ライフサイエンスコーパス: asthma

1 cupational and environmental pollutants, and asthma).

2 m eosinophils and inhibit lung mast cells in asthma.

3 as associated with reduced risk of new-onset asthma.

4 All interventions were for asthma.

5 rgillus may impinge on clinical phenotype in asthma.

6 e that aligned with that of FA alone but not asthma.

7 (TLBW), autism spectrum disorder (ASD), and asthma.

8 ate the airway environment, particularly for asthma.

9 aluated in pediatric patients with bronchial asthma.

10 ng allergic inflammation, but is impaired in asthma.

11 y after 12 to 18 months in those with severe asthma.

12 of human diseases including scrub typhus and asthma.

13 tified black race and progression from AD to asthma.

14 cell junction in the pathological changes of asthma.

15 a-related coughing may identify uncontrolled asthma.

16 l Chinese medicine, in preclinical models of asthma.

17 mation in allergic airway disease, including asthma.

18 used ovalbumin and house dust mite models of asthma.

19 ed corticosteroids and 122 (31%) with severe asthma.

20 mptoms, but not alone to diagnose or monitor asthma.

21 ), to identify individuals with uncontrolled asthma.

22 n reserved for patients with more persistent asthma.

23 s in patients suffering from severe forms of asthma.

24 chanism that licenses tissue inflammation in asthma.

25 esented modest association with eosinophilic asthma.

26 es were associated with clinical features of asthma.

27 eatments and interventions for patients with asthma.

28 e to complex and heterogeneous traits beyond asthma.

29 veolar lavage fluid from individuals without asthma.

30 been shown to be associated with the risk of asthma.

31 106 studies were retrieved, most focused on asthma.

32 way obstruction and inflammation in allergic asthma.

33 seful biomarker for moderate-severe allergic asthma.

34 t of subjects with or without ICS-naive mild asthma.

35 be useful for long-term control of pediatric asthma.

36 hould improve the health of individuals with asthma.

37 and damp air [P = .012]) were more common in asthma.

38 clustering stability in patients with severe asthma.

39 ways capable of promoting or protecting from asthma.

40 are now established biological mechanisms in asthma.

41 hway of complement activation in nonallergic asthma.

42 ciated with adaptive Th2 immune responses in asthma.

43 ion (47%), pharyngitis (18%), and allergy or asthma (11%).

44 n those with nonfatal cases had a history of asthma (13 of 57 [23%] vs. 102 of 1297 [8%]), cardiac di

45 tation 25(OH)D increase in participants with asthma (20.9 nmol/L) and COPD (21.5 nmol/L) was lower th

46 nd girls were equally likely to has resolved asthma (33% vs 29%).

47 or sputum from 175 children: 99 with chronic asthma, 39 with acute asthma and 37 controls.

48 umonia (41% vs 28%; p = 0.02) and less often asthma (8% vs 23%; p < 0.01).

49 novel therapeutic target for obesity-related asthma, a disease that is suboptimally responsive to cur

50 We hypothesized that asthma acquisition from pre- to post-adolescence was ass

51 aboratory-confirmed influenza in people with asthma across all seasons.

52 erventions included the Triple A (Adolescent Asthma Action) programme and a peer-led camp based on th

53 for all-cause pneumonia, bronchiolitis, and asthma admissions in children aged 2-23 months.

54 Clinical factors, including asthma, allergic rhinitis, eosinophil count of at least

55 Asthma, allergic rhinitis, eosinophil count of at least

56 allergic diseases such as atopic dermatitis, asthma, allergic rhinitis, food allergy, contact allergy

57 No subject had a history of asthma/allergic rhinitis: all had negative results for a

58 responses in human diseases such as cancer, asthma, allergy, neurodegeneration, and autoimmune disea

59 s from 10 patients with moderate, persistent asthma and 10 matched, nonallergic controls, and then in

60 ldren: 99 with chronic asthma, 39 with acute asthma and 37 controls.

61 ys a significant role in the pathogenesis of asthma and allergic airway disease (AAD).

62 ithelial cells from children and adults with asthma and allergic rhinitis.

63 ted milk products is associated with reduced asthma and atopic dermatitis.

64 When the children were 6 years of age, asthma and atopic traits were diagnosed by pediatricians

65 No associations were observed between asthma and B- or T-cell numbers.

66 microRNAs (miRNAs) have been associated with asthma and chronic obstructive pulmonary disease (COPD).

67 iseases including, respiratory diseases like asthma and chronic obstructive pulmonary disease.

68 e pathophysiology of airway diseases such as asthma and chronic obstructive pulmonary disease.

69 ecruited 156 children with severe persistent asthma and controls for nasal transcriptome profiling an

70 for Siglec-8 is increased in sputum cells in asthma and correlates with gene expression for eosinophi

71 were used to assess the associations between asthma and corticosteroid use and the risk of COVID-19-r

72 suggest a novel mechanism of early childhood asthma and demonstrates the importance of phenotype-spec

73 various diseases like cancer, ulcers, tumor, asthma and fever.

74 es examining viral infections and subsequent asthma and from understanding the relationships between

75 ST2 expression was examined in subjects with asthma and healthy controls in bronchial epithelium from

76 d in severe asthma compared to mild-moderate asthma and healthy volunteers.

77 ase eosinophils in sputum from patients with asthma and inhibit FcepsilonR1-activated mast cells in l

78 ic corticosteroid use to manage uncontrolled asthma and its associated healthcare burden may account

79 Among children with persistent asthma and low vitamin D levels, vitamin D3 supplementat

80 fect modification on the association between asthma and lung cancer was identified for the variables

81 Comorbidities were present in 28%, including asthma and overweight.

82 cantly associated with a lower prevalence of asthma and rhinitis at the age of 7(0.41 [0.18:0.97] and

83 cal Study on the Genetics and Environment on Asthma and the European Community Respiratory Health Sur

84 Binding Proteins (IGFBPs)" route in allergic asthma and the lectin pathway of complement activation i

85 type 2 inflammation in patients with severe asthma and those with frequent exacerbations.

86 ance of PD-1 agonistic treatment in allergic asthma and underscore its therapeutic potential.

87 pecies richness at baseline and the onset of asthma and wheezing at the age of 7.

88 ta for clinical research concerning allergy, asthma, and immunology and highlights the potential, cha

89 eterogeneity in research concerning allergy, asthma, and immunology.

90 hospital admissions for respiratory disease, asthma, and pneumonia peaked at lag 3 by 8.85% (95% CI:

91 c vapor product was associated with lifetime asthma, and this association was stronger when an electr

92 e with important roles in allergic diseases, asthma, and tissue fibrosis.

93 th with a strong gradient); diabetes; severe asthma; and various other medical conditions.

94 age, race, and sex in multivariate analysis (asthma aOR = 2.61 [95% CI = 2.14-3.18]; allergic rhiniti

95 vated FeNO was associated with self-reported asthma (aOR, 2.65 [95% CI, 1.66-4.24]; P < .001) but not

96 y of the identified susceptibility genes for asthma are expressed in the airway epithelium, supportin

97 ing the pathogenesis of prenatally triggered asthma are largely unknown.

98 d elevated sputum eosinophils+neutrophils in asthma associated with lowest lung function, greater hea

99 eosinophil recruitment, mucin production and asthma-associated cytokines in the bronchoalveolar lavag

100 d with changes in DNAm during this period at asthma-associated cytosine-phosphate-guanine (CpG) sites

101 In parallel, we show asthma-associated factors are attenuated in human cells

102 Using the top 100 asthma-associated methylation markers as classifiers fro

103 Cleaners are at risk of some asthma-associated symptoms and reduced lung function.

104 es, and we correlated these with presence of asthma at 6, 8, 11, 13, and 18 years of age.

105 t asthma/wheeze in age 0-8 years and current asthma at ages 2, 3, 4, 5 and 6 years.

106 their association with allergic diseases and asthma at the ages of 4 and 7.

107 investigate the role of this inflammasome in asthma at the molecular level.

108 She had daily asthma attacks from the age of fourteen, and the additio

109 In asthma, bronchial epithelium protein expression of ST2 i

110 In intractable bronchial asthma cases, it is necessary to consider the complicati

111 Allergic asthma causes substantial morbidity and constitutes a pu

112 d treatment for respiratory diseases such as asthma, chronic bronchitis, and emphysema.

113 prototype chronic allergic diseases allergic asthma, chronic spontaneous urticaria and atopic eczema.

114 tas was associated with an increased risk of asthma coherently during multiple time points and also w

115 D (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of resp

116 mbers were significantly decreased in severe asthma compared to mild-moderate asthma and healthy volu

117 eolar lavage fluid from patients with severe asthma compared with in bronchoalveolar lavage fluid fro

118 The responses of children with asthma compared with those without asthma were lower for

119 he case of a 66-year-old patient with severe asthma complicated by eosinophilic chronic rhinosinusiti

120 Th17 pathways in the sputum of subjects with asthma.Conclusions: This study of sputum microRNA and mR

121 ary function deficits in obese children with asthma.Conclusions: We found enrichment of Rho-GTPase pa

122 ndertaken to determine the optimal levels of asthma control and the potential value of different trea

123 Secondary endpoints included 6-item asthma control questionnaire (ACQ-6) and lung function.

124 Improved asthma control was particularly evident in allergic asth

125 y such associations were modified by current asthma, current hay fever, pollen sensitization, age, an

126 roRNA and mRNA expression from patients with asthma demonstrates the existence of microRNA networks a

127 Some patients with asthma develop bronchospasm after the ingestion of aspir

128 An immunocompetent adult with asthma developed severe human metapneumovirus (HMPV) ill

129 mmune system plays an essential function for asthma development in both thyroid and lung tissues.

130 an the control group, and the probability of asthma development was significantly lower.

131 hma was based on a validated algorithm using asthma diagnoses from hospital visits and prescribed ast

132 life measure, greater than or equal to 5 or asthma diagnosis, bronchodilator or inhaled steroids, or

133 findings show cholinergic neuroplasticity in asthma driven by TrkB signaling and suggest that the BDN

134 iagnoses from hospital visits and prescribed asthma drugs from nation-wide registers, both as inciden

135 risk of HL associated with allergic disease (asthma, eczema, and allergic rhinitis) and corticosteroi

136 samples of patients according to type 2 (T2)-asthma endotypes.

137 ent in the management of ICU-admitted severe asthma episodes.

138 ic episode can experience a life-threatening asthma event.

139 (14.7%; 95% CI, 11%-19.1%) reported a severe asthma exacerbation in the 4 weeks after immunization, r

140 A trend in annual asthma exacerbation rate reduction favouring benralizuma

141 t significantly improve the time to a severe asthma exacerbation.

142 unlock novel strategies to combat asthma or asthma exacerbation.

143 population included 53,654 participants with asthma exacerbation.

144 with GSDMB expression, asthma severity, and asthma exacerbations (P < .05).

145 Rhinovirus frequently causes asthma exacerbations among children and young adults who

146 Asthma exacerbations are inflammatory events that rarely

147 with rs56151658 were associated with severe asthma exacerbations at a P value of .01 or less in the

148 xteen adults presenting to the ED with acute asthma exacerbations were recruited after giving informe

149 eting biologics (already used for preventing asthma exacerbations) have the potential to circumvent s

150 nfections (URTIs) are important triggers for asthma exacerbations.

151 virus, is strongly associated with childhood asthma exacerbations.

152 Children with both FA and asthma exhibited a metabolomic profile that aligned with

153 ot suffice to increase the severity of these asthma features.

154 irflow obstruction (AO) among adults without asthma from 11 European countries within a 20-year follo

155 ma or recurrent wheeze progression to active asthma from age 3 to 6 years (P(for) (trend) = .04).

156 ce of phenotype-specificity for discovery of asthma genes and epistasis.

157 babilistic causal methods to identify severe asthma genes and their master regulators.

158 ntrolled trial in which patients with severe asthma (GINA 4-5; n = 121) reporting URTI symptoms were

159 from the U-BIOPRED cohort identified severe asthma groups with features consistent with the presence

160 Use of the recommendations in the 2020 Asthma Guideline Update should improve the health of ind

161 According to the Global Initiative for Asthma guidelines, blood eosinophil numbers are one mark

162 pecialist, one is often asked to discuss the asthma guidelines.

163 onventional pharmacological approach to mild asthma has long relied on reliever therapy with as-neede

164 atty acid (PUFA) intake and child wheeze and asthma have been inconsistent.

165 Overweight status and asthma have increased during the last decades.

166 outcomes were greater in adults with current asthma, hay fever, and pollen sensitization.

167 to identify genetic variants associated with asthma hospitalizations.

168 smokers, this sets the stage for more severe asthma if both mother and grandmother had smoked during

169 s practice, the American Academy of Allergy, Asthma & Immunology Primary Immunodeficiency Diseases Co

170 of 2, with good specificity for outcomes of asthma improvement and worsening but poor sensitivity.

171 e relationships to features of atopy or mild asthma in adults is unknown.

172 rospective Copenhagen Prospective Studies on Asthma in Childhood 2010(2010) mother-child cohort of 70

173 ren in the Copenhagen Prospective Studies on Asthma in Childhood birth cohort.

174 known regarding the heterogeneity of severe asthma in children, particularly inflammatory signatures

175 ight gain alters the progression of allergic asthma in mice with females developing airway remodellin

176 Conclusion: A history of asthma in the preceding 10 y was not associated with imp

177 ithm among patients with community-diagnosed asthma in the United States.

178 The outcomes were measured using asthma incidence and consumption of corresponding medica

179 ased cohort of 570,595 children with data on asthma (including severity and control) in Grades 7-8 an

180 Allergic asthma is a chronic inflammatory lung disease associated

181 Asthma is a complicated chronic inflammatory disorder ch

182 Asthma is a disease of reversible airflow obstruction ch

183 al corticosteroid (OCS) treatment for severe asthma is associated with substantial disease burden.

184 s, but it remains unclear whether underlying asthma is associated with worse coronavirus disease 2019

185 Investigation of preschool asthma is important since not all children outgrow their

186 nvolvement of the large and small airways in asthma is not clear.

187 ucing OCS treatment for severe, uncontrolled asthma is not fully characterized.

188 Here we have shown that the fetal origin of asthma is orchestrated by a disrupted airway epithelium

189 resonance imaging ((129)Xe MRI) in pediatric asthma is poised to advance our understanding of disease

190 onically for IL-13 production and consequent asthma-like disease traits that peak and last long after

191 We examined regulation of this asthma-like phenotype by IL-1beta.

192 y play an important role in the induction of asthma-like phenotype.

193 In a sub-study, children with recurrent asthma-like symptoms were randomized to either a 3-day c

194 /systemic corticosteroid use is prevalent in asthma management, and the risks of acute and chronic co

195 proach to pharmacological treatment in adult asthma mandates that asthma treatment is progressively s

196 Asthma may limit imaging for PE because of either worsen

197 e a novel path forward to further uncovering asthma mechanisms and therapy.

198 ells in a house dust mite (HDM)-based murine asthma model.

199 n to be regulated in the lung endothelium in asthma models.

200 PS) and bisphenol F (BPF) is associated with asthma morbidity remains unknown.

201 ith severe asthma (n = 21) and mild/moderate asthma (n = 154) was then performed.

202 testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154) was t

203 included AR progression, asthma progression, asthma occurrence, and therapy adherence.

204 experiences with and approaches to managing asthma, of which little is known in this age group.

205 It has been noted that childhood asthma often improves between childhood and adolescence,

206 during pregnancies in women with and without asthma on childhood asthma or recurrent wheeze developme

207 n attenuating the risk conferred by maternal asthma on childhood asthma or recurrent wheeze developme

208 way hyperresponsiveness, a characteristic of asthma, on exposure to electronic cigarettes, across mou

209 ration into the lung in the rat OVA model of asthma, on the other hand, appears to be dependent on TR

210 ociated with a dose-response reduced risk of asthma onset.

211 c-Myc may unlock novel strategies to combat asthma or asthma exacerbation.

212 s in clinical samples taken from adults with asthma or COPD versus control subjects.Measurements and

213 The primary outcome was offspring with asthma or recurrent wheeze by age 3 years.

214 n women with and without asthma on childhood asthma or recurrent wheeze development.

215 sk conferred by maternal asthma on childhood asthma or recurrent wheeze development.

216 This protective trend was reiterated in asthma or recurrent wheeze progression to active asthma

217 range, 2-18 years) with physician-diagnosed asthma or recurrent wheeze were recruited, including 208

218 Our study shows that families with eczema, asthma, or allergic rhinitis should not use daily emolli

219 hronic obstructive pulmonary disease (COPD), asthma, or urinary incontinence.

220 ationship between classroom NO(2) levels and asthma outcomes by BMI stratification.

221 rant fungi compared with no children without asthma (p =< 0.001).

222 y outcomes among children born to women with asthma (P(interaction) < .05 for all outcomes).

223 .59; 95% CI, 0.33-1.03) of current diagnosed asthma (P(trend) < .05 for all).

224 Our results identify a novel pathway of asthma pathogenesis in patients with obesity/metabolic s

225 deregulated expression of genes involved in asthma pathogenesis, tissue remodeling, and tight juncti

226 affect epithelial function and contribute to asthma pathogenesis.

227 pathway has potential downstream effects on asthma pathophysiology, including on airway epithelial c

228 control was particularly evident in allergic asthma patients and correlated with decreased frequencie

229 peroxide in the exhaled breath condensate of asthma patients and healthy participants.

230 Secondly, ILO and/or asthma patients completed the BrTS prospectively, rating

231 rom peripheral blood of healthy controls and asthma patients or cultured with or without activating c

232 Severe asthma patients with high blood eosinophils or low serum

233 ents (ages 20-83; 30 healthy patients and 30 asthma patients) recruited from the John Peter Smith Hos

234 ated with measures of airflow obstruction in asthma patients.

235 putum microbiota also associated with T2-low asthma phenotype, a subgroup of whom displayed elevation

236 g mechanical properties underlying these two asthma phenotypes and the mechanisms explaining the para

237 on analysis (n = 156) of gene expression and asthma phenotypes, and pathway analysis were performed i

238 in a mouse model of severe steroid resistant asthma, potentially through the accumulation of pathogen

239 llergoid required significantly fewer AR and asthma prescriptions (59.7% vs 10.8%) than the control g

240 Study endpoints included AR progression, asthma progression, asthma occurrence, and therapy adher

241 d the recently published research letter "Is asthma protective of COVID-19?" by Carli et al.(1) with

242 The identified master regulator genes of asthma provide a novel path forward to further uncoverin

243 acologic approaches to managing symptoms and asthma-related coughing may identify uncontrolled asthma

244 d with different early-life risk factors and asthma-related outcomes in adolescence.

245 en units are significantly enriched in known asthma-related pathways.

246 framework is a first step toward developing asthma remission as a treatment target and should be ref

247 who reported having ever an ARDs (including asthma) reporting two or more.

248 In the Severe Asthma Research Program (SARP) III cohort, we determined

249 gh the impact of early life acetaminophen on asthma risk is still not clear, potential interactions w

250 es were decreased in subjects with the 17q21 asthma-risk alleles rs7216389 and rs8076131.

251 lus fumigatus, in the airway correlated with asthma severity and control.

252 Obesity influences asthma severity and may impair response to beta-AR agoni

253 ntly diminished in participants with greater asthma severity and was related to airway wall thickness

254 sites and associated with GSDMB expression, asthma severity, and asthma exacerbations (P < .05).

255 (129)Xe MRI correlates with asthma severity, health care utilization, and oral corti

256 ly methylated regions (DMRs) associated with asthma severity.

257 om-forest classifier for directly predicting asthma severity.

258 d genes that are associated with features of asthma severity.

259 a public health burden, which increases with asthma severity.

260 hway analysis from tissue-specific genes for asthma shows that the immune system plays an essential f

261 The functional consequences of IL33 asthma SNPs remain unknown.

262 As an asthma specialist, one is often asked to discuss the ast

263 ial communities in house dust was similar by asthma status but was lower (P < .05) with atopy or hay

264 d factors are attenuated in human cells from asthma subjects when exogenous SP-A is added during IL-1

265 n models were used to assess associations of asthma subtype and AF.

266 Exacerbation-prone asthma subtype has been reported in studies using data-d

267 and most consistently associated region with asthma susceptibility.

268 tic regulatory mechanisms may be crucial for asthma susceptibility.

269 y remodelling, and consequently might impact asthma symptoms and exacerbations.

270 onships between classroom NO(2) exposure and asthma symptoms and morbidity by body mass index (BMI) c

271 mab, which resulted in marked improvement of asthma symptoms and reduced the peripheral blood eosinop

272 rease in the ICS dose alone for worsening of asthma symptoms is not recommended.

273 sputum, and differentially more abundant in asthma than health.

274 children with adrenal dysfunction or severe asthma that are treated with high doses of inhaled corti

275 used for the treatment of moderate-to-severe asthma that is not controlled by inhaled steroids.

276 isk of recurrent wheezing by age 3 years and asthma that persisted throughout childhood.

277 After ICS treatment of patients with asthma, the compositional structure of sputum microbiota

278 hino-conjunctivitis with or without allergic asthma, the cost-effectiveness of SLIT (tablets, Grazax(

279 Current childhood asthma therapies have little effect on lung function tra

280 he optimal method for measuring adherence to asthma therapy remains unclear.

281 Asthma treatment in high altitude reduced the type 2 imm

282 ical treatment in adult asthma mandates that asthma treatment is progressively stepped up to achieve

283 these type-2 pathways has transformed severe asthma treatment, but necessitates robust clinical evalu

284 corticosteroids have been the foundation for asthma treatment, in a large part because they decrease

285 e and function of EVs in the pathogenesis of asthma via the PRISMA statement method.

286 odds ratio in favor of resolution of severe asthma was 2.75 (95% CI, 1.02-7.43) for those with a per

287 Asthma was based on a validated algorithm using asthma d

288 pproach, epigenome-wide CpGs associated with asthma were identified.

289 dren with asthma compared with those without asthma were lower for both RV-A and RV-C while retaining

290 astigmatism, myopia, allergic rhinitis, and asthma were positively associated with KC with adjusted

291 s with poorly controlled, moderate-to-severe asthma were scanned with hyperpolarized (3)He MRI.

292 34.1% of children with chronic asthma were sensitized to thermotolerant fungi compared

293 tients with chronic lung disease (other than asthma) were excluded.

294 from nation-wide registers, both as incident asthma/wheeze in age 0-8 years and current asthma at age

295 Similar findings are observed in Type 2 Hi asthma, where high levels of both 15LO1-PEBP1 and LC3-II

296 Q4 vs Q1, 1.70; 95% CI, 1.07-2.71) diagnosed asthma, whereas n-3 PUFAs were associated with lower ris

297 th each other to jointly predict the risk of asthma - which suggests the pivotal role of cell-cell ju

298 between patient-reported triggers of ILO and asthma, which may support clinician differential diagnos

299 Children with asthma who had a higher number of defects/slice had a hi

300 ng miRNAs from an early age in children with asthma would be prognostic of reduced lung function grow