Modelo de avaliação de transtornos de aprendizagem por equipe interdisciplinar / Evaluation model of learning disorders by interdisciplinary team

Observa-se um aumento progressivo da evasão escolar e do fracasso acadêmico. A demanda por avaliação e diagnóstico sobre questões de aprendizagem está crescendo nos serviços públicos de saúde. Para direcionar os métodos de intervenção e minimizar as dificuldades de aprendizagem, é necessário identificar os fatores que levam ao fracasso escolar e diferenciar as dificuldades escolares. O presente estudo tem como objetivo descrever o modelo de avaliação interdisciplinar realizado no Ambulatório de Transtornos de Aprendizagem (ATA) do Centro de Neuropediatria do Hospital das Clínicas da Universidade Federal do Paraná e relatar três casos avaliados. Os dados apresentados neste estudo baseiam-se em 56 avaliações realizadas em crianças e adolescentes com queixas de dificuldades de aprendizagem, a fim de caracterizar a população atendida, o modelo de avaliação aplicado e as conclusões da equipe interdisciplinar. Nesta amostra, a maior frequência foi do sexo masculino (78,6%), com idade média de 10 anos e 5 meses. As dificuldades escolares foram percebidas em 44,6% dos casos, o transtorno de aprendizagem em 7,1% e outros transtornos em 17,9%. Esses resultados coincidem com outros estudos sobre dificuldades de aprendizagem e demonstram que o modelo utilizado pelo ATA é eficaz para concluir sobre a proposta diagnóstica e de intervenção.

There is a progressive increase of student evasion as well as of academic failure. The demand for evaluation and diagnosis about learning issues is growing up in the public health service care. In order to direct the intervention methods and minimize the learning difficulties is necessary identify the factors that lead to academic failure and differentiate the learning disabilities. The present study aims to describe the interdisciplinary model for evaluation performed at the Learning Disorder Clinic (ATA) of the Neuropediatrics Center at Hospital das Clínicas from Universidade Federal do Paraná and report three evaluated cases. The data presented in this study are based on 56 evaluations performed in children and adolescents with complaints of learning difficulties in order to characterize the population served, the evaluation model applied and the conclusions from the interdisciplinary team. On this sample, the highest frequency was from males (78.6%) aged on average 10 years and 5 months. The learning difficulties was noticed in 44.6% of the cases, the leaning disorder in 7.1% and other disorders in 17.9%. These results are in agreement with other studies about learning disabilities and demonstrates that the model used by ATA is effective to conclude about diagnostic and intervention proposal.

Anaphylatoxin C5a induces monocyte recruitment and differentiation into dendritic cells by TNF-alpha and prostaglandin E2-dependent mechanisms.

Although monocytes can be directed to develop into dendritic cells (DC) in vitro, the molecular mechanisms that induce their transformation in vivo are largely unknown. In the present study we employed an in vivo SCID mouse model to investigate the impact of two proinflammatory chemotaxins, the anaphylatoxin C5a and the chemokine macrophage inflammatory protein-1alpha (CCL3), on the differentiation of human monocytes and immature DC generated from monocytes in the presence of GM-CSF and IL-4. Both C5a and macrophage inflammatory protein-1alpha recruited human monocytes and immature DC into the peritoneal cavity of SCID mice, but only C5a induced their differentiation into phenotypically mature DC by 48 h after injection. Macrophages derived from monocytes by in vitro culture were resistant to C5a-mediated transformation in vivo. The effect of C5a was indirect, since C5a-stimulated TNF-alpha and PGE(2) were found to be obligatory as well as sufficient to induce differentiation of monocytes. In contrast to monocytes, in vitro generated immature DC required TNF-alpha, but not PGE(2), for their C5a-mediated maturation in vivo. C5a-transformed monocytes represented an inflammatory type of DC, as they constitutively secreted high amounts of TNF-alpha, but also retained the capacity to release the Th1 cytokine IL-12 p70 upon stimulation with CD40 ligand. In summary, we identified for the first time a cascade of inflammatory signals that can induce the transformation of monocytes into DC in vivo. This novel function emphasizes the important immunoregulatory role of C5a at the interface of innate and adaptive immunity.

IL-4 down-regulates anaphylatoxin receptors in monocytes and dendritic cells and impairs anaphylatoxin-induced migration in vivo.

Anaphylatoxins mobilize leukocytes to the sites of inflammation. In the present study we investigated the impact of GM-CSF, IL-4, and IFN-gamma on anaphylatoxin receptor expression in monocytes and dendritic cells (DC). IL-4 was identified as the strongest down-regulator of the receptors for C5a and C3a in monocytes and monocyte-derived DC (MoDC). To study the impact of IL-4 on anaphylatoxin-induced chemotaxis, an in vivo migration model was established. For this purpose, human monocytes and MoDC were injected i.v. into SCID mice that at the same time received anaphylatoxins into the peritoneal cavity. A peritoneal influx of human monocytes could be demonstrated by 4 h after injections of C5a and C3a. In line with receptor down-regulation, IL-4 treatment inhibited in vivo mobilization of human monocytes and MoDC in response to C5a and C3a. In addition to its effects on human cells, IL-4 reduced C5a receptors in murine bone marrow-derived DC and impaired recruitment of labeled bone marrow-derived DC in syngeneic BALB/c mice to i.p. injected C5a. Overall, these data suggest that inhibition of a rapid anaphylatoxin-induced mobilization of monocytes and DC to inflamed tissues represents an important anti-inflammatory activity of the Th2 cytokine IL-4.