2 resultados para Risk-taking (Psychology).

em University of Connecticut - USA


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The transition to high school can be challenging for some adolescents, resulting in drops of academic functioning (Barber & Olsen, 2004; Smith, 2006). While changes in academic demands and the disparity between adolescent needs and the environmental characteristics of high school have both been cited as possible contributors to this decrease in academic and personal functioning (Barber & Olsen, 2004), it is possible that teachers may play an even larger role in undermining these students’ functioning, specifically through labeling. Although labeling, and how it can lead to self-fulfilling prophesies, is a concept that has been thoroughly researched and applied to the field of criminology and deviant behavior, it is the goal of this current study to investigate if labeling also occurs in the classroom setting and how such labels ultimately effect the academic potential of high school students.

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Several genetic linkage and epidemiological studies have provided strong evidence that DCDC2 is a candidate gene for developmental dyslexia, a disorder that impairs a person’s reading ability despite adequate intelligence, education, and socio-economic status. Studies investigating embryonic intra-ventricular RNA interference (RNAi) of Dcdc2, a rat homolog of the DCDC2 gene in humans, indicate disruptions in neuronal migration in the rat cortex during development. Interestingly, these anatomical anomalies are consistent with post mortem histological analysis of human dyslexic patients. Other rodent models of cortical developmental disruption have shown impairment in rapid auditory processing and learning maze tasks in affected subjects. The current study investigates the rapid auditory processing abilities of mice heterozygous for Dcdc2 (one functioning Dcdc2 allele) and mice with a homozygous knockout of Dcdc2 (no functioning Dcdc2 allele). It is important to note that this genetic model for behavioral assessment is still in the pilot stage. However, preliminary results suggest that mice with a genetic mutation of Dcdc2 have impaired rapid auditory processing, as well as non-spatial maze learning and memory ability, as compared to wildtypes. By genetically knocking out Dcdc2 in mice, behavioral features associated with Dcdc2 can be characterized, along with other neurological abnormalities that may arise due to the loss of the functioning gene.