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Sökning: WFRF:(Kircher T)

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1.
  • Han, L. K. M., et al. (författare)
  • Brain aging in major depressive disorder: results from the ENIGMA major depressive disorder working group
  • 2020
  • Ingår i: Molecular Psychiatry. - 1359-4184 .- 1476-5578.
  • Tidskriftsartikel (refereegranskat)abstract
    • Major depressive disorder (MDD) is associated with an increased risk of brain atrophy, aging-related diseases, and mortality. We examined potential advanced brain aging in adult MDD patients, and whether this process is associated with clinical characteristics in a large multicenter international dataset. We performed a mega-analysis by pooling brain measures derived from T1-weighted MRI scans from 19 samples worldwide. Healthy brain aging was estimated by predicting chronological age (18–75 years) from 7 subcortical volumes, 34 cortical thickness and 34 surface area, lateral ventricles and total intracranial volume measures separately in 952 male and 1236 female controls from the ENIGMA MDD working group. The learned model coefficients were applied to 927 male controls and 986 depressed males, and 1199 female controls and 1689 depressed females to obtain independent unbiased brain-based age predictions. The difference between predicted “brain age” and chronological age was calculated to indicate brain-predicted age difference (brain-PAD). On average, MDD patients showed a higher brain-PAD of +1.08 (SE 0.22) years (Cohen’s d = 0.14, 95% CI: 0.08–0.20) compared with controls. However, this difference did not seem to be driven by specific clinical characteristics (recurrent status, remission status, antidepressant medication use, age of onset, or symptom severity). This highly powered collaborative effort showed subtle patterns of age-related structural brain abnormalities in MDD. Substantial within-group variance and overlap between groups were observed. Longitudinal studies of MDD and somatic health outcomes are needed to further assess the clinical value of these brain-PAD estimates. © 2020, The Author(s).
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2.
  • Forstner, A. J., et al. (författare)
  • Genome-wide association study of panic disorder reveals genetic overlap with neuroticism and depression
  • 2019
  • Ingår i: Molecular Psychiatry. - 1359-4184 .- 1476-5578.
  • Tidskriftsartikel (refereegranskat)abstract
    • Panic disorder (PD) has a lifetime prevalence of 2–4% and heritability estimates of 40%. The contributory genetic variants remain largely unknown, with few and inconsistent loci having been reported. The present report describes the largest genome-wide association study (GWAS) of PD to date comprising genome-wide genotype data of 2248 clinically well-characterized PD patients and 7992 ethnically matched controls. The samples originated from four European countries (Denmark, Estonia, Germany, and Sweden). Standard GWAS quality control procedures were conducted on each individual dataset, and imputation was performed using the 1000 Genomes Project reference panel. A meta-analysis was then performed using the Ricopili pipeline. No genome-wide significant locus was identified. Leave-one-out analyses generated highly significant polygenic risk scores (PRS) (explained variance of up to 2.6%). Linkage disequilibrium (LD) score regression analysis of the GWAS data showed that the estimated heritability for PD was 28.0–34.2%. After correction for multiple testing, a significant genetic correlation was found between PD and major depressive disorder, depressive symptoms, and neuroticism. A total of 255 single-nucleotide polymorphisms (SNPs) with p < 1 × 10−4 were followed up in an independent sample of 2408 PD patients and 228,470 controls from Denmark, Iceland and the Netherlands. In the combined analysis, SNP rs144783209 showed the strongest association with PD (pcomb = 3.10 × 10−7). Sign tests revealed a significant enrichment of SNPs with a discovery p-value of <0.0001 in the combined follow up cohort (p = 0.048). The present integrative analysis represents a major step towards the elucidation of the genetic susceptibility to PD. © 2019, The Author(s), under exclusive licence to Springer Nature Limited.
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3.
  • Ching, C. R. K., et al. (författare)
  • What we learn about bipolar disorder from large-scale neuroimaging: Findings and future directions from theENIGMABipolar Disorder Working Group
  • 2020
  • Ingår i: Human Brain Mapping. - 1065-9471.
  • Tidskriftsartikel (refereegranskat)abstract
    • MRI-derived brain measures offer a link between genes, the environment and behavior and have been widely studied in bipolar disorder (BD). However, many neuroimaging studies of BD have been underpowered, leading to varied results and uncertainty regarding effects. The Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) Bipolar Disorder Working Group was formed in 2012 to empower discoveries, generate consensus findings and inform future hypothesis-driven studies of BD. Through this effort, over 150 researchers from 20 countries and 55 institutions pool data and resources to produce the largest neuroimaging studies of BD ever conducted. The ENIGMA Bipolar Disorder Working Group applies standardized processing and analysis techniques to empower large-scale meta- and mega-analyses of multimodal brain MRI and improve the replicability of studies relating brain variation to clinical and genetic data. Initial BD Working Group studies reveal widespread patterns of lower cortical thickness, subcortical volume and disrupted white matter integrity associated with BD. Findings also include mapping brain alterations of common medications like lithium, symptom patterns and clinical risk profiles and have provided further insights into the pathophysiological mechanisms of BD. Here we discuss key findings from the BD working group, its ongoing projects and future directions for large-scale, collaborative studies of mental illness.
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  • Van Leeuwen, W. M. A., et al. (författare)
  • Sleep, Sleepiness, and Neurobehavioral Performance While on Watch in a Simulated 4 Hours on/8 Hours off Maritime Watch System
  • 2013
  • Ingår i: Annual Review of Chronopharmacology. - : Informa Healthcare. - 0743-9539 .- 1525-6073 .- 0742-0528. ; 30:9, s. 1108-1115
  • Tidskriftsartikel (refereegranskat)abstract
    • Seafarer sleepiness jeopardizes safety at sea and has been documented as a direct or contributing factor in many maritime accidents. This study investigates sleep, sleepiness, and neurobehavioral performance in a simulated 4 h on/8 h off watch system as well as the effects of a single free watch disturbance, simulating a condition of overtime work, resulting in 16 h of work in a row and a missed sleep opportunity. Thirty bridge officers (age 30 +/- 6 yrs; 29 men) participated in bridge simulator trials on an identical 1-wk voyage in the North Sea and English Channel. The three watch teams started respectively with the 00-04, the 04-08, and the 08-12 watches. Participants rated their sleepiness every hour (Karolinska Sleepiness Scale [KSS]) and carried out a 5-min psychomotor vigilance test (PVT) test at the start and end of every watch. Polysomnography (PSG) was recorded during 6 watches in the first and the second half of the week. KSS was higher during the first (mean +/- SD: 4.0 +/- 0.2) compared with the second (3.3 +/- 0.2) watch of the day (p
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10.
  • Anund, Anna, et al. (författare)
  • The effects of driving situation on sleepiness indicators after sleep loss : A driving simulator study
  • 2009
  • Ingår i: Industrial Health. - 0019-8366 .- 1880-8026. ; 47:4, s. 393-401
  • Tidskriftsartikel (refereegranskat)abstract
    • Almost all studies of sleepy driving are carried out in driving simulators and with monotonous road conditions (no interaction with other cars). The present study investigated indicators of sleepy driving in a more challenging scenario after a night awake. 17 participants drove a high fidelity moving base driving simulator experiment while sleepiness was monitored physiologically and behaviourally. Short periods of situations of free driving (no other vehicles) alternated with short periods of following another vehicle (car following) with and without the possibility to overtake. The result showed that a night of prior sleep loss increased sleepiness levels at the wheel (eye closure duration and lateral variability) compared to after a night of normal sleep. Blink duration while overtaking was significantly lower compared to the other situations, it was at the same level as after night sleep. Speed when passing a stopped school bus was not significantly affected by sleepiness. However the warning caused a more rapid reduction of speed. In conclusion, a moderately challenging driving contest did not affect sleepiness indicators, but a very challenging one did so (overtaking). This suggests that it is important to monitor the driving situation in field operational tests of sleepy driving.
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