247 resultados para MEA
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Pós-graduação em Ciências da Motricidade - IBRC
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Este artigo trata da relação sociedade-ambiente. Busca-se, por meio da Teoria de Sistemas, estabelecer um referencial que permita o entendimento dessa relação e que possibilite o acesso operacional às suas dinâmicas. A esse arcabouço teórico é associada uma proposta metodológica que se estrutura em torno da contabilização dos fluxos materiais componentes dos processos econômicos. Desse método, o Material Flow Analysis (MFA), foi aprofundado o conceito de Metabolismo Econômico-Ambiental (MEA), por meio do qual é possível quantificar toda a matéria e energia demandada por uma economia. A análise da Demanda Material Total (DMT) possibilita o conhecimento da eficiência ecológica de qualquer processo econômico e a produção de indicadores para avaliar os impactos ambientais das atividades antrópicas. Do estudo resultou um detalhamento metodológico próprio que foi aplicado para medir a DMT do Brasil para comparações com a dos EUA, Alemanha, Japão e Holanda. Os resultados demonstraram que a metodologia é capaz de trazer à tona aspectos ecologicamente relevantes da economia, mediante os quais é possível constatar que os sistemas econômicos são configurados por lógicas crescentemente insustentáveis em relação ao ambiente.
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Pós-graduação em Ciências Biológicas (Microbiologia Aplicada) - IBRC
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Neste trabalho são apresentados os resultados de caracterização das principais argilas usadas pela indústria cerâmica vermelha regional e, também, de alguns resíduos sólidos produzidos na região de Presidente Prudente - SP. Os resultados da incorporação destes resíduos em massas cerâmicas são avaliados através do estudo de suas propriedades tecnológicas. Para a caracterização dos materiais foram utilizadas as seguintes técnicas: análise textural (concentração das frações areia, silte e argila), difratometria de raios X e análise térmica. As propriedades tecnológicas de corpos de prova cerâmicos foram avaliadas através dos seguintes parâmetros: retração linear (RL), perda de massa ao fogo (PF), massa específica aparente (MEA), porosidade aparente (PA), absorção de água (AA) e resistência mecânica à flexão (RMF). Corpos de prova, com diferentes concentrações de resíduos, foram prensados (prensa uniaxial manual) e queimados em temperaturas que variaram de 800 a 1200 oC, usando um forno tipo mufla com controle de temperatura. As argilas sedimentares foram coletadas nas margens do rio Paraná e em áreas de várzea, próximas as cerâmicas. As amostras estudadas, coletadas nos depósitos das cerâmicas, são usadas para produção de tijolos maciços, blocos furados e telhas. Quatro tipos diferentes de resíduos foram estudados: (1) lodo de estação de tratamento de água ETA, (2) torta de filtro de indústria de re-refino de óleo lubrificante, (3) pó de vidro (soda-cal) de garrafa tipo long neck descartável, e (4) cinza de bagaço de cana. Estes resíduos foram incorporados em massas cerâmicas coletadas nas indústrias... (Resumo completo, clicar acesso eletrônico abaixo)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Direct methanol fuel cells (DMFCs) without external pumps or other ancillary devices for fuel and oxidant supply are known as passive DMFCs and are potential candidates to replace lithium-ion batteries in powering portable electronic devices. This paper presents the results obtained from a membrane electrode assembly (MEA) specifically designed for passive DMFCs. Appropriated electrocatalysts were prepared and the effect of their loadings was investigated. Two types of gas diffusion layers (GDL) were also tested. The influence of the methanol concentration was analyzed in each case. The best MEA performance presented a maximum power density of 11.94 mW cm-2.
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The medial amygdaloid nucleus (MeA) is a sub-region of the amygdaloid complex that has been described as participating in food intake regulation. Serotonin has been known to play an important role in appetite and food intake regulation. Moreover, serotonin 5-HT2C and 5-HT1A receptors appear to be critical in food intake regulation. We investigated the role of the serotoninergic system in the MeA on feeding behavior regulation in rats. The current study examined the effects on feeding behavior regulation of the serotonin reuptake inhibitor, zimelidine, administered directly into the MeA or given systemically, and the serotoninergic receptors mediating its effect. Our results showed that microinjection of zimelidine (0.2, 2 and 20 nmol/100 nL) into the MeA evoked dose dependent hypophagic effects in fasted rats. The selective 5-HT1A receptor antagonist WAY-100635 (18.5 nmol/100 nL) or the 5-HT1B receptor antagonist SB-216641 microinjected bilaterally into the MeA did not change the hypophagic effect evoked by local MeA zimelidine treatment. However, microinjection of the selective 5-HT2C receptor antagonist SB-242084 (10 nmol/100 nL) was able to block the hypophagic effect of zimelidine. Moreover, microinjection of the 5-HT2C receptor antagonist SB-242084 into the MeA also blocked the hypophagic effect caused by zimelidine administered systemically. These results suggest that MeA 5-HT2C receptors modulate the hypophagic effect caused by local MeA administration as well as by systemic zimelidine administration. Furthermore, 5-HT2C into the MeA could be a potential target for systemic administration of zimelidine. (C) 2012 Elsevier Ltd. All rights reserved.
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In the present study, we investigated the involvement of beta-adrenoceptors in the medial amygdaloid nucleus (MeA) in cardiovascular responses evoked in rats submitted to an acute restraint stress. We first pretreated Wistar rats with the nonselective beta-adrenoceptor antagonist propranolol microinjected bilaterally into the MeA (10, 15, and 20 nmol/100 nL) 10 min before exposure to acute restraint. The pretreatment with propranolol did not affect the blood pressure (BP) increase evoked by restraint. However, it increased the tachycardiac response caused by acute restraint when animals were pretreated with a dose of 15 nmol, without a significant effect on the BP response. This result indicates that beta-adrenoceptors in the MeA have an inhibitory influence on restraint-evoked heart rate (HR) changes. Pretreatment with the selective beta(2)-adrenoceptor antagonist ICI 118,551 (10, 15, and 20 nmol/100 nL) significantly increased the restraint-evoked tachycardiac response after doses of 15 and 20 nmol, an effect that was similar to that observed after the pretreatment with propranolol at a dose of 15 nmol, without a significant effect on the BP response. Pretreatment of the MeA with the selective beta(1)-adrenoceptor antagonist CGP 20712 (10, 15, and 20 nmol/100 nL) caused an opposite effect on the HR response, and a significant decrease in the restraint-evoked tachycardia was observed only after the dose of 20 nmol, without a significant effect on the BP response. Because propranolol is an equipotent antagonist of both beta(1) and beta(2)-adrenoceptors, and opposite effects were observed after the treatment with the higher doses of the selective antagonists ICI 118,551 and CGP 20712, the narrow window in the dose-response to propranolol could be explained by a functional antagonism resulting from the simultaneous inhibition of beta(1) and beta(2)-adrenoceptors by the treatment with propranolol. The present results suggest that beta(2)-adrenoceptors have an inhibitory influence on the restraint-evoked tachycardiac response, whereas beta(1)-adrenoceptors have a facilitatory influence on the restraint-evoked tachycardiac response. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
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The medial amygdaloid nucleus (MeA) is a part of the limbic system and is involved in cardiovascular modulation. We previously reported that microinjection of noradrenaline (NA) into the MeA of unanesthetized rats caused pressor and bradycardiac responses, which were mediated by acute vasopressin release into the systemic circulation. In the present study, we tested the possible involvement of magnocellular neurons of the paraventricular (PVN) and/or supraoptic (SON) of the hypothalamus that synthesize vasopressin in the cardiovascular pathway activated by the microinjection of NA into the MeA. Pressor and bradycardiac responses to the microinjection of NA (27 nmol/100 nL) into the MeA were blocked by pretreatment of either the PVN or the SON with cobalt chloride (CoCl2, 1 mM/100 nL), thus indicating that both hypothalamic nuclei mediate the cardiovascular responses evoked by microinjection of NA Into the MeA. Our results suggest that the pressor and bradycardiac response caused by the microinjection of NA into the MeA is mediated by magnocellular neurons in both the PVN and SON. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
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We have previously reported that noradrenaline (NA) microinjected into the lateral septal area (LSA) caused pressor and bradicardic responses that were mediated by vasopressin release into the circulation through the paraventricular nucleus of hypothalamus (PVN). Although PVN is the final structure involved in the cardiovascular responses caused by NA in the LSA, there is no evidence of direct connections between these areas, suggesting that some structures could be links in this pathway. In the present study, we verified the effect of reversible synaptic inactivation of the medial amygdaloid nucleus (MeA), bed nucleus of stria terminalis (BNST) or diagonal band of Broca (DBB) with Cobalt Chloride (CoCl2) on the cardiovascular response to NA microinjection into the LSA of unanesthetized rats. Male Wistar rats had guide cannulae implanted into the LSA and the MeA, BNST or DBB for drug administration, and a femoral catheter for blood pressure and heart rate recordings. Local microinjection of CoCl2 (1 mm in 100 nL) into the MeA significantly reduced the pressor and bradycardic responses caused by NA microinjection (21 nmol in 200 nL) into the LSA. In contrast, microinjection of CoCl2 into the BNST or DBB did not change the cardiovascular responses to NA into the LSA. The results indicate that synapses within the MeA, but not in BNST or DBB, are involved in the cardiovascular pathway activated by NA microinjection into the LSA.