FECHAMENTO DE ESCOLAS NO BRASIL (2010-2020): agenda neoliberal?

A presente pesquisa tem o objetivo geral de analisar as relações entre o fechamento de escolas no Brasil e o neoliberalismo, a partir da crítica materialista dialética, pautada em Marx, Engels e Kosik. Investigar as justificativas do poder público para o fechamento de escolas e a distribuição do fenômeno no território nacional são objetivos específicos, buscando-se responder às seguintes questões: os números dos censos educacionais do Instituto Nacional de Estudos e Pesquisas Educacionais Anísio Teixeira (INEP) apontam para aumento do número de fechamento de escolas entre 2010 e 2020? Sãs as escolas públicas, ou as privadas, as mais atingidas pelo fechamento? As justificativas apontadas pelo poder público para o fechamento de escolas apresentam uma lógica neoliberal? Os instrumentos de investigação são a abordagem quantitativa de dados secundários, extraídos dos censos educacionais do INEP,  em triangulação com abordagem qualitativa, a partir da Análise de Conteúdo (BARDIN, 2011) de duas fontes de comunicação: portal da Confederação Nacional dos Trabalhadores em Educação (CNTE) e Portal G1.  A investigação conclui que as escolas rurais e as públicas são as mais atingidas por fechamentos, com maior ocorrência na região nordeste, nos estados do Piauí, da Paraíba e do Ceará. As justificativas do poder público para o fechamento de escolas, segundo as reportagens consultadas, centram-se em razões estruturais, baixo número de matrículas e reestruturação da rede de ensino. Assim, os resultados sugerem indícios de privatização e “desruralização” de ensino, bem como possibilidade de gradativa desescolarização.

Anticancer Targets in the Glycolytic Metabolism of Tumors: A Comprehensive Review

Cancer is a metabolic disease and the solution of two metabolic equations: to produce energy with limited resources and to fulfill the biosynthetic needs of proliferating cells. Both equations are solved when glycolysis is uncoupled from oxidative phosphorylation in the tricarboxylic acid cycle, a process known as the glycolytic switch. This review addresses in a comprehensive manner the main molecular events accounting for high-rate glycolysis in cancer. It starts from modulation of the Pasteur Effect allowing short-term adaptation to hypoxia, highlights the key role exerted by the hypoxia-inducible transcription factor HIF-1 in long-term adaptation to hypoxia, and summarizes the current knowledge concerning the necessary involvement of aerobic glycolysis (the Warburg effect) in cancer cell proliferation. Based on the many observations positioning glycolysis as a central player in malignancy, the most advanced anticancer treatments targeting tumor glycolysis are briefly reviewed

Calpain is required for macroautophagy in mammalian cells

Ubiquitously expressed micro- and millicalpain, which both require the calpain small 1 (CAPNS1) regulatory subunit for function, play important roles in numerous biological and pathological phenomena. We have previously shown that the product of GAS2, a gene specifically induced at growth arrest, is an inhibitor of millicalpain and that its overexpression sensitizes cells to apoptosis in a p53-dependent manner (Benetti, R., G. Del Sal, M. Monte, G. Paroni, C. Brancolini, and C. Schneider. 2001. EMBO J. 20:2702–2714). More recently, we have shown that calpain is also involved in nuclear factor κB activation and its relative prosurvival function in response to ceramide, in which calpain deficiency strengthens the proapoptotic effect of ceramide (Demarchi, F., C. Bertoli, P.A. Greer, and C. Schneider. 2005. Cell Death Differ. 12:512–522). Here, we further explore the involvement of calpain in the apoptotic switch and find that in calpain-deficient cells, autophagy is impaired with a resulting dramatic increase in apoptotic cell death. Immunostaining of the endogenous autophagosome marker LC3 and electron microscopy experiments demonstrate that autophagy is impaired in CAPNS1-deficient cells. Accordingly, the enhancement of lysosomal activity and long-lived protein degradation, which normally occur upon starvation, is also reduced. In CAPNS1-depleted cells, ectopic LC3 accumulates in early endosome-like vesicles that may represent a salvage pathway for protein degradation when autophagy is defective

The Calpain System Is Involved in the Constitutive Regulation of β-Catenin Signaling Functions

Beta-catenin is a multifunctional protein serving both as a structural element in cell adhesion and as a signaling component in the Wnt pathway, regulating embryogenesis and tumorigenesis. The signaling fraction of beta-catenin is tightly controlled by the adenomatous polyposis coli-axin-glycogen synthase kinase 3beta complex, which targets it for proteasomal degradation. It has been recently shown that Ca(2+) release from internal stores results in nuclear export and calpain-mediated degradation of beta-catenin in the cytoplasm. Here we have highlighted the critical relevance of constitutive calpain pathway in the control of beta-catenin levels and functions, showing that small interference RNA knock down of endogenous calpain per se (i.e. in the absence of external stimuli) induces an increase in the free transcriptional competent pool of endogenous beta-catenin. We further characterized the role of the known calpain inhibitors, Gas2 and Calpastatin, demonstrating that they can also control levels, function, and localization of beta-catenin through endogenous calpain regulation. Finally we present Gas2 dominant negative (Gas2DN) as a new tool for regulating calpain activity, providing evidence that it counteracts the described effects of both Gas2 and Calpastatin on beta-catenin and that it works via calpain independently of the classical glycogen synthase kinase 3beta and proteasome pathway. Moreover, we provide in vitro biochemical evidence showing that Gas2DN can increase the activity of calpain and that in vivo it can induce degradation of stabilized/mutated beta-catenin. In fact, in a context where the classical proteasome pathway is impaired, as in colon cancer cells, Gas2DN biological effects accounted for a significant reduction in proliferation and anchorage-independent growth of colon cancer

Teachers' interventions in Mathematical Modelling environments : an experience report

O presente artigo é um relato de experiência e constitui-se como um exercício de reflexão acerca de como, e em que momentos, as intervenções de professores e professoras ocorrem em ambientes de Modelagem Matemática. Para isso, consideramos três pesquisas do Grupo de Estudo e Pesquisa em Educação Matemática, Modelagem e Tecnologias (GEPEMMTec), que propõem ambientes de Modelagem Matemática no Ensino Básico. As pesquisas estão embasadas nas concepções de Modelagem de Barbosa (2001) e Malheiros (2008). Consideramos como dados recortes do caderno de campo dos professores e, seguindo uma abordagem qualitativa, procuramos identificar as intervenções realizadas pelos professores e em que momentos ocorreram. A análise dos dados apontou para a ocorrência de quatro tipos de intervenção. Três delas, conforme Veronez e Castro (2018), são: questionamento, esclarecimento e sugestão. O quarto tipo que observamos foi o que denominamos de "não intervenção". Observamos que as intervenções ocorreram: (i) quando foi preciso dar ouvidos a estudantes; (ii) para esclarecer algum procedimento; (iii) para esclarecer que tipo de informações eram válidas; (iv) quando foi preciso delimitar e/ou aprofundar alguma situaçãoproblema; (v) quando os estudantes estavam em um "beco sem saída".This paper is an experience report and constitutes an exercise in reflection on how and when teachers’ interventions occur in Mathematical Modelling environments. We considered three studies from the research group Grupo de Estudo e Pesquisa em Educação Matemática, Modelagem e Tecnologias (GEPEMMTec), which proposed Mathematical Modelling environments in Basic Education. The studies are based on the Modelling perspectives proposed by Barbosa (2001) and Malheiros (2008). We considered excerpts from the teachers’ field notes as data, and following a qualitative approach, we identified teachers’ interventions and when they occured. Data analysis suggested the occurrence of four types of interventions. Three of them, according to Veronez & Castro (2018), are: questioning, clarification and suggestion. The fourth type we named as “nonintervention”. Besides, we observed that the interventions occurred: (i) when it was necessary to give a voice to students; (ii) to clarify some procedure; (iii) to clarify what kind of information was valid; (iv) when it was necessary to delimit and/or deepen the problem situation; (v) when students were in a “dead-lock”

Targeting the Lactate Transporter MCT1 in Endothelial Cells Inhibits Lactate-Induced HIF-1 Activation and Tumor Angiogenesis

Switching to a glycolytic metabolism is a rapid adaptation of tumor cells to hypoxia. Although this metabolic conversion may primarily represent a rescue pathway to meet the bioenergetic and biosynthetic demands of proliferating tumor cells, it also creates a gradient of lactate that mirrors the gradient of oxygen in tumors. More than a metabolic waste, the lactate anion is known to participate to cancer aggressiveness, in part through activation of the hypoxia-inducible factor-1 (HIF-1) pathway in tumor cells. Whether lactate may also directly favor HIF-1 activation in endothelial cells (ECs) thereby offering a new druggable option to block angiogenesis is however an unanswered question. In this study, we therefore focused on the role in ECs of monocarboxylate transporter 1 (MCT1) that we previously identified to be the main facilitator of lactate uptake in cancer cells. We found that blockade of lactate influx into ECs led to inhibition of HIF-1-dependent angiogenesis. Our demonstration is based on the unprecedented characterization of lactate-induced HIF-1 activation in normoxic ECs and the consecutive increase in vascular endothelial growth factor receptor 2 (VEGFR2) and basic fibroblast growth factor (bFGF) expression. Furthermore, using a variety of functional assays including endothelial cell migration and tubulogenesis together with in vivo imaging of tumor angiogenesis through intravital microscopy and immunohistochemistry, we documented that MCT1 blockers could act as bona fide HIF-1 inhibitors leading to anti-angiogenic effects. Together with the previous demonstration of MCT1 being a key regulator of lactate exchange between tumor cells, the current study identifies MCT1 inhibition as a therapeutic modality combining antimetabolic and anti-angiogenic activities

p65/RelA Modulates BECN1 Transcription and Autophagy▿ †

Recently, autophagy has emerged as a critical process in the control of T-cell homeostasis. Given the pivotal role of NF-κB in the signaling events of T cells, we have analyzed and unveiled a conserved NF-κB binding site in the promoter of the murine and human BECN1 autophagic gene (Atg6). Accordingly, we demonstrate that the NF-κB family member p65/RelA upregulates BECN1 mRNA and protein levels in different cellular systems. Moreover, p65-mediated upregulation of BECN1 is coupled to increased autophagy. The newly identified κB site in the BECN1 promoter specifically interacts with p65 both in vitro and in living Jurkat cells upon phorbol myristate acetate (PMA)-ionomycin stimulation, where p65 induction is coupled to BECN1 upregulation and autophagy induction. Finally, anti-CD3- and PMA-ionomycin-mediated activation of T-cell receptor signaling in peripheral T cells from lymph nodes of healthy mice results in an upregulation of BECN1 expression that can be blocked by the NF-κB inhibitor BAY 11-7082. Altogether, these data suggest that autophagy could represent a novel route modulated by p65 to regulate cell survival and control T-cell homeostasis