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Evaluer des eleves ayant un trouble du spectre de l'autisme (TSA) represente un defi pour les enseignants, ce qui peut affecter leur sentiment d'efficacite personnelle (SEP). Les eleves ayant un TSA presentent des specificites multiples pour lesquelles s'imposent souvent des amenagements dans les pratiques pedagogiques, plus specifiquement dans les pratiques evaluatives. Selon la litterature consultee, le SEP des enseignants a un effet direct sur les pratiques enseignantes et leur sante mentale. Les resultats de notre etude proposent que l'appropriation de pratiques puisse devenir un levier dans l'evolution du SEP des enseignants lorsque ces derniers sont impliques dans un processus de developpement professionnel pour lequel des ressources adaptees et de l'accompagnement sont offerts. Mots-cles : sentiment d'efficacite personnelle, appropriation, pratiques evaluatives, developpement professionnel, trouble du spectre de l'autisme Assessing students with an autism spectrum disorder (ASD) is a constant challenge. It impacts the sense of personal effectiveness of teachers working with these learners who can have multiple specificities and for whom adjustments to pedagogical practices, and specifically assessment practices, are often essential. According to the literature, teachers' self-efficacy has a direct effect on teaching practices and their mental health. The results of our study suggest that the appropriation of practices can improve teachers' self-efficacy when they are involved in a professional development process providing suitable material and support. Keywords: teachers' self-efficacy, appropriation, assessment practices, autism spectrum disorder, professional development, Problematique et questions de recherche L'evaluation des competences scolaires des eleves ayant un trouble du spectre de l'autisme (TSA) (1) est un defi de tous les instants (Ravet, 2013) qui [...]

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Copyright of Revista de Derecho y Genoma Humano is the property of Dykinson SL and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background. Although insulin resistance of glucose is often reported with aging, that of protein metabolism is still debated. We tested if the insulin sensitivity of protein metabolism parallels that of glucose and is altered with aging. Method. Whole-body [sup.13]C-leucine and [sup.13]H glucose kinetics were measured in file postabsorptive stale and during an hyperinsulinemic, euglycemic, isoaminoacidemic clamp in 12 young men (age: 27 [+ or -] 1 years: body mass index [BMI]: 23 [+ or -] 1 kg/[m.sup.2]), 11 young women (age: 25 [+ or -] 1 years: BMI: 21 [+ or -] 1 kg/[m.sup.2]), 9 elderly men (age: 70 [+ or -] 1 years: BMI: 26 [+ or -] 1 kg/[m.sup.2]), and 10 elderly women (age: 69 [+ or -] 2 years: BMI: 23 [+ or -] 1 kg/[m.sup.2]). Results. Postabsorptive leucine flux rates adjusted for fat free mass (FFM) were not different between elderly and young participants. During the clamp, leucine flux and protein synthesis rates increased less in the elderly participants, and protein breakdown decreased equally. Thus, the net anabolic (protein balance) response to hyperinsulinemia was lower in elderly versus young participants (p = .007) and was highly correlated with the clamp glucose rate of disposal (r = 0.671. p < .001), indicating insulin resistance of protein concurrent with that of glucose. From regression analysis. FFM explained 73% of the variance in the anabolic response. Age explained an additional 3%, but was accounted for by markers of adiposity. FFM and percent body fat collectively explained 79% of the variance. Conclusion. Both reduction in absolute FFM and increased adiposity, intrinsic to the aging process, are associated with an altered anabolic action of insulin in stimulating protein synthesis. This alteration may contribute to the progressive muscle loss with aging.

Objective In insulin-resistant states, resistance of protein anabolism occurs concurrently with that of glucose, but can be compensated for by abundant amino acid (AA) provision. This effect and its mechanism were sought in obesity. Methods Pancreatic clamps were performed in 8 lean and 11 obese men, following 5-h postabsorptive, 3-h infusions of octreotide, basal glucagon, and growth hormone, with clamped postprandial-level insulin, glucose, and AA. Whole-body [1-13C]-leucine and [3-3H]-glucose kinetics, skeletal muscle protein (2H5-phenylalanine) fractional synthesis rates, and insulin signaling were determined. Results Clamp Δ insulin and Δ branched-chain AA did not differ; fasting glucagon and growth hormone were maintained. Glucose uptake was 20% less in obese concurrent with less AktSer473, but also less IRS-1Ser636/639 phosphorylation. Stimulation of whole-body, myofibrillar, and sarcoplasmic protein synthesis was similar. Whole-body protein catabolism suppression tended to be less ( P=0.06), resulting in lesser net balance (1.09 ± 0.07 vs. 1.31 ± 0.08 μmol [kg FFM−1] min−1, P = 0.048). Increments in muscle S6K1Thr389 phosphorylation were less in the obese, but 4E-BP1Ser65 did not differ. Conclusions Hyperaminoacidemia with hyperinsulinemia stimulated protein synthesis (possibly via nutrient signaling) normally in obesity, but suppression of proteolysis may be compromised. Whether long-term high protein intakes could compensate for the insulin resistance of protein anabolism remains to be determined. [ABSTRACT FROM AUTHOR]