ライフサイエンスコーパス: childhood-onset

1 with chronic isolated proteinuria and early childhood onset.

2 The Allegheny County (Pennsylvania) childhood-onset (age < 18 years) type 1 diabetes registr

3 ective cohort study of 933 participants with childhood-onset (aged <17 years) type 1 diabetes diagnos

4 he population into five age-at-onset groups: childhood onset (ages <12), adolescent onset (ages 12-17

5 icoagulation is commonly prescribed in acute childhood-onset AIS although practice varies with AIS su

6 ways, only 30-50% of which meet traditional childhood onset allergic criteria.

7 resentation is highly variable, ranging from childhood-onset Alpers-Huttenlocher syndrome to adult-on

8 monogenic systemic lupus erythematosus with childhood onset and anti-dsDNA reactivity.

9 Here we present childhood-onset and actionable adult-onset disease risk,

10 kocyte telomere length in study members with childhood-onset and adolescent/adult-onset asthma was no

11 Childhood-onset and adult-onset asthma differ with respe

12 fy shared and distinct genetic risk loci for childhood-onset and adult-onset asthma, and to identify

13 prototypical yet poorly understood forms of childhood-onset and complex hereditary spastic paraplegi

14 The extent to which childhood-onset and late-onset adult ADHD may reflect di

15 atients were divided into classic infantile, childhood-onset, and adult-onset patients.

16 She has a history of childhood-onset antibody defects, cytopenias, and T lymp

17 Childhood-onset anxiety disorders frequently persist int

18 For childhood-onset arterial ischaemic stroke (AIS), treatme

19 d 25OHD on the risk of asthma (n = 146,761), childhood onset asthma (n = 15,008), atopic dermatitis (

20 imates were more than three times larger for childhood-onset asthma (0.327) than for adult-onset dise

21 dividuals with asthma, including adults with childhood-onset asthma (onset before 12 years of age), a

22 91 genes with a significant joint effect on childhood-onset asthma (P < 10(-5)).

23 d genome-wide association studies (GWAS) for childhood-onset asthma and adult-onset asthma each compa

24 arger studies, particularly in patients with childhood-onset asthma and allergic diseases, in these i

25 Phenotypes of childhood-onset asthma are characterized by distinct tra

26 are largely a subset of the genetic risk for childhood-onset asthma but with overall smaller effects,

27 k assessments might be able to predict which childhood-onset asthma cases remit and which become life

28 ng of the results of a meta-analysis of nine childhood-onset asthma GWASs (5,924 and 6,043 subjects,

29 Overall, we learned that childhood-onset asthma is associated with the most indep

30 er smokers, except that differential %LAA in childhood-onset asthma were not seen in them.

31 Disorders such as esophageal diseases and childhood-onset asthma were recently reported to occur m

32 -21 are associated with an increased risk of childhood-onset asthma, a risk known to be modified by e

33 sthma, 0.95 (95% CI 0.69-1.31, p = 0.76) for childhood-onset asthma, and 1.12 (95% CI 0.92-1.37, p =

34 Of cohort members with childhood-onset asthma, those with higher genetic risk w

35 ergic diseases, particularly with respect to childhood-onset asthma, which involves genes that reflec

36 contribute to sex-specific predisposition to childhood-onset asthma.

37 homeostasis, have been strongly linked with childhood-onset asthma.

38 re largely a subset of those associated with childhood-onset asthma.

39 q to be a highly significant risk factor for childhood-onset asthma.

40 of doctor-diagnosed asthma: 9433 adults with childhood-onset asthma; 21 564 adults with adult-onset a

41 plications (EDC) prospective cohort study of childhood-onset (at <17 years of age) type 1 diabetes, w

42 e, CABC1/ADCK3 mutations, not only in severe childhood-onset ataxia, but also in patients with mild c

43 a, asthma-COPD overlap, obese-comorbid, mild childhood-onset atopic asthma, and mild intermittent.

44 The moderate-to-severe childhood-onset atopic asthma, asthma-COPD overlap, and

45 identified 5 phenotypes: moderate-to-severe childhood-onset atopic asthma, asthma-COPD overlap, obes

46 Cluster 3 (9.7%) female-early-childhood-onset-atopic-wheeze-with-impaired-lung-functio

47 Cluster 6 (9.7%) male-late-childhood-onset-atopic-wheeze-with-impaired-lung-functio

48 Cluster 1 (12.3%) male-early-childhood-onset-atopic-wheeze-with-normal-lung-function

49 ters merit attention and are associated with childhood onset, atopy, impaired lung function and in so

50 Differential diagnosis between childhood onset attention-deficit/hyperactivity disorder

51 ressive neurodegenerative syndrome featuring childhood onset blindness, cerebellar ataxia, nystagmus,

52 ity of cases with detectable mutations had a childhood onset but most are now adults, reflecting the

53 Most patients have childhood onset, but some experience the first symptoms

54 ar family revealed that three offspring with childhood-onset cardiomyopathy had inherited three misse

55 To unravel the genetic cause of childhood-onset cardiomyopathy in a consanguineous popul

56 Childhood-onset cardiomyopathy is a heterogeneous group

57 Cases with childhood-onset cardiomyopathy were consecutively recrui

58 e impact of consanguinity on the genetics of childhood-onset cardiomyopathy, the value of adopting a

59 polymorphisms (SNPs) were analyzed in 2,531 childhood-onset case subjects (median time since diagnos

60 similar and unique clinical presentation of childhood-onset chorea and characteristic brain MRI show

61 ulting in an accumulation of lymphocytes and childhood onset chronic lymphadenopathy, splenomegaly, m

62 Growing numbers of persons with childhood-onset chronic illnesses are surviving to adult

63 eficiency in an otherwise healthy adult with childhood-onset classic KS.

64 d markedly decreased alpha-GalA activity and childhood-onset classic manifestations, except for angio

65 hich genetic risk factors are shared between childhood-onset (COA) and adult-onset (AOA) asthma has n

66 on to spastic paraplegia is characterized by childhood onset cognitive impairment, thin corpus callos

67 ers of young adults surviving congenital and childhood onset conditions following improved multidisci

68 additional information for their child about childhood-onset conditions with low or no clinical actio

69 genetic mechanisms in the manifestations of childhood-onset conditions.

70 al cohort of 885 adult subjects with SLE (90 childhood-onset [cSLE], 795 adult-onset [aSLE]).

71 The prevalence of RAF1 mutations was ~9% in childhood-onset DCM cases in these three cohorts.

72 a rare multisystem disease characterized by childhood-onset diabetes mellitus and progressive neurod

73 tations/deletions are a cause of neonatal or childhood-onset diabetes with or without exocrine insuff

74 to date and demonstrate that they can cause childhood-onset diabetes, with protein instability being

75 tients did not develop neonatal diabetes but childhood-onset diabetes.

76 including seven sporadic patients with early childhood onset disease and four familial cases with lat

77 ional views of asthma have centered around a childhood onset disease with an allergic component, seve

78 Affected members of two families had childhood onset disease with very slow progression.

79 nGS revealed a risk of childhood-onset disease in 15/159 (9.4%) newborns; none

80 , identifies features that are unique to the childhood-onset disease, identifies gaps, and proposes r

81 ecific IgE were more common among those with childhood-onset disease.

82 gest that the clinical course of this common childhood onset disorder impacts the functional connecti

83 activity disorder (ADHD) was thought to be a childhood-onset disorder that has a limited effect on ad

84 nically and genetically highly heterogeneous childhood-onset disorder.

85 The largest associations were observed for childhood-onset disorders (1061 cases [29.7%] vs 1362 co

86 st that CAs are associated with 44.6% of all childhood-onset disorders and with 25.9% to 32.0% of lat

87 tal brain development is more pronounced for childhood-onset disorders, such as autism spectrum disor

88 both diagnostic and treatment approaches to childhood-onset disorders.

89 lated individuals with a complex progressive childhood-onset dystonia, often associated with a typica

90 from five unrelated families presented with childhood-onset dystonia, optic atrophy, and basal gangl

91 timing of myelination in the pathogenesis of childhood-onset dystonia.

92 ism and implicate disturbed lipid biology in childhood-onset DYT1 dystonia.

93 has different risk factor associations than childhood-onset eczema.

94 und that (i) encephalopathies with infantile/childhood onset epilepsies (>/=3 months of age) occur al

95 alopathies are a devastating group of severe childhood onset epilepsies with medication-resistant sei

96 aut syndrome and Dravet syndrome, two severe childhood-onset epilepsies, provide evidence of anti-sei

97 This suggests childhood onset epilepsy preferentially alters maturatio

98 were originally enrolled in the Turku Adult Childhood Onset Epilepsy study at the mean (SD) age of 5

99 t and should be mainstream practice in early childhood onset epilepsy.

100 ssion is less common than in other causes of childhood onset epilepsy.

101 Nine individuals with childhood-onset epilepsy (22%) and 3 control participant

102 uate a cohort of 143 adults with unexplained childhood-onset epilepsy and intellectual disability who

103 croarray analysis in adults with unexplained childhood-onset epilepsy and intellectual disability.

104 o determine whether adults with a history of childhood-onset epilepsy exhibit increased brain amyloid

105 population-based cohort of individuals with childhood-onset epilepsy in southwestern Finland, togeth

106 e of pre-surgical evaluations and surgery in childhood-onset epilepsy patients has not previously bee

107 pharmacoresistant epilepsy, and 52/1 000 000 childhood-onset epilepsy patients undergoing epilepsy ev

108 Adults with childhood-onset epilepsy, particularly APOE epsilon4 car

109 ngly appreciated as part of the phenotype of childhood-onset epilepsy.

110 re developmental delay as well as of ID with childhood onset focal epilepsy.

111 ples (combined N = 5599) yielded evidence of childhood onset for 6 of 12 variants present in both Asi

112 5% CI 1.365-1.448; p=1.45 x 10(-111)) in the childhood-onset GWAS.

113 The requirement of a childhood onset has always been a key criterion for the

114 he adaptor protein complex 4 (AP-4) leads to childhood-onset hereditary spastic paraplegia (AP-4-HSP)

115 Four consanguineous families with childhood-onset humoral immune deficiency and features o

116 Myoclonus dystonia syndrome is a childhood onset hyperkinetic movement disorder character

117 f adulthood, the contribution of genetics to childhood-onset hypertrophy is unknown.

118 Childhood-onset hypertrophy should prompt genetic analys

119 s and nearly two thirds of familial cases of childhood-onset hypertrophy.

120 Most autosomal genetic causes of childhood-onset hypogammaglobulinemia are currently not

121 ies presented with an unusual combination of childhood-onset hypogammaglobulinemia with recurrent inf

122 nd cause-specific mortality in patients with childhood-onset IBD, during childhood and adulthood.

123 nd cause-specific mortality in patients with childhood-onset IBD.

124 Childhood-onset inflammatory bowel disease (IBD) is beli

125 to the development of therapeutics for this childhood-onset interferonopathy and adult systemic auto

126 microcytic anemia, and panniculitis-induced childhood-onset lipodystrophy) in adults.

127 l association results for these 23 SNPs with childhood-onset (<17 years) T1D were extracted from a me

128 the molecular genetic basis and phenotype of childhood onset macular dystrophies and to summarize cur

129 he genes associated with the major causes of childhood onset macular dystrophies have now been identi

130 4 in cluster 4 (n = 82 [17.5%]; ie, moderate childhood-onset male rhinitis with asthma) had high atop

131 specific cutaneous lesions in patients with childhood-onset mastocytosis are associated with other d

132 s might exist, particularly in patients with childhood-onset mastocytosis.

133 is are not useful for distinguishing PN from childhood-onset melanoma as opposed to adult-onset melan

134 Only 1 patient with childhood-onset melanoma had a FISH aberration compared

135 Patients with PNs and the 5 patients with childhood-onset melanoma had numerical chromosomal aberr

136 t patients with PNs and 4 of 5 patients with childhood-onset melanoma showed homogeneous staining for

137 1 mutations are responsible for infantile or childhood-onset mitochondrial disease, hallmarked by the

138 Childhood-onset mitochondrial encephalomyopathies are se

139 Childhood-onset mitochondrial encephalomyopathies are us

140 s, whereas recessive SLC25A4 mutations cause childhood-onset mitochondrial myopathy and cardiomyopath

141 The infant/childhood onset motoneuron disease spinal muscular atrop

142 Childhood onset motor neuron diseases or neuronopathies

143 The childhood-onset motor disorder DYT6 dystonia is caused b

144 PRRT2 mutations have been described in other childhood-onset movement disorders, different forms of s

145 taneous lesions as a prognostic parameter in childhood-onset MPCM.

146 nant BAG3-P209L mutation results in a severe childhood-onset myofibrillar myopathy (MFM) associated w

147 = 49), or glomerular-non-HUS (heterogeneous childhood onset; n = 216).

148 ransporters are also candidate genes for the childhood onset-neural degenerative syndrome Brown-Viale

149 ly compose the most common Mendelian form of childhood-onset neurodegeneration.

150 Niemann-Pick type C disease (NPC) is a childhood onset neurodegenerative disorder arising from

151 that loss of NRROS function causes a severe childhood-onset neurodegenerative condition with feature

152 onal ceroid lipofuscinosis (JNCL) is a fatal childhood-onset neurodegenerative disorder caused by mut

153 This review focuses on childhood-onset neurodegenerative disorders with perturb

154 Rett syndrome is a severe childhood onset neurodevelopmental disorder caused by mu

155 ature and should be reclassified as an early-childhood-onset neurodevelopmental condition in DSM-5.

156 a roadmap is particularly relevant for early-childhood-onset neurodevelopmental conditions, which eme

157 n deficit hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder with a preva

158 a prevailing assumption that adult ADHD is a childhood-onset neurodevelopmental disorder, no prospect

159 with the ADHD symptom picture may not have a childhood-onset neurodevelopmental disorder.

160 Comorbidity with childhood-onset neurodevelopmental disorders and psychia

161 Angelman syndrome (AS) is a childhood-onset neurogenetic disorder characterized by f

162 isorder is a chronic and typically impairing childhood-onset neurologic condition.

163 ataxia of Charlevoix-Saguenay (ARSACS) is a childhood-onset neurological disease resulting from muta

164 n the widely expressed TOR1A gene causes the childhood onset, neurological disease of DYT1 dystonia.

165 In conclusion, we describe a novel childhood-onset neurometabolic disease caused by choline

166 nherited in an autosomal recessive fashion a childhood onset neuropathy and optic atrophy.

167 Tourette Disorder (TD) is a childhood-onset neuropsychiatric and neurodevelopmental

168 Tourette syndrome (TS) is a childhood-onset neuropsychiatric disorder characterized

169 ely accepted, and has long been dominant for childhood-onset neuropsychiatric disorders.

170 ns that represent the most common subtype of childhood onset non-dystrophic muscle disorders.

171 ma was classified as life-course-persistent, childhood-onset not meeting criteria for persistence, an

172 uity, +0.95 [0.34] logMAR [20/180 Snellen]), childhood-onset nyctalopia, myopia (mean [SD] refractive

173 The critical region for childhood-onset obesity in the WAGR syndrome was located

174 Mutation carriers exhibited hyperphagia, childhood-onset obesity, disproportionate insulin resist

175 eostasis universal to hyperphagia-associated childhood-onset obesity.

176 ied in a large cohort of people with severe, childhood-onset obesity.

177 ring the first years of life, as well as for childhood-onset obesity.

178 ch are the leading cause of monogenic severe childhood-onset obesity.

179 ted with lower levels of serum BDNF and with childhood-onset obesity; thus, BDNF may be important for

180 Childhood-onset obsessive-compulsive disorder (OCD) affe

181 Many children with childhood-onset obsessive-compulsive disorder (OCD) fail

182 acy of the serotonin reuptake inhibitors for childhood-onset obsessive-compulsive disorder and the an

183 ere we review the diagnosis and treatment of childhood-onset OCD in light of pediatric and adult stud

184 o have the strongest genetic etiology (i.e., childhood-onset OCD), in 33 Caucasian families with >/=2

185 set OCD), in 33 Caucasian families with >/=2 childhood-onset OCD-affected individuals from the United

186 as an adjunctive treatment for children with childhood-onset OCD.

187 A childhood onset of autosomal dominant CMT2A is the most

188 but tractable Mendelian disorder leading to childhood onset of diffuse skin fibrosis with autosomal

189 plex neurological condition characterized by childhood onset of dysfunction in multiple cognitive dom

190 incidence of non-immune hydrops fetalis and childhood onset of facial and four limb lymphoedema.

191 The childhood onset of idiopathic cardiac hypertrophy that o

192 ferative syndrome (ALPS) is characterized by childhood onset of lymphadenopathy, hepatosplenomegaly,

193 d net of these symptom counts with male sex, childhood onset of PTSD, high exposure to prior (to the

194 le predominance (female/male ratio, 4:1) and childhood onset of the disease (91%) with frequent famil

195 e in IBD incidence worldwide associated with childhood-onset of IBD coupled with the diseases' longev

196 mutations more likely to be associated with childhood onset (P = .0011).

197 hese patients results in rapidly progressive childhood-onset parkinsonism-dystonia with distinctive b

198 at ages 32 and 38 years were used to define childhood-onset persistent asthma (n = 91), late-onset a

199 Childhood-onset persistent asthma is associated with air

200 Smoking history and childhood-onset persistent asthma were both associated w

201 with lower FEV1/FVC ratios among those with childhood-onset persistent asthma.

202 remitting, school age-onset persisting, late childhood-onset persisting, and continuous wheeze.

203 discoveries for asthma are associated with a childhood-onset phenotype.

204 was strongly positive in most patients with childhood-onset PNs (10 of 11 patients) and melanoma (al

205 We present a case of early childhood-onset pork-cat syndrome possibly due to sensit

206 FAHN/SPG35 manifests with early childhood onset predominantly lower limb spastic tetrapa

207 th bi-allelic variants in UNC45B who exhibit childhood-onset progressive muscle weakness.

208 t CDH3-related disease is characterized by a childhood-onset, progressive chorioretinal atrophy confi

209 ractivity disorder (ADHD), which is a common childhood-onset psychiatric disorder with high heritabil

210 associations between HLA-DRB1 SE alleles and childhood-onset RA (76% of patients carried 1 or 2 SE al

211 enotypes were obtained for 204 patients with childhood-onset RA and 373 healthy control subjects.

212 A total of 155 children with childhood-onset RA and 684 healthy controls were genotyp

213 ween TNFAIP3, STAT4, and PTPN22 variants and childhood-onset RA are similar to those observed in RA,

214 estigate the largest cohort of patients with childhood-onset RA for association with SE alleles and t

215 ed in RA, suggesting that adult-onset RA and childhood-onset RA share common genetic risk factors.

216 ation of these variants in susceptibility to childhood-onset RA using a weighted genetic risk score (

217 We tested each locus for association with childhood-onset RA via logistic regression.

218 Childhood-onset RA was associated with TNFAIP3 rs1049919

219 r wGRS was associated with increased risk of childhood-onset RA, especially among males.

220 associated variants are also associated with childhood-onset RA, we investigated RA-associated varian

221 investigated these alleles in patients with childhood-onset RA, which is defined as rheumatoid facto

222 A-associated variants with susceptibility to childhood-onset RA.

223 ession to test the wGRS for association with childhood-onset RA.

224 iants at 5 loci in a cohort of patients with childhood-onset RA.

225 oding HLA-DRB1 alleles and susceptibility to childhood-onset RA.

226 , *0401, *0404, *0405, *0408, and *1001) and childhood-onset RA.

227 ere, we report a 7-year-old Italian boy with childhood-onset rapidly progressive encephalomyopathy an

228 Charlevoix-Saguenay, one of the most common childhood-onset recessive ataxias.

229 5 cause a ciliopathy characterized by severe childhood onset retinal blindness, Leber congenital amau

230 Children with childhood-onset rheumatoid arthritis (RA) include those

231 in cluster 1 (n = 128 [27.4%]; ie, moderate childhood-onset rhinitis) had high atopy and eczema prev

232 LRPAP1 gene mutations confer a high risk of childhood-onset RRD and PVR.

233 Childhood onset schizophrenia (COS), defined as onset be

234 rogressive cortical gray matter (GM) loss in childhood-onset schizophrenia (COS) across both lateral

235 Childhood-onset schizophrenia (COS) is a rare and severe

236 Childhood-onset schizophrenia (COS) is a rare and severe

237 NTEXT Nonpsychotic siblings of patients with childhood-onset schizophrenia (COS) share cortical gray

238 ch subject, in a sample of 106 patients with childhood-onset schizophrenia and 102 age-matched health

239 as independently replicated in patients with childhood-onset schizophrenia as compared with their par

240 ested that deficits in cortical thickness in childhood-onset schizophrenia may normalize over time, s

241 in magnetic resonance scans were obtained in childhood-onset schizophrenia probands (N=89, 198 scans)

242 Childhood-onset schizophrenia probands had a fixed reduc

243 examined large-scale network interactions in childhood-onset schizophrenia, a severe form of the dise

244 hood, by reviewing sibling studies from both childhood-onset schizophrenia, and the more common adult

245 volumes in relation to age for patients with childhood-onset schizophrenia, their nonpsychotic health

246 Fixed hippocampal volume loss seen in childhood-onset schizophrenia, which is not shared by he

247 on-deficit/hyperactivity disorder (ADHD) and childhood-onset schizophrenia.

248 potent stem cells derived from patients with childhood-onset SCZ.

249 tarting at age >/=18 years) as compared with childhood-onset severe asthma (<18 years) were selected

250 n patients with adult-onset as compared with childhood-onset severe asthma were identified in nasal b

251 nd optic atrophy (PEHO) syndrome is an early childhood onset, severe autosomal recessive encephalopat

252 uced gray matter volume in the patients with childhood- onset SLE with neurocognitive deficit versus

253 her incidence of renal disease in those with childhood-onset SLE (78% versus 52% in adults; P = 0.000

254 An inception cohort with childhood-onset SLE (n = 67) was compared with an incept

255 Twenty-two patients with childhood-onset SLE and 19 healthy controls underwent hi

256 Eighty-five percent of patients with childhood-onset SLE and 88% of patients with adult-onset

257 sed SLE risk in two independent populations: childhood-onset SLE and adult-onset SLE.

258 Compared with the control group, the childhood-onset SLE group showed statistically significa

259 Children with childhood-onset SLE have more active disease at presenta

260 Neurocognitive deficit in patients with childhood-onset SLE is associated with multifocal decrea

261 followup, the mean SDI scores in those with childhood-onset SLE were higher than those with adult-on

262 e programs were used in a published study of childhood-onset SLE which yielded novel associations wit

263 ter volume was also reduced in patients with childhood-onset SLE with neurocognitive deficit, and the

264 ive deficit versus controls or patients with childhood-onset SLE without neurocognitive deficit.

265 10(-10), odds ratio >1.5) in both adult- and childhood-onset SLE, in 4 different ethnic groups, with

266 between gray and white matter alterations in childhood-onset SLE, whether the underlying mechanisms r

267 of neurocognitive deficit in 8 patients with childhood-onset SLE.

268 Childhood-onset SMS is a rare but underrecognized and tr

269 We identified 8 patients with childhood-onset SMS, representing 5% of patients with SM

270 hyperglycinemia had normal development with childhood-onset spastic paraplegia, spinal lesion, and o

271 detected 61 independent asthma loci: 23 were childhood-onset specific, one was adult-onset specific,

272 Genes at the childhood onset-specific loci were most highly expressed

273 respiratory and swallowing difficulties and childhood-onset spinal deformities.

274 enotyped cohort of patients with congenital, childhood-onset SRNS.

275 lly banal-appearing melanocytic lesions with childhood onset suggests that the combined lesions with

276 l Assessment Metrics (Ped-ANAM) when used in childhood-onset systemic lupus erythematosus (SLE).

277 agnoses of juvenile idiopathic arthritis and childhood-onset systemic lupus erythematosus are likely

278 Similarly, childhood-onset systemic lupus erythematosus is likely a

279 eatment of juvenile idiopathic arthritis and childhood-onset systemic lupus erythematosus.

280 he NCLs, a group of disorders with infant or childhood onset that are caused by single gene mutations

281 Tourette syndrome (TS) is a childhood-onset tic disorder associated with abnormal de

282 (aged 1-30 years) with severe, intractable, childhood-onset, treatment-resistant epilepsy, who were

283 plications (EDC) prospective cohort study of childhood-onset type 1 diabetes and DCCT/EDIC, we show t

284 nalysis of the life expectancy of those with childhood-onset type 1 diabetes because weighting of ins

285 n monozygotic (MZ) twin pairs discordant for childhood-onset type 1 diabetes could reflect distinct s

286 The incidence of childhood-onset type 1 diabetes has been increasing at a

287 ol subjects (n = 2,235) were genotyped at 20 childhood-onset type 1 diabetes loci and FCRL3, GAD2, TC

288 Patients with childhood-onset type 1 diabetes show abnormal monocyte g

289 Monocytes in childhood-onset type 1 diabetes show distinct gene expre

290 MZ twin pairs (n = 10 pairs) discordant for childhood-onset type 1 diabetes, normal control twin pai

291 In contrast with childhood-onset type 1 diabetes, the genetics of autoimm

292 Of 24 genes abnormally expressed in childhood-onset type 1 diabetes, we revalidated abnormal

293 cy were associated with an increased risk of childhood-onset type 1 diabetes.

294 isease (CAD) in a cohort of individuals with childhood-onset type 1 diabetes.

295 Childhood-onset type 1 diabetes.

296 r can be subtyped according to age at onset (childhood-onset versus adolescent-onset) and the presenc

297 e trajectories (never/infrequent wheeze, mid-childhood onset wheeze, early transient wheeze, and pers

298 Cluster 2 (24.2%) early-childhood-onset-wheeze-with-intermediate-lung-function h

299 Cluster 5 (24.6%) female-late-childhood-onset-wheeze-with-normal-lung-function showed

300 Early childhood-onset wheezing that persists into adolescence