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 of distal lung ventilation reflecting small-airway disease.

3 ncept of disease-specific neurophenotypes in airway disease.

4 oach to treat multiple common pathologies of airway disease.

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

6 eptors in the lung protects against allergic airway disease.

7 ting effects of antifungal drugs on allergic airway disease.

8 also exacerbated the development of allergic airway disease.

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

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

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

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

13 in mice enhance the development of allergic airway disease.

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

15 potentially increase occurrence of allergic airway disease.

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

17 irrespective of smoking behaviour and other airway disease.

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

19 potentially contribute to initiate allergic airway disease.

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

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

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

23 H2 inflammation and exacerbation of allergic airway disease.

24 t defense mechanisms and the pathogenesis of airway disease.

25 ng sepsis, metabolic disease, arthritis, and airway disease.

26 ection and inflammation that characterize CF airway disease.

27 y syncytial virus (RSV)-exacerbated allergic airway disease.

28 c target for reducing the severity of distal airway disease.

29 mplifying viral exacerbation during allergic airway disease.

30 y and thus may have clinical applications in airway disease.

31 had no effect on the development of allergic airway disease.

32 d inflammation in a murine model of allergic airway disease.

33 th AERD, especially for the control of upper airway disease.

34 when developing inhaled treatments for small airway disease.

35 implicated as a modifier of cystic fibrosis airway disease.

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

37 and restored steroid sensitivity to allergic airway disease.

38 y to prevent development of postviral atopic airway disease.

39 sential role in neutrophil-dominant allergic airway disease.

40 he lungs and development of postviral atopic airway disease.

41 abolite for potential prevention of allergic airway disease.

42 ts and NOX inhibitors in mitigating allergic airway disease.

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

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

45 t and chronic phase of experimental allergic airway disease.

46 the development and aggravation of allergic airway diseases.

47 ilia, contributing to pathogenesis of fungal airway diseases.

48 oss of lung function in chronic inflammatory airway diseases.

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

50 loping immune system and initiating allergic airway diseases.

51 for mucociliary dysfunction in inflammatory airway diseases.

52 romising therapeutic intervention in chronic airway diseases.

53 utic approaches in the treatment of allergic airway diseases.

54 in CF and potentially other mucoobstructive airway diseases.

55 ce that previously developed murine allergic airway diseases.

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

57 ssociated asthma and other acute and chronic airway diseases.

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

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

60 pathophysiology of asthma and other allergic airway diseases.

61 ations are increasingly affected by allergic airway diseases.

62 rways, resulting in asthma and other chronic airway diseases.

63 ulating airway immune responses and allergic airway diseases.

64 ection is a leading cause of exacerbation of airway diseases.

65 o anti-eosinophil therapies in patients with airway diseases.

66 ifferent prognosis in these two neutrophilic airway diseases.

67 immunity could be impaired in chronic upper airway diseases.

68 the health of individuals with inflammatory airway diseases.

69 sociation of rhinovirus with exacerbation of airway diseases.

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

71 only for asthma but also for hypersecretory airway diseases.

72 lications in modeling and drug screening for airway diseases.

73 omising potential approach to treat allergic airway diseases.

74 mmation in patients with asthma and allergic airway diseases.

75 on-CF bronchiectasis and chronic obstructive airways disease.

76 asthmatic patients and in mice with allergic airways disease.

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

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

79 uced glycolysis and pathogenesis of allergic airways disease.

80 t a distinct pathological process from small airways disease.

81 tibility to fungal allergen-induced allergic airways disease.

82 uced glycolysis and pathogenesis of allergic airways disease.

83 ndent responses in murine models of allergic airways disease.

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

85 important implications for the treatment of airways disease.

86 aintenance of immune homeostasis in allergic airways disease.

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

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

89 f the OSM expressed in patients with mucosal 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 contributions to COPD: emphysema, and small airways disease (a narrowing of the airways).

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

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

97 mportant role in the progression of allergic airway disease (AAD) or asthma.

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

99 pneumolysoid (T+P), which suppress allergic airways disease (AAD) in mouse models of asthma.

100 HDM-induced allergic airways disease (AAD) in neonatal ST2(-/-) mice lacking

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

102 the development of murine neonatal allergic airways disease (AAD).

103 riven and rhinovirus 1B-exacerbated allergic airways disease (AAD).

104 Asthma is a chronic inflammatory airway disease accounting for severe morbidity and morta

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

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

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

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

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

110 re unnecessary for the induction of allergic airway disease and AHR.

111 roteinase activity to initiate both allergic airway disease and antifungal immunity.

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

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

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

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

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

117 thods are needed to monitor and assess small airway disease and its response to treatment because con

118 5(OH)D concentration on outcomes of allergic airway disease and lung function at 20 to 25 years of ag

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

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

121 fficacious in preclinical models of allergic airway disease and may have potential for treating asthm

122 sts are used in the treatment of obstructive airway disease and overactive bladder syndrome.

123 is to review the clinical relevance of small airway disease and the implications for the treatment of

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

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

126 udies have elucidated heterogeneity in these airway diseases and might represent the best opportunity

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

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

129 CI have different relationships in different airway diseases and that LCI does not appear to be a sen

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

131 sexual activity was associated with chronic airways disease and difficulty walking up the stairs bec

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

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

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

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

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

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

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

139 hosis, micro-gallbladder, vas deferens loss, airway disease, and meconium ileus.

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

141 sease processes, such as pain, inflammation, airway diseases, and malignant melanomas.

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

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

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

145 eatment-related issues of uncontrolled upper airway disease are linked with the correct choice of tre

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

147 Allergic airway diseases are immune disorders associated with hei

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

149 NO2) reduced the severity of murine allergic airway disease, as assessed by various pathological and

150 ze barrier integrity and cytokine release in airway diseases associated with barrier dysfunction.

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

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

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

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

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

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

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

158 whether COX inhibition can promote allergic airway diseases by inhibiting immune tolerance is not kn

159 ir pollution on asthma, allergies, and other airway diseases can identify targets for therapy.

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

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

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

163 topes in virus inoculated mice with allergic airway disease compared to mice treated with virus only.

164 e increased propensity of RSV-induced distal airway disease compared with other commonly encountered

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

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

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

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

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

170 The Airways Disease Endotyping for Personalized Therapeutics

171 gnaling in virus-infected mice with allergic airway disease enhanced pulmonary CD4(+) T cell producti

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

173 Several airway diseases exhibit abnormal MCT, including asthma,

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

175 Research into new treatments for airway disease focuses on severe disease because morbidi

176 ne (dimethylxanthine) has been used to treat airway diseases for more than 80 years.

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

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

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

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

181 relation between different aspects of severe airway disease have hindered new drug development.

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

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

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

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

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

187 CI does not appear to be a sensitive test of airway disease in advanced PCD.

188 es between the components of large and small airway disease in CF and PCD.

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

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

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

192 49d to drive development of postviral atopic airway disease in mice.

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

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

195 factors for the high prevalence of allergic airway disease in the tropical urban environment.

196 e enhanced propensity of RSV to cause severe airway disease in young children and suggest NS2 as a po

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

198 unique insight into the cause of obstructive airways disease in 18-year-olds, and follow-up of this c

199 Visual assessment of emphysema and airways disease in individuals with COPD can provide rep

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

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

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

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

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

205 Chronic airway diseases, including asthma, are characterized by

206 Most airway diseases, including chronic obstructive pulmonary

207 Neutrophilic airway diseases, including cystic fibrosis, are characte

208 or dust-related diffuse fibrosis and chronic airway diseases, including emphysema and chronic bronchi

209 human subjects and mouse models of allergic airway disease indicate a central role of IL-33 signalin

210 As shown here BALB/c mice with preexisting airway disease infected with vaccinia virus developed mo

211 nesia (PCD) is a ciliopathy characterized by airway disease, infertility, and laterality defects, oft

212 y dyskinesia (PCD), characterized by chronic airway disease, infertility, and left-right laterality d

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

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

215 Airway disease is the major source of morbidity and mort

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

217 a (PCD), a disorder characterized by chronic airway disease, laterality defects and male infertility.

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

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

220 rogenic dendritic cells (DCs) in an allergic airways disease model.

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

222 tributes to the pathogenesis of obliterative airway disease (OAD) and whether knockout or pharmacolog

223 describe the latency period for obstructive airway disease (OAD) diagnoses.

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

225 Using a murine model of obliterative airway disease (OAD), we recently demonstrated that Abs

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

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

228 ell established, yet the effects of allergic airway disease on the host response to intra-pulmonary v

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

230 ts in an ovalbumin-induced model of allergic airway disease (OVA-AAD).

231 idiopathic interstitial pneumonias and small airways diseases, owes as much to repeated attempts over

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 is group with so-called severe chronic upper airway disease (SCUAD) represents a therapeutic challeng

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

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

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

253 Features of allergic airway disease such as mucous cell hyperplasia, infiltra

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

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

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

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

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

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

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

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

262 In contrast, using two models of allergic airway disease, Th17 cells from the lungs of diseased mi

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 is elevated in asthma and other inflammatory airway diseases that are commonly treated with glucocort

266 to play pivotal roles in asthma and allergic airway diseases, the immunological mechanisms that initi

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

268 allenged and increasing evidence shows small airway disease to be associated with symptoms, disease s

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

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

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

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

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

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

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

276 rbate or trigger the development of allergic airway diseases via multiple mechanisms depending upon t

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

278 impact of Wnt on the development of allergic airway disease was analyzed.

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

280 An exacerbation model of allergic airway disease was established whereby mice were sensiti

281 gen exposure, or the development of allergic airway disease was evaluated in TLR4 or TRIF knockout mi

282 Airway disease was measured by using the CT airway wall

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

284 , but whether they might ameliorate allergic airway disease was previously untested.

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

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

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

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

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

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

291 TIM1(-/-) mice did not have airways disease when infected with RSV or when repeatedl

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

293 on is to use a new approach to assess severe airway disease, which moves the diagnostic focus from ca

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

295 slates into increased prevalence of allergic airway diseases, which now impact a large proportion of

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

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

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

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

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