ライフサイエンスコーパス: childhood asthma

1 us-C infection and is associated with severe childhood asthma.

2 the strongest known genetic risk factor for childhood asthma.

3 f airway hyperreactivity in a mouse model of childhood asthma.

4 s overproduction in airway diseases, such as childhood asthma.

5 or methylation levels, were associated with childhood asthma.

6 effects on the development and morbidity of childhood asthma.

7 his may be a viable preventative therapy for childhood asthma.

8 evere RSV would be associated with decreased childhood asthma.

9 und, leukotriene B4 (LTB4), in patients with childhood asthma.

10 perinatal stress have not been examined for childhood asthma.

11 or gestational age are at increased risk for childhood asthma.

12 intestinal microbiota in the development of childhood asthma.

13 mising avenue of therapeutic development for childhood asthma.

14 phenotypes to identify potential markers of childhood asthma.

15 or in late pregnancy may be associated with childhood asthma.

16 iations of early growth characteristics with childhood asthma.

17 95% CI, -2.39 to 18.20) in the likelihood of childhood asthma.

18 isms may contribute to the predisposition to childhood asthma.

19 the subsequent risk of developing persistent childhood asthma.

20 ts, such as reducing the risks of obesity or childhood asthma.

21 ses the likelihood of development of classic childhood asthma.

22 h current approaches in 'difficult-to-treat' childhood asthma.

23 wheezing illnesses and hospitalizations for childhood asthma.

24 n the first year of life are associated with childhood asthma.

25 strongly with the presence or future risk of childhood asthma.

26 s also independently associated with risk of childhood asthma.

27 ons between infant antipyretic use and early childhood asthma.

28 c airway inflammation and is associated with childhood asthma.

29 ronchiolitis-are at high risk for developing childhood asthma.

30 ight lead to chronic airway inflammation and childhood asthma.

31 it remains unclear whether AT also improves childhood asthma.

32 ment and subsequently predispose children to childhood asthma.

33 e reported effects of day care attendance on childhood asthma.

34 his technique has limited its application to childhood asthma.

35 of the association between breastfeeding and childhood asthma.

36 e, birth weight, and infant weight gain with childhood asthma.

37 lopment of immune-mediated diseases, such as childhood asthma.

38 tinct genetic factors affect Feno values and childhood asthma.

39 romal lymphopoietin (TSLP) gene variants and childhood asthma.

40 e is associated with increased risk of later childhood asthma.

41 describe the spectrum and natural history of childhood asthma.

42 etween SPINK5 and TSLP, which contributes to childhood asthma.

43 -roadway air pollution (NRP) exposure causes childhood asthma.

44 ransferase P (GSTP1) and PM10 on the risk of childhood asthma.

45 understanding the subsequent development of childhood asthma.

46 onchopulmonary dysplasia, bronchiolitis, and childhood asthma.

47 elated pollutants may be causally related to childhood asthma.

48 zae, is associated with later development of childhood asthma.

49 e GSTP1 gene may alter the susceptibility to childhood asthma.

50 en neonatal total serum bilirubin levels and childhood asthma.

51 tial gene-air pollution interaction model on childhood asthma.

52 luence of gene-air pollution interactions on childhood asthma.

53 f genetic variants at 17q21 near ORMDL3 with childhood asthma.

54 mia was associated with an increased risk of childhood asthma.

55 ted with increased but differential risks of childhood asthma.

56 ich in humans are potential risk factors for childhood asthma.

57 ic variants associated with earlier onset of childhood asthma.

58 3.02-19.26) of ADRB2 methylation and severe childhood asthma.

59 particularly in urban centers, and incident childhood asthma.

60 inatal exposure to UFPs and the incidence of childhood asthma.

61 of patients with mild-to-moderate persistent childhood asthma.

62 ms, including methylation, can contribute to childhood asthma.

63 hylation in newborns and children related to childhood asthma.

64 nt with its substantial genetic influence on childhood asthma.

65 ested a role for Tet1 in the pathogenesis of childhood asthma.

66 ncluding the exacerbation and development of childhood asthma.

67 g food allergy, atopic dermatitis/eczema, or childhood asthma.

68 sma metabolome, and diet in association with childhood asthma.

69 pollutant reduction in reduced incidence of childhood asthma.

70 ome during illnesses were related to risk of childhood asthma.

71 tal life exposure to UFPs and development of childhood asthma.

72 ed from a nationwide Swedish study on severe childhood asthma.

73 ted with the development and exacerbation of childhood asthma.

74 en may be an area for possible prevention of childhood asthma.

75 y associated than body mass index (BMI) with childhood asthma.

76 a greatly increased likelihood of developing childhood asthma.

77 ChRM3 may have disease-modifying benefits in childhood asthma.

78 mean age 61 years, were followed up: 38 with childhood asthma; 53 with childhood wheezy bronchitis; a

79 n SPINK5 (P = .003) and TSLP (P = .006) with childhood asthma; a SPINK5 single nucleotide polymorphis

80 d the involvement of behavioural problems in childhood asthma according to phenotypes.

81 Yearly childhood asthma, allergic rhinitis, and eczema diagnose

82 region of ORMDL3, which are associated with childhood asthma, alter transcriptional regulation of OR

83 Bacterial exposure in house dust determined childhood asthma and allergies.

84 The natural course of childhood asthma and allergy is complex and not fully un

85 blings have been shown to reduce the risk of childhood asthma and allergy, but the mechanism driving

86 early-life farming exposures protect against childhood asthma and allergy; few data exist on asthma a

87 It is increasingly clear that childhood asthma and atopy are not single phenotypes, an

88 Although an association between childhood asthma and chronic obstructive pulmonary disea

89 e results suggest a novel mechanism of early childhood asthma and demonstrates the importance of phen

90 e to environmental chemical contaminants and childhood asthma and eczema.

91 the strongest known genetic determinants for childhood asthma and have been reported to interact with

92 ate pregnancy was negatively associated with childhood asthma and hay fever (adjusted odds ratio [OR]

93 sed parental reports on infantile eczema and childhood asthma and hay fever for 3778 pairs of 7-year-

94 Childhood asthma and obstructive sleep apnea (OSA), both

95 e specific estimates for the heritability of childhood asthma and other allergic diseases, to attempt

96 n DENND1B are associated with development of childhood asthma and other immune disorders.

97 ta sets: transcriptomic data from a study of childhood asthma and proteomic data from a study of Alzh

98 (HRV) have been linked to the development of childhood asthma and recurrent acute asthma exacerbation

99 obacco smoke is a well-known risk factor for childhood asthma and reduced lung function, but the effe

100 To identify trajectories of childhood asthma and to characterize the potential impac

101 om genomewide association studies (GWAS) for childhood asthma and to test the same variants against o

102 an section is associated with higher risk of childhood asthma and wheeze in developed Western setting

103 n is established early in life, manifests as childhood asthma and wheezy bronchitis, and continues in

104 human milk is associated with higher risk of childhood asthma, and 2) among children and adolescents

105 ty production, such as pounds of pollutants, childhood asthma, and cancer, outperform monetary saving

106 y in life acts as a predictive biomarker for childhood asthma, and excess pregnancy weight gain in th

107 RT1 might influence sex-specific patterns of childhood asthma, and its expression in testis tissue an

108 etect effects smaller than an OR of 1.33 for childhood asthma, and the analyses were restricted to wh

109 rgic sensitizations are common in persistent childhood asthma, and thorough assessment of allergy is

110 The COPD risk increased with childhood asthma, and wheezy bronchitis was associated w

111 In conclusion, childhood asthma appears to drive an increase in the ons

112 Morbidity and mortality associated with childhood asthma are driven disproportionately by childr

113 Associations between vitamin D status and childhood asthma are increasingly reported, but direct c

114 Infant respiratory viral infection and childhood asthma are the most common acute and chronic d

115 tial confounders and using time to report of childhood asthma as analysis outcome, risk of asthma was

116 cross-sectionally associated with increased childhood asthma, atopic dermatitis, and allergic rhinit

117 We estimated the cost of childhood asthma attributable to residential NRP exposur

118 The trajectory to childhood asthma begins at birth and involves epigenetic

119 Children in the Urban Environment and Childhood Asthma birth cohort were followed through age

120 irth in 329 subjects in the "Environment and Childhood Asthma" birth cohort study in Oslo by using ti

121 children in the URECA (Urban Environment and Childhood Asthma) birth cohort through age 7 years, refl

122 sociated with infant respiratory disease and childhood asthma, but limited epidemiological data exist

123 nfancy are associated with increased risk of childhood asthma, but little is known about the role of

124 lay an important role in the pathogenesis of childhood asthma, but the potentially modifiable exposur

125 of violence contribute to the occurrence of childhood asthma, but there is little information on the

126 rst year of life increases the likelihood of childhood asthma by 19.87 percentage points (95% confide

127 We developed a Markov simulation model of childhood asthma by using data from the Childhood Asthma

128 population, the effects of air pollution on childhood asthma can be better understood.

129 Childhood asthma clusters, or subclasses, have been deve

130 Recently, results from the CLARA childhood asthma cohort suggested an implication of IL-3

131 off points for well-controlled asthma of the Childhood Asthma Control Test (C-ACT) and the Asthma Con

132 The Childhood Asthma Control Test (C-ACT) is a clinically va

133 improves asthma control, as measured by the Childhood Asthma Control Test and Asthma Control Test in

134 including asthma control, measured based on Childhood Asthma Control Test or the Asthma Control Test

135 There was no difference in the Childhood Asthma Control Test score (difference in chang

136 mber of children with an Asthma Control Test/Childhood Asthma Control Test score of less than the con

137 tilation and microstructure in subjects with childhood asthma could advance our understanding of dise

138 s and their application to study pathways to childhood asthma development.

139 ion were significantly associated with early childhood asthma development.

140 specific mold exposures are associated with childhood asthma development.

141 ity of acute respiratory tract infection and childhood asthma development.

142 ient ultrafine particles (UFPs; <0.1 mum) on childhood asthma development.

143 ntial as an application to study pathways to childhood asthma development.

144 Childhood asthma developmental programming is complex.

145 Childhood asthma develops from a complex interaction amo

146 Childhood asthma diagnosis and medication used.

147 At 18 months, we used parental report of childhood asthma diagnosis, wheeze symptoms, and recurre

148 In conclusion, childhood asthma drives an increase in the onset of obes

149 er vitamin D3 supplementation reduces severe childhood asthma exacerbations is unclear.

150 The rs6967330 SNP confers risk of severe childhood asthma exacerbations, likely through increasin

151 dae Enterovirus, is strongly associated with childhood asthma exacerbations.

152 infections among children and are linked to childhood asthma exacerbations.

153 enetic variants associated specifically with childhood asthma, except for one SNP shared with hay fev

154 re studies highlighting associations between childhood asthma, fetal lung and/or immune development,

155 barrier dysfunction can alter the course of childhood asthma, food allergy, and allergic rhinosinusi

156 iwan in the Genetic and Biomarkers study for Childhood Asthma from 2009-2010.

157 Reports of childhood asthma from ages 9, 11, and 13 and self-report

158 Childhood asthma has become a critical public health pro

159 Racial disparities in childhood asthma have been a long-standing target for in

160 Prior transcriptomic studies of childhood asthma have primarily investigated subjects wh

161 Persons with a childhood-asthma history tended to have a higher educati

162 30 SNP showed a significant association with childhood asthma hospitalization.

163 pollutants play a role in the development of childhood asthma, however, remains uncertain.

164 Novel immune-regulatory mechanisms in childhood asthma identified increased Treg cells in pati

165 iation study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases

166 fy early-life environmental risk factors for childhood asthma in a birth cohort of high-risk inner-ci

167 cillus Calmette-Guerin (BCG) vaccination and childhood asthma in a birth cohort using administrative

168 leotide polymorphisms (SNPs) associated with childhood asthma in a genome-wide association study are

169 associated with increased risk of early life childhood asthma in children less than 3 years old over

170 gene, has been consistently associated with childhood asthma in genome-wide association studies.

171 Early-life NO(2) exposure is associated with childhood asthma in Latinos and African Americans.

172 nner and improve the recognition and care of childhood asthma in practice.

173 Little is known about prematurity and childhood asthma in Puerto Rican subjects.

174 ive analysis of the intestinal metabolome of childhood asthma in this ancillary study of the Vitamin

175 b NO(2) was estimated to result in 20% lower childhood asthma incidence (95% CI, -27% to -11%) compar

176 regnancy remained positively associated with childhood asthma incidence (hazard ratio per interquarti

177 tween exposure to ambient air pollutants and childhood asthma incidence (up to age 6) were estimated

178 Model results indicated that childhood asthma incidence rates would have been statist

179 Problematic severe childhood asthma includes a subgroup of patients who are

180 al cord serum is associated with features of childhood asthma including maternal atopy, early childho

181 y and cough without cold are associated with childhood asthma, independent of infant wheeze.

182 play an important role in the development of childhood asthma, indicating that antibiotics taken duri

183 Childhood asthma is a complex disease with known heritab

184 Childhood asthma is a major public health concern and ha

185 Childhood asthma is a significant public health problem

186 that involvement of epigenetic mechanisms in childhood asthma is already demonstrable at birth.

187 radigm shift brought by the recognition that childhood asthma is an aggregated diagnosis that compris

188 Childhood asthma is characterized by disparities in the

189 Childhood asthma is classified into allergic asthma (AA)

190 Risk for childhood asthma is conferred by alleles within the 17q2

191 -related air pollution exposure and incident childhood asthma is inconsistent and may depend on genet

192 ass index (BMI) should be used in studies of childhood asthma is largely unknown.

193 Childhood asthma is likely the result of gene-by-environ

194 any protective effect of BCG vaccination on childhood asthma is likely to be transient.

195 Persistent childhood asthma is mainly atopy driven.

196 iation between early exposure to animals and childhood asthma is not clear, and previous studies have

197 verweight in the association between LGA and childhood asthma is unclear.

198 ssociation between overweight or obesity and childhood asthma is unknown.

199 e association between lower birth weight and childhood asthma is well established.

200 URECA (Urban Environment and Childhood Asthma) is a birth cohort at high risk for ast

201 rt demonstrated a doubled risk for COPD from childhood asthma-like symptoms.

202 lish a clear association between nonallergic childhood asthma, lower whole-blood sphingolipids, and a

203 children with asthma who participated in the Childhood Asthma Management Cohort.

204 was attempted in 2 independent cohorts, the Childhood Asthma Management Program (CAMP) and the Genet

205 cells derived from asthmatic subjects in the Childhood Asthma Management Program (CAMP) clinical tria

206 obtained at baseline/prerandomization in the Childhood Asthma Management Program (CAMP) could serve a

207 ped 383 asthmatic trios participating in the Childhood Asthma Management Program (CAMP) using a compe

208 e independent and ethnically diverse cohorts-Childhood Asthma Management Program (CAMP); Children, Al

209 erbation in 2 pediatric clinical trials: the Childhood Asthma Management Program (n = 581) and the Ch

210 idence for interaction with dust mite in the Childhood Asthma Management Program (P = .02 to .03), wi

211 acerbations, 3.91 vs 1.53]; P = .0089 in the Childhood Asthma Management Program [mean exacerbations,

212 An application to family data from the Childhood Asthma Management Program Ancillary Genetic St

213 blood of 299 young adult participants in the Childhood Asthma Management Program study.

214 udinal lung function phenotypes in 581 white Childhood Asthma Management Program subjects (P < 10(-4)

215 d-to-moderate asthma who participated in the Childhood Asthma Management Program were followed for a

216 genome-wide association study data from the Childhood Asthma Management Program, a clinical trial in

217 c patients and 846 control subjects from the Childhood Asthma Management Program, with verification b

218 children with asthma who participated in the Childhood Asthma Management Program.

219 41 children with asthma participating in the Childhood Asthma Management Program.

220 ildren with mild-to-moderate asthma from the Childhood Asthma Management Program.

221 pproaches on 403 subjects and trios from the Childhood Asthma Management Program.

222 l of childhood asthma by using data from the Childhood Asthma Management Program.

223 e calculated for children with asthma in the Childhood Asthma Management Program.

224 in three independent validation cohorts; the Childhood Asthma Management Programme (clinical trial, n

225 in lung function in patients with persistent childhood asthma may reveal links between asthma and sub

226 Childhood asthma morbidity and mortality in New Orleans,

227 n of these modifiable risk factors for urban childhood asthma morbidity offers a ripe opportunity for

228 ence-based and evidence-informed guidelines, childhood asthma morbidity remains high.

229 Childhood asthma morbidity remains significant, especial

230 l environment is an important contributor to childhood asthma morbidity.

231 2.5 microns (PM2.5) and maternal stress and childhood asthma (n = 736).

232 Heart, Lung, and Blood Institute; and Merck Childhood Asthma Network sponsored a joint workshop to d

233 xFRC)-have been linked to increased risk for childhood asthma.Objectives: To examine the individual a

234 ssociated with a 61% increase in the risk of childhood asthma (odds ratio = 1.61, 95% confidence inte

235 irth and 3 months were at increased risk for childhood asthma (odds ratio [OR], 4.1; confidence inter

236 It has been noted that childhood asthma often improves between childhood and ad

237 haemoglobin was not associated with risk of childhood asthma or other allergic disorders.

238 ing the risk conferred by maternal asthma on childhood asthma or recurrent wheeze development.

239 gnancies in women with and without asthma on childhood asthma or recurrent wheeze development.

240 odour was associated with increased risk of childhood asthma (OR 1.60; 95% CI 1.17-2.19), and adult

241 He had no history of pneumonia, childhood asthma, or tuberculosis.

242 7 weeks) and low birth weight (<2500 g) with childhood asthma outcomes.

243 gher infant weight gain were associated with childhood asthma outcomes.

244 strongly associated with an earlier onset of childhood asthma (P </= .002), whereas the 16q12 single

245 during development and long-term sequelae of childhood asthma, patient-centered outcomes research, an

246 Associations between childhood asthma phenotypes and genetic, immunological,

247 a novel strategy improved classification of childhood asthma phenotypes but requires validation in e

248 The most important variables for classifying childhood asthma phenotypes comprised novel identified g

249 Childhood asthma phenotypes reflecting underlying develo

250 , limited data exist on the risk factors for childhood asthma phenotypes.

251 pes and prediction of the clinical course of childhood asthma phenotypes.

252 pecially to cat, for attenuating the risk of childhood asthma, pneumonia, and bronchiolitis in geneti

253 in were associated with an increased risk of childhood asthma (pooled odds ratio, 1.34 [95% CI, 1.15-

254 INE and EMBASE (1946-2017) for all available childhood asthma prediction models and focused on extern

255 Childhood asthma prevalence and morbidity varies among L

256 Rationale: Puerto Ricans have the highest childhood asthma prevalence in the United States (23.6%)

257 ernal history of asthma were associated with childhood asthma prevalence up to 15 years of age.

258 life triclosan or paraben concentrations and childhood asthma, recurrent wheeze, or allergic sensitiz

259 predicting who will remit or have persistent childhood asthma remains difficult.

260 Asthma Management Program (n = 581) and the Childhood Asthma Research and Education (n = 205) networ

261 We assessed co-occurrence of childhood asthma, rhinitis and eczema using unsupervised

262 These global findings on sibship size and childhood asthma, rhinoconjunctivitis and eczema suggest

263 ta indicate that the role of antioxidants in childhood asthma risk may have a critical time window of

264 l obesity measures should be incorporated in childhood asthma risk predictions.

265 nteractions between sex and polymorphisms on childhood asthma risk were evaluated in the Multicentre

266 d dogs has shown diverging associations with childhood asthma risk, and gene-environment interaction

267 , especially when it is untreated, increases childhood asthma risk.

268 ions or not at all is associated with higher childhood asthma risk.

269 l hypothyroidism in the perinatal period and childhood asthma risk.

270 of asthmatic mothers and was associated with childhood asthma risk.

271 iet can be a promising strategy for reducing childhood asthma risk.

272 and lean mass (all p-values<0.001) and with childhood asthma (RR 2.56, 95% CI 1.38-4.76 per unit sco

273 fe) and the total score of P-CASES (Parental Childhood Asthma's Self-efficacy Scale).

274 between exposures to household microbes and childhood asthma severity stratified by atopic status.

275 ween an important environmental exposure and childhood asthma severity.

276 The Urban Environment and Childhood Asthma study examined a birth cohort at high r

277 r findings were replicated in an independent childhood asthma study in Latinos (P = 5.3 x 10(-3), com

278 tudies using the latest IlluminaBeadChips: a childhood asthma study with methylation measured in both

279 ation of several prenatal factors to risk of childhood asthma supports the early origins hypothesis f

280 evels, and therefore might contribute to the childhood asthma susceptibility signal from 17q21.

281 osomal SNPs were tested for association with childhood asthma symptoms by logistic regression using a

282 s reached genome-wide significance level for childhood asthma symptoms: the 14q11 region flanking the

283 Other modifiable risk factors in urban childhood asthma that have emerged include dietary and n

284 Current childhood asthma therapies have little effect on lung fu

285 ts in ORMDL3 may confer a risk of developing childhood asthma through dysregulation of sphingolipid s

286 These associations explain the risk of childhood asthma to a substantial extent.

287 ies of how the social environment can affect childhood asthma to include characteristics of earlier g

288 e by cluster could provide new insights into childhood asthma treatment.

289 birth cohort from the Urban Environment and Childhood Asthma (URECA) study.

290 genome-wide scan of G x sex interaction for childhood asthma using data from the Children's Health S

291 tify gene-environment interaction effects on childhood asthma using genome-wide single-nucleotide pol

292 The heritability of any childhood asthma was 0.82 (95% CI 0.79-0.85).

293 In adjusted multivariate analyses, childhood asthma was associated with an increased risk o

294 he inverse associations of birth weight with childhood asthma were explained by gestational age at bi

295 The associations of lower birth weight with childhood asthma were largely explained by gestational a

296 canopy cover with subsequent development of childhood asthma, wheeze, rhinitis, and allergic sensiti

297 Maternal asthma is a strong risk factor for childhood asthma, whereas vitamin D (VD) has emerged as

298 derable minority of patients with persistent childhood asthma will have disease remission by adulthoo

299 on more specific asthma phenotypes, such as childhood asthma with severe exacerbations, and on relev

300 iation between neonatal bilirubin levels and childhood asthma without phototherapy intervention in th