964 resultados para Short circuit in stator


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Synchronous machines with brushless excitation have the disadvantage that the field winding is not accessible for the de-excitation of the machine. This means that, despite the proper operation of the protection system, the slow de-excitation time constant may produce severe damage in the event of an internal short circuit. A high-speed de-excitation system for these machines was developed, and this study presents the continuation of a previously published study. This study presents the design by computer simulation and the results of the first commissioning of this de-excitation system in a commercial 20 MVA hydro-generator. The de-excitation is achieved by inserting resistance in the field circuit, obtaining a dynamic response similar to that achieved in machines with static excitation. In this case, a non-linear discharge resistor was used, making the dynamic response even better.

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The effects of PAR2-activating PAR2-activating peptides, SLIGRL (SL)-NH2, and trans-cinnamoyl-LIGRLO (tc)-NH2 were compared with the action of trypsin, thrombin, and the PAR1 selective-activating peptide: Ala-parafluoroPhe-Arg-cyclohexylAla-Citrulline-Tyr (Cit)-NH2 for stimulating intestinal ion transport. These agonists were added to the serosa of stripped rat jejunum segments mounted in Ussing chambers, and short circuit current (Isc) was used to monitor active ion transport. The relative potencies of these agonists also were evaluated in two bioassays specific for the activation of rat PAR2: a cloned rat PAR2 cell calcium-signaling assay (PAR2-KNRK cells) and an aorta ring relaxation (AR) assay. In the Isc assay, all agonists, except thrombin, induced an Isc increase. The SL-NH2-induced Isc changes were blocked by indomethacin but not by tetrodotoxin. The relative potencies of the agonists in the Isc assay (trypsin≫SL-NH2>tc-NH2>Cit-NH2) were strikingly different from their relative potencies in the cloned PAR2-KNRK cell calcium assay (trypsin≫>tc-NH2 ≅ SL-NH2≫>Cit-NH2) and in the AR assay (trypsin≫>tc-NH2 ≅ SL-NH2). Furthermore, all agonists were maximally active in the PAR2-KNRK cell and AR assays at concentrations that were one (PAR2 -activating peptides) or two (trypsin) orders of magnitude lower than those required to activate intestinal transport. Based on the distinct potency profile for these agonists and the considerable differences in the concentration ranges required to induce an Isc effect in the intestinal assay compared with the PAR2-KNRK and AR assays, we conclude that a proteinase-activated receptor, pharmacologically distinct from PAR2 and PAR1, is present in rat jejunum and regulates intestinal transport via a prostanoid-mediated mechanism.

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Dissection of the primary and secondary response to an influenza A virus established that the liver contains a substantial population of CD8+ T cells specific for the immunodominant epitope formed by H-2Db and the influenza virus nucleoprotein peptide fragment NP366–374 (DbNP366). The numbers of CD8+ DbNP366+ cells in the liver reflected the magnitude of the inflammatory process in the pneumonic lung, though replication of this influenza virus is limited to the respiratory tract. Analysis of surface phenotypes indicated that the liver CD8+ DbNP366+ cells tended to be more “activated” than the set recovered from lymphoid tissue but generally less so than those from the lung. The distinguishing characteristic of the lymphocytes from the liver was that the prevalence of the CD8+ DbNP366+ set was always much higher than the percentage of CD8+ T cells that could be induced to synthesize interferon γ after short-term, in vitro stimulation with the NP366–374 peptide, whereas these values were generally comparable for virus-specific CD8+ T cells recovered from other tissue sites. Also, the numbers of apoptotic CD8+ T cells were higher in the liver. The results overall are consistent with the idea that antigen-specific CD8+ T cells are destroyed in the liver during the control and resolution phases of this viral infection, though this destruction is not necessarily an immediate process.

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Nitric oxide (NO) has diverse roles in intercellular communication and (at higher levels) in immune-mediated cell killing. NO reacts with many cellular targets, with cell-killing effects correlated to inactivation of key enzymes through nitrosylation of their iron-sulfur centers. SoxR protein, a redox-sensitive transcription activator dependent on the oxidation state of its binuclear iron-sulfur ([2Fe-2S]) centers, is also activated in Escherichia coli on exposure to macrophage-generated NO. We show here that SoxR activation by NO occurs through direct modification of the [2Fe-2S] centers to form protein-bound dinitrosyl-iron-dithiol adducts, which we have observed both in intact bacterial cells and in purified SoxR after NO treatment. Functional activation through nitrosylation of iron-sulfur centers contrasts with the inactivation typically caused by this modification. Purified, nitrosylated SoxR has transcriptional activity similar to that of oxidized SoxR and is relatively stable. In contrast, nitrosylated SoxR is short-lived in intact cells, indicative of mechanisms that actively dispose of nitrosylated iron-sulfur centers.

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Bird song, like human speech, is a learned vocal behavior that requires auditory feedback. Both as juveniles, while they learn to sing, and as adults, songbirds use auditory feedback to compare their own vocalizations with an internal model of a target song. Here we describe experiments that explore a role for the songbird anterior forebrain pathway (AFP), a basal ganglia-forebrain circuit, in evaluating song feedback and modifying vocal output. First, neural recordings in anesthetized, juvenile birds show that single AFP neurons are specialized to process the song stimuli that are compared during sensorimotor learning. AFP neurons are tuned to both the bird's own song and the tutor song, even when these stimuli are manipulated to be very different from each other. Second, behavioral experiments in adult birds demonstrate that lesions to the AFP block the deterioration of song that normally follows deafening. This observation suggests that deafening results in an instructive signal, indicating a mismatch between feedback and the internal song model, and that the AFP is involved in generating or transmitting this instructive signal. Finally, neural recordings from behaving birds reveal robust singing-related activity in the AFP. This activity is likely to originate from premotor areas and could be modulated by auditory feedback of the bird's own voice. One possibility is that this activity represents an efference copy, predicting the sensory consequences of motor commands. Overall, these studies illustrate that sensory and motor processes are highly interrelated in this circuit devoted to vocal learning, as is true for brain areas involved in speech.

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β-actin mRNA is localized near the leading edge in several cell types, where actin polymerization is actively promoting forward protrusion. The localization of the β-actin mRNA near the leading edge is facilitated by a short sequence in the 3′ untranslated region, the “zip code.” Localization of the mRNA at this region is important physiologically. Treatment of chicken embryo fibroblasts with antisense oligonucleotides complementary to the localization sequence (zip code) in the 3′ untranslated region leads to delocalization of β-actin mRNA, alteration of cell phenotype, and a decrease in cell motility. To determine the components of this process responsible for the change in cell behavior after β-actin mRNA delocalization, the Dynamic Image Analysis System was used to quantify movement of cells in the presence of sense and antisense oligonucleotides to the zip code. It was found that net path length and average speed of antisense-treated cells were significantly lower than in sense-treated cells. Total path length and the velocity of protrusion of antisense-treated cells were not affected compared with those of control cells. These results suggest that a decrease in persistence of direction of movement and not in velocity results from treatment of cells with zip code-directed antisense oligonucleotides. To test this, direct analysis of directionality was performed on antisense-treated cells and showed a decrease in directionality (net path/total path) and persistence of movement. Less directional movement of antisense-treated cells correlated with a unpolarized and discontinuous distribution of free barbed ends of actin filaments and of β-actin protein. These results indicate that delocalization of β-actin mRNA results in delocalization of nucleation sites and β-actin protein from the leading edge followed by loss of cell polarity and directional movement.

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Ca2+ influx controls multiple neuronal functions including neurotransmitter release, protein phosphorylation, gene expression, and synaptic plasticity. Brain L-type Ca2+ channels, which contain either alpha 1C or alpha 1D as their pore-forming subunits, are an important source of calcium entry into neurons. Alpha 1C exists in long and short forms, which are differentially phosphorylated, and C-terminal truncation of alpha 1C increases its activity approximately 4-fold in heterologous expression systems. Although most L-type calcium channels in brain are localized in the cell body and proximal dendrites, alpha 1C subunits in the hippocampus are also present in clusters along the dendrites of neurons. Examination by electron microscopy shows that these clusters of alpha 1C are localized in the postsynaptic membrane of excitatory synapses, which are known to contain glutamate receptors. Activation of N-methyl-D-aspartate (NMDA)-specific glutamate receptors induced the conversion of the long form of alpha 1C into the short form by proteolytic removal of the C terminus. Other classes of Ca2+ channel alpha1 subunits were unaffected. This proteolytic processing reaction required extracellular calcium and was blocked by inhibitors of the calcium-activated protease calpain, indicating that calcium entry through NMDA receptors activated proteolysis of alpha1C by calpain. Purified calpain catalyzed conversion of the long form of immunopurified alpha 1C to the short form in vitro, consistent with the hypothesis that calpain is responsible for processing of alpha 1C in hippocampal neurons. Our results suggest that NMDA receptor-induced processing of the postsynaptic class C L-type Ca2+ channel may persistently increase Ca2+ influx following intense synaptic activity and may influence Ca2+-dependent processes such as protein phosphorylation, synaptic plasticity, and gene expression.

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Based on our previous transgenic mice results, which strongly suggested that separate cell-specific cis-acting elements of the mouse pro-alpha 1(I) collagen promoter control the activity of the gene in different type I collagen-producing cells, we attempted to delineate a short segment in this promoter that could direct high-level expression selectively in osteoblasts. By generating transgenic mice harboring various fragments of the promoter, we identified a 117-bp segment (-1656 to -1540) that is a minimal sequence able to confer high-level expression of a lacZ reporter gene selectively in osteoblasts when cloned upstream of the proximal 220-bp pro-alpha 1(I) promoter. This 220-bp promoter by itself was inactive in transgenic mice and unable to direct osteoblast-specific expression. The 117-bp enhancer segment contained two sequences that appeared to have different functions. The A sequence (-1656 to -1628) was required to obtain expression of the lacZ gene in osteoblasts, whereas the C sequence (-1575 to -1540) was essential to obtain consistent and high-level expression of the lacZ gene in osteoblasts. Gel shift assays showed that the A sequence bound a nuclear protein present only in osteoblastic cells. A mutation in the A segment that abolished the binding of this osteoblast-specific protein also abolished lacZ expression in osteoblasts of transgenic mice.

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Com o objetivo de orientar e agilizar a busca do local de curto circuitos em redes primárias aéreas de distribuição de energia, esta pesquisa propõe uma metodologia para localização de áreas com maior probabilidade de ser sede do defeito, utilizando variáveis Heurísticas. A metodologia Heurística se aplica em problemas que envolvem variáveis com incertezas, que podem ser avaliadas por meio de recursos empíricos e na experiência de especialistas. Dentre as variáveis influentes no cálculo de curto circuito, foram consideradas como mais relevantes: a resistência de defeito, a tensão pré falta, a impedância do sistema equivalente a montante da subestação e a impedância da rede. A metodologia proposta se fundamenta no conhecimento das correntes e tensões oscilografadas no barramento da subestação por ocasião da ocorrência de um curto circuito e, por outro lado no pré-calculo de correntes de curto circuito heurísticas ao longo da rede. No âmbito da pesquisa foram realizados testes de campo para levantamento da variável heurística resistência de defeito, resumidos neste texto e documentados no CD - ROM em anexo. Foi desenvolvido um software que permitiu a efetiva aplicação da proposta desta pesquisa em vários alimentadores de uma Distribuidora, cujos resultados comprovaram a eficiência da metodologia.

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O uso de materiais inteligentes em problemas de controle de vibração tem sido investigado em diversas pesquisas ao longo dos últimos anos. Apesar de que diferentes materiais inteligentes estão disponíveis, o piezelétrico tem recebido grande atenção devido à facilidade de uso como sensores, atuadores, ou ambos simultaneamente. As principais técnicas de controle usando materiais piezoelétricos são os ativos e passivos. Circuitos piezelétricos passivos são ajustados para uma frequência específica e, portanto, a largura de banda efetiva é pequena. Embora os sistemas ativos possam apresentar um bom desempenho no controle de vibração, a quantidade de energia externa e hardware adicionado são questões importantes. As técnicas SSD (Synchronized Switch Damping) foram desenvolvidas como uma alternativa aos controladores passivos e controladores ativos de vibração. Elas podem ser técnicas semi-ativas ou semi-passivas que introduzem um tratamento não linear na tensão elétrica proveniente do material piezelétrico e induz um aumento na conversão de energia mecânica para energia elétrica e, consequentemente, um aumento no efeito de amortecimento. Neste trabalho, o controle piezoelétrico semi-passivo de uma pá piezelétrica engastada é apresentado e comparado com outros controladores. O modelo não linear electromecânico de uma pá com piezocerâmicas incorporados é determinado com base no método variacional-assintótico (VAM). O sistema rotativo acoplado não linear é resolvido no domínio do tempo, utilizando um método de integração alfa-generalizado afim de garantir a estabilidade numérica. As simulações são realizadas para uma vasta gama de velocidades de rotação. Em primeiro lugar, um conjunto de resistências (variando desde a condição de curto-circuito para a condição de circuito aberto) é considerada. O efeito da resistência ótima (que resulta em máximo amortecimento) sobre o comportamento do sistema é investigado para o aumento da velocidade de rotação. Mais tarde, a técnica SSDS é utilizada para amortecer as oscilações da pá com o aumento da velocidade de rotação. Os resultados mostram que a técnica SSDS pode ser um método útil para o controle de vibrações de vigas rotativas não lineares, tais como pás de helicóptero.

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Esta dissertação tem por propósito analisar os impactos da geração distribuída sobre as correntes de curto-circuito e sobre a proteção das redes de média tensão das concessionárias de distribuição de energia elétrica usando uma abordagem paramétrica. A principal motivação deste trabalho são os recentes incentivos regulatórios que estão fomentando a geração distribuída no Brasil. Contudo, as redes de distribuição convencionais foram projetadas para serem passivas e a introdução da geração poderá causar problemas de ordem técnica que ainda precisam ser resolvidos. Tais problemas foram pesquisados e aqueles relacionados com os impactos sobre as correntes de curto-circuito foram enfatizados. As normas técnicas das concessionárias também foram investigadas porque seus requisitos, como a ligação dos transformadores de acoplamento, influem nas correntes de curto-circuito. Para se calcular as correntes de curto-circuito, desenvolveu-se uma planilha eletrônica cujos resultados foram validados com programas comerciais de análise de redes elétricas. Esta ferramenta foi utilizada para demonstrar, através de exemplos, o impacto causado pela geração distribuída sobre as correntes de curto-circuito e, posteriormente, para realizar as análises paramétricas nas quais a influência de cada variável foi avaliada. A aplicação do método paramétrico permitiu o estudo de possíveis limites para a potência de um gerador distribuído em função dos impactos admissíveis, de seu ponto de conexão, de seus parâmetros elétricos e dos parâmetros elétricos da rede.

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From the Introduction. The present contribution is an attempt to raise awareness between the 'trenches' by juxtaposing the two approaches to subsidiarity. Subsequently, I shall set out why, in economics, subsidiarity is embraced as a key principle in the design and working of the Union and how a functional subsidiarity test can be derived from this thinking. Throughout the paper, a range of illustrations and examples is provided in an attempt to show the practical applicability of a subsidiarity test. This does not mean, of course, that the application of the test can automatically "solve" all debates on whether subsidiarity is (not) violated. What it does mean, however, is that a careful methodology can be a significant help to e.g. national parliaments and the Brussels circuit, in particular, to discourage careless politicisation as much as possible and to render assessments of subsidiarity comparable throughout the Union. The latter virtue should be of interest to national parliaments in cooperating, within just six weeks, about a common stance in the case of a suspected violation of the principle. The structure of the paper is as follows. Section 2 gives a flavour of very different approaches and appreciation of the subsidiarity principle in European law and in the economics of multi-tier government. Section 3 elaborates on the economics of multi-tier government as a special instance of cost / benefit analysis of (de)centralisation in the three public economic functions of any government system. This culminates in a five-steps subsidiarity test and a brief discussion about its proper and improper application. Section 4 applies the test in a non-technical fashion to a range of issues of the "efficiency function" (i.e. allocation and markets) of the EU. After showing that the functional logic of subsidiarity may require liberalisation to be accompanied by various degrees of centralisation, a number of fairly detailed illustrations of how to deal with subsidiarity in the EU is provided. One illustration is about how the subsidiarity logic is misused by protagonists (labour in the internal market). A slightly different but frequently encountered aspect consists in the refusal to recognize that the EU (that is, some form of centralisation) offers a better solution than 25 national ones. A third range of issues, where the functional logic of subsidiarity could be useful, emerges when the boundaries of national competences are shifting due to more intense cross-border flows and developments. Other subsections are devoted to Union public goods and to the question whether the subsidiarity test might trace instances of EU decentralisation: a partial or complete shift of a policy or regulation to Member States. The paper refrains from an analysis of the application of the subsidiarity test to the other two public functions, namely, equity and macro-economic stabilisation.2 Section 5 argues that the use of a well-developed methodology of a functional subsidiarity test would be most useful for the national parliaments and even more so for their cooperation in case of a suspected violation of subsidiarity. Section 6 concludes.

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The European Union, together with other countries, is making a second effort to reach a comprehensive global climate change agreement in Paris in 2015, after the unsuccessful attempt to do so in Copenhagen in 2009. In a Europe still preoccupied with recovery from the economic crisis, why should the EU be tempted to offer leadership in the field of climate change and what would such an agreement bring – in short, what’s in it for the EU? Although the world has changed since the earlier attempt to reach agreement, the EU needs to continue to be a leader in the climate talks, argues the author, both for the sake of the world and for our own EU interest. Others will come and share that leadership and shape it together. It is the only way that we, the EU, can be successful in Paris.

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The European Union, together with all countries, is making a second effort to reach a comprehensive global climate change agreement at the United Nations Climate Change Conference (COP21 or CMP11) in Paris in December 2015, after the unsuccessful attempt to do so in Copenhagen in 2009. At a time when the EU is still preoccupied with recovery from the economic crisis, and is facing geopolitical challenges and a number of conflicts, why should it see the importance of continuing to offer leadership in the field of climate change? And why would such an agreement be important for the EU? In short: “What’s in it for the EU?” This commentary reviews the wider context of the negotiations, looking not only at the geopolitical shifts that have taken place on the road to Paris, but also at the interests of the EU both as far as its domestic climate policy is concerned, as well as its role as a diplomatic ‘soft power’.