ライフサイエンスコーパス: childhood asthma

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

2 wheezing illnesses and hospitalizations for childhood asthma.

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

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

5 s also independently associated with risk of childhood asthma.

6 ons between infant antipyretic use and early childhood asthma.

7 c airway inflammation and is associated with childhood asthma.

8 ight lead to chronic airway inflammation and childhood asthma.

9 it remains unclear whether AT also improves childhood asthma.

10 ment and subsequently predispose children to childhood asthma.

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

12 his technique has limited its application to childhood asthma.

13 of the association between breastfeeding and childhood asthma.

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

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

16 tinct genetic factors affect Feno values and childhood asthma.

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

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

19 describe the spectrum and natural history of childhood asthma.

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

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

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

23 understanding the subsequent development of childhood asthma.

24 onchopulmonary dysplasia, bronchiolitis, and childhood asthma.

25 elated pollutants may be causally related to childhood asthma.

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

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

28 en neonatal total serum bilirubin levels and childhood asthma.

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

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

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

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

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

34 ted with increased but differential risks of childhood asthma.

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

36 ic variants associated with earlier onset of childhood asthma.

37 3.02-19.26) of ADRB2 methylation and severe childhood asthma.

38 a greatly increased likelihood of developing childhood asthma.

39 posure in the pathogenesis and expression of childhood asthma.

40 relation to bronchial inflammation in severe childhood asthma.

41 erse association of bacterial diversity with childhood asthma.

42 ernal factors are implicated in the onset of childhood asthma.

43 regulation contributes to the development of childhood asthma.

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

45 use may be associated with increased risk of childhood asthma.

46 en identified as a potential risk factor for childhood asthma.

47 eptor (beta2AR) agonists in the treatment of childhood asthma.

48 assess the association between H. pylori and childhood asthma.

49 ng early life may be relevant to the risk of childhood asthma.

50 rent knowledge of inhaled glucocorticoids in childhood asthma.

51 ession are determinants of susceptibility to childhood asthma.

52 creased risk for both recurrent wheezing and childhood asthma.

53 tors play a major role in the development of childhood asthma.

54 the strongest known genetic risk factor for childhood asthma.

55 c bacterial products affects the presence of childhood asthma.

56 nfection illness in children and can lead to childhood asthma.

57 rent literature related to the management of childhood asthma.

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

59 virus (RSV) is associated with wheezing and childhood asthma.

60 ed there to investigate the risk factors for childhood asthma.

61 ation between day care-related exposures and childhood asthma.

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

63 or methylation levels, were associated with childhood asthma.

64 effects on the development and morbidity of childhood asthma.

65 evere RSV would be associated with decreased childhood asthma.

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

67 perinatal stress have not been examined for childhood asthma.

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

69 intestinal microbiota in the development of childhood asthma.

70 phenotypes to identify potential markers of childhood asthma.

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

72 iations of early growth characteristics with childhood asthma.

73 95% CI, -2.39 to 18.20) in the likelihood of childhood asthma.

74 isms may contribute to the predisposition to childhood asthma.

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

76 ted with the development and exacerbation of childhood asthma.

77 ses the likelihood of development of classic childhood asthma.

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

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

80 Childhood asthma, a growing health concern, has been ass

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

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

83 n about rates and predictors of remission of childhood asthma after the onset of puberty.

84 Yearly childhood asthma, allergic rhinitis, and eczema diagnose

85 cation in studies of diet and development of childhood asthma/allergies.

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

87 ide association study of the age of onset of childhood asthma among participants in the Childhood Ast

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

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

90 tors affecting the prevention and control of childhood asthma and allergy presented during Experts pr

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

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

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

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

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

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

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

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

99 Childhood asthma and obesity are significant public heal

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

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

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

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

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

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

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

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

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

109 Air pollutants have been associated with childhood asthma and wheeze.

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

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

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

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

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

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

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

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

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

119 water-damaged buildings was associated with childhood asthma at age 7 years.

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

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

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

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

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

125 mall component of the long-term prognosis in childhood asthma, but are not important determinants of

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

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

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

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

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

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

132 Childhood asthma clusters, or subclasses, have been deve

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

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

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

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

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

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

139 nal and extra-intestinal diseases, including childhood asthma development and inflammatory bowel dise

140 ion were significantly associated with early childhood asthma development.

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

142 specific mold exposures are associated with childhood asthma development.

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

144 Childhood asthma develops from a complex interaction amo

145 Childhood asthma diagnosis and medication used.

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

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

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

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

150 hand smoke are associated with occurrence of childhood asthma, few studies have investigated the role

151 and need for oral corticosteroid therapy in childhood asthma for planning and evaluation purposes.

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

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

154 Childhood asthma has become a critical public health pro

155 The risk of developing childhood asthma has been linked to the severity and eti

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

157 on was used to assess associations between a childhood-asthma history and educational level, employme

158 those with no asthma history, persons with a childhood-asthma history tended to achieve a higher educ

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

160 tment for age and race/ethnicity, men with a childhood-asthma history were more likely to work in hea

161 onal occupations, and as cooks; women with a childhood-asthma history were more likely to work in man

162 stimated 6.9% of men and 5.8% of women had a childhood-asthma history.

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

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

165 showed strong association with diagnosis of childhood asthma in 2,320 subjects from a cohort of Germ

166 fied 2 SNPs associated with earlier onset of childhood asthma in 4 independent cohorts.

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

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

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

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 ips between the post-Katrina environment and childhood asthma in NOLA and assess a novel asthma couns

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

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

175 Few recent estimates of childhood asthma incidence exist in the literature, alth

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

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

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

179 Childhood asthma is a complex disease with known heritab

180 Childhood asthma is a significant public health problem

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

182 tigated retrospectively whether a history of childhood asthma is associated with educational level an

183 Childhood asthma is characterized by disparities in the

184 Childhood asthma is classified into allergic asthma (AA)

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

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

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

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

189 Persistent childhood asthma is mainly atopy driven.

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

191 Management of childhood asthma is now being directed to early recognit

192 Childhood asthma is strongly associated with allergic se

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

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

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

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

197 GWA) study of asthma with 359 cases from the Childhood Asthma Management Program (CAMP) and 846 genet

198 B gene, both in 708 children enrolled in the Childhood Asthma Management Program (CAMP) and in their

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

200 f childhood asthma among participants in the Childhood Asthma Management Program (CAMP) and used 3 in

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

202 a subset of families ascertained through the Childhood Asthma Management Program (CAMP) Genetics Anci

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

204 ild trios and 493 trios participating in the Childhood Asthma Management Program (CAMP).

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

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

207 d trial of antiinflammatory medications (the Childhood Asthma Management Program [CAMP]).

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

209 with mild to moderate asthma enrolled in the Childhood Asthma Management Program and in their parents

210 In an ancillary study conducted in 3 of 8 Childhood Asthma Management Program Clinical Centers, ad

211 ained through offspring with asthma from the Childhood Asthma Management Program clinical trial.

212 New data from the Childhood Asthma Management Program cohort show progress

213 From the Childhood Asthma Management Program cohort, which was ra

214 hort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort.

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

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

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

218 ations estimated from the placebo arm of the Childhood Asthma Management Program with covariates of a

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

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

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

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

223 41 children with asthma participating in the Childhood Asthma Management Program.

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

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

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

227 tent asthma at the time of enrollment in the Childhood Asthma Management Program.

228 phase (November 1993-September 1995) of the Childhood Asthma Management Program.

229 t in 943 of 1041 participants (90.6%) in the Childhood Asthma Management Program; adult height was de

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

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

232 Childhood asthma morbidity and mortality in New Orleans,

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

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

235 Childhood asthma morbidity remains significant, especial

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

237 2.5 microns (PM2.5) and maternal stress and childhood asthma (n = 736).

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

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

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

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

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

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

244 7 weeks) and low birth weight (<2500 g) with childhood asthma outcomes.

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

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

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

248 Pre-redesign NHIS childhood asthma period prevalence estimates peaked in 1

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 Childhood asthma prevalence and morbidity varies among L

255 red the difference between 1988 core and CHS childhood asthma prevalence estimates to calculate an in

256 o examine the impact of the NHIS redesign on childhood asthma prevalence estimates, the authors analy

257 l Health Interview Survey (NHIS) affected US childhood asthma prevalence estimates.

258 The rise in childhood asthma prevalence suggests a role for environm

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

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

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

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

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

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

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

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

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

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

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

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

271 l hypothyroidism in the perinatal period and 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 responsiveness to beta-agonist treatment and childhood asthma severity.

277 t to chromosome 22 data from the Mexico City Childhood Asthma Study (1998-2003).

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

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

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

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

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

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

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

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

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

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

288 As part of the Urban Environment and Childhood Asthma (URECA) study, we investigated the deve

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

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

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

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

293 The SNPs associated with childhood asthma were consistently and strongly associat

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 generally normal, even in severe persistent childhood asthma, whereas FEV(1)/FVC declines as asthma

298 ummarize trends in the current literature in childhood asthma with implications for current managemen

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