178 research outputs found
EnquĂȘte visant Ă identifier les fonctions et tĂąches du coordonnateur des plans de services individualisĂ©s
Harmonisation des relations interpersonnelles de l'enseignante avec ses Ă©lĂšves Ă partir de leur profil d'apprentissage
La présente recherche a pour but de tendre vers un certain équilibre à l'intérieur de la pratique quotidienne entre les savoirs obligatoires à transmettre et le respect du profil d'apprentissage de chacun des élÚves. Notre questionnement se situe au niveau de l'ampleur de l'engagement et de la motivation qu'elle engendre. Nous voulons rehausser notre image comme professionnelle de l'enseignement et déterminer les balises de nos interventions. Pour atteindre ces buts, nous faisons notre analyse auprÚs des élÚves faisant partie de notre groupe-classe. Au préalable, nous définissons le concept d'apprentissage et la relation pédagogique qui visent à rendre l'apprentissage davantage intelligent à travers un respect individuel. Nous devons donc, pour y répondre et pour ouvrir chez lui de nouveaux horizons, connaßtre le profil d'apprentissage de chacun. Ces trois concepts sont présentés à travers les écrits de différents auteurs qui ont théorisé sur ceux-ci. Nous utilisons une méthodologie qui a pour but de découvrir les encadrements favorables à l'apprentissage, la façon de décoder l'information et de la
traiter pour chacun des élÚves et pour l'ensemble du groupe. Nous examinons leurs acquis académiques à leur arrivée en cinquiÚme année. Mieux les connaßtre permet de
recourir Ă une organisation pĂ©dagogique signifiante pour eux. Nous dĂ©veloppons des attitudes d'Ă©coute et d'expertise pour Ă©tablir la progression de chaque Ă©lĂšve. Cette prĂ©sence aimante, perspicace pour rĂ©soudre les Ă©nigmes du quotidien, permet d'intĂ©grer une estime de soi rĂ©vĂ©latrice d'une vĂ©ritable compĂ©tence professionnelle. Nous concluons que le respect des diffĂ©rences individuelles comme Ă©lĂ©ment central de nos choix pĂ©dagogiques nous permet d'utiliser avec confiance "une pĂ©dagogie de la rĂ©ussite". Ce sentiment gĂ©nĂ©rera chez nos Ă©lĂšves, une plus grande estime d'eux-mĂȘmes
et un plus grand désir de compétence
Paradoxical Role of an Egr Transcription Factor Family Member, Egr2/Krox20, in Learning and Memory
It is well established that Egr1/zif268, a member of the Egr family of transcription factors, is critical for the consolidation of several forms of memories. Recently, the Egr3 family member has also been implicated in learning and memory. Because Egr family members encode closely related zinc-finger transcription factors sharing a highly homologous DNA binding domain that recognises the same DNA sequence, they may have related functions in brain. Another Egr family member expressed in brain, Egr2/Krox20 is known to be crucial for normal hindbrain development and has been implicated in several inherited peripheral neuropathies; however, due to Egr2-null mice perinatal lethality, its potential role in cognitive functions in the adult has not been yet explored. Here, we generated Egr2 conditional mutant mice allowing postnatal, forebrain-specific Cre-mediated Egr2 excision and tested homozygous, heterozygous and control littermates on a battery of behavioural tasks to evaluate motor capacity, exploratory behaviour, emotional reactivity and learning and memory performance in spatial and non-spatial tasks. Egr2-deficient mice had no sign of locomotor, exploratory or anxiety disturbances. Surprisingly, they also had no impairment in spatial learning and memory, taste aversion memory or fear memory using a trace conditioning paradigm. On the contrary, Egr2-deficient mice had improved performance in motor learning on a rotarod, and in object recognition memory. These results clearly do not extend the phenotypic consequences resulting from either Egr1 or Egr3 loss-of-function to Egr2. In contrast, they indicate that Egr family members may have different, and in certain circumstances antagonistic functions in the adult brain
Distinct Functions of Egr Gene Family Members in Cognitive Processes
The different gene members of the Egr family of transcriptional regulators have often been considered to have related functions in brain, based on their co-expression in many cell-types and structures, the relatively high homology of the translated proteins and their ability to bind to the same consensus DNA binding sequence. Recent research, however, suggest this might not be the case. In this review, we focus on the current understanding of the functional roles of the different Egr family members in learning and memory. We briefly outline evidence from mutant mice that Egr1 is required specifically for the consolidation of long-term memory, while Egr3 is primarily essential for short-term memory. We also review our own recent findings from newly generated forebrain-specific conditional Egr2 mutant mice, which revealed that Egr2, as opposed to Egr1 and Egr3, is dispensable for several forms of learning and memory and on the contrary can act as an inhibitory constraint for certain cognitive functions. The studies reviewed here highlight the fact that Egr family members may have different, and in certain circumstances antagonistic functions in the adult brain
Up-regulation of the expression of the gene for liver fatty acid-binding protein by long-chain fatty acids
BDNF Val66Met polymorphism interacts with sleep consolidation to predict ability to create new declarative memories
It is hypothesized that a fundamental function of sleep is to restore an individual's day-to-day ability to learn and to constantly adapt to a changing environment through brain plasticity. Brain-derived neurotrophic factor (BDNF) is among the key regulators that shape brain plasticity. However, advancing age and carrying the BDNF Met allele were both identified as factors that potentially reduce BDNF secretion, brain plasticity, and memory. Here, we investigated the moderating role of BDNF polymorphism on sleep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years of age. All subjects were tested with 1 night of in-laboratory polysomnography followed by a cognitive evaluation the next morning. We found that in subjects carrying the BDNF Val66Val polymorphism, consolidated sleep was associated with significantly better performance on hippocampus-dependent episodic memory tasks the next morning (ÎČ-values from 0.290 to 0.434, p †0.01). In subjects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not associated with better memory performance in most memory tests (ÎČ-values from -0.309 to -0.392, p values from 0.06 to 0.15). Strikingly, increased sleep consolidation was associated with poorer performance in learning a short story presented verbally in Met allele carriers (ÎČ = -0.585, p = 0.005). This study provides new evidence regarding the interacting roles of consolidated sleep and BDNF polymorphism in the ability to learn and stresses the importance of considering BDNF polymorphism when studying how sleep affects cognition
Mutations and Deletions in PCDH19 Account for Various Familial or Isolated Epilepsies in Females
Mutations in PCDH19, encoding protocadherin 19 on chromosome X, cause familial epilepsy and mental retardation limited to females or Dravet-like syndrome. Heterozygous females are affected while hemizygous males are spared, this unusual mode of inheritance being probably due to a mechanism called cellular interference. To extend the mutational and clinical spectra associated with PCDH19, we screened 150 unrelated patients (113 females) with febrile and afebrile seizures for mutations or rearrangements in the gene. Fifteen novel point mutations were identified in 15 female patients (6 sporadic and 9 familial cases). In addition, qPCR revealed two whole gene deletions and one partial deletion in 3 sporadic female patients. Clinical features were highly variable but included almost constantly a high sensitivity to fever and clusters of brief seizures. Interestingly, cognitive functions were normal in several family members of 2 families: the familial condition in family 1 was suggestive of Generalized Epilepsy with Febrile Seizures Plus (GEFS+) whereas all three affected females had partial cryptogenic epilepsy. These results show that mutations in PCDH19 are a relatively frequent cause of epilepsy in females and should be considered even in absence of family history and/or mental retardation. © 2010 Wiley-Liss, Inc
Link between Intestinal CD36 Ligand Binding and Satiety Induced by a High Protein Diet in Mice
CD36 is a ubiquitous membrane glycoprotein that binds long-chain fatty acids. The presence of a functional CD36 is required for the induction of satiety by a lipid load and its role as a lipid receptor driving cellular signal has recently been demonstrated. Our project aimed to further explore the role of intestinal CD36 in the regulation of food intake. Duodenal infusions of vehicle or sulfo-N-succinimidyl-oleate (SSO) was performed prior to acute infusions of saline or Intralipid (IL) in mice. Infusion of minute quantities of IL induced a decrease in food intake (FI) compared to saline. Infusion of SSO had the same effect but no additive inhibitory effect was observed in presence of IL. No IL- or SSO-mediated satiety occurred in CD36-null mice. To determine whether the CD36-mediated hypophagic effect of lipids was maintained in animals fed a satietogen diet, mice were subjected to a High-Protein diet (HPD). Concomitantly with the satiety effect, a rise in intestinal CD36 gene expression was observed. No satiety effect occurred in CD36-null mice. HPD-fed WT mice showed a diminished FI compared to control mice, after saline duodenal infusion. But there was no further decrease after lipid infusion. The lipid-induced decrease in FI observed on control mice was accompanied by a rise in jejunal oleylethanolamide (OEA). Its level was higher in HPD-fed mice than in controls after saline infusion and was not changed by lipids. Overall, we demonstrate that lipid binding to intestinal CD36 is sufficient to produce a satiety effect. Moreover, it could participate in the satiety effect induced by HPD. Intestine can modulate FI by several mechanisms including an increase in OEA production and CD36 gene expression. Furthermore, intestine of mice adapted to HPD have a diminished capacity to modulate their food intake in response to dietary lipids
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