ライフサイエンスコーパス: asthma

1 included 16,860,716 children (1,534,820 with asthma).

2 -reported or a previous hospital contact for asthma).

3 could be a novel approach to treat allergic asthma.

4 enicity of TH1 cells in patients with severe asthma.

5 ings from healthy controls and patients with asthma.

6 mplementary or steroid-sparing treatment for asthma.

7 used to treat patients with severe allergic asthma.

8 in sputum samples from 48 participants with asthma.

9 nction for patients with severe eosinophilic asthma.

10 ed in uncontrolled as compared to controlled asthma.

11 BMI being seen among females with persistent asthma.

12 nt potential novel genetic associations with asthma.

13 ed in moderate while downregulated in severe asthma.

14 nts with IgE-dependent allergic rhinitis and asthma.

15 unction decline in a subset of children with asthma.

16 n patients with severe or difficult-to-treat asthma.

17 to define the molecular phenotypes of severe asthma.

18 ntified genetic correlation between COPD and asthma.

19 eosinophilic and those with noneosinophilic asthma.

20 lls may help delineate different subtypes of asthma.

21 5-17 years) with severe treatment-refractory asthma.

22 activity as novel therapeutic strategies for asthma.

23 l of severe exacerbation of chronic allergic asthma.

24 rospects for diagnosis and causal therapy of asthma.

25 their evaluation and management in difficult asthma.

26 velopment of respiratory diseases, including asthma.

27 el therapeutic approach for the treatment of asthma.

28 rall, 48 990 children received treatment for asthma.

29 ng therapeutic target against ILC2-dependent asthma.

30 a useful additional indicator of "TH2-high" asthma.

31 limitation and the treatment of people with asthma.

32 ther factors important in the development of asthma.

33 mental interventions for their patients with asthma.

34 to inhaled LPS challenge in volunteers with asthma.

35 ction for patients with severe, uncontrolled asthma.

36 nationwide Swedish study on severe childhood asthma.

37 he development and exacerbation of childhood asthma.

38 in peripheral blood to phenotype and monitor asthma.

39 ance of glycolysis in patients with allergic asthma.

40 e factors that impact the natural history of asthma.

41 e and have a significantly increased risk of asthma.

42 mprove our surveillance and understanding of asthma.

43 L3 are associated with BHR severity in adult asthma.

44 ribution in bronchoconstricted patients with asthma.

45 en proposed as a new therapeutic approach in asthma.

46 ction and likely contributed to neutrophilic asthma.

47 ves lung function in only some patients with asthma.

48 s and perhaps reduce the subsequent risk for asthma.

49 nd might thus impact the T-cell responses in asthma.

50 matory phenotypes, particularly eosinophilic asthma.

51 vesting fruit (rhinoconjunctivitis: 100% and asthma: 67.5%).

52 he United States, the prevalence of allergic asthma (AA) is inexplicably rising and in utero exposure

53 nt of moderate-to-severe persistent allergic asthma (AA) that remains uncontrolled despite high-dose

54 food allergy, those with resolved or current asthma (adjusted odds ratio [aOR], 1.9 [95% CI, 1.1-1.3]

55 march to allergic conditions (food allergy, asthma, allergic rhinitis, allergic conjunctivitis, and

56 The reweighted prevalence of asthma alone was 13.5%, COPD alone 4.1%, and ACOS 2.9%.

57 95% confidence interval, 1.9-17.4), but not asthma alone.

58 metabolites to be used for the prevention of asthma and allergic diseases.

59 o the gut microbiota during infancy precedes asthma and allergy development, possibly indicating an i

60 ldhood asthma and allergy; few data exist on asthma and allergy in adults.

61 and in 2 replication cohorts (the Manchester Asthma and Allergy Study [n = 30] and the Childhood Orig

62 farming exposures protect against childhood asthma and allergy; few data exist on asthma and allergy

63 r type 2 cytokine frequently associated with asthma and atopic dermatitis.

64 betaAR, beta2AR, whose ligands are used for asthma and cardiovascular disease.

65 ray analysis of blood from 610 patients with asthma and control participants in the U-BIOPRED (Unbias

66 The prevalence of asthma and food allergy by 6 years of age was strongly i

67 of allergic rhinoconjunctivitis and allergic asthma and has the potential to alter the natural course

68 nd UK) comprising mild, moderate, and severe asthma and healthy volunteers were evaluated for blood l

69 nown about the specific relationship between asthma and hypertension in young adults.

70 ts with TH2/TH17-low asthma had neutrophilic asthma and increased BAL fluid IL-1alpha, IL-6, IL-8, gr

71 been long identified in the lower airways in asthma and is characterized by epithelial shedding, gobl

72 spanic children: the Puerto Rico Genetics of Asthma and Lifestyle Study (PR-GOAL; n = 306) and the Ge

73 led patients with mild, moderate, and severe asthma and nonatopic healthy control subjects.

74 crobiota in patients with symptomatic stable asthma and relate composition to airway inflammatory phe

75 younger patients with early-onset nonsevere asthma and reversible airflow obstruction and normal air

76 ay be particularly important in eosinophilic asthma and that sputum basophil assessment could be a us

77 Subjects with asthma and the AA/AG genotypes had a 5% decrease in FEV1

78 sed to many risk factors facilitating severe asthma and wheezing, including airborne viruses, smoke,

79 C4 (NLRC4) were associated with neutrophilic asthma and with sputum IL-1beta protein levels, whereas

80 lopment of early life wheezing disorders and asthma, and discuss the external environmental factors w

81 t of inflammatory diseases, such as allergy, asthma, and inflammatory bowel disease.

82 with OVA plus SEA but not OVA alone induced asthma, and SEA exacerbated asthma induced by CDE.

83 tizations are common in persistent childhood asthma, and thorough assessment of allergy is crucial fo

84 medications, previous episodes of near-fatal asthma, and whether the patient has experienced multiple

85 ognised to be comorbid with migraine include asthma, anxiety, depression, and other chronic pain cond

86 he mechanisms by which ORMDL3 predisposes to asthma are unclear.

87 ing on oral glucocorticoids to manage severe asthma associated with eosinophilia.

88 and cross-selection strategy to identify an asthma-associated gene module.

89 xty-seven of 186 genes also have significant asthma-associated methylation changes in nasal epithelia

90 a high-risk birth cohort, the persistence of asthma at age 13 years was most strongly associated with

91 -specific crude and adjusted risk ratios for asthma at ages 5-9 years were calculated using Poisson r

92 d adolescence compared with children without asthma at baseline (hazard ratio, 1.51; 95% confidence i

93 We found that children with a diagnosis of asthma at cohort entry were at 51% increased risk of dev

94 oallergen sensitization increase the risk of asthma at school age.

95 ease network portraits rheumatoid arthritis, asthma, atherosclerosis, pulmonary diseases and Crohn's

96 the role of the microbiome in patients with asthma, atopic dermatitis, and food allergy.

97 itamin D levels were associated with risk of asthma, atopic dermatitis, or elevated serum IgE levels,

98 Survey (n = 696) who were later assessed for asthma, atopic eczema and atopy.

99 ive in both reducing influenza infection and asthma attacks.

100 e assessed, including very poorly controlled asthma based on National Heart, Lung, and Blood Institut

101 At 4.5 years, protection against asthma by farm-milk exposure was partially mediated by r

102 extracellular matrix protein upregulated in asthma by type 2 immunity mediators.

103 alyses were performed in pediatric and adult asthma cases and control subjects with European American

104 chronic inflammatory lung diseases including asthma, chronic obstructive pulmonary disease, and pulmo

105 asthma" patients presenting to a specialist asthma clinic were tracked.

106 degree of severity of the disease within an asthma cohort.

107 , both with and without polyps, and comorbid asthma completed the Mini Asthma QOL Questionnaire (mini

108 Asthma control status was measured using the Asthma Control and Communication Instrument, and asthma-

109 ma treatment, these patients experience poor asthma control and face the greatest risk of asthma morb

110 finding encourages interventions to improve asthma control status and HRQOL in minority children.

111 Asthma control status was measured using the Asthma Cont

112 Mini Asthma QOL Questionnaire (miniAQLQ) and Asthma Control Test (ACT) at baseline and 6 months posto

113 In contrast, poor asthma control typically presents with a diurnal variabi

114 Asthma control was assessed by parent report and child r

115 medication-free days, rhinitis severity and asthma control.

116 in which adult patients with adult-onset of asthma (defined as starting at age >/=18 years) as compa

117 n patients with severe or difficult-to-treat asthma despite standard-of-care treatment.

118 ation in early life are at greatest risk for asthma development.

119 respiratory tract infection is implicated in asthma development.

120 among the poorest individuals for arthritis, asthma, diabetes, edentulism, and >/=4 chronic condition

121 Patients (aged 4-66 years) with mild asthma diagnosed within the previous 2 years and no prev

122 ded to be associated with increased rates of asthma diagnosis (HR=1.23; 95% CI: 0.97, 1.55) and bronc

123 Even in subjects with mild steroid-naive asthma, differences in the bronchial microbiome are asso

124 However, the prevalence of asthma differs worldwide, and in many countries the prev

125 gs show that the diagnosis of cough, LPR, or asthma due to gastroesophageal reflux is difficult, as n

126 R with systemic atopy and the development of asthma during 10 years.

127 lampsia is a shared prenatal risk factor for asthma, eczema, and allergy in childhood pointing toward

128 Asthma encompasses a variety of clinical phenotypes that

129 the clinical features of exacerbation-prone asthma (EPA) remain incompletely defined.

130 RATIONALE: Reducing asthma exacerbation frequency is an important criterion

131 Annual asthma exacerbation rates, lung function, symptoms, and

132 dividuals), rates of hospital attendance for asthma exacerbations (-9.83% [-16.62 to -3.04]; five stu

133 primary end point was the annualized rate of asthma exacerbations (events per patient-year) at week 5

134 l recapitulates all major features of severe asthma exacerbations and can serve to discern driving me

135 that has been shown to significantly reduce asthma exacerbations and improve lung function for patie

136 d those inner-city children with and without asthma exacerbations in the fall period treated with gui

137 itamin D supplementation reduces the rate of asthma exacerbations requiring treatment with systemic c

138 lity, preterm birth, hospital attendance for asthma exacerbations, and hospital attendance for respir

139 ly and rapidly depletes eosinophils, reduces asthma exacerbations, and improves lung function for pat

140 that significantly reduces the incidence of asthma exacerbations, was also effective as an oral gluc

141 tory syncytial virus (RSV) infection induces asthma exacerbations, which leads to worsening of clinic

142 ory tract infections synergistically promote asthma exacerbations.

143 Patients with stable asthma exhibited exaggerated capsaicin-evoked cough resp

144 In this study of inner-city students with asthma, exposure to mouse allergen in schools was associ

145 lic access transcriptomics datasets of human asthma, followed by text mining to evaluate functional m

146 Similarly, in children with asthma, fungal exposure was associated with increased se

147 C), CCL-2 (MCP-1) and CCL-13 (MCP-4) in both asthma groups after oral corticosteroids.

148 A subgroup of patients with TH2/TH17-low asthma had neutrophilic asthma and increased BAL fluid I

149 Only four of 56 children with current asthma had positive results for all three tests (spirome

150 ed approach to treatment decision-making for asthma has the potential to be an effective tool for imp

151 We examined the causal effect of BMI on asthma, hay fever, allergic sensitization, serum total i

152 was associated with concomitant diagnoses of asthma, hay fever, and food allergy and increased diseas

153 models were fitted to assess associations of asthma history with obesity incidence during follow-up.

154 .09) was significantly associated with child asthma hospitalizations independent of human rhinovirus

155 s Measurement Information System's Pediatric Asthma Impact Scale.

156 mette-Guerin (BCG) vaccination and childhood asthma in a birth cohort using administrative databases,

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

158 factors included county prevalence rates for asthma in children and adults, chronic obstructive pulmo

159 tions between specific modes of delivery and asthma in children from 9 European birth cohorts that en

160 d serum periostin as potential biomarkers of asthma in children.

161 lergic diseases are characteristic of severe asthma in children.

162 anagement Program (CAMP) and the Genetics of Asthma in Costa Rica Study.

163 n and correlated inversely with wheezing and asthma in nonatopic subjects.

164 l strategy for achieving clinical control of asthma in obese patients.

165 lactic potential for long-term prevention of asthma in offspring.

166 l outcomes were calculated for children with asthma in the Childhood Asthma Management Program.

167 of patients with documented well-controlled asthma in this study's primary care population increased

168 The timing and mechanisms of asthma inception remain imprecisely defined.

169 Maternal asthma increased the risk of preeclampsia.

170 In children with asthma, indoor classroom NO2 levels can be associated wi

171 VA alone induced asthma, and SEA exacerbated asthma induced by CDE.

172 For asthma induction, mice were intratracheally sensitized w

173 For persons with asthma, influenza vaccination may be effective in both r

174 define obstruction phenotypes that relate to asthma instability.

175 Asthma is a chronic airway disease characterized by infl

176 Allergic asthma is a chronic Th2 inflammation in the lungs that c

177 Asthma is a common chronic lung disease characterized by

178 Asthma is a common disease in childhood and is often pre

179 vement of epigenetic mechanisms in childhood asthma is already demonstrable at birth.

180 Differentiation from bronchial asthma is also important.

181 Neutrophilic asthma is associated with airway microbiology that is si

182 Asthma is characterized by airway inflammation, mucus se

183 rated that epithelial barrier dysfunction in asthma is characterized by persistent underlying de-diff

184 Conversely, a reduced risk for asthma is consistently found in children growing up on t

185 Prevalence of asthma is higher in women than in men, but the mechanism

186 Persistent childhood asthma is mainly atopy driven.

187 Asthma is one of the most common chronic diseases of chi

188 We found that this "core" signature of asthma is shared by mild, moderate, and severe forms of

189 RATIONALE: Severe, steroid-resistant asthma is the major unmet need in asthma therapy.

190 mitigated both early-life viral disease and asthma-like features, highlighting HMGB1 as a possible n

191 rolled weeks (WCWs) have been used to assess asthma long-term control but have never been validated f

192 ars) as compared with childhood-onset severe asthma (<18 years) were selected from the U-BIOPRED coho

193 pted in 2 independent cohorts, the Childhood Asthma Management Program (CAMP) and the Genetics of Ast

194 ed for children with asthma in the Childhood Asthma Management Program.

195 progress in the diagnosis and management of asthma, many patients have poorly controlled or refracto

196 the Igf1r plays an important role in murine asthma, mediating both AHR and mucus secretion after HDM

197 story of chronic pulmonary disease or use of asthma medication in the past 5 years.

198 Specifically, asthma medication usage and respiratory symptoms increas

199 A murine transgenerational asthma model was used to identify involved pathways.

200 asthma control and face the greatest risk of asthma morbidity and mortality.

201 ocioeconomic status (SES) is associated with asthma morbidity in observational studies, but the facto

202 We used an HDM-driven asthma mouse model to compare the capacity of Jagged 1 a

203 Comparisons to severe asthma multicenter studies and available registries show

204 ons between severe asthma (SA) and nonsevere asthma (NONSA) may be confounded by differential adheren

205 c IgE (sIgE), which may lead to occupational asthma (OA).

206 Asthma-one of the most common chronic, non-communicable

207 etween microorganisms including pathogens in asthma onset, severity and exacerbation, yet with the ex

208 ice did not contribute to the enhancement of asthma or arthritis and seemed to be due to alterations

209 in was not associated with risk of childhood asthma or other allergic disorders.

210 ere significantly correlated with changes in asthma outcomes.

211 The Epidemiology and Natural History of Asthma: Outcomes and Treatment Regimens (TENOR I) study

212 In some patients with moderate-to-severe asthma, particularly those with noneosinophilic inflamma

213 cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeut

214 2 responses of allergen-specific T cells and asthma pathogenesis by activating Treg cells.

215 Our results suggest that asthma pathophysiology might be differentially associate

216 Work-related asthma patients exposed to protein allergens and isocyan

217 We classified problems of asthma patients into biological, psychological and adher

218 Two hundred twenty two well-controlled asthma patients receiving ICS or ICS/LABA were assessed

219 ted using commercial artus assay in 10.7% of asthma patients, but was negative in all control individ

220 severe exacerbation rates among "problematic asthma" patients and develop a risk score to predict the

221 n rates over five years for 177 "problematic asthma" patients presenting to a specialist asthma clini

222 a2ARs on airway epithelial cells promote the asthma phenotype and that the proinflammatory pathway do

223 a-arrestin-2 (betaarr-2(-/-)) attenuates the asthma phenotype as in beta2AR(-/-) mice.

224 activation is required for expression of the asthma phenotype in mice, but the cell types involved ar

225 ion and could contribute to the eosinophilic asthma phenotype.

226 d airflow obstruction associated with severe asthma phenotypes.

227 ssociated with increased risk for persistent asthma, potentially through modulating susceptibility to

228 liary clearance, a characteristic feature of asthma, produces spontaneous type 2 airway inflammation

229 The Finnish Asthma Program resulted in significant cost savings at b

230 lyps, and comorbid asthma completed the Mini Asthma QOL Questionnaire (miniAQLQ) and Asthma Control T

231 atients have poorly controlled or refractory asthma (RA).

232 n lower estradiol, with odds ratios (OR) for asthma ranging from 1.25 for PFOS (95% Confidence Interv

233 Ethyl-paraben was associated with increased asthma rate [hazard rate (HR)=1.10; 95% confidence inter

234 In this review, eight major asthma-related comorbidities are discussed: rhinitis, ch

235 ependently associated with increased risk of asthma-related ED visits and hospitalizations.

236 7A enhanced IL-13-induced gene expression in asthma-relevant murine and human cells.

237 omal lymphopoietin (TSLP), in patients whose asthma remained uncontrolled despite treatment with long

238 se patterns were investigated in relation to asthma, rhinitis, and eczema.

239 Longitudinal associations between prevalent asthma, rhinitis, and IgE sensitization and mold or damp

240 tion and RV wheezing had additive effects on asthma risk at adolescence.

241 It determined high asthma risk through excessive sIgE production and direct

242 an association between Asp358Ala and COPD or asthma risk, and to explore the role of the Asp358Ala va

243 t was associated with increased or decreased asthma risk.

244 ssive sIgE production early in life affected asthma risk.

245 oidism in the perinatal period and childhood asthma risk.

246 % CI, 1.20-27.83) scales in association with asthma risk.

247 NALE: Phenotypic distinctions between severe asthma (SA) and nonsevere asthma (NONSA) may be confound

248 he ARIA (Allergic Rhinitis and its Impact on Asthma) score ranging from 0 to 4 of the Allergy Diary w

249 n to measure cytokine production relevant to asthma (secondary outcomes).

250 n phenotypes that are indicators of risk for asthma severity and instability.

251 muscle/mast cell interactions contribute to asthma severity by transiently increasing MMP activation

252 rpg phenotype also had the highest Composite Asthma Severity Index score, the highest asthma treatmen

253 sis, gene expression networks in relation to asthma severity provided potentially new insight into bi

254 as similar across health and the spectrum of asthma severity, but the percentage of neutrophils expre

255 irways disease and have been associated with asthma severity.

256 iated with increased serum IL-17A levels and asthma severity.

257 ma Control and Communication Instrument, and asthma-specific HRQOL was assessed using the Patient-Rep

258 ictive value for NLP algorithm in predicting asthma status were 97%, 95%, 90%, and 98%, respectively.

259 iated with the risk genotype was modified by asthma status.

260 mediating pediatric severe therapy-resistant asthma (STRA).

261 Study [n = 30] and the Childhood Origins of Asthma Study [n = 28]) was analyzed by using bisulfite s

262 Children enrolled in the School Inner-City Asthma Study were followed for 1 academic year.

263 hildren enrolled in the Childhood Origins of ASThma study were followed prospectively from birth.

264 EACAM6 was significantly increased in severe asthma, suggesting the presence of an altered neutrophil

265 gen in schools was associated with increased asthma symptoms and decreased lung function.

266 environment factors that are associated with asthma symptoms beyond the residential address.

267 We detected increased reporting of asthma symptoms in regions affected by heat, pollen, and

268 Only subjects with "active asthma" (symptoms or medication in the last year, n = 74

269 E as a novel regulatory molecule in allergic asthma that acts upstream of proallergic events and sugg

270 may be less likely to respond to traditional asthma therapies (ie, corticosteroids).

271 As the armamentarium of pharmacologic asthma therapies expands, it will be critical to include

272 cy is an important criterion for approval of asthma therapies, but the clinical features of exacerbat

273 ronchodilator treatments are the mainstay of asthma therapy and are used in a stepwise approach.

274 -resistant asthma is the major unmet need in asthma therapy.

275 association between bacterial diversity and asthma to a large extent.

276 hma with that in normal-weight children with asthma to identify key differentially expressed genes as

277 ging the gap between identifying subtypes of asthma to understand causal mechanisms and translating t

278 ified and validated multiple TFs influencing asthma treatment response.

279 ite Asthma Severity Index score, the highest asthma treatment step, the greatest variability in FEV1

280 Despite high-intensity asthma treatment, these patients experience poor asthma

281 tom control remains the primary objective of asthma treatment.

282 The primary end point was the development of asthma until age 12 years.

283 ld or dampness indicator was associated with asthma up to 16 years of age (OR 1.31; 95% CI 1.08-1.59)

284 L-1beta protein levels, whereas eosinophilic asthma was associated with an IL-13-induced TH2 signatur

285 METHOD: Asthma was determined in 370 participants (218 HIV-infec

286 Asthma was inversely associated with richness [aOR = 0.4

287 s obtained to determine how the diagnosis of asthma was originally made in the community.

288 Asthma was solely associated with pattern 1 (odds ratio

289 Participants in whom a diagnosis of current asthma was ultimately ruled out were followed up clinica

290 ic rhinitis (AR) related to mite allergy and asthma were based on yearly interviews at the ages of 1

291 vels, associations between PFAS exposure and asthma were consistently stronger among children with hi

292 Participants with mild asthma were enrolled in a double-blinded, placebo-contro

293 isorders involving marked eosinophilia (e.g. asthma), were particularly elevated in the peritoneum.

294 airways, the actual site of inflammation in asthma, which is hardly accessible in population studies

295 Of 434 children with asthma who consented, 286 (mean age, 7.7 yr; male sex, 6

296 The stronger inverse association of asthma with bacterial diversity in mattress dust as comp

297 Offspring asthma with hayfever was more strongly associated with p

298 he use of NPPV in children with acute severe asthma with respiratory muscle fatigue and failure of me

299 T-cell transcriptome in obese children with asthma with that in normal-weight children with asthma t

300 t differed between children with and without asthma, with the highest BMI being seen among females wi