ライフサイエンスコーパス: late-onset

1 of 22q11DS-related psychosis and control its late onset.

2 /low sensitization; (2) early onset; and (3) late onset.

3 rly persistent-410 ml, 95%CI -533; -287; and late onset-148 ml, 95%CI -237; -58).

4 nts (25 men) with Ala97Ser transthyretin and late onset (59.9 +/- 6.0 years) disabling neuropathy.

5 (DEGs) in published datasets comprising 450 late onset AD (LOAD) brains and 212 controls.

6 on myeloid cells 2, in the increased risk of late onset AD.

7 To the extent that sporadic late-onset AD (LOAD) also results from dysregulated beta

8 an order of magnitude more likely to develop late-onset AD (LOAD) than ApoE3/E3 carriers.

9 1524 patients with EOAD, 7046 patients with late-onset AD (LOAD), and 7001 cognitively intact contro

10 oxyglucose uptake between early-onset AD and late-onset AD groups were detectable.

11 tic risk locus BIN1 rs744373 confers risk to late-onset AD has yet to be determined.

12 A number of common variants associated with late-onset AD have been identified including apolipoprot

13 patients with early-onset AD, patients with late-onset AD have more comorbid small vessel disease (S

14 The greater extent of SVD in late-onset AD influences the association between neurona

15 Patients with late-onset AD showed a significantly greater amount of S

16 r models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contribute

17 e at-risk gene polymorphisms responsible for late-onset AD, all indicate a direct and early role of A

18 epsilon4 allele are a major risk factor for late-onset AD.

19 ene is the strongest genetic risk factor for late-onset AD.

20 llele, the strongest genetic risk factor for late-onset AD.

21 of at least part of the genetic component in late-onset AD.

22 tion study or identified as genetic nodes in late-onset AD.

23 s from multiple generations of a family with late-onset ADAD and 12 noncarrier family members were fo

24 f the PSEN1 A79V carriers in the family with late-onset ADAD, 4 were female (57%); among those with L

25 False positive late-onset ADHD cases are common without careful assessm

26 However, at age 18 years, those with late-onset ADHD demonstrated comparable ADHD symptoms an

27 ive on symptom checklists were excluded from late-onset ADHD diagnosis.

28 n such that this group consisted of a large, late-onset ADHD group with no childhood diagnosis, and a

29 Individuals seeking treatment for late-onset ADHD may be valid cases; however, more common

30 regressions indicated that individuals with late-onset ADHD showed fewer externalizing problems (OR,

31 Among individuals with impairing late-onset ADHD symptoms, the most common reason for dia

32 to clinics seeking stimulant medication for late-onset ADHD symptoms.

33 t birth-cohort studies support the notion of late-onset ADHD, but these investigations are limited by

34 The extent to which childhood-onset and late-onset adult ADHD may reflect different causes has i

35 ogen storage disorder type IV (GSDIV) or the late-onset adult polyglucosan body disease (APBD).

36 of the LT and Wnt pathways during early- or late-onset allergic airway inflammation and to address r

37 rcoma (FUS) gene can cause both juvenile and late onset ALS.

38 in the SORL1 gene have been associated with late onset Alzheimer disease (LOAD), but causal variants

39 th early onset Alzheimer's disease (75%) and late onset Alzheimer's disease (73%) assigned to one clu

40 major risk factors for cognitive decline and late onset Alzheimer's disease (AD).

41 ntified as the major genetic risk factor for late onset Alzheimer's disease (AD).

42 's disease (ADAD) is far less prevalent than late onset Alzheimer's disease (LOAD), but enables well-

43 etic polymorphisms have been associated with Late Onset Alzheimer's Disease (LOAD), but there has bee

44 The most significant genetic risk factor for late onset Alzheimer's disease is a variant of the apoli

45 Late-onset Alzheimer disease (AD), the most common form

46 BIN1 is a genetic risk factor of late-onset Alzheimer disease (AD), which was identified

47 tion 673 (A673T), appears to protect against late-onset Alzheimer disease (AD).

48 , we found strong genetic covariance between late-onset Alzheimer disease (LOAD) and amyotrophic late

49 and cerebrovascular disease to the risk for late-onset Alzheimer disease (LOAD) has been long debate

50 ignificant association between microglia and late-onset Alzheimer disease and an association between

51 ironmental factors that increase the risk of late-onset Alzheimer disease are now well recognized but

52 Our findings are consistent with a model of late-onset Alzheimer disease in which beta-amyloidosis a

53 N1 is implicated in cancers, arrhythmia, and late-onset Alzheimer disease, these findings may trigger

54 was recently identified as a risk factor for late-onset Alzheimer disease.

55 ene is the strongest genetic risk factor for late-onset Alzheimer disease.

56 OE4 is the strongest genetic risk factor for late-onset Alzheimer disease.

57 articipants: The National Institute on Aging Late-Onset Alzheimer Disease/National Cell Repository fo

58 We review the genetic risk factors for late-onset Alzheimer's disease (AD) and their role in AD

59 the microglia gene TREM2 increases risk for late-onset Alzheimer's disease (AD) but the mechanisms r

60 r aging-related cognitive decline as well as late-onset Alzheimer's disease (AD) compared to the comm

61 y patterns from voxelwise structural MRIs of late-onset Alzheimer's disease (AD) dementia patients.

62 ic risk factor influencing susceptibility to late-onset Alzheimer's disease (AD) is apolipoprotein E

63 in hippocampi of patients at early stages of late-onset Alzheimer's disease (AD), CAR levels are sign

64 Hyperinsulinemia is a risk factor for late-onset Alzheimer's disease (AD).

65 orLA expression in the brain and the risk of late-onset Alzheimer's disease (AD).

66 POE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD).

67 immune signalling molecules are involved in late-onset Alzheimer's disease (LOAD) risk.

68 y receptor Siglec-3/CD33 influences risk for late-onset Alzheimer's disease (LOAD), an apparently hum

69 important contributing mechanism underlying late-onset Alzheimer's disease (LOAD).

70 Furthermore, we applied NETAM on late-onset Alzheimer's disease data and identified 477 s

71 Early-onset and late-onset Alzheimer's disease exhibited different patte

72 opment of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear w

73 Despite close similarities with late-onset Alzheimer's disease, individuals with Down's

74 phisms are associated with increased risk of late-onset Alzheimer's disease, its role in axon growth

75 Similar to studies of late-onset Alzheimer's disease, we demonstrated increase

76 ly increases the risk for the development of late-onset Alzheimer's disease.

77 e who had nattou-(fermented-soybean) induced late-onset anaphylaxis following SCUBA diving to about 2

78 Nattou-induced late-onset anaphylaxis following SCUBA diving was suspec

79 These cases are of late onset and likely result from the interaction of man

80 in MAPKBP1 as a genetic cause of juvenile or late-onset and cilia-independent NPH.

81 ng mild or moderate toxicities as well as to late-onset and cumulative toxicities.

82 tions resulting in age-related disease, both late-onset and progressive.

83 t and progressive motor deficits, as well as late-onset and selective neuropathology in the striatum,

84 The late-onset and variable severity of the symptoms may hav

85 to classify schizophrenia into early-onset, late-onset, and very-late-onset subtypes now should be t

86 ropsychiatric disturbances (memory problems, late-onset anxiety or depression, cognitive decline, and

87 We document that T2D, both early and late onset, are characterized by reduced muscle expressi

88 ent asthma', 'early persistent asthma', and 'late onset asthma'.

89 childhood-onset persistent asthma (n = 91), late-onset asthma (n = 93), asthma in remission (n = 85)

90 in individuals with asthma-COPD overlap with late-onset asthma was 49.6 mL (3.0) per year, higher tha

91 orter in those with asthma-COPD overlap with late-onset asthma, 10.1 years (8.6-11.5) shorter in thos

92 7 (61.67-112.98) in asthma-COPD overlap with late-onset asthma, 23.80 (17.43-33.50) in COPD, and 14.7

93 ents with asthma were phenotyped and 80% had late-onset asthma, 50% had fixed airflow obstruction, an

94 sthma, and 202 with asthma-COPD overlap with late-onset asthma.

95 1.20-2.50), but not with early-transient or late-onset asthma.

96 onset transient, early-onset persistent, and late-onset asthma.

97 "Difficult," "Early-onset mild atopic," and "Late-onset asthma." Children with moderate-to-severe ast

98 e another important cause, albeit rare, of a late-onset ataxic PEO phenotype due to a disturbance of

99 n leucine-rich repeat kinase 2 (LRRK2) cause late-onset, autosomal dominant familial Parkinson's dise

100 leucine-rich repeat kinase 2 (LRRK2) lead to late-onset, autosomal dominant Parkinson's disease, char

101 Late-onset axonal Charcot-Marie-Tooth neuropathy (CMT2)

102 tein disassembly, attenuates both early- and late-onset BBB impairment, and improves long-term histol

103 ed (cnj) confer identical defects, including late onset blockage near the terminal cell-stalk cell ju

104 endogenous levels of mutant CHMP2B developed late-onset brain volume loss associated with frank neuro

105 Most late-onset cases displayed onset in adolescence and an a

106 sms was different from that implicated among late-onset cases.

107 and substance use before treating potential late-onset cases.

108 wed that some compounds specifically trigger late-onset cell death after 72 h with a unique correlati

109 nstrate that the C3H/HeSnJ inbred strain has late onset cerebellar degeneration due to this mutation.

110 Late-onset chronic (low-grade) periprosthetic joint infe

111 ased the risk of membership in the early and late-onset chronic asthma trajectories, relative to subj

112 recognized: acute, early-onset chronic, and late-onset chronic.

113 to demographic data (non-white origin, very late onset), clinical features (limited recovery from ON

114 We screened 51 index case subjects with late-onset CMT2 for mutations by whole-exome (WES) and S

115 f mutations in a so far unknown gene causing late-onset CMT2.

116 langiectasia Type 2 (MacTel) is an uncommon, late-onset complex retinal disease that leads to central

117 adiologists should be aware of this rare and late onset complication, even after many years from surg

118 ed as a differential diagnosis in cases with late-onset corneal edema post-cataract surgery.

119 ections to A1 that differ between early- and late-onset deaf animals, suggesting that potential cross

120 Myosin IIIa, defective in the late-onset deafness form DFNB30, has been proposed to tr

121 AF in hearing cats and those with early- and late-onset deafness.

122 A1 in hearing cats and those with early- and late-onset deafness.

123 R signaling in Leydig cells protects against late-onset degeneration of the seminiferous epithelium i

124 cell lineage predisposes individuals to this late-onset degeneration remains unknown.

125 Three signals explained late-onset degradation: miR-430 seeds, AU-rich sequences

126 (DMN) underlying the cognitive impairment in Late-onset depression (LOD), 32 LOD patients and 39 norm

127 Subgroup analyses showed that late-onset depression was more strongly associated with

128 ardiovascular disease than did patients with late-onset diabetes (11.1% vs 4.9%; p<0.0001).

129 at the Ins2(Akita) mouse is a good model for late-onset diabetic retinopathy.

130 ulopharyngeal muscular dystrophy (OPMD) is a late onset disease caused by polyalanine expansion in th

131 ch presents specific challenges for modeling late onset disease.

132 nts with early-onset T2DM than in those with late-onset disease (193 [56.9%] vs 110 [50.2%]; P = .02)

133 nset disease (EOD, </=7 days) or compared to late-onset disease (LOD, >7 days).

134 isease incidence was 0.41 (95% CI, .36-.47); late-onset disease incidence was 0.26 (95% CI, .21-.30).

135 the strategies and challenges for triggering late-onset disease phenotypes.

136 Strikingly, late-onset disease was associated with increased numbers

137 t photoreceptor loss except in patients with late-onset disease who had a focal preservation of the e

138 t disease and 114000 (UR, 44000-326000) with late-onset disease, of whom a minimum of 7000 (UR, 0-190

139 of 48 [54.2%]; P = .04) than did those with late-onset disease.

140 ptomatic children as compared to babies with late-onset disease.

141 eate the mechanistic links between aging and late-onset disorders, describe efforts to develop compou

142 lains how they can contribute to the risk of late-onset disorders.

143 rneal venting incision with air tamponade in late-onset DMD cases not responding to pneumatic desceme

144 ponents, with temporal differences (early vs late onset) dominant in grass and diverging patterns of

145 g, peanut and sesame; early (< 4 months) and late-onset eczema; and wheeze in the first year of life.

146 These results suggest that when large, even late-onset effects are kept at low frequency by purifyin

147 Late-onset effects of exposure to ionising radiation on

148 from fatal neonatal multisystemic disease to late-onset encephalopathy.

149 tions were exclusively seen in patients with late onset epilepsies and lack of response to sodium cha

150 ing from early onset familial AD (EOFAD) and late onset familial AD (LOAD).

151 several large family-based and case-control late-onset familial Alzheimer's disease (LOAD) samples o

152 inase 2 (LRRK2) contribute to development of late-onset familial Parkinson's disease (PD), with clini

153 Adrenomyeloneuropathy is the late-onset form of X-linked adrenoleukodystrophy, and is

154 In contrast, mutations in patients with late-onset forms and an insufficient response to sodium

155 On the other hand, susceptibility to late-onset forms of AD (LOAD) is indisputably associated

156 ping, disease-associated loci for early- and late-onset forms of myasthenia gravis.

157 ) distinct phenotypes can be seen within the late onset group, including myoclonic-atonic epilepsy (t

158 with protection against both early-onset and late-onset group B streptococcus disease.

159 more focal medial temporal lobe loss in the late-onset group.

160 EV1 was observed in the early persistent and late onset groups.

161 ears), intermediate onset (15-24 years), and late onset (>/=25 years), which were compared for clinic

162 r in Ile107Val and in Val30Met mutation with late onset (>50 years; LateMet30) FAP (p = 0.0005).

163 early-onset (<34 gestational week, n=26) and late-onset (>/=34 gestational week, n=24) samples from p

164 , or -DR had a significantly reduced risk of late-onset (>2 years after transplantation), but not ear

165 ral genetic factors have been found to cause late-onset hemochromatosis, many patients have unexplain

166 These novel models of late-onset HPP can inform on long-term skeletal and dent

167 eaning, we aimed to generate mouse models of late-onset HPP with extended life spans by engineering a

168 nocopy skeletal and dental manifestations of late-onset HPP.

169 immunodeficiency (CVID) is characterized by late-onset hypogammaglobulinemia in the absence of predi

170 ovirus seropositivity increased the risk for late-onset IA (ie, occurred >3 months after transplant)

171 Other neurodegenerative diseases with late onset in which variant segregation cannot be verifi

172 cur despite antiviral prophylaxis, including late-onset infection or recurrent disease, and patients

173 achieve the rate from the best quartile for late-onset infection, 6 years to achieve the rate from t

174 nts with sporadic inclusion body myositis, a late-onset inflammatory myopathy with prominent mitochon

175 increase susceptibility to mild-to-moderate late-onset iron overload.

176 ducing neutrophils/macrophages, resulting in late-onset, irreversible BBB damage.

177 ions in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC

178 et (present as early as 4 days after birth), late-onset lymphoid cancer development, and premature de

179 Early-onset presentations in infancy and late-onset manifestations in adults older than 70 years

180 ekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degenera

181 phic lateral sclerosis (ALS), a devastating, late-onset motor neuronal disease, with more than 150 AL

182 ith early-onset mtDNA depletion in liver and late-onset multiple deletions in brain of Mpv17-/- mice.

183 r dystrophy (OPMD) is an autosomal dominant, late-onset muscle disorder characterized by ptosis, swal

184 ive phenotype similar to human patients with late-onset muscle weakness.

185 pidermolysis bullosa simplex associated with late-onset muscular dystrophy (EBS-MD) is an autosomal r

186 mutations in families with multiple cases of late onset myelodysplastic syndrome (MDS) and/or acute m

187 e of PD-ligands, both TS1 TEM and TN induced late-onset myocarditis.

188 OPMD is a dominant, late-onset myopathy, caused by an alanine-expansion muta

189 ); "Early-onset mild non-atopic: (n = 153); "Late-onset" (n = 105); and "Exacerbation-prone asthma" (

190 ase, but were 4.43 times more likely to have late-onset neonatal GBS disease.

191 y leading to preterm births, stillbirths, or late-onset neonatal infections.

192 impaired adult hippocampal neurogenesis and late-onset neurodegeneration in mouse brains.

193 utation in the EMP lineage in mice can drive late-onset neurodegeneration.

194 associated tremor/ataxia syndrome (FXTAS), a late-onset neurodegenerative condition.

195 Late-onset neurodegenerative disease observed in patient

196 implication of other autophagy regulators in late-onset neurodegenerative disease.

197 rs using patient-specific cells, modeling of late-onset neurodegenerative diseases such as Parkinson'

198 sociated tremor/ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder affecting carriers

199 target sites in Huntington's disease (HD), a late-onset neurodegenerative disorder due to a toxic dom

200 of tissue-resident macrophages and a severe late-onset neurodegenerative disorder.

201 al neuropathy due to ATP7A mutations and the late-onset neurodegenerative disorders Alzheimer's disea

202 nowledging aging as a contributing factor in late-onset neurodegenerative disorders represents an imp

203 ging is a major risk factor in many forms of late-onset neurodegenerative disorders.

204 ar muscular atrophy (SBMA) is a progressive, late onset neuromuscular disease causing motor dysfuncti

205 Amyotrophic lateral sclerosis (ALS) is a late-onset neuromuscular disease characterized by progre

206 n TNF and BDNF, and this is accompanied by a late onset neuropathic pain behavior and increased dorsa

207 iffers notably from CVID and B(-) CVID: very late onset, no familial cases, and absence of lymphoid h

208 owever, there are no detailed assessments of late-onset, non-communicable diseases.

209 ht individuals from five families presenting late-onset NPH with massive renal fibrosis.

210 ucleotide polymorphism in a DISC1 intron and late onset of AD.

211 About 30% showed late onset of asthma diagnosis/symptoms (>40 years); the

212 , and this function may be important for the late onset of cardiac damage in DMD.

213 However, a late onset of demyelination and axonal degeneration occu

214 The late onset of limb ossification suggests that the juveni

215 rimarily characterized by nail dystrophy and late onset of mild skin fragility and acral blistering.

216 We show that the late onset of neurogenesis has a profound effect on the

217 patient with Pierson syndrome and unusually late onset of proteinuria.

218 ung adulthood and risk factors for early and late onset of sensitization.

219 e most deadly gynaecologic malignancy due to late onset of symptoms and propensity towards drug resis

220 d R161Q, which are associated with early and late onset of the CblC disorder, respectively.

221 Cluster 4 patients were late-onset older male subjects with persistent airflow o

222 In some situations (such as studies of late-onset or rapidly lethal diseases), it may be more p

223 among subjects without asthma and those with late-onset or remittent asthma, but smoking was not asso

224 rneal Dystrophy (FECD) is a highly prevalent late-onset oxidative stress disorder characterized by pr

225 Late-onset painful sensory neuropathies are usually acqu

226 -Canadian family with a dominantly inherited late-onset painful sensory neuropathy.

227 in VPS35 (PARK17) cause autosomal dominant, late onset Parkinson's disease (PD).

228 loss of functional protein in a patient with late onset Parkinson's disease.

229 , and in more patients with early-onset than late-onset Parkinson's disease (p=0.005).

230 ore patients with early-onset (p<0.0001) and late-onset Parkinson's disease (p=0.016) than in control

231 patients (n=137; 1.17 points [0.22]) than in late-onset patients (n=100; 0.56 points [0.10]).

232 rast, self-rated emotional symptoms showed a late-onset pattern with minimal differences versus UK co

233 and leucine-rich repeat kinase 2 (LRRK2) in late-onset PD.

234 set PE (EO-PE; symptom onset < 34 weeks) and late-onset PE (LO-PE; symptom onset > 34 weeks) cohorts.

235 ; 13 with early-onset PE (eoPE); and 11 with late-onset PE (loPE).

236 n in term placentas from pregnant women with late-onset PE and GDM compared to controls.

237 Few regulated genes were found in late-onset PE and GDM placentas, which may suggest that

238 Late-onset peanut allergy at age 4 years was rare (0.2%)

239 udinal wheezing phenotypes (early-transient, late-onset, persistent) and asthma were defined at age 7

240 The late onset phenotype of the NSE-Fig4(Cys486Ser) transgen

241 157 pedigrees analysed, out of which 27 are late-onset phenotypes across a range of physiological sy

242 44 of these mutant phenotypes, including 12 late-onset phenotypes.

243 n clinically variable disease with early- to late-onset phenotypic presentation.

244 berrant retinal pigment epithelium (RPE) and late-onset photoreceptor cell loss in the mutant retina.

245 phenotypes, including abnormal RPE cells and late-onset photoreceptor cell loss.

246 expected to increase the diagnostic yield in late-onset polyneuropathies, and it will be tempting to

247 ratio, 4.2; confidence interval, 1.3-13.1); late-onset preeclampsia (after week 34, hazard ratio, 2.

248 Compared with infants of women with late-onset preeclampsia, those with early onset (<34 wee

249 ccurs in treatment responders; children with late-onset presentation, lower ALT, and intracellular BS

250 maternally encoded early-onset program and a late-onset program that accelerated degradation after zy

251 c acidosis to childhood (cardio)myopathy and late-onset progressive external ophthalmoplegia.

252 trinucleotide repeats are known to cause 10 late-onset progressive neurodegenerative disorders as th

253 phy (SFD) as a syndromic condition including late-onset pulmonary disease.

254 etin protein, which has been associated with late-onset restrictive amyloid cardiomyopathy and increa

255 Late-onset retinal degeneration (L-ORD) is a rare autoso

256 fecta, nail abnormalities, and occasional or late-onset retinal pigmentation.

257 Of the 10 patients, 4 had a progressive late-onset rod-cone dystrophy, with a mean (range) age a

258 and impaired cognitive skill acquisition, or late onset SCA13, which typically produces cerebellar de

259 21 males; mean age 15.5 [11-26] years) with late-onset scoliosis requiring corrective surgery were e

260 REGgamma knockout (REGgamma-/-) mice exhibit late-onset sensorimotor gating and cognitive deficiencie

261 S) was identified in a single patient with a late-onset, sensory-predominant peripheral neuropathy; h

262 prevention of necrotising enterocolitis and late-onset sepis in very preterm infants.

263 ics may reduce necrotising enterocolitis and late-onset sepsis after preterm birth.

264 Late-onset sepsis and nonsurvivors had an immune exhaust

265 e no improvement from 1993 to 2004, rates of late-onset sepsis declined between 2005 and 2012 for inf

266 in parallel with a reduction in the rate of late-onset sepsis from 19.0% in 2010 to 13.8% in 2014 du

267 f prematurity, necrotizing enterocolitis, or late-onset sepsis) by 36 weeks of postmenstrual age.

268 BBG-001 to reduce necrotising enterocolitis, late-onset sepsis, and death in preterm infants.

269 n 14 days for any indication; a composite of late-onset sepsis, necrotising enterocolitis (modified B

270 ing 8824 infants without early-onset sepsis, late-onset sepsis, or NEC, a 10% increase in the AUR was

271 the patient's condition was observed due to late-onset sepsis.

272 mortality, and termination of pregnancy; and late onset sequelae.

273 oad in blood at birth and the development of late-onset sequelae in asymptomatic congenital CMV infec

274 6%) patients initially seen with an isolated late-onset seroma and 7 of 83 (8%) with an isolated new

275 ereas cluster T2 is a group of patients with late-onset severe asthma with a history of smoking and c

276 ntify the responsible gene defect underlying late onset spinal motor neuronopathy (LOSMoN/SMAJ; Onlin

277 Late-onset, sporadic Alzheimer disease (AD) is a common

278 Late-onset, sporadic PD is thought to result from the co

279 renia into early-onset, late-onset, and very-late-onset subtypes now should be tempered by the recogn

280 (UPLC-MS) to identify urinary biomarkers for late-onset T2D in the elderly.

281 e elderly, the pathogenesis and phenotype of late-onset T2D is not well studied.

282 f urine samples from people with and without late-onset T2D using ultra-performance liquid-chromatogr

283 ion of metabolite biomarkers associated with late-onset T2D.

284 se with early-onset T2DM and 50.6 (6.5) with late onset T2DM.

285 0.01], respectively) than did patients with late-onset T2DM (36.7 [7.5] and 8.2% [1.6%], respectivel

286 ents (339 with early-onset T2DM and 219 with late-onset T2DM) with a body mass index (calculated as w

287 achieved greater weight loss than those with late-onset T2DM, although the difference was not statist

288 nts with early-onset T2DM than in those with late-onset T2DM.

289 ing studies of MTAs should take into account late-onset toxicities to ensure that a tolerable dose is

290 asthma and diminished lung function, and the late-onset trajectory was associated with rhinitis.

291 Recurrent disease, second malignancy, or late-onset treatment effects in any patient who reports

292 Failure to diagnose late-onset type 1 diabetes can have serious consequences

293 l cardiovascular disease than did those with late-onset type 2 diabetes (OR 1.91, 95% CI 1.81-2.02).

294 e investigated effects of early-onset versus late-onset type 2 diabetes on risk of non-fatal cardiova

295 disease in patients with early-onset versus late-onset type 2 diabetes.

296 disease in patients with early-onset versus late-onset type 2 diabetes.

297 itiligo (<12 years) compared with those with late-onset vitiligo (OR, 3.54; 95% CI, 2.24-5.63, P < .0

298 sthma phenotypes (transient, persistent, and late-onset) were defined by timing of onset and remissio

299 Longer breastfeeding was protective against late-onset wheeze in the IoW cohort.

300 D) with early onset is distinct from AD with late onset with regard to amyloid pathology and neuronal