O movimento corporal na educação infantil

Body movement is an essential practice for the integral development of the child. The realization of the corporal movement in the Infantile Education must be reconciled with the physical, psychological, intellectual and social aspects of the child. Therefore, this study aimed to verify how the movement is present in the pedagogical practice of the teachers of Early Childhood Education, besides emphasizing the importance of the corporal movement in the development of the children. The work is qualitative and was carried out in a Child Education Institution in the city of João Pessoa with children from 2 to 5 years of age, through observations and informal conversation with the teachers of the respective classes: Maternal I, Maternal II and Pre I. To give us support, we did some reading with authors who investigated the subject, namely: Sarmento, Furlan, Iza and Mello, Tosatto, among others. In the work carried out, we noticed that the teachers of the researched CREI have experience of working with the children, but they lack the knowledge of how to work educational activities with Movement and, therefore, prioritize the maintenance of children in situation of Non-Movement. Such practices of keeping children quiet and silent reveal the conceptions of the child and the movement of the teachers, indicating the urgency of reformulating the processes and courses of initial and continuing training of teachers of Early Childhood Education, as well as the improvement of working conditions for care And the education of young children.O movimento corporal é uma prática essencial para o desenvolvimento integral da criança. A realização do movimento corporal na Educação Infantil deve ser conciliada com os aspectos físico, psicológico, intelectual e social da criança. Sendo assim, este trabalho teve como objetivo verificar como o movimento está presente na prática pedagógica da Educação Infantil, além de ressaltar a importância do movimento corporal no desenvolvimento das crianças. O trabalho é de cunho qualitativo e foi realizado em uma Instituição de Educação Infantil na cidade de João Pessoa com crianças de 2 a 5 anos de idade, através de observações e conversa informa com as professoras das respectivas turmas: Maternal I, Maternal II e Pré I. Para nos dar suporte, fizemos algumas leituras com autores que investigaram sobre a temática, a saber: Sarmento, Furlan, Iza e Mello, Tosatto, entre outros. No trabalho realizado, percebemos que as professoras do CREI investigado têm experiência de trabalho com as crianças, mas falta-lhes o conhecimento de como trabalhar atividades educativas com Movimento e, portanto, priorizam a manutenção das crianças em situação de Não-Movimento. Tais práticas de manter as crianças quietas e caladas revelam as concepções de criança e movimento das professoras, indicando a urgência de reformulação dos processos e cursos de formação inicial e continuada de professoras de Educação Infantil, bem como a melhoria das condições de trabalho para o cuidado e a educação de crianças pequenas

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration

Background The angiotensin-I converting enzyme (ACE) plays a central role in the renin-angiotensin system, acting by converting the hormone angiotensin-I to the active peptide angiotensin-II (Ang-II). More recently, ACE was shown to act as a receptor for Ang-II, and its expression level was demonstrated to be higher in melanoma cells compared to their normal counterparts. However, the function that ACE plays as an Ang-II receptor in melanoma cells has not been defined yet. Aim Therefore, our aim was to examine the role of ACE in tumor cell proliferation and migration. Results We found that upon binding to ACE, Ang-II internalizes with a faster onset compared to the binding of Ang-II to its classical AT1 receptor. We also found that the complex Ang-II/ACE translocates to the nucleus, through a clathrin-mediated process, triggering a transient nuclear Ca2+ signal. In silico studies revealed a possible interaction site between ACE and phospholipase C (PLC), and experimental results in CHO cells, demonstrated that the beta 3 isoform of PLC is the one involved in the Ca2+ signals induced by Ang-II/ACE interaction. Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. In addition, we found that stimulation of ACE by Ang-II caused the melanoma cells to migrate, at least in part due to decreased vinculin expression, a focal adhesion structural protein. Conclusion ACE activation regulates melanoma cell proliferation and migration.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)INCT Nanocarbono - UFMG (Brazil)Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, BrazilUniv Fed Sao Joao del Rei, Dept Nat Sci, Sao Joao Del Rei, MG, BrazilUniv Fed Ceara, Dept Phys, Fortaleza, CE, BrazilUniv Fed Sao Paulo, Dept Biophys, Sao Paulo, SP, BrazilUniv Fed Minas Gerais, Dept Phys, Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Morphol, Belo Horizonte, MG, BrazilDepartment of Biophysics, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, BrazilWeb of Scienc

Common variable immunodeficiency in two kindreds with heterogeneous phenotypes caused by novel heterozygous NFKB1 mutations

NFKB1 haploinsufficiengcy was first described in 2015 in three families with common variable immunodeficiency (CVID), presenting heterogeneously with symptoms of increased infectious susceptibility, skin lesions, malignant lymphoproliferation and autoimmunity. The described mutations all led to a rapid degradation of the mutant protein, resulting in a p50 haploinsufficient state. Since then, more than 50 other mutations have been reported, located throughout different domains of NFKB1 with the majority situated in the N-terminal Rel homology domain (RHD). The clinical spectrum has also expanded with possible disease manifestations in almost any organ system. In silico prediction tools are often used to estimate the pathogenicity of NFKB1 variants but to prove causality between disease and genetic findings, further downstream functional validation is required. In this report, we studied 2 families with CVID and two novel variants in NFKB1 (c.1638-2A>G and c.787G>C). Both mutations affected mRNA and/or protein expression of NFKB1 and resulted in excessive NLRP3 inflammasome activation in patient macrophages and upregulated interferon stimulated gene expression. Protein-protein interaction analysis demonstrated a loss of interaction with NFKB1 interaction partners for the p.V263L mutation. In conclusion, we proved pathogenicity of two novel variants in NFKB1 in two families with CVID characterized by variable and incomplete penetrance.Peer reviewe

Common variable immunodeficiency in two kindreds with heterogeneous phenotypes caused by novel heterozygous NFKB1 mutations

NFKB1 haploinsufficiengcy was first described in 2015 in three families with common variable immunodeficiency (CVID), presenting heterogeneously with symptoms of increased infectious susceptibility, skin lesions, malignant lymphoproliferation and autoimmunity. The described mutations all led to a rapid degradation of the mutant protein, resulting in a p50 haploinsufficient state. Since then, more than 50 other mutations have been reported, located throughout different domains of NFKB1 with the majority situated in the N-terminal Rel homology domain (RHD). The clinical spectrum has also expanded with possible disease manifestations in almost any organ system. In silico prediction tools are often used to estimate the pathogenicity of NFKB1 variants but to prove causality between disease and genetic findings, further downstream functional validation is required. In this report, we studied 2 families with CVID and two novel variants in NFKB1 (c.1638-2A>G and c.787G>C). Both mutations affected mRNA and/or protein expression of NFKB1 and resulted in excessive NLRP3 inflammasome activation in patient macrophages and upregulated interferon stimulated gene expression. Protein-protein interaction analysis demonstrated a loss of interaction with NFKB1 interaction partners for the p.V263L mutation. In conclusion, we proved pathogenicity of two novel variants in NFKB1 in two families with CVID characterized by variable and incomplete penetrance.Peer reviewe

O primeiro ano do ensino fundamental de nove anos: uma revisão teórica

Resumo O artigo revisa publicações brasileiras que tratam do tema do primeiro ano do ensino fundamental de nove anos. Foram realizadas buscas nas bases de dados SciELO - Scientific Electronic Library Online e no Portal de Periódicos da CAPES, considerando o período 2005-2015 e utilizando-se os termos: “Ensino Fundamental de Nove Anos” e “Primeiro Ano do Ensino Fundamental”. A pesquisa resultou em 43 artigos na base do SciELO e 37 no Portal de Periódicos da CAPES. Do total, 16 artigos foram selecionados para compor a análise de conteúdo, da qual resultaram três categorias temáticas: Política Educacional, Implantação do Ensino Fundamental de Nove Anos e Alfabetização e Letramento. Os resultados revelaram preocupações, especialmente, quanto ao descompasso entre a política educacional e a prática pedagógica.Embora essas questões não possam ser generalizadas, faz-se importante considerar que a ampliação do tempo de escolarização não é, necessariamente, um indicador de qualidade no ensino

Alterações físico, mecânicas e microestruturais em concretos sujeitos a resfriamento lento e rápido em situação de incêndio simulado

Concrete, when exposed to high temperatures, has its properties changed, and the recovery processes depend on the intensity of these changes. This paper aimed to evaluate the influence of high temperatures on concrete properties and verify the effects generated in the material when submitted to natural and fast cooling. Three different concrete mixes were exposed to temperatures of 100 °C, 300 ºC, 450 ºC, and 600 ºC, subdivided into slow and fast cooling groups. With the increase in temperature, cracking processes and microstructural alterations intensified, generating reductions in mechanical strength and increases in absorptions. This study has identified that the elastic modulus was the property most affected by these changes. The correlations between the elastic modulus and the other properties were accompanied by increased concrete micro-cracking, water loss, and decomposition of paste phases. Also, it was found an effect of ettringite rehydration during concrete cooling.O concreto quando exposto a elevadas temperaturas tem suas propriedades alteradas e os processos de recuperação são dependentes da intensidade destas modificações. O objetivo deste artigo foi avaliar a influência das altas temperaturas nas propriedades do concreto, em uma faixa na qual a estrutura ainda pode ser recuperada, e a verificação dos efeitos gerados no material quando submetidos a resfriamento natural e resfriamento rápido. Para isto se desenvolveu o programa experimental com três traços de concreto, os quais foram expostos a temperaturas de 100 ºC, 300 ºC, 450 ºC e 600 ºC; subdivididos em grupos de resfriamento lento e rápido. Com a elevação da temperatura, intensificam-se os processos de fissuração e alterações microestruturais, as quais geram redução nas resistências mecânicas e o aumento da absorção. Verificou-se que o módulo de elasticidade foi a propriedade mais afetada por estas alterações. As correlações entre o módulo de elasticidade e as demais propriedades foram acompanhadas pelo aumento da microfissuração do concreto, perda de água e decomposição das fases da pasta, sendo observada posterior reidratação da etringita durante o resfriamento do concreto

MOLECULAR FRACTIONATION WITH CONJUGATE CAPS STUDY OF THE INTERACTION OF THE ANACARDIC ACID WITH THE ACTIVE SITE OF TRYPANOSOMA CRUZI GAPDH ENZYME: A QUANTUM INVESTIGATION

Objective: The objective of this study was to use the molecular fractionation with conjugate caps (MFCC) method to elucidate the possible interaction mechanism of anacardic acid (AA) with the saturated alkyl chain (AA0) in the Trypanosoma cruzi glyceraldehyde-3-phosphate dehydrogenase (TcGAPHD) enzyme. Methods: Initially, the geometry optimization of the AA three-dimensional structure (with the pentadecyl chain) was performed using density functional theory (B3LYP) calculations. With the AA0 optimization data, it was possible to plot the molecular electrostatic potential (MESP) surface. Molecular docking simulation was performed using automated coupling with the AutoDock Vina program. The best-fit conformation in the docking simulation of AA0 is the binding site used for the construction of the TcGAPHD-AA0 complex. Interaction energies between the AA0 molecule and the amino acid residues of the TcGAPHD enzyme were estimated using the MFCC strategy. Results: To obtain more reliable quantitative information on the interaction of AA with the active site of the TcGAPHD enzyme, the fragmentation method was combined with conjugated layers (MFCC) and molecular docking. It can be observed that the AA0 molecule occupies a region near the active site of the chalepin molecule in the TcGAPHD enzyme, and the Ile13 residue has the strongest binding energy of approximately 25 kcal/mol with AA0, through a strong Van der Waals interaction. Conclusion: The paper presents an improved quantitative analysis approach for assessing the contribution of individual amino acids to the free energy of interaction between AA and TcGAPHD. Specifically, the paper illustrates the advantageous approach of combining molecular docking with the MFCC method

Angiotensin Converting Enzyme Regulates Cell Proliferation and Migration.

The angiotensin-I converting enzyme (ACE) plays a central role in the renin-angiotensin system, acting by converting the hormone angiotensin-I to the active peptide angiotensin-II (Ang-II). More recently, ACE was shown to act as a receptor for Ang-II, and its expression level was demonstrated to be higher in melanoma cells compared to their normal counterparts. However, the function that ACE plays as an Ang-II receptor in melanoma cells has not been defined yet.Therefore, our aim was to examine the role of ACE in tumor cell proliferation and migration.We found that upon binding to ACE, Ang-II internalizes with a faster onset compared to the binding of Ang-II to its classical AT1 receptor. We also found that the complex Ang-II/ACE translocates to the nucleus, through a clathrin-mediated process, triggering a transient nuclear Ca2+ signal. In silico studies revealed a possible interaction site between ACE and phospholipase C (PLC), and experimental results in CHO cells, demonstrated that the β3 isoform of PLC is the one involved in the Ca2+ signals induced by Ang-II/ACE interaction. Further studies in melanoma cells (TM-5) showed that Ang-II induced cell proliferation through ACE activation, an event that could be inhibited either by ACE inhibitor (Lisinopril) or by the silencing of ACE. In addition, we found that stimulation of ACE by Ang-II caused the melanoma cells to migrate, at least in part due to decreased vinculin expression, a focal adhesion structural protein.ACE activation regulates melanoma cell proliferation and migration