100 research outputs found

    NeuroStratE: An educational neuroscience intervention to reduce procrastination behavior and improve executive planning function in higher students

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    This study aimed to evaluate the impact of an educational cognitive neuroscience intervention (NeuroStratE) focusing on teaching the functioning of the brain and practical tools to address the procrastination behavior of 199 students enrolled at university from 2019 to 2021. The evolution of procrastination behavior is measured by specific scales and the planning ability through the Tower of Hanoi test. We compared the change in procrastination behaviors and planning ability between the pre and post-test to those of a control group. Procrastination behavior reduction and planning ability improved more in the students who followed the intervention (N = 179) than those in the control group (N = 20). Using mixed methods, these results were qualitatively refined with student feedback on the value of the intervention program, along with individual student interviews. This study highlights that it is particularly courses of procrastination and associated practical tools which contributed to reduced procrastination behavior and improved the planning ability

    A nearly optimal randomized algorithm for explorable heap selection

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    Explorable heap selection is the problem of selecting the nth smallest value in a binary heap. The key values can only be accessed by traversing through the underlying infinite binary tree, and the complexity of the algorithm is measured by the total distance traveled in the tree (each edge has unit cost). This problem was originally proposed as a model to study search strategies for the branch-and-bound algorithm with storage restrictions by Karp, Saks and Widgerson (FOCS '86), who gave deterministic and randomized n⋅exp(O(logn−−−−√)) time algorithms using O(log(n)2.5) and O(logn−−−−√) space respectively. We present a new randomized algorithm with running time O(nlog(n)3) using O(logn) space, substantially improving the previous best randomized running time at the expense of slightly increased space usage. We also show an Ω(log(n)n/log(log(n))) for any algorithm that solves the problem in the same amount of space, indicating that our algorithm is nearly optimal

    Professional quality of life and burnout amongst radiation oncologists:The impact of alexithymia and empathy

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    Background and purpose: Different factors may influence the professional quality of life of oncology professionals. Among them, personality traits, as alexithymia and empathy, are underinvestigated. Alexithymia is about deficits in emotion processing and awareness. Empathy is the ability to understand another's 'state of mind'/emotion. The PROject on BurnOut in RadiatioN Oncology (PRO BONO) assesses professional quality of life, including burnout, in the field of radiation oncology and investigates alexithymia and empathy as contributing factors. Material and methods: An online survey was conducted amongst ESTRO members. Participants completed 3 validated questionnaires for alexithymia, empathy and professional quality of life: (a) Toronto Alexithymia Scale; (b) Interpersonal Reactivity Index; (c) Professional Quality of Life Scale. The present analysis, focusing on radiation/clinical oncologists, evaluates Compassion Satisfaction (CS), Secondary Traumatic Stress (STS) and Burnout and correlates them with alexithymia and empathy (empathic concern, perspective taking and personal distress) with generalized linear modeling. Significant covariates on univariate linear regression analysis were included in the multivariate linear regression model. Results: A total of 825 radiation oncologists completed all questionnaires. A higher level of alexithymia was associated to decreased CS (beta:-0.101; SE: 0.018; p <0.001), increased STS (beta: 0.228; SE: 0.018; p <0.001) and burnout (beta: 0.177; SE: 0.016; p <0.001). A higher empathic concern was significantly associated to increased CS (beta: 0.1.287; SE: 0.305; p = 0.001), STS (beta: 0.114; SE: 0.296; p <0.001), with no effect on burnout. Personal distress was associated to decreased CS (beta:-1.423; SE: 0.275; p <0.001), increased STS (beta: 1.871; SE: 0.283; p <0.001) and burnout (beta: 1.504; SE: 0.245; p <0.001). Conclusions: Alexithymic personality trait increased burnout risk, with less professional satisfaction. Empathic concern was associated to increased stress, without leading to burnout, resulting in higher professional fulfillment. These results may be used to benchmark preventing strategies, such as work-hour restrictions, peer support, debriefing sessions, and leadership initiatives for professionals at risk. (c) 2020 Elsevier B.V. All rights reserved. Radiotherapy and Oncology 147 (2020) 162-16

    Thymus‐derived regulatory T cells restrain pro‐inflammatory Th1 responses by downregulating CD

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    The severity and intensity of autoimmune disease in Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) patients and in scurfy mice emphasizes the critical role played by thymus-derived regulatory T cells (tTregs) in maintaining peripheral immune tolerance. However, although tTregs are critical to prevent lethal autoimmunity and excessive inflammatory responses, their suppressive mechanism remains elusive. Here we demonstrate that tTregs selectively inhibit CD27/CD70-dependent Th1 priming, while leaving the IL-12-dependent pathway unaffected. Immunized mice depleted of tTregs showed an increased response of IFN-Îł-secreting CD4+ T cells that was strictly reliant on a functional CD27/CD70 pathway. In vitro studies revealed that tTregs downregulate CD70 from the plasma membrane of dendritic cells (DCs) in a CD27-dependent manner. CD70 downregulation required contact between Tregs and DCs and resulted in endocytosis of CD27 and CD70 into the DC. These findings reveal a novel mechanism by which tTregs can maintain tolerance or prevent excessive, proinflammatory Th1 responsesin pressSCOPUS: ar.jFLWINinfo:eu-repo/semantics/publishe

    Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

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    Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

    Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

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    Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska LĂ€karesĂ€llskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD

    Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

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    Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk

    The role and uses of antibodies in COVID-19 infections: a living review

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    Coronavirus disease 2019 has generated a rapidly evolving field of research, with the global scientific community striving for solutions to the current pandemic. Characterizing humoral responses towards SARS-CoV-2, as well as closely related strains, will help determine whether antibodies are central to infection control, and aid the design of therapeutics and vaccine candidates. This review outlines the major aspects of SARS-CoV-2-specific antibody research to date, with a focus on the various prophylactic and therapeutic uses of antibodies to alleviate disease in addition to the potential of cross-reactive therapies and the implications of long-term immunity
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