ライフサイエンスコーパス: asthmatic

1 on study (GWAS) on the slope of BHR in adult asthmatics.

2 arker of eosinophilic airway inflammation in asthmatics.

3 and the complex immune response in blood of asthmatics.

4 id-sensitive (SS) and steroid-resistant (SR) asthmatics.

5 biopsy sections from smoking and non-smoking asthmatics.

6 mation in all compartments in both groups of asthmatics.

7 ced sensitivity of ASM cells to GC in severe asthmatics.

8 hmatic adults aged under 56 than among older asthmatics.

9 thelial and bronchial lavage cells in atopic asthmatics.

10 ronchial hyperresponsiveness in adult stable asthmatics.

11 Cross-sectional study of 431 asthmatics.

12 cies of total DCs and pDCs in both SS and SR asthmatics.

13 hilic inflammation compared to mild/moderate asthmatics.

14 une response in a large proportion of atopic asthmatics.

15 rsecretion and decreased ciliary function of asthmatics.

16 bundles in endobronchial biopsies in severe asthmatics.

17 requency of mDCs in SS, but reduced it in SR asthmatics.

18 re analysed in a cohort of poorly controlled asthmatics.

19 om control and airflow obstruction in severe asthmatics.

20 (EoP) were assayed in 21 severe eosinophilic asthmatics, 19 mild asthmatics, eight COPD patients and

21 Thirty-two mild/moderate asthmatics, 50 severe asthmatics and 35 healthy subjects

22 Eighty-five elderly asthmatics, 74 younger asthma patients, and 114 age-matc

23 asthma, a total of 231 asthmatic and 225 non-asthmatic adolescents were selected from northern Taiwan

24 sensitization are more common among Finnish asthmatic adults aged under 56 than among older asthmati

25 metabolism sustains arginine availability in asthmatic airway epithelium with consequences for bioene

26 se (iNOS) and arginase (ARG), are typical in asthmatic airway epithelium; however, little is known ab

27 A role for smooth muscle ARHGEF1 in asthmatic airway hyper-responsiveness is worthy of furth

28 tial therapeutic target for the treatment of asthmatic airway hyper-responsiveness.

29 n periostin-rich extracellular matrix in the asthmatic airway in an ADAM8-dependent manner, making AD

30 airway obstruction in the context of chronic asthmatic airway inflammation.

31 To investigate the role of calpain in asthmatic airway remodelling as well as the underlying m

32 Asthmatic airways are inflamed and undergo remodelling.

33 Our data suggest that BPIFA1 deficiency in asthmatic airways promotes Orai1 hyperactivity, increase

34 nslational modification (PTM) of proteins in asthmatic airways through a process called carbamylation

35 own to be co-localized with EPO within human asthmatic airways.

36 rmones and associated asthma, a total of 231 asthmatic and 225 non-asthmatic adolescents were selecte

37 In a nested case-control study of 35 asthmatic and 49 nonasthmatic children, 42 FAs were quan

38 ed for sncRNA profiling in BSM cells (from 8 asthmatic and 6 nonasthmatic subjects).

39 ral infections (CCL8/CXCL11), we screened 92 asthmatic and 69 healthy children without illness for re

40 Asthmatic and allergic inflammation is mediated by TH2 c

41 ated with reduced ST2 in blood cells of both asthmatic and control children and reduced IL-33 levels

42 nti-bacterial immune responses in pre-school asthmatic and control children within the EU-wide study

43 this interaction remained in both groups of asthmatic and non-asthmatic subjects.

44 Lung biopsy specimens from asthmatic and nonasthmatic patients revealed a predomina

45 DNA from blood of asthmatic and normal subjects was genotyped for Tollip S

46 helial brushings from healthy, steroid-naive asthmatic and steroid-treated asthmatic subjects.

47 condary assay identified CMV DNA in 41.5% of asthmatics and 13.3% of control subjects (P < .001).

48 irty-two mild/moderate asthmatics, 50 severe asthmatics and 35 healthy subjects took part.

49 /bronchial IL-17F for discriminating between asthmatics and controls, between MAs and SAs and between

50 ease in nitrotyrosine in HBECs in cells from asthmatics and controls.

51 uman bronchial epithelial cells (HBECs) from asthmatics and healthy controls to evaluate: (i) ADMA-me

52 nt in uncontrolled as compared to controlled asthmatics and healthy controls.

53 The severity of BHR varies between asthmatics and is associated with lack of asthma control

54 PP5 were increased in ASM cells from severe asthmatics and PP5 knockdown using siRNA restored flutic

55 ghest loads of fungus are observed in severe asthmatics and the most common fungus is Aspergillus fum

56 frequency is elevated in SR compared with SS asthmatics, and mDC shows a differential response to ora

57 a few studies involving healthy individuals, asthmatics, and smokers.

58 Elderly asthmatics are at a higher risk for morbidity and mortal

59 Evidence suggests that elderly asthmatics are more likely to be underdiagnosed and unde

60 from ASMCs was increased in the presence of asthmatic ASMCs that expressed more mRNA for FGF2b compa

61 In asthmatics, basophils were positively correlated with sp

62 Asthmatic bronchial biopsies were immunostained for CD48

63 In asthmatic bronchial biopsies, mCD48 was expressed predom

64 e immunity and increased localization to the asthmatic bronchial epithelium, we investigated whether

65 to diagnose or evaluate effect of therapy in asthmatics, but invasive.

66 m basophil numbers are increased in allergic asthmatics, but it is unclear what role airway basophils

67 The mycobiome was highly varied with severe asthmatics carrying higher loads of fungus.

68 re validated in an independent population of asthmatic children (n = 30) by using a shared healthy co

69 Asthmatic children aged 6 to 17 years underwent baseline

70 A total of 229 dyads of asthmatic children and their parents enroled in public i

71 pment of eosinophilic airway inflammation in asthmatic children at school age.

72 Furthermore, asthmatic children had more episodes of infection that r

73 Obese asthmatic children have nonatopic TH1-polarized systemic

74 nts (n = 196) were selected from a cohort of asthmatic children in Connecticut and Massachusetts.

75 Over 89% of asthmatic children in underdeveloped countries demonstra

76 ylated regions, was selectively increased in asthmatic children of asthmatic mothers and was associat

77 ide differential gene expression among obese asthmatic children was enriched for genes, including VAV

78 IL33R-ST2 was found induced in the blood of asthmatic children with additional Gram + bacteria in th

79 health-related quality of life (HRQOL) among asthmatic children, especially from low-income families,

80 These data suggest that, in asthmatic children, Gram- bacteria, which persist after

81 In this cohort of pre-school asthmatic children, nasopharyngeal colonization with Gra

82 get that is upregulated in TH cells of obese asthmatic children, suggesting its role in nonatopic TH1

83 We performed HC in a rich data set from 613 asthmatic children, using 45 clinical variables (Model 1

84 in the blood of control children but not of asthmatic children.

85 n and reduced IL-33 levels in the airways of asthmatic children.

86 ed in epidemiologic studies mainly including asthmatic children.

87 e and dexamethasone in ASM cells from severe asthmatic compared to that in healthy subjects.

88 gnificantly reduced in ASM cells from severe asthmatics compared to responses in healthy subjects.

89 -beta, IFN-lambda1/IL-29, OAS and viperin in asthmatics compared with healthy subjects, while IL-28 w

90 gative answers to all three questions as non-asthmatic controls.

91 In poorly controlled asthmatics, DARC SNPs were associated with worse asthma

92 features more usually associated with severe asthmatic disease.

93 Neutrophilic, but not eosinophilic, asthmatics display overexpression of IFN-beta, IFN-lambd

94 ident in eosinophils derived from atopic and asthmatic donors; (iii) enhanced F-actin formation; (iv)

95 ed form in eosinophils from healthy, but not asthmatic, donors (143 +/- 21% and 108 +/- 11% of contro

96 n 21 severe eosinophilic asthmatics, 19 mild asthmatics, eight COPD patients and eight normal subject

97 In the smoking asthmatics, eosinophil numbers also correlated with expr

98 P2X5 receptors were expressed in healthy and asthmatic eosinophils.

99 ions closely approximated gene expression in asthmatic epithelial brushings.

100 The lasting alteration of the asthmatic epithelial cell transcriptome implicates regul

101 findings in epithelial brushings and primary asthmatic epithelial cells cultured in different biologi

102 re not required for development of pulmonary asthmatic features yet contributed to TH2 expansion in t

103 Exosomes of severe eosinophilic asthmatics' fibroblasts can contribute to airway remodel

104 Overexpression of TGF-beta2 in severe asthmatics' fibroblasts induced enhanced TGF-beta2 in ex

105 We performed a GWAS on BHR severity in adult asthmatics from the Dutch Asthma GWAS cohort (n = 650),

106 of subjects into type 2-high and type 2-low asthmatic groups, but in the ADEPT study population CCL2

107 At baseline, both groups of asthmatics had a lower FEV1 and Pc20 and increased eosin

108 Severely asthmatic horses (6 horses/group) were treated with flut

109 secreted basolaterally from healthy, but not asthmatic human bronchial epithelial cultures (HBECs), w

110 ands, it will be critical to include elderly asthmatics in large clinical trials so that therapy may

111 d viperin in unstimulated sputum cells in 57 asthmatics (including 16 mild, 19 moderate and 22 severe

112 In a murine model of ASIT for allergic asthmatic inflammation, we found that OVA released from

113 ma and may contribute to the pathogenesis of asthmatic inflammation.

114 clinical glucocorticoid sensitivity of these asthmatics is reflected in differences in peripheral blo

115 alance also occurs in bronchial epitheliumof asthmatics is unknown.

116 ate from obese asthmatic (OA) patients, lean asthmatic (LA) patients, and obese nonasthmatic (ONA) su

117 ate from obese asthmatic (OA) patients, lean asthmatic (LA) patients, and obese nonasthmatic (ONA) su

118 ore, RV1B infection led to susceptibility to asthmatic lung disease when mice subsequently re-encount

119 Fibroblasts from asthmatic lung exhibited increased TRPV4 activity and en

120 and that this can lead to susceptibility to asthmatic lung inflammation.

121 sue enhances M2-mediated inflammation in the asthmatic lung.

122 al/bronchial biopsies from controls and mild asthmatics (MAs) to severe asthmatics (SAs) in relation

123 lectively increased in asthmatic children of asthmatic mothers and was associated with childhood asth

124 istent asthma was observed among children of asthmatic mothers with mild uncontrolled (PR, 1.19; 95%

125 etons, of which 15,014 children were born to asthmatic mothers.

126 evels were determined in control (n = 9) and asthmatic (n = 27) bronchial biopsies using immunohistoc

127 asophils were significantly increased in all asthmatics (n=26) compared with healthy controls (n=8) (

128 mics of exhaled breath condensate from obese asthmatic (OA) patients, lean asthmatic (LA) patients, a

129 mics of exhaled breath condensate from obese asthmatic (OA) patients, lean asthmatic (LA) patients, a

130 the odds of airway obstruction by 75% within asthmatics only.

131 ased with farm exposure and increased within asthmatics, opposite to age 4.5 years.

132 bserved in the blood of SR as compared to SS asthmatics (P = .03).

133 stering was applied to a training set of 266 asthmatic participants from the European Unbiased Biomar

134 y disease but crucial in maintaining chronic asthmatic pathology.

135 presence of allergy and eosinophilia in each asthmatic patient.

136 ents with COPD (mean, 0.922 [SD, 0.037]) and asthmatic patients (mean, 0.852 [SD, 0.061]) compared wi

137 independent population of white adult atopic asthmatic patients (n = 12) and control subjects (n = 12

138 In asthmatic patients (n = 63) CNTO3157 provided no protect

139 le patients (P = .0001) and 71% lower in all asthmatic patients (P = .0008).

140 ma had a 21% lower Emax value than nonatopic asthmatic patients (P = .04).

141 This was a retrospective cohort study of asthmatic patients 18 years and older in the 2000-2014 M

142 In asthmatic patients abnormalities in many aspects of epit

143 In asthmatic patients airway microbial composition was asso

144 We studied human blood and lung ILC2s from asthmatic patients and control subjects using flow cytom

145 ed with small hairpin RNA lentivirus in both asthmatic patients and control subjects with BSM cell pr

146 e uniquely expressed in patients with AR and asthmatic patients and have potential for use as noninva

147 patients and in peripheral blood of allergic asthmatic patients and healthy control subjects.

148 AECs were obtained from asthmatic patients and healthy subjects and treated with

149 EF1 expression was also enhanced in ASMCs of asthmatic patients and in lungs of ovalbumin-sensitized

150 role of p53 in proliferation of BSM cells in asthmatic patients and mitochondrial biogenesis.

151 s also enhanced in airway smooth muscle from asthmatic patients and ovalbumin-sensitized mice.

152 odeling, air trapping, and emphysema between asthmatic patients and patients with COPD and explore th

153 sthma review, we discuss viral infections in asthmatic patients and potential therapeutic agents, the

154 rations in glycolysis in sputum samples from asthmatic patients and primary human nasal cells and use

155 A1 levels are reduced in sputum samples from asthmatic patients and that BPIFA1 is secreted basolater

156 istance of human blood and airway ILC2s from asthmatic patients and to examine its mechanism of induc

157 olyclonal autoimmune event in the airways of asthmatic patients and to identify associated clinical a

158 inflammatory patterns of aged versus younger asthmatic patients are associated with increased sputum

159 BSM cells of asthmatic patients are characterized by aberrant sncRNA

160 ng function, asthma control, and symptoms in asthmatic patients but suppressed cold symptoms in healt

161 nt knowledge on pathogenic CD4(+) T cells in asthmatic patients by drawing on observations in mouse m

162 tion and progression of airway remodeling in asthmatic patients by recruiting fibroblasts that produc

163 [alpha-SMA](+)) fibrocytes were increased in asthmatic patients compared with control subjects.

164 vWF (142% vs 87%, overall P < .01) levels in asthmatic patients compared with healthy control subject

165 levels were increased in induced sputum from asthmatic patients compared with that from control subje

166 nd IFN-lambda levels were lower in AECs from asthmatic patients compared with those from healthy subj

167 counts are often increased in the airways of asthmatic patients despite their typical association wit

168 Aged asthmatic patients experience increased morbidity and mo

169 -SMA(+)CXCR4(+) fibrocytes were increased in asthmatic patients experiencing an asthma exacerbation i

170 rentiated fibrocytes in circulating blood of asthmatic patients experiencing an exacerbation in the p

171 A total of 36.2% of asthmatic patients expressed at least 1 sign of asthma s

172 Asthmatic patients had higher Emax and lower ED50 values

173 Aged asthmatic patients had higher sputum IL-6 (P < .01) and

174 Aged asthmatic patients had higher sputum neutrophil (30.5 x

175 BAL fluid from asthmatic patients had increased TSLP but not IL-7 level

176 unger (mean age, 30.8 +/- 5.9 years; n = 37) asthmatic patients had significantly worse asthma contro

177 Nonatopic asthmatic patients had the highest cough responses, sugg

178 A substantial subgroup of asthmatic patients have "nonallergic" or idiopathic asth

179 Asthmatic patients have higher microbiome diversity and

180 of phenotypic signs of asthma severity among asthmatic patients in a general population and to descri

181 eated rolling cohorts of pediatric and adult asthmatic patients in the Mini-Sentinel Distributed Data

182 In aged asthmatic patients increased sputum IL-6 and macrophage

183 Primary nasal epithelial cells from asthmatic patients intrinsically produced more lactate c

184 Cough in asthmatic patients is a common and troublesome symptom.

185 r data demonstrate that barrier leakiness in asthmatic patients is induced by TH2 cells, IL-4, and IL

186 Sputum analysis in asthmatic patients is used to define airway inflammatory

187 Consistently, in asthmatic patients pDC numbers were markedly increased d

188 can contribute to IL-13-driven pathology in asthmatic patients remain unclear.

189 More than 1 in 3 asthmatic patients show at least 1 sign of asthma severi

190 HBECs from asthmatic patients showed a significantly low TJ integri

191 ronchial hyperresponsiveness in adult stable asthmatic patients taking inhaled corticosteroids.

192 ercome barriers to T-cell discovery in human asthmatic patients that could transform our understandin

193 synthesis of TJ molecules in epithelium from asthmatic patients to the level seen in HBECs from contr

194 A total of 240 asthmatic patients were categorized into the four phenot

195 Asthmatic patients were grouped as having nonsevere dise

196 Four reproducible and stable clusters of asthmatic patients were identified.

197 patients were obese, 62% (178/289) of obese asthmatic patients were IL-6 low.

198 Although 80% (111/138) of IL-6 high asthmatic patients were obese, 62% (178/289) of obese as

199 ronchoalveolar lavage (BAL) fluid ILC2s from asthmatic patients were resistant to dexamethasone.

200 62 adult-onset asthmatic patients who had prolonged coughs and chest di

201 the ability to provide personalized care to asthmatic patients will follow.

202 rring in the airways of prednisone-dependent asthmatic patients with increased eosinophil activity, r

203 BAL fluid ILC2s from asthmatic patients with increased TSLP levels were stero

204 onas, and Aeribacillus species compared with asthmatic patients with more eosinophils and healthy con

205 Sputum from asthmatic patients with stable disease or acute exacerba

206 ith the lowest levels of eosinophils but not asthmatic patients with the highest levels of eosinophil

207 Asthmatic patients with the lowest levels of eosinophils

208 rall composition of the airway microbiome of asthmatic patients with the lowest levels of eosinophils

209 t cohort (n = 60; 10 healthy subjects and 50 asthmatic patients).

210 In a previously reported cohort of 60 asthmatic patients, 16 patients were immunophenotyped wi

211 role of TH1 cells and other non-TH2 types in asthmatic patients, and the features of T-cell pathogeni

212 techniques being used for the evaluation of asthmatic patients, both from a clinical and research pe

213 tic resonance imaging (MRI) are prevalent in asthmatic patients, but the clinical importance of venti

214 Epidemiologic studies have shown that asthmatic patients, in particular those with severe dise

215 philic inflammation, and disease severity in asthmatic patients, metabolomics (using target aliphatic

216 ificantly higher in sputum supernatants from asthmatic patients, notably those with greater than 61%

217 However, unlike older asthmatic patients, OW preschool children do not demonst

218 he concept of the environmental epigenome in asthmatic patients, summarize previous publications of r

219 tanding the origins of atypical TH2 cells in asthmatic patients, the role of TH1 cells and other non-

220 ount for the majority of hospitalizations in asthmatic patients, there is still very little known abo

221 tes with variations in the microbiome across asthmatic patients, whereas neutrophilic airway inflamma

222 tive inspiration and expiration scans of 248 asthmatic patients.

223 r when implementing personalized medicine in asthmatic patients.

224 tions of these alterations in SP-A levels in asthmatic patients.

225 he aberrant phenotype observed in ASMCs from asthmatic patients.

226 repeated in a separate validation set of 152 asthmatic patients.

227 during experimental rhinovirus infection of asthmatic patients.

228 een shown to work with TH2 cells from atopic asthmatic patients.

229 moral immune responses in healthy adults and asthmatic patients.

230 and 7 were significantly high in HBECs from asthmatic patients.

231 l HRV-16 inoculation in healthy subjects and asthmatic patients.

232 resting new topical treatment opportunity in asthmatic patients.

233 to identify and target lung inflammation in asthmatic patients.

234 g to increased proliferation of BSM cells in asthmatic patients.

235 the pathophysiology of airway obstruction in asthmatic patients.

236 reported in bronchoalveolar lavage fluids of asthmatic patients.

237 controlled asthma in a large cohort of young asthmatic patients.

238 nt increase in ERp57 levels in epithelium of asthmatic patients.

239 therapeutic target against BSM remodeling in asthmatic patients.

240 NAs could be used to characterize or subtype asthmatic patients.

241 orticosteroids indicates disease severity in asthmatic patients.

242 from control subjects but not in HBECs from asthmatic patients.

243 patients and in peripheral blood of allergic asthmatic patients.

244 e effective in reducing airway remodeling in asthmatic patients.

245 on changes in nasal epithelia of adult white asthmatic patients.

246 ter segmental allergen challenge in allergic asthmatic patients.

247 Spls elicited IgE antibody responses in most asthmatic patients.

248 urs almost exclusively in cystic fibrosis or asthmatic patients.

249 The results showed that, among asthmatics, PFASs were positively associated with estrad

250 acteristics can be used to identify specific asthmatic phenotypes and provide a more detailed underst

251 olled despite optimal treatment represent an asthmatic population that requires further study for pot

252 quid interface (ALI) cultures of control and asthmatic primary human bronchial epithelial cells (HBEC

253 Fifty severe asthmatics received prednisone 40 mg/d for 2 weeks and m

254 is sufficient to mediate key features of the asthmatic responses to IL-13 in murine models.

255 controls and mild asthmatics (MAs) to severe asthmatics (SAs) in relation to exacerbation rate.

256 with peach leaf extract was positive in the asthmatic sensitized patients tested.

257 ntly elevated in the bronchial mucosa of the asthmatic smokers compared to the non-smokers.

258 The data support the hypothesis that asthmatic smokers develop neutrophilic inflammation of t

259 tum neutrophils >/= 76%), while eosinophilic asthmatics (sputum eosinophils >/= 3%) did not differ fr

260 verexpression was restricted to neutrophilic asthmatics (sputum neutrophils >/= 76%), while eosinophi

261 Adult severe asthmatics (SS n = 12; SR n = 23) were assessed for thei

262 levels were most predictive of allergic and asthmatic status.

263 lls from 36 children (18 nonasthmatic and 18 asthmatic subjects by age 9 years) from the Infant Immun

264 ell proliferation of both healthy and severe asthmatic subjects compared to healthy controls' exosome

265 In obese asthmatic subjects conventional biomarkers of inflammati

266 Obese asthmatic subjects have lower cut points for IgE levels

267 ate the type of lung inflammation present in asthmatic subjects is increasingly common.

268 ed to delineate eosinophilic inflammation in asthmatic subjects should be approached with caution in

269 smooth muscle cells from healthy and severe asthmatic subjects were treated with TNF-alpha and respo

270 Asthmatic subjects were uniquely enriched in members of

271 Exosomes of severe asthmatic subjects' fibroblasts showed a lower level of

272 protected bronchial brushings from 42 atopic asthmatic subjects, 21 subjects with atopy but no asthma

273 mong these genes in an independent cohort of asthmatic subjects, and identified the presence of commo

274 y on conventional markers of inflammation in asthmatic subjects.

275 steroid-naive asthmatic and steroid-treated asthmatic subjects.

276 remained in both groups of asthmatic and non-asthmatic subjects.

277 anced activation potential of Th2 cells from asthmatic subjects.

278 HI is highly prevalent in poorly controlled asthmatics suggesting small airway dysfunction and may r

279 was diagnosed based on a typical history of asthmatic symptoms and lung function tests.

280 After switching to FP/FM-pMDI, asthmatic symptoms and plural values of small-airways fu

281 cal features in bronchial biopsies of severe asthmatics that could be related to symptom control and

282 r outpatient clinic, we recruited 115 stable asthmatics that were being treated with inhaled corticos

283 In asthmatics, the risk genotype (AA/AG) was associated wit

284 We evaluated 14 non-smoking asthmatics using an open-label, randomized crossover des

285 ion of airway proteins recovered from atopic asthmatics versus healthy controls in response to segmen

286 sm with asthma and airway obstruction within asthmatics via multivariate logistic regression.

287 In bronchial epithelial cells recovered from asthmatic vs healthy human subjects, we found FOXa2 and

288 Tregs from asthmatics vs nonasthmatics suppressed IFN-gamma (P = 0.

289 The most common fungus in asthmatics was Aspergillus fumigatus complex and this ta

290 Symptom control in severe asthmatics was not associated with airway tissue inflamm

291 lation-based sample of largely mild-moderate asthmatics was symptomatically uncontrolled.

292 ession of these receptors is higher in human asthmatics, we determined whether engagement of CD36 or

293 Severe (n = 40) and controlled (n = 31) asthmatics were assessed for allergic sensitization by t

294 Asthmatics were more likely to be hospitalized but less

295 Mild asthmatics who smoke cigarettes may develop unstable dis

296 and Pc20 for both mild/ moderate and severe asthmatics with a correlation between the baseline eosin

297 Treatment of severe asthmatics with mepolizumab significantly attenuated blo

298 rting continuous positive airway pressure in asthmatics with moderate to severe obstructive sleep apn

299 ial in asthma pathogenesis, predominantly in asthmatics with neutrophilia and severe refractory disea

300 Asthmatics with persistent airflow obstruction had great