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2 of GM to total cerebral volume declined with age at a slower rate in autistic boys and girls relative
3 tween 2013 and 2017 were eligible (77% men); age at admission was 47 years [interquartile range (IQR)
5 After adjustment for potential covariates, ages at alcohol initiation (AAIs) of 18.1-29.0 years, 29
7 age 9.4 y), classified as early treated (ET; age at ART initiation <=0.5 y, n = 14) or late treated (
9 lation-based cohort studies (1983-2018; mean age at baseline = 46 years; median follow-up, 19 years).
11 19 male) with a mean (+/-standard deviation) age at baseline of 76.60+/-6.65 years and median (interq
12 n and no history of CVD and cancer, the mean age at baseline was 50.9 (SD 10.4) years, and 40.8% were
13 ts from the UK Biobank (55% were women, mean age at baseline, 56 years [SD, 8 years]), 4607 CHD and 3
14 pooled sample included 252 745 women (median age at baseline, 57 years) with 38% self-reporting use o
17 in a cohort of n = 64 preterm infants (mean age at birth = 32.0 weeks), we tested whether cortical a
18 RI) in n = 292 healthy newborn infants (mean age at birth = 39.9 weeks) with regional patterns of gen
19 nates who were at least 34 weeks gestational age at birth and enrolled within 48 h of birth, born to
22 socioeconomic status, birth weight, maternal age at birth, anisometropia, astigmatism, spherical equi
25 p analysis according to age at diagnosis and age at blood draw revealed increased methylation levels
26 l hazards regression, declined steadily with age at BMI assessment, from 1.25 (95% confidence interva
28 lating drug dose, and an interaction between age at cancer diagnosis and haematopoietic stem-cell tra
30 erse mental health included younger maternal age at cancer diagnosis, low socioeconomic status, and r
33 Potential confounding variables; maternal age at conception, maternal education level, parental so
35 cases with cerebral amyloid angiopathy (mean age at death 73 years, nine males) and three controls (m
36 years, nine males) and three controls (mean age at death 91 years, one male) were included in the st
41 death, and r=0.40 individual and mean family age at death) or the GRN group (r=0.22 individual and pa
42 nd r=0.69 between individual and mean family age at death) than in either the C9orf72 group (r=0.32 i
43 CI 35-62, for age at onset; 61%, 47-73, for age at death), and even more by family membership (66%,
46 dels to explore differences in age at onset, age at death, and disease duration between genetic group
47 , we collected data on age at symptom onset, age at death, and disease duration for patients with pat
48 international study of age at symptom onset, age at death, and disease duration in individuals with m
49 age at onset, r=0.22 individual and parental age at death, and r=0.32 individual and mean family age
50 age at onset, r=0.38 individual and parental age at death, and r=0.40 individual and mean family age
51 nset, r=0.58 between individual and parental age at death, and r=0.69 between individual and mean fam
53 neuropathologic burden was weakly related to age at death; it occurred in only about one-third of par
56 two clusters demonstrated lower gestational age at delivery (p = 0.049), increased protein excretion
61 six clinical parameters (GAD autoantibodies, age at diabetes onset, HbA(1c), BMI, and measures of ins
62 OR: 2.4), glaucoma (P = .04; OR: 4.09), and age at diagnosis (P = .005; OR: 1.02) were independent r
65 12.2 and 12.6 years in the PCG (53%, median age at diagnosis = 5 months) and secondary glaucoma grou
73 sed with glaucoma (9/11, 81.8%), with a mean age at diagnosis of 9.22+/-14.89 years, and all individu
75 4% (according to both criteria), and younger age at diagnosis of glaucoma (18-39 years) was predictiv
78 rter period than previously assumed, and the age at diagnosis of pineal TRb is independent of the age
81 unique clinical variables such as patients' age at diagnosis or information regarding lymph nodes, w
84 ard deviation (SD), range 0.2-5.0], the mean age at diagnosis was 10.2 +/- 8.5 years (SD, range 0.1-4
89 hundred sixty patients were identified (mean age at diagnosis was 68 years and 49% were females): 122
92 t of smoking), (ii) among women with cancer, age at diagnosis was positively related to 2D:4D, i.e. w
96 dentified 1699 cases of cardiomyopathy (mean age at diagnosis, 46.2 [SD 9.1] years) during the follow
97 oma cohort included 1295 patients (mean [SD] age at diagnosis, 59.8 [15.6] years; 488 [37.7%] women;
98 e cancer cohort included 1072 men (mean [SD] age at diagnosis, 63.7 [7.9] years; 857 [79.9%] with Eur
101 erformed using (1) individual INPC criteria (age at diagnosis, histologic category, mitosis-karyorrhe
102 included total number of tumors per patient, age at diagnosis, laterality at presentation and later,
107 = 0.44), suggesting independence between the ages at diagnosis of intraocular retinoblastoma and pine
108 nome-wide genotyping in 145 patients (median age-at-diagnosis of 3.5 years), in whom no Mendelian dis
112 wed significantly stronger associations with age-at-disease-onset, clinical progression, amyloid depo
114 ated with longer dystonia duration and older age at dystonia onset in DYT-TOR1A, longer dystonia dura
115 cipants of the Penn Medicine Biobank (median age at enrollment 63 years, interquartile range 55-72; 3
118 cohort of 57,053 individuals 50-64 years of age at enrollment, we identified 21,241 individuals who
123 Medical records of 65 patients >50 years of age at first diagnosis of IIH were reviewed based on the
126 found between the two study groups regarding age at first IAC injection, disease grouping at diagnosi
127 ith anti-VEGF agent according to the patient age at first injection ($78 323.19-$292 449.87) and freq
128 ositions based on the agent modeled, patient age at first injection, frequency of injections, and cli
130 otective effect of pregnancy is dependent on age at first pregnancy, with young mothers receiving the
131 10% of variance in the ratio of fertility to age at first reproduction (F/alpha) and lifetime reprodu
135 d Main Results: For all 4,240 subjects, mean age at follow up was 65.4 years, 3,486 (82.0%) were male
136 ore inpatient days during childhood, younger age at Fontan surgery, and longer time since Fontan proc
139 r associated with both maternal and paternal age at Holocaust exposure were in the same direction.
140 ent, parental posttraumatic stress disorder, age at Holocaust exposure) and offspring characteristics
145 AF, 21% required de novo pacemakers (median age at implantation 37 years; IQR: 29 to 48 years), 14%
146 ards models (controlling for patient gender, age at index diagnosis of IC, and diagnosis with diabete
151 pact of lipid lowering as a function of age, age at initiation, and non-high-density lipoprotein chol
154 lity analyses were restricted to women whose age at last birth (ALB) was >= 30 years, the age when fe
155 g age at menarche, current menstrual status, age at last menstruation, and menopausal aetiology) info
158 rials.gov identifier: NCT02953678), patients aged at least 12 years with grades II to IV steroid-refr
159 tes in 26 countries) trial enrolled patients aged at least 18 years with active psoriatic arthritis.
160 ncluded patients with stage III colon cancer aged at least 18 years with an Eastern Cooperative Oncol
161 patients from 49 hospitals in six countries aged at least 18 years with histologically confirmed, ad
162 South Korea, and Republic of Ireland, women (aged at least 18 years) with newly diagnosed, histologic
163 omised trial, patients with advanced cancer, aged at least 18 years, admitted to the palliative and s
165 ed pregnant women in South Africa and Uganda aged at least 18 years, with untreated but confirmed HIV
166 ICIPANTS: Representative sample of US adults aged at least 40 years in the National Health and Nutrit
167 patients from 29 trials, 21 492 (8.8%) were aged at least 75 years, of whom 11 750 (54.7%) were from
169 factors of long-term (beyond 12 mo) CVE were age at LT (hazard ratio [HR], 1.04; 95% confidence inter
173 x (BMI), smoking, alcohol intake, parity and age at menarche with changes in hormones by reproductive
174 ects of LDL, TGs, body mass index (BMI), and age at menarche, corroborated this observation for HDL (
175 re and adequate menstrual history (including age at menarche, current menstrual status, age at last m
176 od collection for premenopausal women) minus age at menarche, subtracting years of oral contraceptive
180 in myopia prevalence and ORs with increasing age at migration were observed, most prominent in immigr
182 years (22 years before the estimated median age at mild cognitive impairment onset of 44 years), alt
183 if they had clinical data available on sex, age at motor symptom onset, disease duration (from motor
184 and matched with each case for center, sex, age at MPN diagnosis, date of diagnosis, and MPN disease
185 ht loss >= 5%, tobacco use at LEMS onset and age at onset >= 50 years were independent predictors for
186 testing in Parkinson's disease patients with age at onset < 40 years, especially in those from famili
188 omy was significantly affected by 3 factors: age at onset (HR 1.047, p = 0.006), body mass index < 20
189 the CAG repeat expansion and to the residual age at onset (RAO): The difference between the observed
190 on, whereas 14% (9-22) of the variability of age at onset and 20% (12-30) of that of age at death was
191 group, only 2% (0-10) of the variability of age at onset and 9% (3-21) of that of age of death was e
192 significantly correlated with both parental age at onset and at death and with mean family age at on
193 vestigate the extent to which variability in age at onset and at death could be accounted for by fami
194 e at onset and at death and with mean family age at onset and at death in all three groups, with a st
195 Modelling showed that the variability in age at onset and at death in the MAPT group was explaine
196 We also assessed correlations between the age at onset and at death of each individual and the age
198 nset and at death of each individual and the age at onset and at death of their parents and the mean
202 y lower than that of non-carriers, while the age at onset of carriers with other gene pathogenic/like
205 n in ductal cells of the pancreas delays the age at onset of diabetes, suggesting a CFTR-agnostic tre
208 ies have detected genetic loci modifying the age at onset of motor symptoms in HD, but genetic factor
213 xed effects models to explore differences in age at onset, age at death, and disease duration between
214 he GRN group (r=0.22 individual and parental age at onset, r=0.18 individual and mean family age at o
215 at onset, r=0.18 individual and mean family age at onset, r=0.22 individual and parental age at deat
216 9orf72 group (r=0.32 individual and parental age at onset, r=0.36 individual and mean family age at o
217 at onset, r=0.36 individual and mean family age at onset, r=0.38 individual and parental age at deat
218 t, r=0.63 between individual and mean family age at onset, r=0.58 between individual and parental age
219 roup (r=0.45 between individual and parental age at onset, r=0.63 between individual and mean family
222 he specific mutation (48%, 95% CI 35-62, for age at onset; 61%, 47-73, for age at death), and even mo
224 linical practice and research by considering age-at-onset and changes over time as well as different
225 Recent genome-wide association studies of age-at-onset in Huntington's disease (HD) point to disti
226 nock-out of Mlh1, the ortholog of a third HD age-at-onset modifier gene (MLH1), which suppresses soma
227 , we evaluated the mouse orthologs of two HD age-at-onset modifier genes, FAN1 and RRM2B, for an infl
228 ciated with individual-specific variation in age-at-onset not accounted for by ePAL, further highligh
229 A higher PRS was associated with earlier age at PD diagnosis and inclusion of the PRS in the PRED
230 bertal body weight and BMI at 8 y of age and age at peak height velocity (PHV; an objective measure o
231 -0.19, -0.17) were inversely associated with age at PHV but the association for body weight was signi
232 ody weight explained more of the variance in age at PHV than BMI in both the old cohort and the recen
233 In 32 patients identified with ARS (median age at presentation 6.9 years, 0-58.7 years; median foll
237 emale, with a mean (standard deviation [SD]) age at presentation of 35.2 (14.2) years, and mean refra
238 was 8 years (range, 1-22 years), and median age at presentation of Coats-like exudative vitreoretino
241 Cox analysis revealed that for PCa patients, age at presentation, older age, single marital status, l
243 models, infant vaccination increased average age at primary infection as a result of decreased second
248 e tested whether song traits were related to age at recording, future survival, longevity, and territ
251 length over time not accounted for by ePAL, age-at-sampling and time was inversely associated with i
253 34 had perinatal HIV infection, and reported age at sexual debut and history of heterosexual vaginal
254 ecific mechanisms underlying primate ovarian aging at single-cell resolution, revealing new diagnosti
255 lationship with duration of progestogen use, age at start and last use, and time since first and last
256 al [CI], 0.09-0.99, P = 0.03) and increasing age at surgery (OR, 0.97, 95% CI, 0.95-0.99, P = 0.02) w
257 and glaucoma or GS correlated strongly with age at surgery (P = 0.011/0.004) and glaucoma correlated
258 vents and glaucoma correlated with a younger age at surgery and glaucoma correlated with the presence
267 en histopathology, duration of epilepsy, and age at surgery, and the primary outcomes using random ef
268 were 81% male and 50% nonwhite with a median age at switch of 50 years, CD4+ T-cell count 512 cells/m
272 c studies by doing an international study of age at symptom onset, age at death, and disease duration
273 ospective cohort study, we collected data on age at symptom onset, age at death, and disease duration
274 it may be possible to achieve the biological age at the ground zero lower than that achieved naturall
279 risk for failure was associated with younger age at the time of implantation (<1 year; HR, 27; P = 0.
281 mpared with that to timothy extract at all 3 ages: at the age of 4 years, 9.7% versus 6.8%; at the ag
282 lyses were performed on the basis of patient age at time of first injection and frequency interval of
287 tween host genetics, dose of the at-risk GH, age at treatment onset, and duration of the incubation p
288 gender, ROP treatment method, postmenstrual age at treatment, and coincident nonocular procedures du
293 her age-constant or age-varying FOI, and the age at which 50% and 80% of children had been infected.
294 veloping, whether its onset is linked to the age at which intraocular retinoblastomas develop, and th
295 trations and age, and establish the earliest age at which NfL concentrations begin to diverge between
298 perienced no cardiac events until 4 years of age, at which point she was hospitalized because of thre
299 older mothers tended to die before reaching ages at which such senescent decreases could be observed
300 nstrate differences in retinopathy outcomes, age at worst ROP stage, or postnatal growth failure.