ライフサイエンスコーパス: childhood-onset

1 correlates of decision making in adults with childhood-onset ADHD and in healthy adults.

2 th full ADHD who met all DSM-IV criteria for childhood-onset ADHD, 79 subjects with late-onset ADHD w

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

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

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

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

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

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

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

10 rum disorders among parents of patients with childhood-onset and adult-onset schizophrenia and parent

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

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

13 Childhood-onset anxiety disorders frequently persist int

14 mosome instability syndrome characterized by childhood-onset aplastic anemia, cancer or leukemia susc

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

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

17 n 317,000 SNPs in DNA from 994 patients with childhood onset asthma and 1,243 non-asthmatics, using f

18 tide polymorphisms (SNPs) on the presence of childhood onset asthma by genome-wide association.

19 be strongly and reproducibly associated with childhood onset asthma in family and case-referent panel

20 91 genes with a significant joint effect on childhood-onset asthma (P < 10(-5)).

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

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

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

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

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

26 -21 are associated with an increased risk of childhood-onset asthma, a risk known to be modified by e

27 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 =

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

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

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

31 se locus described in a French pedigree with childhood-onset ataxia and cognitive delay.

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

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

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

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

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

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

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

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

40 e typically arises in young adults, although childhood-onset BD has also been reported.

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

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

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

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

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

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

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

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

49 er (ADHD) is a highly heritable, disruptive, childhood-onset condition, the aetiology and pathogenesi

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

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

52 d IQ.Main Outcome Measure DSM-IV symptoms of childhood-onset conduct disorder rated by trained interv

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

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

55 -onset Charcot-Marie-Tooth disease type 1 to childhood-onset Dejerine-Sottas neuropathy and congenita

56 e-Tooth disease, as well as the more severe, childhood-onset Dejerine-Sottas neuropathy and congenita

57 ive observational Pittsburgh Epidemiology of Childhood-Onset Diabetes Complications Study.

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

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

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

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

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

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

64 stem inflammatory disease (NOMID) is a rare, childhood-onset disease that is characterized by chronic

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

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

67 nically and genetically highly heterogeneous childhood-onset disorder.

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

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

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

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

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

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

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

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

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

77 This suggests childhood onset epilepsy preferentially alters maturatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 Childhood-onset hypertrophy should prompt genetic analys

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

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

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

99 greater influence of perinatal exposures on childhood-onset illness.

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

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

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

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

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

105 4 in cluster 4 (n = 82 [17.5%]; ie, moderate childhood-onset male rhinitis with asthma) had high atop

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

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

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

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

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

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

112 1 mutations are responsible for infantile or childhood-onset mitochondrial disease, hallmarked by the

113 Childhood-onset mitochondrial encephalomyopathies are se

114 Childhood-onset mitochondrial encephalomyopathies are us

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

116 The infant/childhood onset motoneuron disease spinal muscular atrop

117 Childhood onset motor neuron diseases or neuronopathies

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

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

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

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

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

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

124 Cockayne syndrome (CS) is a rare recessive childhood-onset neurodegenerative disease, characterized

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

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

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

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

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

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

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

132 Comorbidity with childhood-onset neurodevelopmental disorders and psychia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Childhood onset of "adult" psychiatric disorders may be

156 ic phenotypes in the 1st year of life in the Childhood Onset of Asthma (COAST) cohort of children.

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

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

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

160 The childhood onset of idiopathic cardiac hypertrophy that o

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

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

163 rticularly if the lesion was associated with childhood onset of seizures, were impaired relative to a

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

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

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

167 rmation on 19 additional parents (parents of childhood-onset patients, N=2; parents of adult-onset pa

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

169 Childhood-onset persistent asthma is associated with air

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 Childhood-onset RA was associated with TNFAIP3 rs1049919

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

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

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

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

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

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

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

193 , *0401, *0404, *0405, *0408, and *1001) and childhood-onset RA.

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

195 The clinical characteristics of childhood-onset restless legs syndrome are described.

196 strong family history are characteristic of childhood-onset restless legs syndrome.

197 5 cause a ciliopathy characterized by severe childhood onset retinal blindness, Leber congenital amau

198 our understanding of the immunopathology of childhood-onset rheumatic diseases; however, considerabl

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

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

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

202 with schizophrenia, parents of patients with childhood-onset schizophrenia (95 parents), patients wit

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

204 atter (GM) loss is marked and progressive in childhood-onset schizophrenia (COS) during adolescence b

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

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

207 f cortical gray matter (GM) in patients with childhood-onset schizophrenia (COS), which appears great

208 ing scans were acquired for 60 subjects with childhood-onset schizophrenia (mean age=14.5 years, SD=2

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

210 mately 2-year intervals for 39 subjects with childhood-onset schizophrenia and 43 healthy subjects.

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

212 Parents of patients with childhood-onset schizophrenia had a significantly higher

213 Parents of patients with childhood-onset schizophrenia have a higher rate of schi

214 Childhood-onset schizophrenia is a rare but severe form

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

216 of some neurodevelopmental disorders such as childhood-onset schizophrenia or autism.

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

218 Childhood-onset schizophrenia probands had a fixed reduc

219 ne whether healthy siblings of patients with childhood-onset schizophrenia show structural brain abno

220 Childhood-onset schizophrenia shows progressive brain ma

221 tected a dynamic wave of gray matter loss in childhood-onset schizophrenia that started in parietal a

222 te of gray matter reduction in patients with childhood-onset schizophrenia was examined in relation t

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

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

225 ared with olanzapine in treatment-refractory childhood-onset schizophrenia, the study suggests that c

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

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

228 ttern of abnormalities seen in patients with childhood-onset schizophrenia.

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

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

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

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

233 blindness (RDH5) and an autosomal recessive, childhood-onset severe retinal dystrophy (RDH12).

234 ed to be associated with autosomal recessive childhood-onset severe retinal dystrophy.

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

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

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

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

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

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

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

242 investigate gene expression in patients with childhood-onset SLE and both of their parents.

243 erns for each FMRI paradigm in patients with childhood-onset SLE and to compare these patterns with t

244 subjects, corresponding to 251 full trios of childhood-onset SLE families, were genotyped and analyze

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

246 Patients with childhood-onset SLE had significantly higher NGAL levels

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

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

249 with those observed in controls suggest that childhood-onset SLE may be associated with abnormalities

250 y NGAL is a promising potential biomarker of childhood-onset SLE nephritis.

251 ps showing differences in activation between childhood-onset SLE patients and controls were generated

252 during times of the paradigm control tasks, childhood-onset SLE patients consistently undersuppresse

253 sensitive and 100% specific for identifying childhood-onset SLE patients with biopsy-proven nephriti

254 Ten patients with childhood-onset SLE underwent formal neuropsychological

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

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

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

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

259 agnosed as having SLE prior to age 16 years (childhood-onset SLE) was assessed for disease activity (

260 10(-10), odds ratio >1.5) in both adult- and childhood-onset SLE, in 4 different ethnic groups, with

261 FMRI abnormalities are present in childhood-onset SLE, manifesting as an imbalance between

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

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

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

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

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

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

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

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

270 Childhood-onset systemic lupus erythematosus (SLE) prese

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

272 neuropsychological testing, in patients with childhood-onset systemic lupus erythematosus (SLE).

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

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

275 been made in the diagnosis and treatment of childhood-onset systemic lupus erythematosus, juvenile i

276 This review will focus on childhood-onset systemic lupus erythematosus, juvenile i

277 risk for atherosclerosis has been studied in childhood-onset systemic lupus erythematosus.

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

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

280 disease (BBGD) is a recessive disorder with childhood onset that presents as a subacute encephalopat

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

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

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

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

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

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

289 demiology of Diabetes Complications Study of childhood-onset type 1 diabetes, first seen in 1986-1988

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 Childhood-onset type 1 diabetes.

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

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

296 of the co-occurrence of severe congenital or childhood-onset visual impairment with bone fragility or

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

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

299 Early childhood-onset wheezing that persists into adolescence

300 results in severe retinal degeneration with childhood onset when in compound heterozygous form with