chronic phase of experimental allergic airway disease.

14 ncept of disease-specific neurophenotypes in airway disease.

15 oach to treat multiple common pathologies of airway disease.

16 d in an HDM-induced murine model of allergic airway disease.

17 ting effects of antifungal drugs on allergic airway disease.

18 also exacerbated the development of allergic airway disease.

19 t of uricase inhibited NO2-promoted allergic airway disease.

20 n subjects and with mouse models of allergic airway disease.

21 ng in AEC regulated key features of allergic airway disease.

22 ly active alveolar-like macrophages to treat airway disease.

23 sets with unique roles in promoting allergic airway disease.

24 in mice enhance the development of allergic airway disease.

25 y reduces the manifestations of mite-induced airway disease.

26 potentially increase occurrence of allergic airway disease.

27 ndard for demonstrating cystic fibrosis (CF) airway disease.

28 irrespective of smoking behaviour and other airway disease.

29 IL-4 and IL-13 and is activated in allergic airway disease.

30 potentially contribute to initiate allergic airway disease.

31 he current unmet needs in work-related upper airway disease.

32 S in vitro and in a murine model of allergic airway disease.

33 ctor phase in the ovalbumin-induced allergic airway disease.

34 is pathway in mice with established allergic airway disease.

35 rventions might have benefit in subgroups of airway disease.

36 cellular matrix formation) in the context of airway disease.

37 ential for understanding the pathogenesis of airway disease.

38 sthma, and its activity tracks that of lower airway disease.

39 atory scans has enabled measurement of small airway disease.

40 r the host susceptible to the development of airway disease.

41 h impaired ciliary function leads to chronic airway disease.

42 ects and mice, ultimately promoting allergic airway disease.

43 ion of CFTR leads to mucus stasis and severe airway disease.

44 ions in the pathogenesis of mucoinflammatory airway disease.

45 ch Gimap5 deficiency predisposes to allergic airway disease.

46 of distal lung ventilation reflecting small-airway disease.

47 ts and NOX inhibitors in mitigating allergic airway disease.

48 eptors in the lung protects against allergic airway disease.

49 ulating airway immune responses and allergic airway diseases.

50 the health of individuals with inflammatory airway diseases.

51 ine involved in type 2 immunity and allergic airway diseases.

52 only for asthma but also for hypersecretory airway diseases.

53 lications in modeling and drug screening for airway diseases.

54 omising potential approach to treat allergic airway diseases.

55 mmation in patients with asthma and allergic airway diseases.

56 the development and aggravation of allergic airway diseases.

57 ilia, contributing to pathogenesis of fungal airway diseases.

58 oss of lung function in chronic inflammatory airway diseases.

59 ermatitis (AD), allergic conjunctivitis, and airway diseases.

60 loping immune system and initiating allergic airway diseases.

61 for mucociliary dysfunction in inflammatory airway diseases.

62 romising therapeutic intervention in chronic airway diseases.

63 utic approaches in the treatment of allergic airway diseases.

64 in CF and potentially other mucoobstructive airway diseases.

65 ce that previously developed murine allergic airway diseases.

66 ons to our understanding of asthma and other airway diseases.

67 ssociated asthma and other acute and chronic airway diseases.

68 and are linked to asthma and other reactive airway diseases.

69 e roles of MMP-12 and PAR2 in PCFs mediating airway diseases.

70 pathophysiology of asthma and other allergic airway diseases.

71 ations are increasingly affected by allergic airway diseases.

72 or therapeutic intervention in patients with airway diseases.

73 uced glycolysis and pathogenesis of allergic airways disease.

74 tibility to fungal allergen-induced allergic airways disease.

75 uced glycolysis and pathogenesis of allergic airways disease.

76 s), mainly pneumonia and chronic obstructive airways disease.

77 important implications for the treatment of airways disease.

78 aintenance of immune homeostasis in allergic airways disease.

79 patients with house dust mite (HDM)-induced airways disease.

80 tion of RSV-induced exacerbation of allergic airways disease.

81 f the OSM expressed in patients with mucosal airways disease.

82 ccur early in the development of obstructive airways disease.

83 on-CF bronchiectasis and chronic obstructive airways disease.

84 asthmatic patients and in mice with allergic airways disease.

85 a in a mast cell-dependent model of allergic airways disease.

86 t a distinct pathological process from small airways disease.

87 or the management and prevention of allergic airways disease.

88 eterogeneous effects on features of allergic airways disease.

89 Rho kinases (ROCKs) contribute to allergic airways disease.

90 linical assessment and monitoring of chronic airways diseases.

91 est of the epidemic of allergies and chronic airways diseases.

92 erance compromised in patients with allergic airway diseases?

93 ) of 614 had a history of asthma or reactive airway disease; 200 (66%) of 304 patients with a history

94 Animal models of allergic airway disease (AAD) and virus-induced AAD exacerbations

95 Asthma is an allergic airway disease (AAD) caused by aberrant immune responses

96 e in the pathogenesis of asthma and allergic airway disease (AAD).

97 sponses and have been implicated in allergic airway disease (AAD).

98 responses during the development of allergic airway disease (AAD).

99 cles (DEP) predisposed offspring to allergic airway disease (AAD, murine counterpart of human asthma)

100 -sensitive, house dust mite-induced allergic airways disease (AAD) model and a steroid-insensitive mo

101 and inflammation in mouse models of allergic airways disease (AAD), associated with induction of Foxp

102 may unravel mechanistic targets for chronic airway disease across the lifespan.

103 lt life may reflect the underlying course of airway disease activity.

104 en proposed as "treatable traits" in chronic airways disease, adding impetus to their evaluation and

105 esistance; however, their role in persistent airway diseases after RSV is unexplored.

106 ential 3 (TRPC3) channel in allergen-induced airway disease (AIAD) and its underlying signaling mecha

107 ic progress in treating cystic fibrosis (CF) airway disease, airway inflammation with associated muco

108 a, but the role of Th17 response in allergic airway disease and aging is not well understood.

109 mechanisms responsible for RSV-induced acute airway disease and associated long-term consequences rem

110 ular mechanisms underlying RSV-induced acute airway disease and associated long-term consequences rem

111 ng that precedes the development of juvenile airway disease and corroborates observations that have b

112 CT-assessed functional small airway disease and emphysema are associated with FEV1 de

113 cellular epigenome may serve as biomarker of airway disease and environmental response.

114 great progress in the understanding of upper airway disease and in its management.

115 5(OH)D concentration on outcomes of allergic airway disease and lung function at 20 to 25 years of ag

116 H]D) concentrations and outcomes of allergic airway disease and lung function in offspring with 20 to

117 nally, at age 20 years, outcomes of allergic airway disease and lung function were assessed in a subs

118 nically exposed to HDM to establish allergic airway disease and then treated with the EGFR inhibitor

119 elated conditions, inhalants for obstructive airway diseases and glucocorticoid use.

120 can help in understanding these obstructive airway diseases and provide guidance for disease managem

121 (TRAP) exposure is associated with allergic airway diseases and reduced lung function in children, b

122 genotyped in 259 Yale Center for Asthma and Airways Disease and 919 Severe Asthma Research Program s

123 anced analysis techniques to dissect (small) airways disease and emphysema were not available.

124 linked mechanistically in models of allergic airways disease and have been associated with asthma sev

125 und to be protected from developing allergic airways disease and showed a marked decrease in pathophy

126 subjects from the Yale Center for Asthma and Airways Disease and the Severe Asthma Research Program.

127 is implicated in obesity, diabetes, allergic airway disease, and altered immune function.

128 Asthma is a frequent airway disease, and asthma control determinants have bee

129 or CF (PRAGMA-CF), a quantitative measure of airway disease, and compared it with the commonly used C

130 therapeutic effects, on established allergic airway disease, and prevented the development of ovalbum

131 hydrocephalus internus, chronic destructive airway disease, and randomization of left/right body asy

132 ice, deletion of Blimp-1 in T cells worsened airway disease, and this worsening was inhibited by IL-9

133 equency is increased in chronic inflammatory airway diseases, and its role in inflammatory and immune

134 ising biomarker of corticosteroid responsive airways disease, and evaluation of this biomarker in spu

135 alter the progression of childhood allergic airways disease; and (4) propose a study design to deter

136 that the severity and character of allergic airway disease are age dependent, with a bias towards a

137 for evaluating presence and degree of small airway disease are lacking.

138 ain idea and goals of the symposium: chronic airway diseases are a major and growing health problem i

139 Severe inflammatory airway diseases are associated with inflammation that do

140 Allergic airway diseases are immune disorders associated with hei

141 microbial profiles at acute exacerbation of airways disease are reflected by the gammaProteobacteria

142 cted to induction of allergy had exacerbated airway disease as juveniles, in which exacerbated airway

143 Asthma is a chronic inflammatory airway disease associated with type 2 cytokines interleu

144 k peptides may have therapeutic potential in airway diseases associated with chronic mucous hypersecr

145 ction results related to emphysema and small airways disease, both of which were unexpectedly present

146 as a physician diagnosis of asthma, reactive airways disease, BPD exacerbation, bronchiolitis, or pne

147 irflow limitation caused by a combination of airways disease (bronchiolitis) and parenchymal destruct

148 cells are dispensable for acute OVA-induced airway disease but crucial in maintaining chronic asthma

149 protects against the development of allergic airway disease but may be overcome to induce allergic se

150 vity reactions, and association with chronic airway diseases, but also with environmental factors.

151 treatment has proven benefit in inflammatory airways diseases, but whether it leads to changes in the

152 trol alleviates NTHi-induced inflammation in airway disease by up-regulating the negative regulator o

153 crucial role in the pathogenesis of allergic airways disease by increasing IL-1beta-induced proinflam

154 ocioeconomic impact of allergies and chronic airways diseases cannot be underestimated, as they repre

155 Asthma is a chronic allergic inflammatory airway disease caused by aberrant immune responses to in

156 a mouse model of persistent and exacerbating airway disease characterized by a mixed inflammatory phe

157 Asthma is a chronic airway disease characterized by inflammation, mucus hype

158 Asthma is a heterogeneous airway disease characterized by typical symptoms in comb

159 as been on the role of these clocks in adult airway diseases, clock biology is also likely to be impo

160 stipulated that the phenotype of obstructive airway disease could be affected by sex and changes with

161 tulate cystic fibrosis-like mucoinflammatory airway disease, deficient in innate lymphoid (Il2rg knoc

162 In untreated rats, marked obliterative airway disease developed over 60 days.

163 alpha, those induced in vivo during allergic airway disease did not, possibly rendering them unrespon

164 Allergic asthma is a chronic inflammatory airway disease driven predominantly by a T(H) 2 immune r

165 In mice with established allergic airway disease, EGFR inhibition reduced levels of GM-CSF

166 the IL-1R family genes was validated in the Airway Disease Endotyping for Personalized Therapeutics

167 The Airways Disease Endotyping for Personalized Therapeutics

168 um for Research and Education in Allergy and Airway Diseases (EUFOREA) organized a multidisciplinary

169 were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmark

170 ovel quantitative measures for emphysema and airway disease, evaluation of dose reduction techniques,

171 of innate lymphoid cells (ILCs) in allergic airway disease exacerbation caused by high-fat diet (HFD

172 HFD feeding exacerbated allergic airway disease features, including humoral response, air

173 g component, referred to as functional small airways disease (fSAD).

174 e, but the association with functional small airway disease has greatest importance in mild-to-modera

175 AMs for therapeutic use in acute and chronic airway diseases has yet to be investigated.

176 arefully phenotype patients with obstructive airways diseases has been adopted by many current resear

177 russels on Precision Medicine in Allergy and Airways Diseases, hosted by MEP David Borrelli, and with

178 istance at 20 Hz (R20) is a measure of small airway disease; however, there has been limited validati

179 of human conditions associated with chronic airway diseases, hydrocephalus and infertility.

180 tal factors and immune responses in allergic airway diseases, identification of new allergens, and ri

181 During acute allergic airway disease, IL-4 deficiency did not prevent the onse

182 n contrast, TNF was dispensable for allergic airway disease in a protease-mediated model of asthma.

183 These findings may also explain the risk of airway disease in CF carriers.

184 have measured functional characteristics of airway disease in cleaners.

185 The excess risk of small airway disease in female mice after chronic smoke exposu

186 ed with significant exacerbation of allergic airway disease in mice, including an increase in epithel

187 49d to drive development of postviral atopic airway disease in mice.

188 t wild-type mice develop an eosinophilic Th2 airway disease in response to A. alternata exposure, whe

189 Famotidine treatment resulted in more severe airway disease in the OVA model, while dimaprit treatmen

190 on for the increasing prevalence of allergic airway diseases in Europe.

191 ogenesis of house dust mite-induced allergic airways disease in C57BL/6NJ mice.

192 To determine the role of DARC in allergic airways disease in mice, and the association between DAR

193 ettes, with or without nicotine, on allergic airways disease in mice.

194 allergen was assessed in a model of allergic airways disease in which treated mice were protected fro

195 Current therapeutic strategies to treat airway disease include the use of muscarinic and leukotr

196 However, reactive airways disease including asthma (1.36, 0.82-2.26) and o

197 xhibited characteristic features of allergic airway disease, including airway eosinophilia and methac

198 ent of eosinophilic inflammation in allergic airway disease, including asthma.

199 erval) than controls for incidence of: upper airway diseases, including adenotonsillitis (3.29, 2.41-

200 tic bacteria for prevention and treatment of airway diseases, including allergies.

201 Most airway diseases, including chronic obstructive pulmonary

202 Neutrophilic airway diseases, including cystic fibrosis, are characte

203 tions that characterize acquired and genetic airway diseases, including the mucus metaplasia of asthm

204 nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity

205 In a percentage of LAR subjects, the upper airway disease is also associated with lower airway symp

206 reshold gas trapping representing mild small airway disease is prevalent in normal-appearing lung reg

207 Airway disease is the major source of morbidity and mort

208 The airway epithelium in asthma and upper airway diseases is dysfunctional due to disturbed tight

209 dotypes are identified and a new taxonomy of airway diseases is generated.

210 Lower lobe-predominant small-airways disease is a major driver of clinically measured

211 isplay infertility as well as severe chronic airway disease leading to postnatal death.

212 uction is a hallmark of cystic fibrosis (CF) airway disease, leading to chronic infection, dysregulat

213 ) was used to calculate the functional small-airways disease marker PRM(fSAD) and Hounsfield unit (HU

214 ced expiratory volume in 1 second (FEV1) and airway disease measurements were not.

215 ithelial cells and an ovine model of CF-like airway disease.Methods: Losartan's antiinflammatory effe

216 nted IFN-gamma responses in the HDM allergic airway disease model were accompanied by increased disru

217 Of interest especially for allergic airway disease, mucosal germs might not just elicit a cl

218 f molecular networks underlying inflammatory airway disease needs to be translated into new therapies

219 Abnormal mPRM measurements of small airways disease (normal CT, not ventilated) and mild emp

220 fraction of abnormal voxels, including small airways disease (normal CT, not ventilated: 5% vs 6% [no

221 urine model of anti-MHC-induced obliterative airway disease (OAD), a correlate of obliterative bronch

222 trapping largely because emphysema and small airways disease occurred in different smokers.

223 CS-exposed NHPs can be used as a model of airway disease occurring in COPD patients.

224 r PMBF were independent of measures of small airways disease on CT and gas trapping largely because e

225 ased airway obstruction and functional small airways disease on quantitative chest CT.

226 wer alpha-1 antitrypsin and functional small airway disease (P = 0.007).Conclusions: In this integrat

227 of 270 with no history of asthma or reactive airway disease (p=0.0004).

228 tients with no history of asthma or reactive airway disease (p=0.039).

229 ither the "British" or "Dutch" hypotheses of airway disease pathogenesis.

230 y and the European Federation of Allergy and Airway Diseases Patients Associations in the European Pa

231 RS), the European Federations of Allergy and Airways Diseases Patients Associations (EFA), the Global

232 ar and lung function, leading to severity in airway disease phenotypes.

233 ), an important mediator in the pathology of airway disease, plays a central role in bronchoconstrict

234 clusters were identified across the combined airways disease population.

235 rs including maternal diet may predispose to airway disease, possibly by impacting on fetal airway de

236 Use of inhalants for obstructive airway diseases (PR = 0.79; 95% CI = 0.74-0.85) also dec

237 computed tomography (CT) biomarker of small airway disease predicts FEV1 decline.

238 ography metrics quantifying functional small airways disease (PRM(fSAD)) and parenchymal disease (PRM

239 e emphysema (PRM(emph)) and functional small airways disease (PRM(fSAD)), a measure of nonemphysemato

240 iven exacerbation of chronic murine allergic airway diseases remain elusive.

241 ich barrier dysfunction leads to early onset airway diseases, remain unclear.

242 atients with a history of asthma or reactive airway disease required intensive care compared with 138

243 atients with a history of asthma or reactive airway disease required ventilator support compared with

244 ion of gene- and cell-based therapies for CF airway disease requires knowledge of relationships among

245 In a mast cell model of allergic airways disease, ROCK1 and ROCK2 both contribute to AHR,

246 he pathobiology of respiratory virus-induced airway disease severity and exacerbations.

247 nduced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed an

248 bited the development of OVA-driven allergic airway disease subsequent to OVA challenge, as well as t

249 centrally involved in the pathophysiology of airway diseases such as asthma and chronic obstructive p

250 Chronic airway diseases such as asthma and chronic obstructive p

251 elivery of many therapeutics for respiratory airway diseases such as asthma, COPD, and cystic fibrosi

252 ng rehydration in patients with debilitating airway diseases such as COPD.

253 story of imminent pediatric muco-obstructive airway diseases such as cystic fibrosis remains unclear.

254 de of TIGIT suppressed hallmarks of allergic airway disease, such as lung eosinophilia, goblet cell h

255 cytokine IL-13 is a key mediator of allergic airway diseases, such as asthma, and is up-regulated in

256 exacerbating factor contributing to chronic airway diseases, such as asthma, via mechanisms that are

257 eatment strategy for mucus overproduction in airway diseases, such as childhood asthma.

258 its role in patients with evidence of other airway diseases, such as chronic obstructive pulmonary d

259 r targets to stimulate improved clearance in airway diseases, such as cystic fibrosis and chronic rhi

260 a (MCM), but their roles in mucoinflammatory airway diseases, such as cystic fibrosis, remain unknown

261 evels are elevated in patients with allergic airway diseases suggest that IL-33 plays an important ro

262 r data suggest that in patients with chronic airway diseases, TGF-beta can elevate the HIV viral rese

263 and a history of underlying asthma/reactive airway disease than patients without viremia.

264 , but there has been less on the genetics of airways disease than in previous years possibly reflecti

265 role of ceramide in mouse models of allergic airway disease that recapitulate the cardinal clinical f

266 IVIg alleviates allergic airways disease through interaction of SA-IgG with DCIR.

267 rgen mucosal sensitization model of allergic airway disease to investigate the role of alveolar macro

268 role of ORMDL3 in the generation of allergic airways disease to the fungal aeroallergen Alternaria al

269 e airway wall thickening, inflammatory small airways disease, tracheal abnormalities, interstitial lu

270 Chronic oxidative injury produced by airway disease triggers a transforming growth factor-bet

271 olytic reprogramming contributes to allergic airway disease using a murine house dust mite model.

272 ay of life 3 induced or exacerbated juvenile airway disease using an ovalbumin (OVA) allergy model of

273 role of STAT6 in Th2/Th17-mediated allergic airway disease using STAT6(-/-) mice.

274 del of chronic obstructive pulmonary disease airway disease utilizing adenoviral delivery of IL-1beta

275 e 1/3 inhibitor R507 to prevent obliterative airway disease was analyzed in preclinical airway transp

276 y disease as juveniles, in which exacerbated airway disease was defined as increased cellular infiltr

277 Allergic airway disease was induced in mice by repeated intranasa

278 Allergic airway disease was induced in wild-type, IL-10 reporter,

279 Airway disease was measured by using the CT airway wall

280 Increased sensitivity to AF-induced airway disease was not observed.

281 Allergic airways disease was assessed 24 hours and 7 days followi

282 The role of LRP-1 in modulating HDM-induced airways disease was assessed in mice with deletion of LR

283 murine model of neutrophil-dominant allergic airway disease, we demonstrate that BET inhibition limit

284 transfer studies in mouse models of allergic airway disease, we examined the effects of Act-A-iTreg c

285 By using a mouse model of allergic airway disease, we have defined in this study that s.c.

286 Both OVA and HDM-induced airway diseases were more severe in H2 R-deficient anima

287 The mechanisms by which RGMb causes airways disease were also examined.

288 of microRNAs (miRNAs) has been implicated in airway diseases where transforming growth factor-beta (T

289 ion can be the predominant cause of allergic airway diseases, whereas in other environments, polysens

290 her medical domains like allergy and chronic airway diseases, which face an urgent need to improve th

291 sputum microbiomic clusters exist in stable airways disease, which can be differentiated by the sput

292 odel of RSV-induced exacerbation of allergic airways disease, which mimics hallmark clinical features

293 e available literature on occupational upper airway disease with a focus on pathophysiological mechan

294 ssant that similarly diminished obliterative airway disease with systemic or inhaled administration.

295 drive the exacerbation of a murine allergic airway diseases with an eosinophilic phenotype.

296 0 inhibitors may be a therapeutic option for airway diseases with goblet cell metaplasia of unknown m

297 individuals with different types of chronic airway disease, with a special focus on individuals with

298 a novel therapeutic option to abate allergic airway disease without altering life-saving autonomic hy

299 Asthma is a common chronic airway disease worldwide.

300 cific regionalization of topographical small-airway disease would best account for IOS- and MBW-measu