965 resultados para Normal degree in Garça SP


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Relatório de estágio apresentado para a obtenção do grau de mestre na especialidade profissional de Educação pré-escolar e ensino do 1º ciclo do ensino básico

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While Lloyd Gaines, who was now enrolled at the University of Michigan, worked on a Masters degree in Economics, Houston, Redmond and Espy planned their next step. The decisions in Missouri were not made on a level playing field, so to speak. They needed to take their case to place where justice was blind and unbiased; the Supreme Court of the United States.

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A presente pesquisa propõe analisar o contexto educacional ocorrido no período da ditadura militar, buscando extrair aspectos históricos e educacionais referentes ao período (1964- 1985). Trata-se de uma pesquisa realizada com professores do antigo segundo grau da rede pública de ensino do Município de Santo André (S.P). Optou-se por entrevistar seis professores que atuaram durante esse contexto histórico. Para investigar, foi utilizada a abordagem histórica-metodológica de cunho qualitativo, elegendo a memória como fonte principal de estudo. Para tanto, recorreu-se às contribuições de Bosi (Memória e sociedade: lembranças de velhos, 1984), Thompson (A voz do Passado, 1992), Romanelli (História da Educação no Brasil, 1978), Freitag (Escola Estado e Sociedade, 1980), Góes (O golpe na Educação, 1996), Cunha (Educação e Desenvolvimento Social no Brasil, 1977), Cardoso (Para uma crítica do presente, 2001), Vieira (Estado e miséria social no Brasil, 1995), Minguili (Direção de Escola de 2º grau no Estado de São Paulo, 1984), Arelaro (A extensão do ensino básico no Brasil, 1988), Teixeira (Política e administração de pessoal docente, 1988), Hilsdorf (História da educação brasileira, 2005), Gadotti (Educação e poder, 2001), Germano (Estado militar e educação no Brasil, 1990), Saviani (Escola e democracia, 1986), Santos (Professoras em tempos de mudanças, 2003). A hipótese trabalhada centra-se em interpretar a postura dos professores que atuaram no período em questão, relativa ao regime político que se instalou no País durante esta época, e de que forma isso repercutiu no seu trabalho docente. Na análise do contexto político/social e educacional, recorreu-se à revisão que forneceram subsídios para compreender e explicitar a voz do professor.

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A presente pesquisa propõe analisar o contexto educacional ocorrido no período da ditadura militar, buscando extrair aspectos históricos e educacionais referentes ao período (1964- 1985). Trata-se de uma pesquisa realizada com professores do antigo segundo grau da rede pública de ensino do Município de Santo André (S.P). Optou-se por entrevistar seis professores que atuaram durante esse contexto histórico. Para investigar, foi utilizada a abordagem histórica-metodológica de cunho qualitativo, elegendo a memória como fonte principal de estudo. Para tanto, recorreu-se às contribuições de Bosi (Memória e sociedade: lembranças de velhos, 1984), Thompson (A voz do Passado, 1992), Romanelli (História da Educação no Brasil, 1978), Freitag (Escola Estado e Sociedade, 1980), Góes (O golpe na Educação, 1996), Cunha (Educação e Desenvolvimento Social no Brasil, 1977), Cardoso (Para uma crítica do presente, 2001), Vieira (Estado e miséria social no Brasil, 1995), Minguili (Direção de Escola de 2º grau no Estado de São Paulo, 1984), Arelaro (A extensão do ensino básico no Brasil, 1988), Teixeira (Política e administração de pessoal docente, 1988), Hilsdorf (História da educação brasileira, 2005), Gadotti (Educação e poder, 2001), Germano (Estado militar e educação no Brasil, 1990), Saviani (Escola e democracia, 1986), Santos (Professoras em tempos de mudanças, 2003). A hipótese trabalhada centra-se em interpretar a postura dos professores que atuaram no período em questão, relativa ao regime político que se instalou no País durante esta época, e de que forma isso repercutiu no seu trabalho docente. Na análise do contexto político/social e educacional, recorreu-se à revisão que forneceram subsídios para compreender e explicitar a voz do professor.

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O contexto batista é predominantemente marcado por lideranças masculinas, destinando às mulheres apenas lugares e comportamentos socialmente estabelecidos, como a casa, o cuidado, a maternidade, a submissão, entre outras características que enfatizam a hierarquia de gênero. Mesmo diante do desenvolvimento econômico e da ocupação que as mulheres estão conquistando no campo público, a igreja e principalmente as igrejas batistas, permanecem fundadas em alicerces que exaltam o poder masculino em detrimento do lugar que deve ser ocupado pelas mulheres, ou seja, onde elas decidirem atuar. Caso elas decidam atuar num campo predominantemente masculino, terão que lidar com a desconstrução de um pensamento socialmente permeado de dominação masculina e com a árdua construção de um pensamento que vise a igualdade de gênero. O objeto desta pesquisa é o ministério pastoral feminino no contexto batista brasileiro. O texto analisa o discurso das Pastoras Batistas do Estado de São Paulo e o discurso dos líderes da Ordem dos Pastores Batistas de São Paulo (OPBB-SP) a respeito do ministério pastoral feminino e a não filiação de mulheres na OPBB-SP. A importância deste trabalho é a de demostrar as relações de micro poder existentes entre pastores e pastoras e concomitantemente as desigualdades dentro do contexto batista com relação ao ministério pastoral feminino. Essa afirmação se consolida por meio das análises das entrevistas semiestruturadas que realizei na pesquisa de campo, com sete pastoras batistas do Estado de São Paulo, bem como com três líderes da OPPB-SP. Esta é uma pesquisa qualitativa, em que foram analisados documentos oficiais da igreja, como pautas de convenções, atas, sites institucionais, periódicos e documentos não oficiais encontrados em redes sociais, blogs, jornais online, entre outros. Posso afirmar que as pastoras batistas estão se mobilizando para cumprir sua vocação, usando argumentos transcendentes que impedem qualquer pessoa de desafiar ou duvidar de seu chamado pastoral, pois: “O vento sopra onde quer; ouve-se o ruído, mas não sabes de onde vem, nem para onde vai. Assim acontece com aquele(a) que nasceu do Espírito.” (João 3.8).

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For analyzing the mechanism of energy transduction in the “motor” protein, myosin, it is opportune both to model the structural change in the hydrolytic transition, ATP (myosin-bound) + H2O → ADP⋅Pi (myosin-bound) and to check the plausibility of the model by appropriate site-directed mutations in the functional system. Here, we made a series of mutations to investigate the role of the salt-bridge between Glu-470 and Arg-247 (of chicken smooth muscle myosin) that has been inferred from crystallography to be a central feature of the transition [Fisher, A. J., Smith, C. A., Thoden, J. B., Smith, R., Sutoh, K., Holden, H. M., & Rayment, I. (1995) Biochemistry 34, 8960–8972]. Our results suggest that whether in the normal, or in the inverted, direction an intact salt-bridge is necessary for ATP hydrolysis, but when the salt-bridge is in the inverted direction it does not support actin activation. Normally, fluorescence changes result from adding nucleotides to myosin; these signals are reported by Trp-512 (of chicken smooth muscle myosin). Our results also suggest that structural impairments in the 470–247 region interfere with the transmission of these signals to the responsive Trp.

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Mutations in the gene encoding rhodopsin, the visual pigment in rod photoreceptors, lead to retinal degeneration in species from Drosophila to man. The pathogenic sequence from rod cell-specific mutation to degeneration of rods and cones remains unclear. To understand the disease process in man, we studied heterozygotes with 18 different rhodopsin gene mutations by using noninvasive tests of rod and cone function and retinal histopathology. Two classes of disease expression were found, and there was allele-specificity. Class A mutants lead to severely abnormal rod function across the retina early in life; topography of residual cone function parallels cone cell density. Class B mutants are compatible with normal rods in adult life in some retinal regions or throughout the retina, and there is a slow stereotypical disease sequence. Disease manifests as a loss of rod photoreceptor outer segments, not singly but in microscopic patches that coalesce into larger irregular areas of degeneration. Cone outer segment function remains normal until >75% of rod outer segments are lost. The topography of cone loss coincides with that of rod loss. Most class B mutants show an inferior-nasal to superior-temporal retinal gradient of disease vulnerability associated with visual cycle abnormalities. Class A mutant alleles behave as if cytotoxic; class B mutants can be relatively innocuous and epigenetic factors may play a major role in the retinal degeneration.

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We performed a comprehensive analysis of T cell receptor (TCR) γ rearrangements in T cell precursors of the mouse adult thymus. Using a sensitive quantitative PCR method, we show that TCRγ rearrangements are present in CD44+CD25+ Pro-T thymocytes much earlier than expected. TCRγ rearrangements increase significantly from the Pro-T to the CD44−CD25+ Pre-T cell transition, and follow different patterns depending on each Vγ gene segment, suggesting that ordered waves of TCRγ rearrangement exist in the adult mouse thymus as has been described in the fetal mouse thymus. Recombinations of TCRγ genes occur concurrently with TCRδ and D-Jβ rearrangements, but before Vβ gene assembly. Productive TCRγ rearrangements do not increase significantly before the Pre-T cell stage and are depleted in CD4+CD8+ double-positive cells from normal mice. In contrast, double-positive thymocytes from TCRδ−/− mice display random proportions of TCRγ rearranged alleles, supporting a role for functional TCRγ/δ rearrangements in the γδ divergence process.

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We have developed a proton magnetic resonance spectroscopy method that selectively can sample cortical gray matter and adjacent white matter in the frontal lobe. We have used this approach to study a group of patients (n = 7) infected with HIV and clinical manifestations of the AIDS dementia complex (ADC), a group of patients (n = 8) infected with HIV without any indications of ADC, and seven controls. The patients without ADC had a statistically significant increase in the ratio of myo-inositol to creatine in white matter compared with normal controls. In contrast, the group of patients with ADC had almost normal levels of myo-inositol to creatine in both gray matter and white matter and showed a statistically significant decrease in the N-acetylaspartate to creatine ratio in gray matter compared with either the normal controls or the patients without ADC. Patterns of spectral abnormalities correlated with neuropsychological measures of frontal lobe dysfunction, suggesting that the evaluation of frontal lobe metabolism by magnetic resonance spectroscopy can play a role in the early detection of ADC, in determining its progression, and in assessing responses to therapeutic interventions.

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Application of exogenous retinoic acid (RA) to zebrafish during the initial stages of photoreceptor differentiation results in a precocious development of rod photoreceptors and an inhibition of cone photoreceptor maturation. The acceleration of rod differentiation is observed initially within the ventral retina 3 days after fertilization, following 24 hr of RA application, and within the dorsal retina 4 days after fertilization, following 48 hr of RA application. The differentiation of rods was impeded significantly when the synthesis of endogenous retinoic acid was inhibited by citral prior to the initial stage of rod differentiation. RA-treated embryos labeled for bromodeoxyuridine (BrdU) uptake revealed that RA exerts its effect on a postmitotic cell population within the developing retina. During normal development in zebrafish, rod differentiation is most robust within the ventral retina, a region previously shown to be rich in RA. Our data suggest that the RA signaling pathway is involved in the differentiation and maturation of both the rod and cone photoreceptors within the developing zebrafish retina.

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Cpefat mice carry a mutation in the carboxypeptidase E/H gene which encodes an exopeptidase that removes C-terminal basic residues from endoproteolytically cleaved hormone intermediates. These mice have endocrine disorders including obesity, infertility, and hyperproinsulinemia–diabetes syndrome, but the etiology remains an enigma. Because studies have identified membrane carboxypeptidase E as a sorting receptor for targeting prohormones to the regulated secretory pathway for processing and secretion, the intracellular routing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pituitary cells were investigated in Cpefat mice. In Cpefat mice, pro-opiomelanocortin was accumulated 24-fold above normal animals in the pituitary and it was poorly processed to adrenocorticotropin. Furthermore, pro-opiomelanocortin was secreted constitutively at high levels, showing no response to stimulation by corticotropin-releasing hormone. Similarly, growth hormone release was constitutive and did not respond to high K+ stimulation. Both pro-opiomelanocortin and growth hormone levels were elevated in the circulation of Cpefat mice versus normal mice. These data provide evidence that the lack of carboxypeptidase E, the sorting receptor, results in the intracellular misrouting and secretion of pro-opiomelanocortin and growth hormone via the constitutive pathway in the pituitary of Cpefat mice.

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In the South West Pacific region, the striking geographical correlation between the frequency of α+-thalassemia and the endemicity of Plasmodium falciparum suggests that this hemoglobinopathy provides a selective advantage against malaria. In Vanuatu, paradoxically, α+-thalassemia increases the incidence of contracting mild malaria in the first 2 years of life, but severe disease was too uncommon to assess adequately. Therefore, we undertook a prospective case-control study of children with severe malaria on the north coast of Papua New Guinea, where malaria transmission is intense and α+-thalassemia affects more than 90% of the population. Compared with normal children, the risk of having severe malaria was 0.40 (95% confidence interval 0.22–0.74) in α+-thalassemia homozygotes and 0.66 (0.37–1.20) in heterozygotes. Unexpectedly, the risk of hospital admission with infections other than malaria also was reduced to a similar degree in homozygous (0.36; 95% confidence interval 0.22–0.60) and heterozygous (0.63; 0.38–1.07) children. This clinical study demonstrates that a malaria resistance gene protects against disease caused by infections other than malaria. The mechanism of the remarkable protective effect of α+-thalassemia against severe childhood disease remains unclear but must encompass the clear interaction between this hemoglobinopathy and both malarial and nonmalarial infections.

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Vascular endothelial cells are important in a variety of physiological and pathophysiological processes. The growth and functions of vascular endothelial cells are regulated both by soluble mitogenic and differentiation factors and by interactions with the extracellular matrix; however, relatively little is known about the role of the matrix. In the present study, we investigate whether integrin-mediated anchorage to a substratum coated with the extracellular matrix protein fibronectin regulates growth factor signaling events in human endothelial cells. We show that cell adhesion to fibronectin and growth factor stimulation trigger distinct initial tyrosine phosphorylation events in endothelial cells. Thus, integrin-dependent adhesion of endothelial cells leads to tyrosine phosphorylation of both focal adhesion kinase and paxillin, but not of several growth factor receptors. Conversely, EGF stimulation causes receptor autophosphorylation, with no effect on focal adhesion kinase or paxillin tyrosine phosphorylation. Adhesion to fibronectin, in the absence of growth factors, leads to activation of MAPK. In addition, adhesion to fibronectin also potentiates growth factor signaling to MAPK. Thus, polypeptide growth factor activation of MAPK in anchored cells is far more effective than in cells maintained in suspension. Other agonists known to activate MAPK were also examined for their ability to activate MAPK in an anchorage-dependent manner. The neuropeptide bombesin, the bioactive lipid lysophosphatidic acid (LPA), and the cytokine tumor necrosis factor α, which signal through diverse mechanisms, were all able to activate MAPK to a much greater degree in fibronectin-adherent cells than in suspended cells. In addition, tumor necrosis factor α activation of c-Jun kinase (JNK) was also much more robust in anchored cells. Together, these data suggest a cooperation between integrins and soluble mitogens in efficient propagation of signals to downstream kinases. This cooperation may contribute to anchorage dependence of mitogenic cell cycle progression.

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The putative role of sorting early endosomes (EEs) in synaptic-like microvesicle (SLMV) formation in the neuroendocrine PC12 cell line was investigated by quantitative immunoelectron microscopy. By BSA-gold internalization kinetics, four distinct endosomal subcompartments were distinguished: primary endocytic vesicles, EEs, late endosomes, and lysosomes. As in other cells, EEs consisted of vacuolar and tubulovesicular subdomains. The SLMV marker proteins synaptophysin and vesicle-associated membrane protein 2 (VAMP-2) localized to both the EE vacuoles and associated tubulovesicles. Quantitative analysis showed that the transferrin receptor and SLMV proteins colocalized to a significantly higher degree in primary endocytic vesicles then in EE-associated tubulovesicles. By incubating PC12 cells expressing T antigen-tagged VAMP (VAMP-TAg) with antibodies against the luminal TAg, the recycling pathway of SLMV proteins was directly visualized. At 15°C, internalized VAMP-TAg accumulated in the vacuolar domain of EEs. Upon rewarming to 37°C, the labeling shifted to the tubular part of EEs and to newly formed SLMVs. Our data delineate a pathway in which SLMV proteins together with transferrin receptor are delivered to EEs, where they are sorted into SLMVs and recycling vesicles, respectively.

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Hepatic lipid synthesis is known to be regulated by food consumption. In rodents fasting decreases the synthesis of cholesterol as well as fatty acids. Refeeding a high carbohydrate/low fat diet enhances fatty acid synthesis by 5- to 20-fold above the fed state, whereas cholesterol synthesis returns only to the prefasted level. Sterol regulatory element binding proteins (SREBPs) are transcription factors that regulate genes involved in cholesterol and fatty acid synthesis. Here, we show that fasting markedly reduces the amounts of SREBP-1 and -2 in mouse liver nuclei, with corresponding decreases in the mRNAs for SREBP-activated target genes. Refeeding a high carbohydrate/low fat diet resulted in a 4- to 5-fold increase of nuclear SREBP-1 above nonfasted levels, whereas nuclear SREBP-2 protein returned only to the nonfasted level. The hepatic mRNAs for fatty acid biosynthetic enzymes increased 5- to 10-fold above nonfasted levels, a pattern that paralleled the changes in nuclear SREBP-1. The hepatic mRNAs for enzymes involved in cholesterol synthesis returned to the nonfasted level, closely following the pattern of nuclear SREBP-2 regulation. Transgenic mice that overproduce nuclear SREBP-1c failed to show the normal decrease in hepatic mRNA levels for cholesterol and fatty acid synthetic enzymes upon fasting. We conclude that SREBPs are regulated by food consumption in the mouse liver and that the decline in nuclear SREBP-1c upon fasting may explain in part the decrease in mRNAs encoding enzymes of the fatty acid biosynthetic pathway.