Letramento em Matemática: um estudo a partir dos dados do PISA2003

Neste trabalho partimos do pressuposto de que os resultados das avaliações em larga escala são instrumentos adequados para compreender o currículo aprendido. Entendemos, ainda, que os resultados obtidos por distintos países em avaliações internacionais constituem-se uma boa estratégia para captar ênfases diferenciadas no currículo ensinado. A partir dos resultados do Programa Internacional de Avaliação dos Estudantes - PISA 2003, buscou-se comparar diferenças nas ênfases curriculares em Matemática entre Brasil e Portugal. Para isto, a pesquisa utilizou como metodologia a análise do Funcionamento Diferencial do Item (DIF). Esta metodologia possibilita identificar itens que violam um dos principais pressupostos da Teoria de Resposta ao Item (TRI), segundo o qual, alunos de grupos distintos, mas de mesma habilidade cognitiva, têm a mesma probabilidade de acertar um item. A análise em 84 itens da prova de Matemática do PISA 2003 mostrou que alguns itens apresentam DIF entre alunos brasileiros e portugueses. De modo sintético, podemos dizer que alguns itens mostram-se mais fáceis aos alunos brasileiros, em especial os que se referem à subárea Quantidade. Já os itens da subárea Mudança e Relações são, aparentemente, mais fáceis aos alunos portugueses. Ao mesmo tempo, itens envolvendo contextos científicos mostram-se mais fáceis aos alunos portugueses, enquanto os que envolvem contextos da vida pessoal são mais fáceis aos brasileiros. Os resultados desta pesquisa evidenciam a relevância e necessidade da ampliação do debate curricular no campo da educação matemática. A compreensão dos resultados dos testes de avaliação em larga escala pode fornecer novas questões sobre o como e o quê os alunos aprendem Matemática

Group B Streptococcus GAPDH Is Released upon Cell Lysis, Associates with Bacterial Surface, and Induces Apoptosis in Murine Macrophages

Glyceraldehyde 3-phosphate dehydrogenases (GAPDH) are cytoplasmic glycolytic enzymes that, despite lacking identifiable secretion signals, have been detected at the surface of several prokaryotic and eukaryotic organisms where they exhibit non-glycolytic functions including adhesion to host components. Group B Streptococcus (GBS) is a human commensal bacterium that has the capacity to cause life-threatening meningitis and septicemia in newborns. Electron microscopy and fluorescence-activated cell sorter (FACS) analysis demonstrated the surface localization of GAPDH in GBS. By addressing the question of GAPDH export to the cell surface of GBS strain NEM316 and isogenic mutant derivatives of our collection, we found that impaired GAPDH presence in the surface and supernatant of GBS was associated with a lower level of bacterial lysis. We also found that following GBS lysis, GAPDH can associate to the surface of many living bacteria. Finally, we provide evidence for a novel function of the secreted GAPDH as an inducer of apoptosis of murine macrophages

A mouse model reproducing the pathophysiology of neonatal group B streptococcal infection

Group B streptococcal (GBS) meningitis remains a devastating disease. The absence of an animal model reproducing the natural infectious process has limited our understanding of the disease and, consequently, delayed the development of effective treatments. We describe here a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection. We show that GBS strain BM110, belonging to the CC17 clonal complex, is more virulent in this vertical transmission model than the isogenic mutant BM110∆cylE, which is deprived of hemolysin/cytolysin. Pups exposed to the more virulent strain exhibit higher mortality rates and lung inflammation than those exposed to the attenuated strain. Moreover, pups that survive to BM110 infection present neurological developmental disability, revealed by impaired learning performance and memory in adulthood. The use of this new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced meningitis.The authors gratefully acknowledge the help of Encarnaca̧ ̃o Ribeiro for excellent technical assistance, Joana Tavares for assisting with IVIS Lumina LT, Susana Roque for the luminex instrument experiments, the Molecular Microbiology group at i3S for microscope use, and the Portuguese architect and artist Gil Ferreira da Silva for the artworks included in the last figure. This work was supported by funds from Foundation for Science and Technology (FCT), European Regional Development Fund (FEDER) and Compete under project POCI-01-0145-FEDER-016607 (PTDC/IMI-MIC/1049/2014) and from the project NORTE-01-0145-FEDER-000012, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). T.S. and A.M. were supported by Investigador FCT (IF/00875/2012 and IF/00753/2014), POPH and Fundo Social Europeu. E.B.A. and C.C.P. hold postdoctoral fellowships from FCT (PTDC/IMI-MIC/1049/2014 and SFRH/BPD/91962/2012). Ar.F. and P.T.C. were supported by Laboratoire d’Excellence (LABEX) Integrative Biology of Emerging Infectious Diseases (grant ANR-10-LABX-62-IBEID).info:eu-repo/semantics/publishedVersio