ライフサイエンスコーパス: severe asthma

1 sought to define the molecular phenotypes of severe asthma.

2 cell numbers and activation in patients with severe asthma.

3 ignificantly higher in mild while reduced in severe asthma.

4 ters 3 and 4 were dominated by patients with severe asthma.

5 mechanism driving GC insensitivity in ASM in severe asthma.

6 mily members in the bronchi of patients with severe asthma.

7 ng epithelial cell proliferation observed in severe asthma.

8 clinical features in children with mild and severe asthma.

9 non-obese patients, are associated with more severe asthma.

10 ntelukast alone in patients with moderate-to-severe asthma.

11 and Equ c 3 with persistent rhinitis, AD and severe asthma.

12 with symptoms ranging from mild rhinitis to severe asthma.

13 signature gene associated with moderate and severe asthma.

14 er understanding of non-type 2 mechanisms of severe asthma.

15 vage from healthy subjects and patients with severe asthma.

16 ondria-dependent pathway in individuals with severe asthma.

17 roblasts on epithelial cell proliferation in severe asthma.

18 lic dysfunction in a subset of patients with severe asthma.

19 lopment of more effective drugs for treating severe asthma.

20 is highly correlated with the development of severe asthma.

21 pared with the non-eosinophilic phenotype in severe asthma.

22 low in mechanically ventilated patients with severe asthma.

23 directed to any subject with a diagnosis of severe asthma.

24 ed, and then read to adults with moderate-to-severe asthma.

25 ent a major advancement in the management of severe asthma.

26 cted from patients with mild-to-moderate and severe asthma.

27 opamil on airway remodeling in patients with severe asthma.

28 on potential, were observed in patients with severe asthma.

29 care costs and resource use in patients with severe asthma.

30 ls and neutrophils, such as in patients with severe asthma.

31 nonsevere asthma but not from patients with severe asthma.

32 has been shown to play an important role in severe asthma.

33 ct and in sputum from patients with moderate-severe asthma.

34 fy gene profiles associated with adult-onset severe asthma.

35 of healthy donors and patients with mild and severe asthma.

36 attenuated in fibrocytes from patients with severe asthma.

37 p=0.02), and carboxypeptidase A3 (p=0.02) in severe asthma.

38 OSM-producing cells in patients with CRS and severe asthma.

39 was performed in 62 patients diagnosed with severe asthma.

40 ls from women (n = 14) and men (n = 15) with severe asthma.

41 d biologics, may be required in moderate and severe asthma.

42 C-HA was only observed in a patient with non-severe asthma.

43 promoters, may underlie CS insensitivity of severe asthma.

44 nonsevere asthma but not from patients with severe asthma.

45 diseases, such as bronchial thermoplasty for severe asthma.

46 roliferation of BSM cells from patients with severe asthma.

47 describe a novel deficiency of MAIT cells in severe asthma.

48 h SCS-related complications in patients with severe asthma.

49 een the bronchial microbiome and features of severe asthma.

50 f SCS-related complications in patients with severe asthma.

51 ful targets for the treatment of adult-onset severe asthma.

52 teria included eosinophilic oesophagitis and severe asthma.

53 nd radiological abnormalities in moderate to severe asthma.

54 cross the United States, including many with severe asthma.

55 ung injury were less enriched in adult-onset severe asthma.

56 ic landscape in the airways of children with severe asthma.

57 pathogenicity of TH1 cells in patients with severe asthma.

58 elevated in moderate while downregulated in severe asthma.

59 of radiological abnormalities in moderate to severe asthma.

60 lls contribute to the pathobiologic basis of severe asthma.

61 to the emergency department with moderate to severe asthma.

62 n observed in CD8 T cells from patients with severe asthma.

63 position document on the role of allergy in severe asthma.

64 evels in biopsy specimens from patients with severe asthma.

65 ontrol was maintained in adult patients with severe asthma.

66 in patients with corticosteroid-insensitive severe asthma.

67 and IL-6 release in ASMCs from patients with severe asthma.

68 the management of patients with uncontrolled severe asthma.

69 ence of AERD was highest among patients with severe asthma (14.89% [95% CI, 6.48% to 23.29%]).

70 logy, clinical diagnosis, asthma phenotypes, severe asthma, acute exacerbations, and clinical managem

71 Severe asthma AMs also expressed increased levels of thr

72 ression of TLR7 was significantly reduced in severe asthma AMs and was associated with reduced rhinov

73 Sixty patients with mild-to-severe asthma and 24 control subjects underwent detailed

74 male and female volunteers (60 with mild-to-severe asthma and 24 healthy, non-atopic controls) aged

75 Twenty-nine patients with moderate-to-severe asthma and 26 control subjects were enrolled in t

76 A total of 22 subjects with severe asthma and 27 subjects with no asthma were recrui

77 ruited patients with persistent, moderate-to-severe asthma and an elevated sputum eosinophil count (>

78 reased twofold (RR 1.96 (95% CI 1.25-3.07)); severe asthma and asthma attacks was increased by 60% (R

79 asthma control in patients with moderate-to-severe asthma and deserves further study for this indica

80 and safety of benralizumab for patients with severe asthma and elevated eosinophils, which are uncont

81 In patients with severe asthma and healthy control subjects, IL-17A produ

82 y tissue obtained from patients with mild-to-severe asthma and healthy control subjects.

83 the UK, we assessed volunteers with mild-to-severe asthma and healthy non-atopic controls using clin

84 avage fluid was collected from patients with severe asthma and healthy subjects, and the level of PTX

85 s (IL and UK) comprising mild, moderate, and severe asthma and healthy volunteers were evaluated for

86 k allele A at rs12141494 was associated with severe asthma and higher YKL-40 expression in the airway

87 9-3p is increased in sputum of patients with severe asthma and is linked to neutrophilic airway infla

88 articipants without asthma in the nonsmoking severe asthma and mild/moderate asthma subgroups were si

89 y profiled patients with mild, moderate, and severe asthma and nonatopic healthy control subjects.

90 Here we report that mice with severe asthma and OVA-sensitized/challenged mice had inc

91 fferentially expressed between patients with severe asthma and participants without asthma.

92 le of HDM on BSM remodeling in patients with severe asthma and points out different therapeutic targe

93 profiles were compared between patients with severe asthma and previously studied healthy control sub

94 summary, CEACAM6 expression is increased in severe asthma and primarily associated with airway epith

95 ated in patients with persistent moderate-to-severe asthma and raised sputum eosinophil counts despit

96 late inflammatory processes in patients with severe asthma and related phenotypes.

97 IL-17A is associated with severe asthma and requires IL-23 receptor (IL-23R) signa

98 In contrast, symptoms of severe asthma and severe eczema were positively associat

99 bjects and patients with mild-to-moderate or severe asthma and to identify specific clinical and path

100 l, and molecular phenotypes in patients with severe asthma and to investigate the potential role of s

101 Patients aged 18-75 years with severe asthma and two to six exacerbations in the previo

102 icantly increased in sputum of patients with severe asthma and were positively associated with sputum

103 be exposed to many risk factors facilitating severe asthma and wheezing, including airborne viruses,

104 to glucocorticoid therapy can be blunted in severe asthma and will describe some of the factors and

105 patients with mild asthma, 32 patients with severe asthma, and 30 patients with prednisolone-depende

106 Treatment options are limited for severe asthma, and the need for additional therapies rem

107 Patients with severe asthma appear relatively corticosteroid resistant

108 Airway dysbiosis in patients with severe asthma appears to differ from that observed in th

109 We propose that fibrocytes in severe asthma are different from those in nonsevere asth

110 r eosinopenic response to glucocorticoids in severe asthma are poorly defined.

111 ellular pathways driving the pathogenesis of severe asthma are poorly defined.

112 Patients with severe asthma are responsible for a significant proporti

113 orticoid (GC) insensitivity in patients with severe asthma are still unknown.

114 These patients, labeled severe asthma, are responsible for a substantial fractio

115 s with nonsevere asthma and 19 subjects with severe asthma as comparative groups (COBRA cohort [Cohor

116 perresponsiveness, a physiological marker of severe asthma, as well as on airway mast-cell numbers an

117 etic approaches support a role for IL1RL1 in severe asthma, as well as TH2-lke asthma, suggesting tha

118 ts relying on oral glucocorticoids to manage severe asthma associated with eosinophilia.

119 We show that a severe asthma-associated polymorphism in the gene encodi

120 s with moderate asthma, and 26 patients with severe asthma based on airway mucosal expression of (1)

121 We stratified patients with moderate-to-severe asthma based on clinicophysiologic parameters and

122 014, new biologic therapies are emerging for severe asthma based on identification of relevant phenot

123 Poor asthma control is often driven by severe asthma biology, which has appropriately been the

124 d mast cell mediator levels in patients with severe asthma both in its atopic (type 2 cytokine-high)

125 In patients with severe asthma, bronchial bacterial composition was assoc

126 tients, with a few patients falling into the severe asthma category.

127 ts with clinical and therapeutic criteria of severe asthma; cluster 2, with an high proportion of res

128 The severe asthma clusters (T2, T3, and T4) had higher sputu

129 lls and lamina propria inflammatory cells in severe asthma compared with healthy control subjects.

130 Women have an increased prevalence of severe asthma compared with men.

131 ulated (>2-fold) in nonsmoking patients with severe asthma compared with MMAs, including IL-1 recepto

132 antly upregulated in sputum of patients with severe asthma compared with that in healthy control subj

133 Severe asthma comprises a heterogeneous group of phenoty

134 nd myeloid cell trafficking in patients with severe asthma, decreased B-lymphocyte development and he

135 sthma, as well as subgroups of patients with severe asthma defined by transcript profiles, show the v

136 alyses across ASM quartiles in patients with severe asthma demonstrated that patients with the highes

137 Self-management of moderate-to-severe asthma depends on the patient's ability to (1) na

138 present in the airways of patients who have severe asthma despite glucocorticoid treatment; these ce

139 cy of asthma exacerbations, and frequency of severe asthma differed between IL-6 low and IL-6 high as

140 The lower airways of children with severe asthma display a dominant TH1 signature and atypi

141 h improved clinical classification show that severe asthma does not identify a specific patient pheno

142 A small population of patients with severe asthma does not respond to glucocorticoids (stero

143 The term 'Severe Asthma' encompasses a highly heterogeneous group

144 dust) were assessed at baseline, and (>/=1) severe asthma exacerbation (emergency department visit o

145 (10.0%) in the fluticasone-alone group had a severe asthma exacerbation (hazard ratio, 0.86; 95% CI,

146 nificantly reduced the risk of a moderate or severe asthma exacerbation compared with placebo (hazard

147 dications improved time to first moderate or severe asthma exacerbation during ICS reduction, with an

148 rimary outcome was time to first moderate or severe asthma exacerbation during the ICS reduction peri

149 9 polymorphisms were more likely to report a severe asthma exacerbation if exposed to increased dust

150 All the patients had a history of a severe asthma exacerbation in the year before randomizat

151 79; 95% CI, 0.70 to 0.89), with at least one severe asthma exacerbation occurring in 480 of 5834 pati

152 The main efficacy end point was the first severe asthma exacerbation that led to treatment with sy

153 The risk of a severe asthma exacerbation was 21% lower in the fluticas

154 rom healthy subjects, while in patients with severe asthma exacerbation, this activity was lower.

155 The efficacy end point was the first severe asthma exacerbation.

156 n its mRNA expression, both in patients with severe asthma exacerbation.

157 The primary outcome was any protocol-defined severe asthma exacerbation.

158 y outcome was time to first protocol-defined severe asthma exacerbation.

159 is model recapitulates all major features of severe asthma exacerbations and can serve to discern dri

160 of the evaluation of asthma management, but severe asthma exacerbations are rare events.

161 Occurrence of severe asthma exacerbations are the cornerstone of the e

162 act with environmental dust mite to increase severe asthma exacerbations in children.

163 t mite-impermeable bedding and its impact on severe asthma exacerbations in children.

164 s receiving fluticasone-salmeterol had fewer severe asthma exacerbations than did those in the flutic

165 month intervention period, the occurrence of severe asthma exacerbations was investigated.

166 for uncontrolled asthma at 3 months and for severe asthma exacerbations within 12 months of commenci

167 rnata, a fungal aeroallergen associated with severe asthma exacerbations, endogenous PGI2 signaling s

168 al response to budesonide versus placebo for severe asthma exacerbations, lung function, and asthma s

169 Identifying patients at risk of future severe asthma exacerbations, those whose asthma might be

170 ould suggest interventions to prevent future severe asthma exacerbations.

171 nic diseases worldwide, and individuals with severe asthma experience recurrent exacerbations.

172 Discriminant analysis distinguished severe asthma from COPD completely using a combination o

173 t metrics when differentiating patients with severe asthma from those with nonsevere asthma and healt

174 Patients with severe asthma generally benefit from consultation with a

175 brocytes was primarily seen in patients with severe asthma (Global Initiative for Asthma steps 4-5) a

176 (r = 0.76), with a larger effect size in the severe asthma group.

177 21 previously described schoolchildren with severe asthma (group 3, 5-11.2 yr).

178 way mucosal CCL26 expression and moderate-to-severe asthma had Feno values (>/=35 ppb) and/or high bE

179 Patients with severe asthma had increased HA levels in bronchoalveolar

180 In the human population, patients with severe asthma had increased levels of anti-Pneumocystis

181 Severe asthma has also been associated with bronchial re

182 ut its efficacy in patients with moderate-to-severe asthma has not been assessed.

183 Patients with severe asthma have elevated numbers of circulating fibro

184 uss our current state of knowledge regarding severe asthma, highlighting different molecular and immu

185 17A production has been associated with more severe asthma; however, the mechanisms whereby IL-17A ca

186 In patients with severe asthma, imatinib decreased airway hyperresponsive

187 asthma in childhood is often associated with severe asthma in adulthood.

188 ed development of TH17-mediated neutrophilic severe asthma in both acute and chronic HDM-driven model

189 The pathogenesis of severe asthma in childhood remains poorly understood.

190 rbid allergic diseases are characteristic of severe asthma in children.

191 013, enrolling black adults with moderate to severe asthma in the United States.

192 itamin D levels, especially in patients with severe asthma in whom bronchoalveolar lavage regulatory

193 al mechanism for the increased prevalence of severe asthma in women compared with men.

194 Severe asthma is a complex heterogeneous disease associa

195 Severe asthma is a major public health issue throughout

196 Severe asthma is associated with a striking deficiency o

197 does not therefore support the concept that severe asthma is associated with corticosteroid resistan

198 Severe asthma is characterized by difficulty to achieve

199 Adult-onset severe asthma is characterized by highly symptomatic dis

200 Adult-onset severe asthma is characterized by inflammatory pathways

201 n recent years has been the recognition that severe asthma is heterogeneous with respect to clinical

202 e for a role for TH17 cells in patients with severe asthma is limited.

203 a may be a separate asthma endotype and that severe asthma is not a single entity, but an extreme end

204 Unlike milder disease, severe asthma is poorly controlled by the current standa

205 Furthermore, this severe asthma is resistant to steroids and characterized

206 However, the role of allergy in severe asthma is still under debate.

207 ilar relationships exist among patients with severe asthma is unknown.

208 aracteristic feature of airway remodeling in severe asthma, is associated with resistance to high-int

209 oclonal antibody registered for treatment of severe asthma, is only active in patients with active eo

210 /=18 years) as compared with childhood-onset severe asthma (<18 years) were selected from the U-BIOPR

211 on]) than did the measures for patients with severe asthma (mean SVP segmental ventilation percentage

212 Severe asthma might be associated with overexpression of

213 Highly selected patients with severe asthma might benefit from bronchial thermoplasty.

214 Comparisons to severe asthma multicenter studies and available registri

215 ng patients with SA, smokers/ex-smokers with severe asthma, nonsmoking patients with mild/moderate as

216 e asthma with fungal sensitization (n = 16), severe asthma not sensitized to fungi (n = 9), mild asth

217 Severe asthma often coclusters with highly allergic chil

218 nophilic inflammation, whereas patients with severe asthma often present with TH17-mediated neutrophi

219 Other patients have severe asthma or are asthmatic patients who smoke with f

220 of continuous OCS exposure in patients with severe asthma, our results suggest that each OCS prescri

221 ST2L expression was increased in severe asthma (P = .02) and associated with multiple ind

222 In some patients with moderate-to-severe asthma, particularly those with noneosinophilic i

223 an adverse role for neutrophils in pediatric severe asthma pathophysiology.

224 atics (including 16 mild, 19 moderate and 22 severe asthma patients) and compared them with 19 health

225 lugs and airflow obstruction associated with severe asthma phenotypes.

226 l role of sputum periostin as a biomarker of severe asthma phenotypes.

227 osis, chronic obstructive pulmonary disease, severe asthma, pre-existing pulmonary lesions, and sever

228 flammation in some but not all patients with severe asthma predicts responsiveness to current treatme

229 utcomes for this analysis were time to first severe asthma-related event (SARE; hospital admission, e

230 Many patients with severe asthma rely on oral glucocorticoids to manage the

231 Subsets of patients with severe asthma remain symptomatic despite prolonged, high

232 Severe asthma remains poorly characterized, although it

233 The mechanism underlying nonsevere and severe asthma remains unclear, although it is commonly a

234 derstand the clinical features and to manage severe asthma, representing a non-negligible socioeconom

235 Severe asthma represents a major unmet clinical need; un

236 Many patients with severe asthma require maintenance treatment with systemi

237 nature and mechanistic role in patients with severe asthma requires further evaluation.

238 Baseline data from the NHLBI Severe Asthma Research Program (SARP)-3 were analyzed.

239 (UCSF) and mainly severe asthmatics from the Severe Asthma Research Program (SARP).

240 to less than 18 years (107 SA) in the NHLBI Severe Asthma Research Program III were characterized be

241 enter for Asthma and Airways Disease and 919 Severe Asthma Research Program subjects.

242 h asthma and healthy control subjects in the Severe Asthma Research Program was analyzed by weighted

243 enter for Asthma and Airways Disease and the Severe Asthma Research Program.

244 to which eosinophilic airway inflammation in severe asthma responds to treatment with systemic cortic

245 Severe asthma (SA) afflicts a heterogeneous group of ast

246 RATIONALE: Phenotypic distinctions between severe asthma (SA) and nonsevere asthma (NONSA) may be c

247 Patients with severe asthma (SA) are less responsive to the beneficial

248 ression in sputum samples from patients with severe asthma (SA) compared with nonsmoking patients wit

249 Severe asthma (SA) is a challenge to control, as patient

250 RATIONALE: Severe asthma (SA) is a heterogeneous disease with multi

251 Severe asthma (SA) is associated with neutrophil recruit

252 atients with respiratory diseases, including severe asthma (SA), display defective generation of lipo

253 This implies that currently recognized severe asthma subphenotypes could meet the criteria of r

254 Aspirin-exacerbated respiratory disease, a severe asthma subtype, is characterized by exaggerated e

255 ssing CEACAM6 was significantly increased in severe asthma, suggesting the presence of an altered neu

256 f several new biologics for the treatment of severe asthma-targeting specific endotypes and phenotype

257 n the upper tercile were more likely to have severe asthma than children in the lower terciles (P = .

258 s study identifies an autoimmune endotype of severe asthma that can be identified by the presence of

259 nts with eosinophils >/=300/muL or with more severe asthma, this rate reduction was significantly mor

260 iR-19a enhances cell proliferation of BEC in severe asthma through targeting TGF-beta receptor 2 mRNA

261 In patients with severe asthma, tiotropium improves lung function and exa

262 In severe asthma, TLR7 deficiency drives impaired innate im

263 New biological therapies for treatment of severe asthma, together with developments in biomarkers,

264 , we enrolled patients aged 12-75 years with severe asthma uncontrolled by medium-dosage to high-dosa

265 mild-to-moderate asthma, and 9 patients with severe asthma using high-throughput, stem-loop, reverse

266 had similar demographic characteristics, but severe asthma was more common in the omalizumab versus t

267 ssion on B, T, and NK cells and monocytes in severe asthma was significantly increased.

268 ld-to-moderate asthma, and 105 patients with severe asthma were analyzed for ASM area, basement membr

269 l brushings of 107 subjects with moderate to severe asthma were annotated by gene set variation analy

270 children aged 5 to 17 years with moderate to severe asthma were enrolled in a 12-month randomized con

271 Subjects with uncontrolled and severe asthma were excluded from the trials.

272 adult-onset as compared with childhood-onset severe asthma were identified in nasal brushings (5 sign

273 six healthy volunteers and 10 patients with severe asthma were imaged in compliance with HIPAA regul

274 Patients with mild/moderate and severe asthma were investigated before and after 2 weeks

275 ate-onset asthma." Children with moderate-to-severe asthma were present in each cluster.

276 ents with moderate asthma, and patients with severe asthma were stained for OSM and neutrophil elasta

277 ] vs 3.9% [1.3-5.3%], p=0.02), especially in severe asthma where BAL regulatory T cells were also red

278 reptococcus pneumoniae, in particular during severe asthma where high levels of the glycoprotein, ost

279 of patients with well-controlled moderate-to-severe asthma, whereas cluster T2 is a group of patients

280 hoid cells were more enriched in adult-onset severe asthma, whereas signatures associated with induce

281 ients and twice that number in patients with severe asthma, which underscores the importance of recog

282 ical benefits for patients with uncontrolled severe asthma who are refractory to glucocorticoid thera

283 reation of subgroups among the patients with severe asthma who differed in molecular responses to ora

284 imatinib in patients with poorly controlled severe asthma who had airway hyperresponsiveness despite

285 residual volume compared with patients with severe asthma who had low anti-Pneumocystis IgG.

286 acologic intervention to treat patients with severe asthma who present with TH17-mediated neutrophili

287 er T2 is a group of patients with late-onset severe asthma with a history of smoking and chronic airf

288 Patients with severe asthma with elevated anti-Pneumocystis IgG levels

289 Bronchopulmonary aspergillosis (n = 16), severe asthma with fungal sensitization (n = 16), severe

290 The mechanism underlying severe asthma with fungal sensitization (SAFS) is unknow

291 ic bronchopulmonary aspergillosis (ABPA) and severe asthma with fungal sensitization (SAFS).

292 allergic bronchopulmonary aspergillosis and severe asthma with fungal sensitization.

293 allergic bronchopulmonary aspergillosis and severe asthma with fungal sensitization.

294 d of obese female patients with uncontrolled severe asthma with increased exacerbations but with norm

295 ts with a mix of patients with nonsevere and severe asthma with marginal inflammation who exhibited a

296 athways, characterizes younger patients with severe asthma with poor asthma control.

297 in-13 monoclonal antibodies in patients with severe asthma with recurrent exacerbations and high bloo

298 ed by the use of NPPV in children with acute severe asthma with respiratory muscle fatigue and failur

299 asty (BT) has been reported in patients with severe asthma, yet its effect on different bronchial str

300 ponent of airway remodeling in patients with severe asthma, yet the pathobiological mechanisms and cl