880 resultados para Developmental Neuroscience


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The purpose of this paper is to examine how child psychologists' specialized training inhuman development may make them more prone to stigmatize the parents of their young clients. The stigmatization of parents may lead to fewer parents seeking treatment for their children and to poorer treatment outcomes for those who work with a child psychologist. The process of stigmatization is summarized to provide context for the method through which parents receive stigma. A commonly used theory of child development, Erik Erikson's stages of ego development, is outlined to provide background on how child psychologists may interpret and evaluate a child'sdevelopment. Child psychologists' may identify parenting practices that seem to hinder or stunt children's emotional development, which would make the psychologist more aptto stigmatize and isolate parents from the treatment process. To demonstrate the unique ways in which a child psychologist may stigmatize parents of children at different developmental stages two case studies are included. Finally, a theoretical model of treatment is described that may be more inclusive, and less stigmatizing of parents. This model outlines how the parents' concerns about and observations of their children should be validated and reflected in the treatment process. This treatment modality would allow for child psychologists to more actively involve parents in treatment and provide more education and support around their children's unique emotional development needs. Through this treatment model and child psychologists' awareness of and attempts to reduce the stigmatization of parents, treatment outcomes for young clients may improve.

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This project examines rural Indian women and discusses the strong correlation between gender inequity and the setbacks that have crippled development. The embedded caste system has created a distinct social hierarchy, which has incidentally deprived women of their freedom and voice. Gender inequity and social stratification are direct causes of the AIDS epidemic, research revealing a contingency between lack of empowerment and exposure to the disease. Additionally, the HIV/AIDS virus carries a strong cultural stigma, which influences whether or not women will seek treatment if infected, since AIDS victims face extreme social isolation and discrimination, in India. This project discusses several cause-and-effect frameworks related to gender inequity, which have stunted the growth and success of India.

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Robotics is a field that presents a large number of problems because it depends on a large number of disciplines, devices, technologies and tasks. Its expansion from perfectly controlled industrial environments toward open and dynamic environment presents a many new challenges, such as robots household robots or professional robots. To facilitate the rapid development of robotic systems, low cost, reusability of code, its medium and long term maintainability and robustness are required novel approaches to provide generic models and software systems who develop paradigms capable of solving these problems. For this purpose, in this paper we propose a model based on multi-agent systems inspired by the human nervous system able to transfer the control characteristics of the biological system and able to take advantage of the best properties of distributed software systems.

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The purpose of the present study was to determine whether adolescent females had unique developmental experiences in different types of basketball programs. The Youth Experiences Survey 2.0 [YES] (Hansen & Larson, 2005) was used to measure the learning experiences of 14 and 15 year old females (n = 212) who were enrolled in a school, recreational, or competitive basketball program. Interviews with organization representatives were conducted to determine the structure of each basketball program (n= 16) from which participants were drawn. One-way ANOVAs and Bonferroni comparisons were used to compare YES 2.0 positive experience scale scores of participants in school, recreational and competitive basketball programs. Results revealed that females in recreational programs had significantly lower scores than those in competitive and school programs on numerous positive experiences scales. Mann-Whitney U tests found that those in school and competitive programs reported higher stress levels. Interview results indicate that four characteristics of competitive and school programs may contribute to participants in these programs reporting more growth experiences: 1) time commitment, 2) coaches’ training and background, 3) competition, and 4) volunteer opportunities.

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Despite the popularity of youth sport programs, little research has examined the psychosocial benefits assumed to stem from involvement. Some studies suggest birthplace influences the development of elite athletes, but little work has examined other influences of community contexts. The purpose of this study was to examine relationships between young athletes’ community size, developmental assets, and sport involvement. Current and recently withdrawn competitive swimmers (N = 181) completed the Developmental Assets Profile (Search Institute, 2004). Athletes from smaller cities had significantly higher developmental asset scores for support, commitment to learning, and boundaries/expectations. Further, community size was a significant predictor of withdrawal. Findings suggest community context should be given additional attention in youth sport literature.

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The purpose of this exploratory study was to compare the developmental profiles of successful high-school sport coaches, and to determine if elements of a coach’s developmental profile were associated with coaching success. Sixteen high-school coaches in the United States – nine who coach basketball and seven cross-country running – participated in structured retrospective quantitative interviews. All coaches had accumulated extensive experience as an athlete (M = 19.6 seasons; 2,428.8 hours) and were better than average athletes in relation to their peers. Positive significant relationships were found between time (seasons and hours) spent as an athlete in the sport that the participants now coach and five measures of coaching success. The results are discussed in relation to the ongoing dialogue about coach development, coaching effectiveness, and coach education.

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This study examined youth sport dropout and prolonged engagement from a developmental perspective focusing on physical and psychosocial factors. Twenty-five dropout and 25 engaged adolescent swimmers, matched on key demographic variables, participated in a retrospective interview. Results indicated that dropouts were involved in fewer extra-curricular activities, less unstructured swimming play, and received less one-on-one coaching throughout development. Dropouts reached several developmental milestones (i.e., started training camps, started dry land training, and were top in club) earlier than engaged athletes. Dropouts were more likely to have had parents who were high-level athletes in their youth, were more likely to be the youngest in their training group, and were less likely to have a best friend at swimming. Findings are discussed in relation to past research; future directions and implications for researchers, sport programmers, coaches, and parents are suggested.

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Background: Studies suggest that expert performance in sport is the result of long-term engagement in a highly specialized form of training termed deliberate practice. The relationship between accumulated deliberate practice and performance predicts that those who begin deliberate practice at a young age accumulate more practice hours over time and would, therefore, have a significant performance advantage. However, qualitative studies have shown that a large amount of sport-specific practice at a young age may lead to negative consequences, such as dropout, and is not necessarily the only path to expert performance in sport. Studies have yet to investigate the activity context, such as the amount of early sport participation, deliberate play and deliberate practice within which dropout occurs. Purpose: To determine whether the nature and amount of childhood-organized sport, deliberate play and deliberate practice participation influence athletes' subsequent decisions to drop out or invest in organized sport. It was hypothesized that young athletes who drop out will have sampled fewer sports, spent less time in deliberate play activities and spent more time in deliberate practice activities during childhood sport involvement. Participants: The parents of eight current, high-level, male, minor ice hockey players formed an active group. The parents of four high-level, male, minor ice hockey players who had recently withdrawn from competitive hockey formed a dropout group. Data collection: Parents completed a structured retrospective survey designed to assess their sons' involvement in organized sport, deliberate play and deliberate practice activities from ages 6 to 13. Data analysis: A complete data-set was available for ages 6 through 13, resulting in a longitudinal data-set spanning eight years. This eight-year range was divided into three levels of development corresponding to the players' progress through the youth ice hockey system. Level one encompassed ages 6–9, level two included ages 10–11 and level three covered ages 12–13. Descriptive statistics were used to report the ages at which the active and dropout players first engaged in select hockey activities. ANOVA with repeated measures across the three levels of development was used to compare the number of sports the active and dropout players were involved in outside of hockey, the number of hours spent in these sports, and involvement in various hockey-related activities. Findings: Results indicated that both the active and dropout players enjoyed a diverse and playful introduction to sport. Furthermore, the active and dropout players invested similar amounts of time in organized hockey games, organized hockey practices, specialized hockey training activities (e.g. hockey camps) and hockey play. However, analysis revealed that the dropout players began off-ice training at a younger age and invested significantly more hours/year in off-ice training at ages 12–13, indicating that engaging in off-ice training activities at a younger age may have negative implications for long-term ice hockey participation. Conclusion: These results are consistent with previous research that has found that early diversification does not hinder sport-specific skill development and it may, in fact, be preferable to early specialization. The active and dropout players differed in one important aspect of deliberate practice: off-ice training activities. The dropout players began off-ice training at a younger age, and participated in more off-ice training at ages 12 and 13 than their active counterparts. This indicates a form of early specialization and supports the postulate that early involvement in practice activities that are not enjoyable may ultimately undermine the intrinsic motivation to continue in sport. Youth sport programs should not focus on developing athletic fitness through intense and routine training, but rather on sport-specific practice, games and play activities that foster fun and enjoyment.

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The purpose of this study was to analyze the development of four 20 year-old elite hockey players through an in-depth examination of their sporting activities. The theoretical frameworkof deliberate practice (Ericsson, Krampe, & Tesch-Romer, 1993) and the notion of deliberate play (Côté, 1999) served as the theoretical foundations. Interviews were conducted to providea longitudinal and detailed account of each participant.s involvement in various sporting activities. The interviewer asked questions about the conditions and sporting activities for eachyear of development. The data obtained were validated through independent interviews conducted with three parents of three different athletes. The results were consistent with Côté.s(1999) three stages of development in sport: the sampling (age 6.12), specializing (age 13. 15), and investment (age 16+) years

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The purpose of this research report is to present an overview of an ongoing, international project designed to chart the developmental paths and activities of sport coaches. This brief report includes three sections: (a) conceptual framework used to guide the project, (b) project design and methodology, and (c) results from pilot studies with a sample of 15 successful coaches working in different sport contexts in the United States Unlike the findings for athletic profiles, where several trends across coaching contexts were evident, only one trend was found in how these diverse groups of coaches invested their time in coach developmental activities. In relation to other coaching activities very little time was devoted to formal coach education on an annual basis. The results reinforce the need to consider the coaching context when examining coach development and when designing coach development initiatives.

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The purpose of this study was to gain understanding of adolescents’ positive and negative developmental experiences in sport. Twenty-two purposefully sampled adolescent competitive swimmers participated in a semistructured qualitative interview. Content analysis led to the organization of meaning units into themes and categories (Patton, 2002). Athletes suggested their sport involvement facilitated many positive developmental experiences (i.e., related to challenge, meaningful adult and peer relationships, a sense of community, and other life experiences) and some negative developmental experiences (i.e., related to poor coach relationships, negative peer influences, parent pressure, and the challenging psychological environment of competitive sport). Findings underline the important roles of sport programmers, clubs, coaches, and parents in facilitating youths’ positive developmental experiences in sport, while highlighting numerous important directions for future research. Implications for coach training and practice are outlined.

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This chapter examines the personal and contextual factors of youth sport that affect sport expertise and developmental outcomes. The developmental model of sport participation (DMSP) is used as a comprehensive framework that outlines different pathways of involvement in sport. Activities and contexts that promote continued sport participation and expert performance are discussed as the building blocks of all effective youth sport programs. This chapter provides evidence that performance in sport, participation, and psychological development should be considered as a whole instead of as separate entities by youth sport programmers. Adults in youth sports (i.e. coaches, parents, sport psychologists, administrators) must consider the differing implications of concepts such as deliberate play, deliberate practice, sampling, specialization, and program structure at different stages of an athlete's talent development. Seven postulates are presented regarding important transitions in youth sport and the role that sampling and deliberate play, as opposed to specialization and deliberate practice, can have during the childhood in promoting continued participation and elite performance in sport

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La déficience intellectuelle est la cause d’handicap la plus fréquente chez l’enfant. De nombreuses évidences convergent vers l’idée selon laquelle des altérations dans les gènes synaptiques puissent expliquer une fraction significative des affections neurodéveloppementales telles que la déficience intellectuelle ou encore l’autisme. Jusqu’à récemment, la majorité des mutations associées à la déficience intellectuelle a été liée au chromosome X ou à la transmission autosomique récessive. D’un autre côté, plusieurs études récentes suggèrent que des mutations de novo dans des gènes à transmission autosomique dominante, requis dans les processus de la plasticité synaptique peuvent être à la source d’une importante fraction des cas de déficience intellectuelle non syndromique. Par des techniques permettant la capture de l’exome et le séquençage de l’ADN génomique, notre laboratoire a précédemment reporté les premières mutations pathogéniques dans le gène à transmission autosomique dominante SYNGAP1. Ces dernières ont été associées à des troubles comportementaux tels que la déficience intellectuelle, l’inattention, des problèmes d’humeur, d’impulsivité et d’agressions physiques. D’autres patients sont diagnostiqués avec des troubles autistiques et/ou des formes particulières d’épilepsie généralisée. Chez la souris, le knock-out constitutif de Syngap1 (souris Syngap1+/-) résulte en des déficits comme l’hyperactivité locomotrice, une réduction du comportement associée à l’anxiété, une augmentation du réflexe de sursaut, une propension à l’isolation, des problèmes dans le conditionnement à la peur, des troubles dans les mémoires de travail, de référence et social. Ainsi, la souris Syngap1+/- représente un modèle approprié pour l’étude des effets délétères causés par l’haploinsuffisance de SYNGAP1 sur le développement de circuits neuronaux. D’autre part, il est de première importance de statuer si les mutations humaines aboutissent à l’haploinsuffisance de la protéine. SYNGAP1 encode pour une protéine à activité GTPase pour Ras. Son haploinsuffisance entraîne l’augmentation des niveaux d’activité de Ras, de phosphorylation de ERK, cause une morphogenèse anormale des épines dendritiques et un excès dans la concentration des récepteurs AMPA à la membrane postsynaptique des neurones excitateurs. Plusieurs études suggèrent que l’augmentation précoce de l’insertion des récepteurs AMPA au sein des synapses glutamatergiques contribue à certains phénotypes observés chez la souris Syngap1+/-. En revanche, les conséquences de l’haploinsuffisance de SYNGAP1 sur les circuits neuronaux GABAergiques restent inconnues. Les enjeux de mon projet de PhD sont: 1) d’identifier l’impact de mutations humaines dans la fonction de SYNGAP1; 2) de déterminer si SYNGAP1 contribue au développement et à la fonction des circuits GABAergiques; 3) de révéler comment l’haploinsuffisance de Syngap1 restreinte aux circuits GABAergiques affecte le comportement et la cognition. Nous avons publié les premières mutations humaines de type faux-sens dans le gène SYNGAP1 (c.1084T>C [p.W362R]; c.1685C>T [p.P562L]) ainsi que deux nouvelles mutations tronquantes (c.2212_2213del [p.S738X]; c.283dupC [p.H95PfsX5]). Ces dernières sont toutes de novo à l’exception de c.283dupC, héritée d’un père mosaïque pour la même mutation. Dans cette étude, nous avons confirmé que les patients pourvus de mutations dans SYNGAP1 présentent, entre autre, des phénotypes associés à des troubles comportementaux relatifs à la déficience intellectuelle. En culture organotypique, la transfection biolistique de l’ADNc de Syngap1 wild-type dans des cellules pyramidales corticales réduit significativement les niveaux de pERK, en fonction de l’activité neuronale. Au contraire les constructions plasmidiques exprimant les mutations W362R, P562L, ou celle précédemment répertoriée R579X, n’engendre aucun effet significatif sur les niveaux de pERK. Ces résultats suggèrent que ces mutations faux-sens et tronquante résultent en la perte de la fonction de SYNGAP1 ayant fort probablement pour conséquences d’affecter la régulation du développement cérébral. Plusieurs études publiées suggèrent que les déficits cognitifs associés à l’haploinsuffisance de SYNGAP1 peuvent émerger d’altérations dans le développement des neurones excitateurs glutamatergiques. Toutefois, si, et auquel cas, de quelle manière ces mutations affectent le développement des interneurones GABAergiques résultant en un déséquilibre entre l’excitation et l’inhibition et aux déficits cognitifs restent sujet de controverses. Par conséquent, nous avons examiné la contribution de Syngap1 dans le développement des circuits GABAergiques. A cette fin, nous avons généré une souris mutante knockout conditionnelle dans laquelle un allèle de Syngap1 est spécifiquement excisé dans les interneurones GABAergiques issus de l’éminence ganglionnaire médiale (souris Tg(Nkx2.1-Cre);Syngap1flox/+). En culture organotypique, nous avons démontré que la réduction de Syngap1 restreinte aux interneurones inhibiteurs résulte en des altérations au niveau de leur arborisation axonale et dans leur densité synaptique. De plus, réalisés sur des coupes de cerveau de souris Tg(Nkx2.1-Cre);Syngap1flox/+, les enregistrements des courants inhibiteurs postsynaptiques miniatures (mIPSC) ou encore de ceux évoqués au moyen de l’optogénétique (oIPSC) dévoilent une réduction significative de la neurotransmission inhibitrice corticale. Enfin, nous avons comparé les performances de souris jeunes adultes Syngap1+/-, Tg(Nkx2.1-Cre);Syngap1flox/+ à celles de leurs congénères contrôles dans une batterie de tests comportementaux. À l’inverse des souris Syngap1+/-, les souris Tg(Nkx2.1-Cre);Syngap1flox/+ ne présentent pas d’hyperactivité locomotrice, ni de comportement associé à l’anxiété. Cependant, elles démontrent des déficits similaires dans la mémoire de travail et de reconnaissance sociale, suggérant que l’haploinsuffisance de Syngap1 restreinte aux interneurones GABAergiques dérivés de l’éminence ganglionnaire médiale récapitule en partie certains des phénotypes cognitifs observés chez la souris Syngap1+/-. Mes travaux de PhD établissent pour la première fois que les mutations humaines dans le gène SYNGAP1 associés à la déficience intellectuelle causent la perte de fonction de la protéine. Mes études dévoilent, également pour la première fois, l’influence significative de ce gène dans la régulation du développement et de la fonction des interneurones. D’admettre l’atteinte des cellules GABAergiques illustre plus réalistement la complexité de la déficience intellectuelle non syndromique causée par l’haploinsuffisance de SYNGAP1. Ainsi, seule une compréhension raffinée de cette condition neurodéveloppementale pourra mener à une approche thérapeutique adéquate.

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Le co-transporteur KCC2 spécifique au potassium et chlore a pour rôle principal de réduire la concentration intracellulaire de chlore, entraînant l’hyperpolarisation des courants GABAergic l’autorisant ainsi à devenir inhibiteur dans le cerveau mature. De plus, il est aussi impliqué dans le développement des synapses excitatrices, nommées aussi les épines dendritiques. Le but de notre projet est d’étudier l’effet des modifications concernant l'expression et la fonction de KCC2 dans le cortex du cerveau en développement dans un contexte de convulsions précoces. Les convulsions fébriles affectent environ 5% des enfants, et ce dès la première année de vie. Les enfants atteints de convulsions fébriles prolongées et atypiques sont plus susceptibles à développer l’épilepsie. De plus, la présence d’une malformation cérébrale prédispose au développement de convulsions fébriles atypiques, et d’épilepsie du lobe temporal. Ceci suggère que ces pathologies néonatales peuvent altérer le développement des circuits neuronaux irréversiblement. Cependant, les mécanismes qui sous-tendent ces effets ne sont pas encore compris. Nous avons pour but de comprendre l'impact des altérations de KCC2 sur la survenue des convulsions et dans la formation des épines dendritiques. Nous avons étudié KCC2 dans un modèle animal de convulsions précédemment validé, qui combine une lésion corticale à P1 (premier jour de vie postnatale), suivie d'une convulsion induite par hyperthermie à P10 (nommés rats LHS). À la suite de ces insultes, 86% des rats mâles LHS développent l’épilepsie à l’âge adulte, au même titre que des troubles d’apprentissage. À P20, ces animaux presentent une augmentation de l'expression de KCC2 associée à une hyperpolarisation du potentiel de réversion de GABA. De plus, nous avons observé des réductions dans la taille des épines dendritiques et l'amplitude des courants post-synaptiques excitateurs miniatures, ainsi qu’un déficit de mémoire spatial, et ce avant le développement des convulsions spontanées. Dans le but de rétablir les déficits observés chez les rats LHS, nous avons alors réalisé un knock-down de KCC2 par shARN spécifique par électroporation in utero. Nos résultats ont montré une diminution de la susceptibilité aux convulsions due à la lésion corticale, ainsi qu'une restauration de la taille des épines. Ainsi, l’augmentation de KCC2 à la suite d'une convulsion précoce, augmente la susceptibilité aux convulsions modifiant la morphologie des épines dendritiques, probable facteur contribuant à l’atrophie de l’hippocampe et l’occurrence des déficits cognitifs. Le deuxième objectif a été d'inspecter l’effet de la surexpression précoce de KCC2 dans le développement des épines dendritiques de l’hippocampe. Nous avons ainsi surexprimé KCC2 aussi bien in vitro dans des cultures organotypiques d’hippocampe, qu' in vivo par électroporation in utero. À l'inverse des résultats publiés dans le cortex, nous avons observé une diminution de la densité d’épines dendritiques et une augmentation de la taille des épines. Afin de confirmer la spécificité du rôle de KCC2 face à la région néocorticale étudiée, nous avons surexprimé KCC2 dans le cortex par électroporation in utero. Cette manipulation a eu pour conséquences d’augmenter la densité et la longueur des épines synaptiques de l’arbre dendritique des cellules glutamatergiques. En conséquent, ces résultats ont démontré pour la première fois, que les modifications de l’expression de KCC2 sont spécifiques à la région affectée. Ceci souligne les obstacles auxquels nous faisons face dans le développement de thérapie adéquat pour l’épilepsie ayant pour but de moduler l’expression de KCC2 de façon spécifique.