Soutenir la motivation scolaire des adolescents : comprendre et agir sur base de principes neuroéducatifs.

peer reviewedLa motivation est un facteur clé largement reconnu pour assurer l’engagement et la persévérance dans l’action. C’est également le cas dans le domaine des apprentissages scolaires.  De nombreux modèles théoriques de la motivation, souvent complémentaires, sont disponibles dans la littérature. Cependant, les articles qui envisagent le processus motivationnel sous l’angle de la neuroéducation sont encore peu nombreux. C’est l’objectif de cet article, dans lequel la motivation à apprendre est présentée comme le résultat d’un calcul de probabilité de type couts – bénéfices. Le focus est placé sur les élèves du secondaire, avec une attention particulière aux spécificités de leur développement cérébral d’adolescents. Des pistes d’intervention sont avancées, en vue de créer des conditions propices à la motivation d’apprendre, soit en réduisant la perception des coûts de l’engagement dans l’apprentissage, soit en augmentant la perception de ses bénéfices

Inégalités vues par les sociologues de l’éducation et les psychologues cognitifs : pour une fertilisation croisée au service de l’équité scolaire

La question des inégalités scolaires est traitée depuis plus d'un siècle par les sociologues de l'éducation et par les psychologues de l'apprentissage (en particulier les psychologues d'orientation cognitiviste et neuroscientifique), de manière très autonome. En effet, chacun de ces deux domaines reste très étanche aux travaux de l'autre, voire l'observe avec méfiance. Depuis quelques années toutefois, des points de fertilisation croisée semblent s'amorcer. Ils sont envisagés surtout par des sociologues (e.g., Draelants & Cattonar, 2022 ; Duru-Bellat & Fournier, 2007 ; Morel, 2021), puis par des neuroscientifiques (Farah, 2017; Noble et al., 2021; Thomas, 2017). Aussi, l'objectif de cette conférence est double : (1) Alimenter le débat en faveur d'une fertilisation croisée de ces deux approches des inégalités scolaires, avec davantage de sources psycho-cognitives et, (2) Identifier des perspectives pour la formation initiale et continue des enseignants en Fédération Wallonie-Bruxelles

Les enjeux de la réforme de la formation initiale des enseignants (RFIE) : impact sur l’organisation des stages et évolution du rôle de maître de stage

Communication centrée sur la justification de l’évolution de la formation initiale des enseignants, l’identification de quelques changements de fonds dans les compétences attendues du futur enseignant ainsi que l’identification des changements principaux dans la formation et plus précisément concernant l’accompagnement de stages

Comment développer le portfolio étudiant au supérieur ? Analyse de dispositifs innovants à l’Université de Liège

Depuis 2008, l’Institut de Formation et de Recherche en Enseignement Supérieur de l’Université de Liège (IFRES) accompagne des innovations pédagogiques qui consistent, notamment, en l’implantation de portfolios pour des étudiants de master. Ces initiatives, venant de quatre équipes d’enseignants-chercheurs (Psychologie sociale des groupes et des organisations, Formation d’adultes, Pharmacie et Logopédie), poursuivent des objectifs centrés sur l’articulation théorie-pratique, l’accompagnement de démarches réflexives, le développement et l’évaluation de compétences. Notre communication se focalisera principalement sur la mise en œuvre de ces initiatives au travers des questions suivantes : Comment intégrer un portfolio étudiant dans le cadre d’une formation universitaire? Comment en évaluer son contenu? Comment accompagner les étudiants dans la collecte de preuves significatives ? Des perspectives concernant l’accompagnement de tels projets pédagogiques seront également abordées pour qu’au delà de l’analyse de quelques dispositifs portfolio, notre communication apporte un regard plus critique sur les conditions optimales d’implantation et d’accompagnement d’innovations pédagogiques telles que la mise en place d’un portfolio pour les étudiants

How to Support the Development of Clinical Reasoning in Students in Psychology?

peer reviewedClinical reasoning (CR) is defined as “the thinking and decision-making processes that allow the clinician to take the most appropriate actions in a specific clinical problem-solving context” (Nendaz et al., 2005). This process is thoroughly addressed in the literature concerning medical students (e.g., Audétat et al., 2017; Cairo Notari et al., 2020). Since clinical reasoning is poorly discussed regarding the education of future clinical psychologists, our objective is to illustrate a pedagogic design which aims at its development throughout the cursus in clinical psychology in the Faculty of Psychology of ULiège. Indeed, as Wilcox and Schroeder stated in 2015, “graduate school is an ideal time to provide clear, immediate feedback not only about students’ diagnostic accuracy but, more importantly, about their clinical reasoning: teaching students how to think like psychologists”. In the Bachelor's program, students are made aware of the clinical reasoning through different educational devices, including two MOOCs (Massive Open Online Course), namely 1 : "Acting for one's health", and 2 : "Psychologist and speech therapist: EBP at the service of the patient". These MOOCS develop diverse theoretical knowledges through different learning paths (e.g., videos, expert interviews, quizzes). Also, they train several practical skills (e.g., literature research, cases analysis). In the Master’s program, Jstudents in clinical psychology participate in a course which aims at developing an integrate approach of clinical psychology, beyond different theoretical perspectives in clinical psychology (e.g., psychodynamic, cognitive and behavioral, systemic, humanist). Concretely, students are trained to recourse to an evidence-based approach in their practice through – for instance - modeling, role-playing, and flipped classes. In Master 1, students focus their clinical reasoning on patients’ assessment while in Master 2, they focus on the elaboration of the therapeutic plan. In parallel to this integrate course, they participate in two internships and seminars supporting the development of the clinical reasoning through presentations of clinical cases and an introduction to the supervision via the "7-eyed model of supervision". This communication will present in detail the different pedagogic designs used. Prospects for development will be discussed, particularly in view of the year of supervised practice that future clinical psychologists will have to complete

Genetic association study of QT interval highlights role for calcium signaling pathways in myocardial repolarization.

The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD

Genetics of the thrombomodulin-endothelial cell protein C receptor system and the risk of early-onset ischemic stroke

Background and purpose Polymorphisms in coagulation genes have been associated with early-onset ischemic stroke. Here we pursue an a priori hypothesis that genetic variation in the endothelial-based receptors of the thrombomodulin-protein C system (THBD and PROCR) may similarly be associated with early-onset ischemic stroke. We explored this hypothesis utilizing a multi-tage design of discovery and replication. Methods Discovery was performed in the Genetics-of-Early-Onset Stroke (GEOS) Study, a biracial population-based case-control study of ischemic stroke among men and women aged 1549 including 829 cases of first ischemic stroke (42.2% African-American) and 850 age-comparable stroke-free controls (38.1% African-American). Twenty-four single-nucleotide-polymorphisms (SNPs) in THBD and 22 SNPs in PROCR were evaluated. Following LD pruning (r(2)>= 0.8), we advanced uncorrelated SNPs forward for association analyses. Associated SNPs were evaluated for replication in an early-onset ischemic stroke population (onset-ge Results Among GEOS Caucasians, PROCR rs9574, which was in strong LD with 8 other SNPs, and one additional independent SNP rs2069951, were significantly associated with ischemic stroke (rs9574, OR = 1.33, p = 0.003; rs2069951, OR = 1.80, p = 0.006) using an additive-model adjusting for age, gender and population-structure. Adjusting for risk factors did not change the associations; however, associations were strengthened among those without risk factors. PROCR rs9574 also associated with early-onset ischemic stroke in the replication sample (OR = 1.08, p = 0.015), but not older-onset stroke. There were no PROCR associations in African-Americans, nor were there any THBD associations in either ethnicity. Conclusion PROCR polymorphisms are associated with early-onset ischemic stroke in Caucasians.Peer reviewe

Cystatin C and Cardiovascular Disease

Background Epidemiological studies show that high circulating cystatin C is associated with risk of cardiovascular disease (CVD), independent of creatinine-based renal function measurements. It is unclear whether this relationship is causal, arises from residual confounding, and/or is a consequence of reverse causation. Objectives The aim of this study was to use Mendelian randomization to investigate whether cystatin C is causally related to CVD in the general population. Methods We incorporated participant data from 16 prospective cohorts (n = 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n = 252,216) with 63,292 CVD events. We used the common variant rs911119 in CST3 as an instrumental variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, ischemic stroke, and heart failure. Results Cystatin C concentrations were associated with CVD risk after adjusting for age, sex, and traditional risk factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13; p = 2.12 × 10−14). The minor allele of rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p = 5.95 × 10−211), explaining 2.8% of the observed variation in cystatin C. Mendelian randomization analysis did not provide evidence for a causal role of cystatin C, with a causal relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p = 0.994), which was statistically different from the observational estimate (p = 1.6 × 10−5). A causal effect of cystatin C was not detected for any individual component of CVD. Conclusions Mendelian randomization analyses did not support a causal role of cystatin C in the etiology of CVD. As such, therapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CVD

Contribution of Common Genetic Variants to Risk of Early-Onset Ischemic Stroke

Background and Objectives Current genome-wide association studies of ischemic stroke have focused primarily on late-onset disease. As a complement to these studies, we sought to identify the contribution of common genetic variants to risk of early-onset ischemic stroke. Methods We performed a meta-analysis of genome-wide association studies of early-onset stroke (EOS), ages 18-59 years, using individual-level data or summary statistics in 16,730 cases and 599,237 nonstroke controls obtained across 48 different studies. We further compared effect sizes at associated loci between EOS and late-onset stroke (LOS) and compared polygenic risk scores (PRS) for venous thromboembolism (VTE) between EOS and LOS. Results We observed genome-wide significant associations of EOS with 2 variants in ABO, a known stroke locus. These variants tag blood subgroups O1 and A1, and the effect sizes of both variants were significantly larger in EOS compared with LOS. The odds ratio (OR) for rs529565, tagging O1, was 0.88 (95% confidence interval [CI]: 0.85-0.91) in EOS vs 0.96 (95% CI: 0.92-1.00) in LOS, and the OR for rs635634, tagging A1, was 1.16 (1.11-1.21) for EOS vs 1.05 (0.99-1.11) in LOS; p-values for interaction = 0.001 and 0.005, respectively. Using PRSs, we observed that greater genetic risk for VTE, another prothrombotic condition, was more strongly associated with EOS compared with LOS (p = 0.008). Discussion The ABO locus, genetically predicted blood group A, and higher genetic propensity for venous thrombosis are more strongly associated with EOS than with LOS, supporting a stronger role of prothrombotic factors in EOS.Peer reviewe

The origins and spread of domestic horses from the Western Eurasian steppes

This is the final version. Available on open access from Nature Research via the DOI in this recordData availability: All collapsed and paired-end sequence data for samples sequenced in this study are available in compressed fastq format through the European Nucleotide Archive under accession number PRJEB44430, together with rescaled and trimmed bam sequence alignments against both the nuclear and mitochondrial horse reference genomes. Previously published ancient data used in this study are available under accession numbers PRJEB7537, PRJEB10098, PRJEB10854, PRJEB22390 and PRJEB31613, and detailed in Supplementary Table 1. The genomes of ten modern horses, publicly available, were also accessed as indicated in their corresponding original publications57,61,85-87.NOTE: see the published version available via the DOI in this record for the full list of authorsDomestication of horses fundamentally transformed long-range mobility and warfare. However, modern domesticated breeds do not descend from the earliest domestic horse lineage associated with archaeological evidence of bridling, milking and corralling at Botai, Central Asia around 3500 BC. Other longstanding candidate regions for horse domestication, such as Iberia and Anatolia, have also recently been challenged. Thus, the genetic, geographic and temporal origins of modern domestic horses have remained unknown. Here we pinpoint the Western Eurasian steppes, especially the lower Volga-Don region, as the homeland of modern domestic horses. Furthermore, we map the population changes accompanying domestication from 273 ancient horse genomes. This reveals that modern domestic horses ultimately replaced almost all other local populations as they expanded rapidly across Eurasia from about 2000 BC, synchronously with equestrian material culture, including Sintashta spoke-wheeled chariots. We find that equestrianism involved strong selection for critical locomotor and behavioural adaptations at the GSDMC and ZFPM1 genes. Our results reject the commonly held association between horseback riding and the massive expansion of Yamnaya steppe pastoralists into Europe around 3000 BC driving the spread of Indo-European languages. This contrasts with the scenario in Asia where Indo-Iranian languages, chariots and horses spread together, following the early second millennium BC Sintashta culture