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1 ing criteria for persistence, and adolescent/adult-onset.
2 2q11.2, a rate higher than that reported for adult onset (0.3-1%) (P<0.001) or autism spectrum disord
3 ere we show that mice with tamoxifen-induced adult-onset ablation of P/Q channel alpha subunit (iKOp/
4                                              Adult-onset ablation of Sh2b1 in the mediobasal hypothal
5                    There was no evidence for adult-onset ADHD independent of a complex psychiatric hi
6             Importantly, we demonstrate that adult-onset administration of the drug trametinib, a hig
7 ense or in-frame mutation is associated with adult onset and slow progression.
8 and peripheral postmortem tissues from seven adult-onset and one juvenile-onset HD individual.
9 t clinical exome sequencing in patients with adult-onset and sporadic presentations of ataxia is a hi
10 eproduce important clinical features such as adult-onset and stereotypical patterns of progression.
11 are shared between childhood-onset (COA) and adult-onset (AOA) asthma has not been estimated.
12 ly enriched gene signatures in patients with adult-onset as compared with childhood-onset severe asth
13 (not observed in spastin knockout mice) were adult onset, as is typical of human patients.
14  (onset before 12 years of age), adults with adult-onset asthma (onset between 26 and 65 years of age
15                      The association between adult-onset asthma and >= 1 allergic multimorbidity decr
16 groups of asthma and allergic disease cases; adult-onset asthma and moderate-to-severe asthma are ass
17                     Genetic risk factors for adult-onset asthma are largely a subset of the genetic r
18 ociation between allergic multimorbidity and adult-onset asthma considering the number of allergic di
19                          Childhood-onset and adult-onset asthma differ with respect to severity and c
20 tudies (GWAS) for childhood-onset asthma and adult-onset asthma each compared with shared controls, a
21                       One in 6 patients with adult-onset asthma experiences remission within the firs
22                A proportion of patients with adult-onset asthma have severe disease.
23 n BMI and physical activity with the risk of adult-onset asthma in 76,470 asthma-free women from the
24 ergens distinguish subjects with and without adult-onset asthma in Finland.
25 vity may have a modest impact on the risk of adult-onset asthma in this population of US women.
26                      Compared to nonatopics, adult-onset asthma increased with the number of allergic
27                                              Adult-onset asthma is an important but relatively unders
28 ctive or passive smoking to the incidence of adult-onset asthma is inconsistent with both positive an
29 barrier function genes, whereas the cause of adult-onset asthma is more lung-centred and environmenta
30 etween air pollutants and immune markers and adult-onset asthma using mixed-effects (logistic) regres
31 5% of the effect of air pollution on risk of adult-onset asthma was mediated through the immune syste
32  members with childhood-onset and adolescent/adult-onset asthma was not different from leukocyte telo
33                                              Adult-onset asthma was positively associated with the nu
34 p, active smoking increased the incidence of adult-onset asthma, and passive smoke exposure increased
35 ct genetic risk loci for childhood-onset and adult-onset asthma, and to identify the genes that might
36  respiratory disease (AERD) is manifested by adult-onset asthma, nasal polyposis, chronic rhinosinusi
37                                           In adult-onset asthma, the level of FEV(1) reached during t
38 y predictors of persistence and remission of adult-onset asthma.
39 have a beneficial effect on the incidence of adult-onset asthma.
40  depression as a marker of risk for incident adult-onset asthma.
41 te the association between air pollution and adult-onset asthma.
42 greater role for non-genetic risk factors in adult-onset asthma.
43 f IL-1RA [OR 1.37; 95% CI (1.09, 1.73)] with adult-onset asthma.
44 in the association between air pollution and adult-onset asthma.
45 h childhood-onset asthma; 21 564 adults with adult-onset asthma; and an additional 6849 young adults
46                                           62 adult-onset asthmatic patients who had prolonged coughs
47                                      To date adult-onset asthmatic patients who lack a clear stridor
48                      Affected members showed adult onset asymmetric distal muscle weakness with initi
49 opic eczema remain high after childhood, and adult-onset atopic eczema has different risk factor asso
50                    Schnitzler syndrome is an adult-onset autoinflammatory disease characterized by ur
51                             When compared to adult onset autosomal dominant CMT2A, it is associated w
52 cipants from a 3-generation family with pure adult-onset autosomal dominant HSP of unknown genetic or
53 man lamin B1 (LMNB1) gene has been linked to adult-onset autosomal dominant leukodystrophy, and mouse
54 n of the LMNB1 gene encoding lamin B1 causes adult-onset autosomal-dominant leukodystrophy (ADLD) sta
55 Several heterozygous SLC25A4 mutations cause adult-onset autosomal-dominant progressive external opht
56 ers were categorized as adolescent-onset and adult-onset based on when they were first exposed to ket
57 ) is a neurodegenerative disease that causes adult-onset blindness.
58 ology and pathophysiologic features of human adult-onset branching enzyme deficiency.
59 f CVD risk in 36,232 >/= 2-year survivors of adult-onset cancer compared with matched (age, sex, and
60                                 Follow-up of adult-onset cancer survivors given cisplatin should incl
61 en comprehensively evaluated in survivors of adult-onset cancer.
62 nt primary cancers (SPCs) among survivors of adult-onset cancers are limited.
63                           Among survivors of adult-onset cancers in the United States, several types
64 oring of cardiac dysfunction in survivors of adult-onset cancers.
65 c expression of NSML-associated SHP2 induced adult-onset cardiac hypertrophy.
66  growth restriction (IUGR) enhances risk for adult onset cardiovascular disease (CVD).
67 th that correlates positively with increased adult-onset cardiovascular, metabolic and behavioural di
68 ation of the amyloid beta peptide and delays adult-onset cellular dysfunction.
69 tations, linked in two different families to adult-onset cerebellar ataxia, and a de novo truncation
70                                              Adult-onset CFLD lacks sufficient characterization and d
71                                              Adult-onset CFLD may be more prevalent than previously d
72  health, predicting mortality, stunting, and adult-onset chronic conditions.
73                                              Adult-onset CI included approximately 1 in 6 adults who
74                                 In contrast, adult-onset ciliary dysgenesis in POMC neurons causes no
75 the adult mouse facial nerve crush model and adult-onset conditional disruption of the CNTF receptor
76 egenerative diseases ranging from well-known adult onset conditions such as Alzheimer and Parkinson d
77 jority thought that incidental results about adult-onset conditions (62%) and carrier status (62%) sh
78 linical actionability, clinically actionable adult-onset conditions, and carrier status for autosomal
79 ng (WES) for the diagnosis and management of adult-onset constitutional disorders has not been adequa
80 dity and health-care costs in paediatric and adult onset Crohn's disease.
81 from patients with pediatric IBD (n = 45) or adult-onset Crohn's disease (n = 20) and healthy individ
82 gous mice of both sexes (Atoh1(lacZ/+)) have adult-onset deafness.
83 ned in hearing cats, and cats with early- or adult-onset deafness.
84 Ub(G76V)-GFP-Syb2 mice developed progressive adult-onset degeneration of motor nerve terminals, where
85    Amyotrophic lateral sclerosis (ALS) is an adult-onset degeneration of motor neurons that is common
86 he central nervous system (CNS), causing the adult-onset degenerative disease amyotrophic lateral scl
87 omal dominant leukodystrophy (ADLD), a fatal adult onset demyelinating disease.
88  B1 (LMNB1) gene underlie autosomal dominant adult-onset demyelinating leukodystrophy (ADLD), a rare
89 alent asthma is not associated with incident adult-onset depression.
90  between low birth weight (LBW; <2.5 kg) and adult-onset diabetes in 12,525 participants from the Bra
91 resistance and insulin secretion) to cluster adult-onset diabetes patients into five subtypes.
92 linical phenotypes that include neonatal and adult-onset diabetes using CRISPR (clustered regularly i
93  mutations have also recently been linked to adult-onset diabetes, with subclinical or no exocrine in
94 IR are two physiologically distinct forms of adult-onset diabetes.
95 ndow for therapeutic intervention to prevent adult-onset diabetes.
96 obal Id3 ablation (Id cDKOs), which develops adult-onset dilated cardiomyopathy.
97 ommon variants to congenital abnormality and adult onset disease are considered in light of a new ker
98  epigenetic transgenerational inheritance of adult onset disease.
99  for childhood-onset asthma (0.327) than for adult-onset disease (0.098).
100 yotrophic lateral sclerosis (ALS) is a fatal adult-onset disease characterized by upper and lower mot
101 in the pathological range of repeats causing adult-onset disease in humans.
102 od, and the frequency and characteristics of adult-onset disease remain controversial.
103                 nGS also revealed actionable adult-onset disease risk in 3/85 (3.5%) newborns whose p
104 re we present childhood-onset and actionable adult-onset disease risk, carrier status, and pharmacoge
105 ey disease (ADPKD) is a common, progressive, adult-onset disease that is an important cause of end-st
106 hose eczema started in childhood, those with adult-onset disease were more likely to be women, from S
107 CARD9 deficiency caused by p.Y91H results in adult-onset disease with variable penetrance and express
108 pically more severe than infantile-onset and adult-onset disease, long-term morbidity has not been as
109   While this pathogenesis model accounts for adult-onset disease, the molecular basis of congenital D
110 at of infantile-onset (ie, <6 years old) and adult-onset disease, with genetic cause characterised by
111 reening programs and reduce the incidence of adult onset diseases via genetic risk identification and
112 children and their parents: implications for adult onset diseases.
113 d mortality and a greater risk of developing adult-onset diseases in later life, understanding the ro
114 are serious caveats to their use in modeling adult-onset diseases such as cardiomyopathies and Alzhei
115 cause or increase the risk for childhood and adult-onset diseases, finding genes that influence how p
116                                         Some adult-onset disorders may be linked to dysregulated embr
117 rse environments can also be associated with adult-onset disorders.
118  and, although most are also misregulated in adult-onset DM1, dysregulation is significantly more sev
119   In this study, we analyzed consequences of adult-onset DR (24 h to 1 yr) on hematopoietic stem cell
120                                     Using an adult-onset Drosophila model of Abeta (amyloid beta) tox
121         Both models recreate the progressive adult-onset dysfunction and degeneration of a neuronal n
122 sm (XDP) is a neurodegenerative disease with adult onset dystonia and subsequent parkinsonism.
123 dystonia pathogenesis.SIGNIFICANCE STATEMENT Adult-onset dystonia DYT25 is caused by dominant loss-of
124 atric-onset EGPA has a poorer prognosis than adult-onset EGPA, which can be attributed to a high prev
125                      Sera of 4 patients with adult onset epilepsy and suspected encephalitis of unres
126               In the serum of a patient with adult onset epilepsy and suspected encephalitis, a stron
127 company the motor manifestations of isolated adult-onset focal dystonias.
128 0) and complex inheritance evident in common adult-onset forms of disease.
129 ing from severe childhood variants to milder adult-onset forms, were collected in 17 neuromuscular re
130 h age-related macular degeneration (AMD) and adult-onset foveomacular vitelliform dystrophy (AOFVD) w
131    Thus, mutations in PAX2 may contribute to adult-onset FSGS in the absence of overt extrarenal mani
132 s, in addition to other suggested actionable adult-onset genetic conditions, opportunistic screening
133                                              Adult-onset genetic leukoencephalopathies and leukodystr
134           The number of identified causes of adult-onset genetic leukoencephalopathies has recently i
135 MRI scans may help indicate the diagnosis of adult-onset genetic leukoencephalopathies.
136 ent GWAS completed for three types of common adult-onset glaucoma have identified novel loci for POAG
137                                         Many adult-onset glomerulopathies also feature alterations in
138 elopmental irregularities that manifested as adult-onset glomerulosclerosis and proteinuria.
139 were separated into infantile, childhood and adult-onset groups.
140 nown regarding CVD in long-term survivors of adult-onset (&gt;/= 40 years) cancer.
141 enome-wide significant locus associated with adult-onset (&gt;27 years) MDD (rs7647854, odds ratio: 1.16
142 of Htt CAG repeats, in the juvenile- and the adult-onset HD ranges, whereas knock-out of Rrm2b did no
143 enile onset hearing loss (89 Hz) relative to adult onset hearing loss (64 Hz).
144                                              Adult-onset hearing loss is very common, but we know lit
145  during cardiac development leads to CHD and adult-onset heart hypertrophy.
146                                              Adult-onset hemophagocytic lymphohistiocytosis (HLH) is
147                                Therefore, an adult-onset, hepatocyte-specific, GH receptor (GHR) knoc
148 deficiency manifesting a complicated form of adult-onset hereditary spastic paraparesis partially res
149 t that CH is more common in individuals with adult-onset HLH and can contribute to the pathophysiolog
150                                    Using the adult-onset HLH mouse model in which repeated treatments
151 rant inflammatory state, could contribute to adult-onset HLH.
152 ulates hallmark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impai
153     Mice with either LepR neuron-specific or adult-onset, hypothalamus-specific ablation of Sh2b1 dev
154 is believed to be a more severe disease than adult-onset IBD, but there is little information on all-
155     Compared with patients with pediatric or adult-onset IBD, elderly patients used fewer biologics a
156 tic targets for patients with very early and adult-onset IBD.
157 etic factors associated very early onset and adult-onset IBD.
158 l presentation of specific gene defects (eg, adult-onset idiopathic T-cell lymphopenia and early-onse
159                          More significantly, adult-onset inducible expression of TAK1DeltaN protected
160                                              Adult-onset inflammatory syndromes often manifest with o
161 a disorder that connects seemingly unrelated adult-onset inflammatory syndromes.
162                                              Adult-onset inherited myopathies with similar pathologic
163 rt our review by arguing that in contrast to adult-onset injury, developmental brain insults alter th
164    The exception is FKRP mutations, in which adult onset is a common presentation.
165 cterise risk of spread in recently diagnosed adult-onset isolated focal dystonia patients.
166                                              Adult-onset KD (AKD) is rare and often misdiagnosed.
167      PODXL heterozygosity is associated with adult-onset kidney disease and podocalyxin shedding into
168 SF1R mutations account for 10% of idiopathic adult onset leukodystrophies and that genetic testing fo
169                                              Adult-onset leukodystrophies and genetic leukoencephalop
170 atients from the UK, Greece and Ireland with adult onset leukodystrophy of unknown cause.
171 euroaxonal spheroids (HDLS) is a hereditary, adult onset leukodystrophy which is characterised by the
172 pigmented glia (ALSP) is a frequent cause of adult-onset leukodystrophy known to be caused by autosom
173 roposed to improve the diagnostic process of adult-onset leukoencephalopathies.
174                                  Importance: Adult-onset leukoencephalopathy with axonal spheroids an
175                                    The term "adult-onset leukoencephalopathy with axonal spheroids an
176 dominant adult-onset neurological condition (adult-onset leukoencephalopathy with axonal spheroids an
177                                              Adult-onset leukoencephalopathy with axonal spheroids, a
178                                              Adult-onset leukoencephalopathy with spheroids and pigme
179 o improved diagnostic rates in patients with adult-onset leukoencephalopathy.
180 ural abnormalities and intellectual delay to adult-onset limb-girdle muscular dystrophies without men
181 c transformation of intestinal fate, whereas adult-onset loss compromises crucial physiological funct
182 ared genetic risk exists between earlier and adult-onset MDD with commonly comorbid disorders of schi
183 r to schizophrenia and bipolar disorder than adult-onset MDD.
184 provides a refined estimate of the burden of adult onset, medically actionable incidental findings ex
185 SH) in distinguishing PNs from childhood and adult-onset melanoma arising in CMN.
186 ISH aberration compared with 4 patients with adult-onset melanoma.
187 ll patients) but negative in 4 patients with adult-onset melanoma.
188  from childhood-onset melanoma as opposed to adult-onset melanoma.
189 g for HMB45 was seen in 3 of 6 patients with adult-onset melanoma.
190 h may contribute to their increased risk for adult onset metabolic diseases, such as diabetes and obe
191 n these regions) are at risk of stunting and adult-onset metabolic conditions.
192 metabolome accompany heritable IUGR, precede adult-onset MetS, and are partially amenable to dietary
193  a neonatal-onset, very severe disease to an adult-onset, milder form.
194 ogue lap could rescue Abeta42 toxicity in an adult-onset model of AD, without affecting Abeta42 level
195                                To develop an adult-onset model of BRAF-mutant ATC, we generated a thy
196 hic lateral sclerosis (ALS), the most common adult-onset motor neuron (MN) disease.
197 ral sclerosis (ALS), the most common form of adult-onset motor neuron disease and the third most comm
198 ey cyst formation in vivo in both early- and adult-onset mouse models of ADPKD, we used conditional i
199 atus at birth may be associated with risk of adult onset multiple sclerosis, but this link has not be
200  muscular atrophy (SBMA) is characterized by adult-onset muscle weakness and lower motor neuron degen
201 ily with 13 affected members presenting with adult-onset muscle weakness, and we provide clinical, me
202 trophy type 1 (DM1), the most common form of adult-onset muscular dystrophy, is caused by an expanded
203 ophy type 1 (DM1) is the most common form of adult-onset muscular dystrophy, which is characterised b
204                              In contrast, an adult-onset mutation did not significantly alter basal t
205                Purkinje cells expressing the adult-onset mutation matured normally and did not degene
206 h, we tested the hypothesis that infant- and adult-onset mutations differentially affect the excitabi
207        A recent study of a sibling pair with adult onset NCL and retinal degeneration showed linkage
208 in a mouse (termed decrepit) that results in adult-onset neurodegeneration with a stereotypical neuro
209 pted "RNA-only" repeats in Drosophila caused adult-onset neurodegeneration.
210 ic lateral sclerosis (ALS) is a progressive, adult onset neurodegenerative disease that is always fat
211 eurodegenerative disease, is the most common adult onset neurodegenerative disorder affecting motor n
212  Huntington's disease (HD) is a progressive, adult-onset neurodegenerative disease caused by a polygl
213 EMENT The development of novel therapies for adult-onset neurodegenerative disease has been impeded b
214 use amyotrophic lateral sclerosis is a fatal adult-onset neurodegenerative disease produced by mutati
215 pinal and bulbar muscular atrophy (SBMA), an adult-onset neurodegenerative disease that affects males
216 yotrophic lateral sclerosis is a progressive adult-onset neurodegenerative disease that primarily aff
217 ike 2 (HDL2) and Huntington disease (HD) are adult-onset neurodegenerative diseases characterized by
218  of this pathological hallmark shared across adult-onset neurodegenerative diseases.
219 ted tremor/ataxia syndrome (FXTAS) is a late adult-onset neurodegenerative disorder that affects move
220 ociated tremor/ataxia syndrome (FXTAS) is an adult-onset neurodegenerative disorder that affects prem
221 hic lateral sclerosis (ALS) is a devastating adult-onset neurodegenerative disorder with a poor progn
222  Multiple system atrophy is a fatal sporadic adult-onset neurodegenerative disorder with no symptomat
223 elopment and is an early hallmark of several adult-onset neurodegenerative disorders.
224 a gene previously associated with a dominant adult-onset neurological condition (adult-onset leukoenc
225 otrophic lateral sclerosis (ALS) is a fatal, adult-onset neurological disease characterized by a prog
226 he pathogenesis of several developmental and adult-onset neurological disorders that affect the hippo
227 ogued genome-wide association study hits for adult-onset neurological disorders.
228                  This locus for this form of adult onset neuronal ceroid lipofuscinosis was designate
229                                              Adult onset neuronal lipofuscinosis (ANCL) is a human ne
230                           Autosomal-dominant adult-onset neuronal ceroid lipofuscinosis (ANCL) is cau
231 -alpha (CSPalpha) cause dominantly inherited adult-onset neuronal ceroid lipofuscinosis (ANCL), a rap
232 generation (FTLD) and nullizygosity produces adult-onset neuronal ceroid lipofuscinosis.
233 families have relatively mild, childhood- to adult-onset NM with slowly progressive muscle weakness.
234 post-neonatal mortality, growth failure, and adult-onset non-communicable diseases.
235 rocyte ablation during early life results in adult-onset O(2) chemoreflex deficiency.
236 ctivity as low as 5-20% leads to juvenile or adult onset of a disorder that primarily affects the cen
237                  This report dealing with an adult onset of atypical KD may be of benefit to physicia
238 cline in cognitive function, as well as with adult onset of psychosis and anxiety.
239 tients with ataxia present sporadically with adult onset of symptoms and the contribution of genetic
240 henotype in mouse models of developmental or adult-onset of ADPKD.
241 rvational study in which adult patients with adult-onset of asthma (defined as starting at age >/=18
242 explain many of its key aspects, such as its adult onset or its specificity for the corticospinal tra
243 m brain samples from individuals with either adult-onset or juvenile-onset HD.
244 ietic-stem-cell chimerism, and can rescue an adult-onset osteopetrotic phenotype caused by cathepsin
245 iants were identified in family members with adult-onset parkinsonism.
246                          In 11 childhood and adult onset patients, clinical measures stabilized or im
247 associated with refractory celiac disease in adult onset patients.
248 ts were most pronounced in first episode and adult-onset patients (>21 years).
249 ompared with their healthy siblings and with adult-onset patients (AOS), carry significantly more rar
250 ompared with their healthy siblings and with adult-onset patients (AOS), carry significantly more rar
251 into classic infantile, childhood-onset, and adult-onset patients.
252   Unexpectedly, unlike the inborn model, the adult-onset pattern of excitability changes believed to
253 opmentally impaired myelination, whereas the adult-onset phenotype reflects axonal degeneration witho
254     Unbiased transcriptional profiling in an adult-onset Pkd2 mouse model before cysts formed reveale
255 N=20); intraneural B-cell lymphoma (N=20) or adult-onset polyglucosan body disease (APBD: N=6) in com
256                                              Adult onset primary torsion dystonia (AOPTD) is a poorly
257 ariants from previously published studies in adult-onset primary CNS tumors and replicated these in s
258 revalence and phenomenology in patients with adult-onset primary dystonia is limited.
259 inical correlates of tremor in patients with adult-onset primary dystonia.
260  tremor is a common feature of patients with adult-onset primary dystonia.
261 consecutive patients with different types of adult-onset primary dystonia.
262 entions against fetal growth restriction and adult-onset programmed hypertension in an animal model o
263 FUS protein at physiological levels and have adult onset progressive motor neuron loss and denervatio
264 eukoencephalopathy with spheroids (HDLS), an adult-onset progressive neurodegenerative disorder.
265 nt identification of a dominantly inherited, adult-onset, progressive dementia associated with inacti
266  patients aged 18 years or older with active adult-onset psoriatic arthritis and symptoms for at leas
267 eurodegenerative diseases, epilepsy or other adult-onset psychiatric diseases.
268 nd Dec 31, 2017, on incidence of non-organic adult-onset psychotic disorder.
269 adic amyotrophic lateral sclerosis (ALS), an adult-onset, rapidly progressing neurodegenerative disea
270            GBE1 mutations can cause an early adult-onset relapsing-remitting form of polyglucosan bod
271 ere we describe five families affected by an adult-onset retinal dystrophy with early macular involve
272 resembled those seen in juvenile- (rHD1) and adult-onset (rHD7) HD.
273 es collected from twenty-three patients with adult-onset RRP every three months for one year.
274 ng of cerebellar degeneration in infant- and adult-onset SCA13.
275  rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or
276                                              Adult-onset severe asthma is characterized by highly sym
277                                              Adult-onset severe asthma is characterized by inflammato
278  innate lymphoid cells were more enriched in adult-onset severe asthma, whereas signatures associated
279 ht to identify gene profiles associated with adult-onset severe asthma.
280 epresent useful targets for the treatment of adult-onset severe asthma.
281 th induced lung injury were less enriched in adult-onset severe asthma.
282 nsidered when patients show a combination of adult-onset spastic ataxia and a thin corpus callosum.
283 i: 23 were childhood-onset specific, one was adult-onset specific, and 37 were shared.
284 in, blood, and small intestine; genes at the adult onset-specific loci were most highly expressed in
285 ockout (MCM-Speg(fl/fl)) model revealed that adult-onset SPEG deficiency results in heart failure (HF
286 tigator-driven, real-life follow-up study of adult-onset steroid-naive, newly diagnosed asthma (162 p
287 2 patients with Schnitzler syndrome, 12 with adult-onset Still's disease, 7 with cryopyrin-associated
288 id arthritis, juvenile idiopathic arthritis, adult-onset Still's disease, giant cell arteritis and Ta
289              All of the most common forms of adult-onset strabismus increased with age, especially af
290 r period, constituting 15.7% of all forms of adult-onset strabismus observed in this population.
291                             The incidence of adult-onset strabismus overall and its 4 most common for
292 early-life stress, (2) in adulthood to model adult-onset stress, or (3) across the entire postnatal l
293 e sequencing in a case-control cohort of 600 adult-onset sudden cardiac death cases and 600 matched c
294 ivity and extent at diagnosis in consecutive adult-onset UC patients diagnosed at The Ottawa Hospital
295 vels of total disease burden at diagnosis in adult-onset UC patients.
296 l Disease outpatient clinic and compare with adult-onset UC.
297 duals, including one family with exclusively adult-onset upper motor neuron features, consistent with
298 chopathy) differs from that of patients with adult-onset ventromedial prefrontal cortex lesions--the
299 set analyses were performed for childhood vs adult-onset vitiligo and alopecia totalis or alopecia un
300 nclude limb-girdle muscular dystrophies with adult onset with or without intellectual disability, or

 
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