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1 of 22q11DS-related psychosis and control its late onset.
2 tress results in at least some of the hira-1 late-onset abnormalities.
3 on myeloid cells 2, in the increased risk of late onset AD.
4  1524 patients with EOAD, 7046 patients with late-onset AD (LOAD), and 7001 cognitively intact contro
5 ge of APOE-epsilon4 is a key risk factor for late-onset AD and has been believed to be the only risk
6 m data of a genome-wide association study of late-onset AD cases and controls (n = 17,008 and 37,154,
7                                  Over 50% of late-onset AD heritability has been captured, allowing r
8 gating with an autosomal-dominant pattern of late-onset AD in one family.
9  the mechanism underlying the development of late-onset AD is largely unknown.
10 trong role in Alzheimer's disease (AD), with late-onset AD showing heritability of 58-79% and early-o
11 r models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contribute
12 nd most significant susceptibility locus for late-onset AD.
13 tein E4 (APOE4), the principle risk gene for late-onset AD.
14 ene is the strongest genetic risk factor for late-onset AD.
15 llele, the strongest genetic risk factor for late-onset AD.
16 of at least part of the genetic component in late-onset AD.
17 tion study or identified as genetic nodes in late-onset AD.
18 ive on symptom checklists were excluded from late-onset ADHD diagnosis.
19            Individuals seeking treatment for late-onset ADHD may be valid cases; however, more common
20             Among individuals with impairing late-onset ADHD symptoms, the most common reason for dia
21  to clinics seeking stimulant medication for late-onset ADHD symptoms.
22 t birth-cohort studies support the notion of late-onset ADHD, but these investigations are limited by
23  of the LT and Wnt pathways during early- or late-onset allergic airway inflammation and to address r
24 rcoma (FUS) gene can cause both juvenile and late onset ALS.
25                                              Late onset Alzheimer disease (LOAD) is traditionally con
26 s acquired on 17 older adults with sporadic, late onset Alzheimer disease.
27      Dozens of genes have been implicated in late onset Alzheimer's disease (AD) risk, but none has a
28        Pyk2 genetic variation contributes to late onset Alzheimer's disease (AD) risk.
29 tion at the Pyk2 (PTK2B) locus is a risk for late onset Alzheimer's disease (AD), but the pathophysio
30 tains both the major common risk variant for late onset Alzheimer's disease (AD), e4, and the major n
31 major risk factors for cognitive decline and late onset Alzheimer's disease (AD).
32 is a main genetic risk factor for developing late onset Alzheimer's disease (LOAD) and is thought to
33 The most significant genetic risk factor for late onset Alzheimer's disease is a variant of the apoli
34                                              Late onset Alzheimer's disease is currently a disease wi
35 tatistically-significant locus associated to Late Onset Alzheimer's Disease, its role in disease path
36 indicate that most of the risk of developing late onset Alzheimer's disease, the most common form of
37 P) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognit
38 trations are associated with a lower risk of late-onset Alzheimer disease (AD) in observational studi
39  gene is a major genetic risk determinant of late-onset Alzheimer disease (AD), with the APOE*epsilon
40 tes HSV type 1 (HSV1) in the pathogenesis of late-onset Alzheimer disease (AD).
41 , we found strong genetic covariance between late-onset Alzheimer disease (LOAD) and amyotrophic late
42        The RV-NPL was applied to analyze 107 late-onset Alzheimer disease (LOAD) pedigrees of Caribbe
43                                     Sporadic late-onset Alzheimer disease (LOAD) preceded by mild cog
44 N1 is implicated in cancers, arrhythmia, and late-onset Alzheimer disease, these findings may trigger
45 4 (APOE4) is a major genetic risk factor for late-onset Alzheimer disease.
46 ene is the strongest genetic risk factor for late-onset Alzheimer disease.
47 OE4 is the strongest genetic risk factor for late-onset Alzheimer disease.
48 is associated with reduced susceptibility to late-onset Alzheimer's disease (AD) and causal for eleva
49 ion, but the molecular mechanisms underlying late-onset Alzheimer's disease (AD) are unclear.
50                                              Late-onset Alzheimer's disease (AD) can, in part, be con
51 r aging-related cognitive decline as well as late-onset Alzheimer's disease (AD) compared to the comm
52 2DM) is a risk factor for the development of late-onset Alzheimer's disease (AD).
53 the major genetic risk factor for developing late-onset Alzheimer's disease (AD).
54 ted by the BACE2 locus to the development of late-onset Alzheimer's disease (AD).
55 ele is the strongest genetic risk factor for late-onset Alzheimer's disease (AD).
56  myeloid cells 2 (TREM2) are associated with late-onset Alzheimer's disease (AD).
57 POE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD).
58 trongest genetic risk factor associated with late-onset Alzheimer's disease (AD).
59                                              Late-Onset Alzheimer's Disease (LOAD) is a leading form
60 tion that implicate causal genes in sporadic late-onset Alzheimer's disease (LOAD) pathogenesis, ther
61 n illumination microscopy (SIM) to study the late-onset Alzheimer's disease (LOAD) risk factor BIN1,
62 y receptor Siglec-3/CD33 influences risk for late-onset Alzheimer's disease (LOAD), an apparently hum
63                                     Risk for late-onset Alzheimer's disease (LOAD), the most prevalen
64  mechanisms and novel therapeutic targets of late-onset Alzheimer's Disease (LOAD), we performed an i
65 dominant genetic risk factor associated with late-onset Alzheimer's disease (LOAD).
66  alleles is a strong genetic risk factor for late-onset Alzheimer's disease (LOAD).
67  important contributing mechanism underlying late-onset Alzheimer's disease (LOAD).
68 common genome-wide significant risk loci for late-onset Alzheimer's disease (LOAD).
69 in brain glucose metabolism is a hallmark of late-onset Alzheimer's disease (LOAD).
70 idence indicates that the polygenic basis of late-onset Alzheimer's disease can be harnessed to ident
71                              Early-onset and late-onset Alzheimer's disease exhibited different patte
72                     Categorizing people with late-onset Alzheimer's disease into biologically coheren
73                                The cause for late-onset Alzheimer's disease is unknown.
74 issue samples from a subset of patients with late-onset Alzheimer's disease that exhibit higher gamma
75 opment of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear w
76                    When T-GEN was applied to late-onset Alzheimer's disease, we identified 96 genes l
77 windows of opportunity to reduce the risk of late-onset Alzheimer's disease.
78 ring APP/Abeta metabolism has been linked to late-onset Alzheimer's disease.
79 etase activity in samples from patients with late-onset Alzheimer's disease.
80 associated with increased risk for sporadic, late-onset Alzheimer's disease.
81 ly increases the risk for the development of late-onset Alzheimer's disease.
82 mbly complexes can prevent the expression of late-onset anatomical, physiologic, and behavioral abnor
83                           These cases are of late onset and likely result from the interaction of man
84                                          The late onset and mild phenotype observed confirms presenta
85 in MAPKBP1 as a genetic cause of juvenile or late-onset and cilia-independent NPH.
86 riggers intervention, but also in predicting late-onset and progressive hearing loss and identifying
87         We document that T2D, both early and late onset, are characterized by reduced muscle expressi
88 ciated with a reduced risk of development of late onset asthma in menopausal women.
89                The subjects in cluster 3 had late-onset asthma and low lung function, high baseline e
90  1.20-2.50), but not with early-transient or late-onset asthma.
91 onset transient, early-onset persistent, and late-onset asthma.
92 "Difficult," "Early-onset mild atopic," and "Late-onset asthma." Children with moderate-to-severe ast
93 ive progressive retinal atrophy (PRA) with a late onset at 3-6 years of age or older.
94 lexia syndrome (CANVAS) and a major cause of late onset ataxia.
95                                              Late-onset ataxia is common, often idiopathic, and can r
96 e of familial CANVAS and a frequent cause of late-onset ataxia, particularly if sensory neuronopathy
97 GGG expansion in RFC1 is a frequent cause of late-onset ataxia.
98  affected members of the index family with a late-onset autosomal-dominant parkinsonism and polyneuro
99 5 ortholog (VPS35) gene represent a cause of late-onset, autosomal dominant familial Parkinson's dise
100 inase 2 (LRRK2) are the most common cause of late-onset, autosomal-dominant familial Parkinson's dise
101 endogenous levels of mutant CHMP2B developed late-onset brain volume loss associated with frank neuro
102 erations to the transformation process while late-onset cancers are more driven by somatic mutations.
103 utic agents, and age at exposure on risk for late-onset cardiac disease in survivors of childhood can
104                       Further, septic shock, late-onset cardiac dysfunction, and multiorgan system fa
105 ute ventricular dysfunction, and also induce late-onset cardiomyopathy and heart failure.
106                                         Most late-onset cases displayed onset in adolescence and an a
107  and substance use before treating potential late-onset cases.
108 xon 2 splicing and is found in two-thirds of late-onset cases.
109                                           No late-onset cCMVI-related HL was detected during a median
110 wed that some compounds specifically trigger late-onset cell death after 72 h with a unique correlati
111 nd 5hmC in human frontal cortex tissues from late-onset Chinese AD patients and cognitively normal co
112 ased the risk of membership in the early and late-onset chronic asthma trajectories, relative to subj
113 ine specific immune parameters predictive of late-onset CMV disease with AP.
114                                  Regardless, late-onset CMV disease, specifically pneumonia, remains
115 d spectrum of immune manifestations, such as late-onset combined immunodeficiency and autoimmunity.
116 langiectasia Type 2 (MacTel) is an uncommon, late-onset complex retinal disease that leads to central
117 bclassified into early-onset CRC (EOCRC) and late-onset CRC (LOCRC), and patients with multiple prima
118 hermore, mutants lacking histone H3.3 have a late-onset defect similar to a defect of hira-1, pqn-80,
119                                        These late-onset defects can be maternally rescued, and matern
120 tochondrial stress likely contributes to the late-onset defects, given that hira-1 mutants display mi
121                      Three signals explained late-onset degradation: miR-430 seeds, AU-rich sequences
122                                              Late onset depression (LOD) may precede the diagnosis of
123                Subgroup analyses showed that late-onset depression was more strongly associated with
124 family (78 members) with ASD combined with a late-onset dilated cardiomyopathy and further characteri
125 ation identified in association with ASD and late-onset dilated cardiomyopathy in a large, multi-gene
126  implications with regard to monitoring for (late-onset) dilated cardiomyopathy.
127 ulopharyngeal muscular dystrophy (OPMD) is a late onset disease caused by polyalanine expansion in th
128 owing that, in contrast, much of the risk of late onset disease is encoded by loci involved in lipid
129 disease (case fatality rate 5.2%) and 26 had late-onset disease (case fatality rate 7.7%).
130 ibodies in breast milk and the occurrence of late-onset disease (LOD) in young infants.
131 BS), the hypervirulent clone responsible for late-onset disease (LOD), remains elusive.
132 nset disease (EOD, </=7 days) or compared to late-onset disease (LOD, >7 days).
133  1000 livebirths (95% CI 0.52-0.62), and for late-onset disease (n=339) was 0.37 per 1000 livebirths
134 often showing the mild phenotype (CORD) with late-onset disease (sixth decade).
135 comprehensive protection, as early onset and late-onset disease and maternal complications potentiall
136 disease complications have incomplete and/or late-onset disease expression.
137 ong partners for traits such as longevity or late-onset disease have been found to be comparable to p
138 isease incidence was 0.41 (95% CI, .36-.47); late-onset disease incidence was 0.26 (95% CI, .21-.30).
139 cts trigger the molecular changes that cause late-onset disease is important for understanding diseas
140                             PCP was mostly a late-onset disease occurring after complete course of pr
141 t photoreceptor loss except in patients with late-onset disease who had a focal preservation of the e
142 m to explain the relative protection against late-onset disease with PET.
143 t disease and 114000 (UR, 44000-326000) with late-onset disease, of whom a minimum of 7000 (UR, 0-190
144 portant consequences for both congenital and late-onset disease.
145                                              Late-onset diseases (LOD) occur between 7 and 89 days of
146  diseases tend to have lower prevalence than late-onset diseases (Spearman's rho = 0.32, p < 10(-16))
147 ribution of genetic variants associated with late-onset diseases in different species.
148 arents especially suited for the analysis of late-onset diseases such as Alzheimer's Disease (AD).
149  These results suggest that when large, even late-onset effects are kept at low frequency by purifyin
150 ube exposure was a necessary risk factor for late-onset endophthalmitis and required surgical removal
151 tions were exclusively seen in patients with late onset epilepsies and lack of response to sodium cha
152                                              Late-onset exudation and fibrovascular proliferation in
153 rom 2000 through 2018, 5 (3.6%) demonstrated late-onset exudation or vasoproliferation.
154     Amyotrophic lateral sclerosis (ALS) is a late-onset fatal neurodegenerative disorder that is pred
155                                              Late-onset FECD is a uniquely advantageous model for stu
156  in female than male mice, characteristic of late-onset FECD.
157 confidence interval (CI) 0.87-1.00), but not late-onset FGR (AUC 0.70, 95% CI 0.64-0.75).
158 f the Alzheimer's patients have the sporadic late-onset form (LOAD).
159                           It is considered a late-onset form of muscular dystrophy and leads to asymm
160 reptococcus (GBS) is the cause of early- and late-onset GBS disease in neonates and can present as se
161 aryngeal muscular dystrophy (OPMD) is a rare late onset genetic disease leading to ptosis, dysphagia
162  of the P322S/+ metabolic phenotype revealed late-onset glucose intolerance.
163             Toxicity included persistent and late-onset grade 3 or higher TRAEs.
164 ) distinct phenotypes can be seen within the late onset group, including myoclonic-atonic epilepsy (t
165 with protection against both early-onset and late-onset group B streptococcus disease.
166 me individuals although the etiology of this late-onset group is unclear.
167  more focal medial temporal lobe loss in the late-onset group.
168 ociation is with early-onset (< 34 weeks) or late-onset (&gt; 34 weeks) FGR; as a result there is no con
169 cated no clear differences between early and late onset HCM mutations.
170 te the lack of distinction between early and late onset HCM, the predicted occupancy of the force-hol
171 th outcomes are subsequently associated with late-onset health conditions.
172                              One sibling had late onset hearing loss and both siblings had symmetric
173  Cdh23(ahl) (C57BL/6J and C57BL/6NTac), from late-onset hearing loss mice (C3H/HeJ), and from mice co
174                                              Late-onset heart failure (HF) is a known side effect of
175              A combined phenotype of ASD and late-onset heart failure was caused by a heterozygous, n
176 eaning, we aimed to generate mouse models of late-onset HPP with extended life spans by engineering a
177 nocopy skeletal and dental manifestations of late-onset HPP.
178 ts might explain the missing heritability of late-onset human diseases, such as Alzheimer's disease,
179 uman IOPD, displaying skeletal myopathy with late-onset hypertrophic cardiomyopathy.
180                                              Late-onset hypogonadism is a clinical condition in the a
181  lifelong, whereas testosterone treatment of late-onset hypogonadism remains a matter of debate becau
182 ncreased risk of prostate cancer in men with late-onset hypogonadism.
183 ncreased risk of prostate cancer in men with late-onset hypogonadism.
184  zebrafish scospondin (sspo) mutants develop late-onset idiopathic-like spinal curvatures in the abse
185 K2 alleles that predispose their carriers to late-onset idiotypic Parkinson's disease (PD) and also t
186  achieve the rate from the best quartile for late-onset infection, 6 years to achieve the rate from t
187 perforin-deficient CAR T cells recapitulated late-onset inflammatory toxicities occurring in human CA
188                                              Late-onset inflammatory toxicities resembling hemophagoc
189 unctival surgical (MICS) technique to repair late-onset leaking blebs after trabeculectomy.
190 rocedure is an effective option for treating late-onset leaking blebs without cutting or excising con
191 c.1000G>C;p.G334R, in a family with multiple late-onset LFS-spectrum cancers.
192 nd cognitive diagnosis (P = 3.5 x 10(-7)) of late-onset (LO) AD.
193 ptococcus (GBS) is an important precursor to late-onset (LO) disease in infants.
194 partum antibiotic prophylaxis guidelines but late-onset (LOGBS) rates remain unchanged.
195 et (present as early as 4 days after birth), late-onset lymphoid cancer development, and premature de
196    Macular telangiectasia type 2 (MacTel), a late-onset macular degeneration, has been linked to a lo
197 ociation of a dominant splicing variant with late-onset mild maculopathy was established.
198 ciency, a pathological hallmark of aging and late-onset mitochondrial disease.
199 phenotype and prognosis of RTD patients with late-onset MN.
200 ekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degenera
201 ith early-onset mtDNA depletion in liver and late-onset multiple deletions in brain of Mpv17-/- mice.
202 ions in the HSP70 cochaperone DNAJB6 cause a late-onset muscle disease termed limb-girdle muscular dy
203 r dystrophy (OPMD) is an autosomal dominant, late-onset muscle disorder characterized by ptosis, swal
204 ystrophy (OPMD) is a rare autosomal dominant late-onset muscular dystrophy affecting approximately 1:
205 e of PD-ligands, both TS1 TEM and TN induced late-onset myocarditis.
206                Differences between early and late-onset myopia were confirmed with DNA methylation pa
207 ); "Early-onset mild non-atopic: (n = 153); "Late-onset" (n = 105); and "Exacerbation-prone asthma" (
208 ase, but were 4.43 times more likely to have late-onset neonatal GBS disease.
209 y leading to preterm births, stillbirths, or late-onset neonatal infections.
210  to explore the association between HMOs and late-onset neonatal sepsis.
211 tect infants with very low birth weight from late-onset neonatal sepsis.
212  impaired adult hippocampal neurogenesis and late-onset neurodegeneration in mouse brains.
213 utation in the EMP lineage in mice can drive late-onset neurodegeneration.
214                                              Late-onset neurodegenerative disease observed in patient
215 Autophagy defects are implicated in multiple late-onset neurodegenerative diseases including Amyotrop
216  of tissue-resident macrophages and a severe late-onset neurodegenerative disorder.
217 areflexia syndrome (CANVAS) is a progressive late-onset, neurological disease.
218 We also further quantified newly-identified, late-onset neuromuscular phenotypes of this mutant line,
219 11C-PBB3 binding capacity is associated with late-onset neuropsychiatric symptoms following TBI, and
220 rent regional pattern of binding compared to late onset, non-familial Alzheimer's disease.
221 gic moderate-to-severe remodeled asthma, (3) late-onset nonallergic eosinophilic asthma, and (4) late
222 set nonallergic eosinophilic asthma, and (4) late-onset nonallergic noneosinophilic asthma.
223 ht individuals from five families presenting late-onset NPH with massive renal fibrosis.
224                             About 30% showed late onset of asthma diagnosis/symptoms (>40 years); the
225 able ocular appearance during second decade, late onset of nystagmus and dyschromatopsia (after 20 ye
226  patient with Pierson syndrome and unusually late onset of proteinuria.
227 ung adulthood and risk factors for early and late onset of sensitization.
228 ase disorder (DSPD), characterized by a very late onset of sleep.
229  and after 60 years (reflecting an early and late-onset of AF) to assess the risk of incident AF by g
230                      Cluster 4 patients were late-onset older male subjects with persistent airflow o
231 hylaxis, Pneumocystis pneumonia has become a late-onset opportunistic infection requiring indications
232 psia: an early-onset or placental type and a late-onset or maternal type.
233 's disease (age at onset <= 50) and 1799 had late onset Parkinson's disease.
234 loss of functional protein in a patient with late onset Parkinson's disease.
235 her Sanger and/or exome sequencing; and 1701 late-onset patients were genotyped with the LRRK2 'Kompe
236 rast, self-rated emotional symptoms showed a late-onset pattern with minimal differences versus UK co
237 set PE (EO-PE; symptom onset < 34 weeks) and late-onset PE (LO-PE; symptom onset > 34 weeks) cohorts.
238                                              Late-onset peanut allergy at age 4 years was rare (0.2%)
239 ter recapitulates the expression pattern and late onset phenotype characteristic of FSHD patients.
240 ore to evaluate risk factors associated with late-onset Pneumocystis pneumonia.
241 e (PI(MAX)) reflects inspiratory weakness in late-onset Pompe disease (LOPD).
242 ecompensation of the maternal circulation in late-onset preeclampsia, thus sharing the pathophysiolog
243  earlier and more severely in early- than in late-onset preeclampsia; however, some very specific dys
244 ulopharyngeal muscular dystrophy (OPMD) is a late-onset, primarily autosomal dominant disease caused
245 maternally encoded early-onset program and a late-onset program that accelerated degradation after zy
246 lear tuning and sensitivity and give rise to late-onset progressive hearing loss.
247  trinucleotide repeats are known to cause 10 late-onset progressive neurodegenerative disorders as th
248 myelin protein biosynthesis; and resulted in late-onset, progressive myelin thinning in the CNS of ad
249 associations of topology of tau lesions with late-onset psychiatric symptoms due to TBI have not been
250  remain at increased risk for development of late-onset pulmonary hypertension, and may be particular
251                                              Late-onset PXE extends the spectrum of ectopic calcifica
252  phenotyping of obelix(td15) fish revealed a late onset retinal degeneration at 12 months.
253                                              Late-onset retinal degeneration (L-ORD) is a rare autoso
254      Of the 10 patients, 4 had a progressive late-onset rod-cone dystrophy, with a mean (range) age a
255                                      Whereas late-onset RTD may mimic different acquired or genetic c
256 s remained stable, except for a reduction in late-onset sepsis (0.94 [0.89, 0.99]).
257 factor 3 in colostrum with a reduced risk of late-onset sepsis (HR: 0.63; 95% CI: 0.41, 0.97).
258                                              Late-onset sepsis (LOS) is a highly consequential compli
259                                              Late-onset sepsis (LOS) is thought to result from system
260 s a major risk factor for the development of late-onset sepsis (LOS), a main cause of mortality and m
261 considered to play a role in the etiology of late-onset sepsis (LOS).
262 ith an increased risk for the development of late-onset sepsis (LOS).
263 robiotics for improving growth or preventing late-onset sepsis in moderately preterm neonates.
264 tween human milk oligosaccharides (HMOs) and late-onset sepsis in very-low-birth-weight infants, and
265                                              Late-onset sepsis occurred in 414 of 1389 infants (29.8%
266 nt improvements in survival and reduction of late-onset sepsis of extreme preterm infants in South Wa
267 r-age (-0.133 SD; 95% CI: -0.380, 0.114), or late-onset sepsis probability (-1.175 percentage points;
268 f prematurity, necrotizing enterocolitis, or late-onset sepsis) by 36 weeks of postmenstrual age.
269  the primary outcome, confirmed or suspected late-onset sepsis, necrotizing enterocolitis, and cerebr
270 izing enterocolitis but an increased risk of late-onset sepsis.
271  the patient's condition was observed due to late-onset sepsis.
272 ght-for-age z scores at discharge as well as late-onset sepsis.
273 age and height-for-age z scores) and risk of late-onset sepsis.
274 mortality, and termination of pregnancy; and late onset sequelae.
275 6%) patients initially seen with an isolated late-onset seroma and 7 of 83 (8%) with an isolated new
276 ereas cluster T2 is a group of patients with late-onset severe asthma with a history of smoking and c
277 LL treatment include resistance, relapse and late-onset side effects due to the chemotherapy.
278 .3%), (2) patients without CAV at 1 year and late-onset slow CAV progression (7.6%), (3) patients wit
279 sorders is pseudoxanthoma elasticum (PXE), a late-onset, slowly progressing disorder with multisystem
280 ring at birth, but are at risk of developing late-onset SNHL.
281  followed for 3 years to assess emergence of late-onset SNHL.
282               Neuronal EAAT2 loss results in late-onset spatial reference long-term memory deficit.
283 estioning the etiologic role of Abeta in the late-onset, sporadic form of AD, and reciting either of
284 ns, somatic mutation may also play a role in late-onset, sporadic neurodegenerative diseases, such as
285 n lead to hearing loss that is congenital or late onset, stable or progressive, drug related, noise i
286 asures can achieve results highly similar to late-onset stringent mandates.
287 cal and psychiatric disorders with early and late onset such as autism, schizophrenia and depression
288 he TBI patients, 14 were diagnosed as having late-onset symptoms based on the criteria of traumatic e
289 e elderly, the pathogenesis and phenotype of late-onset T2D is not well studied.
290 ion of metabolite biomarkers associated with late-onset T2D.
291                 Inclusion body myositis is a late onset treatment-refractory autoimmune disease of sk
292 observable decades prior to the diagnosis of late-onset trinucleotide repeat disease.
293                          Failure to diagnose late-onset type 1 diabetes can have serious consequences
294 to early defibrotide access for treatment of late-onset VOD in current treatment guidelines.
295                  Twenty percent (n = 2/8) of late-onset VOD patients were anicteric and 42% (n = 8) c
296 around 30% (n = 8/27) of cases classified as late-onset VOD presenting at median of 46 (22-93) days b
297 criteria failed to recognize the syndrome of late-onset VOD.
298 d as disease in the first 6 days of life and late onset was defined as 7-89 days of life.
299 ated BMI or obesity loci, for both early and late onset, we uncovered one completely novel locus in t
300 sthma phenotypes (transient, persistent, and late-onset) were defined by timing of onset and remissio

 
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