999 resultados para Ottimizzazione banco prova alte quote motori pistoni


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Banco Nacional: Ponzi game, PROER and FCVS. This paper analyses the causes of the failure of Banco Nacional and the resolution method adopted by the Brazilian central bank. The program (PROER) designed by the central bank and its legal framework allowed the failed bank to buy " defaulted securities" , financed by the central bank, and to use them as borrowing collateral. The paper also analyses the private and social costs of this bank failure.

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Central Bank transparency: an analysis of the Brazilian case. Nowadays there is a tendency among central banks of increasing transparency in the conduction of the monetary policy. After the adoption of inflation targeting in Brazil there was an increase in the communication of the Central Bank of Brazil with the public. This paper makes a brief review of the recent theoretical and empirical literature concerning this subject. Furthermore, an analysis due to the transparency in the conduction of Brazilian monetary policy on important macroeconomic variables is made. The findings denote that an increase in transparency improves the behavior of several macroeconomic variables.

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The Banco Central do Brazil (BACEN) adopted inflation targeting in 1999. This monetary policy regime originates in institutional design which remains crucial today for the expectations management, and is in permanent evolution. After 10 years, the BACEN institutional framework is assessed, asking if there is still room for improvement. Various institutional procedures are analysed, and lessons are drawn from the international experience of a panel of sixteen countries. Some proposals for the BACEN institutional framework are made.

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The current crisis shed a new light on issues that, previously, were not perceived as serious or important. It highlighted the close ties between fiat currency and government bonds denominated in it or, in other words, the relationship between Treasury and Central Bank. Two ill-conceived views of the "new consensus" on money that had turned into taboos were put in evidence. The first, derived from the quantitative theory, concerns the rejection of unsterilized monetary expansion; the second, directly related to the neoliberal ideology, prohibits or imposes strict limits on the role of central banks in the financing of public debts.

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Dirección de Canales / Operaciones

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Dirección de Canales / Operaciones

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Dirección de Canales / Operaciones

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Dirección de Canales / Operaciones

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Dirección de Canales / Operaciones

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UANL

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Le couplage neurovasculaire (CNV) est un mécanisme d’homéostasie cérébrale régulant le débit sanguin cérébral (CBF) en fonction de l’activité neuronale. La manière dont il est altéré par l’angiotensine II (Ang II), une hormone synthétisée et relâchée dans la circulation systémique ou, alternativement, produite dans le cerveau grâce aux astrocytes, demeure à élucider. Ces cellules expriment le récepteur AT1 (rAT1) et participent à l’orchestration du CNV en relâchant des agents vasoactifs suivant la réponse calcique astrocytaire. Nous avons donc étudié le rôle de cette réponse dans l’altération du CNV induite par l’Ang II. Nous avons trouvé par fluxmétrie par laser Doppler que l’Ang II atténue (p<0.05) la réponse du CBF engendrée par l’activation des récepteurs métabotropes du glutamate du groupe I (mGluRI) du cortex chez la souris C57BL/6. De manière similaire, l’Ang II diminue l'élévation du CBF induite par la stimulation des vibrisses (p<0.05). Sur tranches de cerveaux en aiguë, la polarité de la réponse vasculaire induite par un agoniste mGluRI dans les artérioles parenchymateuses a été significativement renversée par l’Ang II de la vasodilatation vers la vasoconstriction. En parallèle, l’Ang II a augmenté les niveaux de calcium astrocytaire basaux et l’amplitude des réponses calciques (p<0.05). L’altération des réponses vasculaires et calciques maximales a été prévenue par le candesartan, antagoniste des rAT1. Nos résultats suggèrent que l’Ang II potentialise via les rAT1 la réponse calcique qui atteint un seuil favorisant la vasoconstriction par rapport à la vasodilatation, altérant ainsi l’augmentation du CBF en réponse à l’activité neuronale.