Desenvolvimento de um modelo de gerenciamento de redes de telecomunicações utilizando a plataforma CORBA

Orientador: Edmundo Roberto Mauro MadeiraDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de ComputaçãoResumo: O gerenciamento de rede é uma tarefa muito importante para o funcionamento de uma rede, principalmente as redes de telecomunicações. A causa disto é o aumento do tamanho e da complexidade das redes que dificultam a deteção de fallias e baixo desempenho. Outro fator de importância na gerência é permitir que este seja feito de fonna descentralizada. O grupo OMG, analisando a possibilidade de se utilizar a sua platafonna CORBA para permitir esta forma de gerenciamento, lançou um conjunto de serviços para auxiliar a construção de aplicações para o gerenciamento de redes de telecomunicações. Neste traballio será apresentada uma arquitetura para o gerenciamento de redes de telecomunicações que utiliza objetos distribuídos. Esta arquitetura utiliza-se dos recursos existentes no Serviço de Notificação CORBA, várias ferramentas foram desenvolvidasAbstract: The network management is a task very important to its operation, mainly in telecommunication networks. This fact is caused by increasing of size and complexity of the networks which raises difficulties to detect faults and low performance. Other important fact in network management is the decentralization of the managers, so in case of faults there will be a manager receiving the events. The CORBA architecture allows the decentralized network management, using the CORBA services. In this dissertation an architecture to the management of telecommunication networks using distributed objects is presented. This architecture uses the existent resources in the CORBA Notification Service, many tools were developed.MestradoMestre em Ciência da Computaçã

Role of the energy offset in the charge photogeneration and voltage loss of nonfullerene acceptor-based organic solar cells

The trade-off between short-circuit current density (JSC) and open-circuit voltage (VOC) has been one of the largest challenges in improving the power conversion efficiencies (PCEs) of organic solar cells (OSCs). Although the energy offset between the excited and charge transfer (CT) states should remain minimal to achieve a high VOC, a very small energy offset typically leads to degradation of JSC, even when novel nonfullerene acceptors (NFAs), such as Y6, are used. Therefore, understanding the limit to what extent the energy offset can be minimized and the physics underlying the trade-off relationship is important to optimize the design of new materials and further improve the PCEs. This study provides a threshold energy that can ensure high charge photogeneration quantum efficiencies for Y-series NFA-based OSCs and discusses the role of the energy offset in device performances. We found that an insufficient energy offset led to not only slow hole transfer at the donor:acceptor interfaces, but also inefficient long-range spatial dissociation of the CT states and degradation of the fill factor (FF). This study also discusses the interplay of the energy levels of the two NFAs that constitute ternary blend OSCs. We found that, by introducing a low-efficiency NFA into a high-efficiency donor:acceptor blend, the voltage loss can be reduced while maintaining a high charge photogeneration quantum efficiency. Our findings highlight the importance of overcoming the trade-off between FF and VOC for further improving the PCE

Role of Energy Offset in Nonradiative Voltage Loss in Organic Solar Cells

The voltage loss incurred by nonradiative charge recombination should be reduced to further improve the power conversion efficiency of organic solar cells (OSCs). This work discusses the nonradiative voltage loss in OSCs with systematically controlled energy offset between optical bandgap and charge transfer (CT) states. It is demonstrated that the nonradiative voltage loss is a function of the energy offset; it drops sharply with decreasing energy offset. By measuring the quantum yields of electroluminescence from OSCs and decay kinetics of CT states, it is found that the radiative decay rate of CT states becomes larger when the energy offset is negligible compared with those in conventional OSCs with sufficient energy offset. This behavior is rationalized by hybridization between CT and local excited states, resulting in a considerable enhancement of the oscillator strength of CT states. Based on a trend observed in this study, the precise mechanism by which the energy offset affects the nonradiative voltage loss is discussed

Numerical investigations on shock oscillations ahead of a hemispherical shell in supersonic flow

A clear understanding of the mechanism responsible for large amplitude shock pulsations ahead of a hemispherical cavity in supersonic flow is presented for the first time in this article. This has applications in supersonic parachute decelerators during the atmospheric descent stage of aerospace vehicles. A cell-centered finite volume code FaSTAR is used to solve the full Navier–Stokes equations on a hemispherical shell facing a Mach 4.0 supersonic free stream. The numerical method is validated against earlier experimental results. First, Flow Configuration A appears consisting of an axisymmetric shock that undergoes low-amplitude oscillations. This flow transitions to Flow Configuration B that has an asymmetric shock structure and undergoes large-amplitude non-stationary shock pulsations. The shock stand-off distance in Flow Configuration B is 1.65 times that in Flow Configuration A. The generation of vortices from the curved shock, amplification of vortices of one kind due to the dynamics of the cavity flow, and further interaction of these amplified vortices with the shock in a loop causes the large-amplitude shock pulsations. The oscillation frequencies as determined from cavity pressure and shock stand-off distance signals extracted from the unsteady results are 1.26 kHz during Flow Configuration A, and 859 and 863 Hz during the non-stationary pulsations of Flow Configuration B. The Helmholtz resonator model predicts quite accurately the frequency of Flow Configuration A (1.27 kHz), and to a good extent the frequency in Flow Configuration B (916.7 Hz).Conference: 21st International Shock Interaction Symposium (ISIS)Location: Riga, LATVIADate: AUG 03-08, 201

Identification of novel mast cell genes by serial analysis of gene expression in cord blood-derived mast cells

AbstractThe gene expression profile of human cord blood-derived mast cells (MCs) was investigated using serial analysis of gene expression (SAGE). A total of 22 914 tags, representing 9181 unique transcripts, were sequenced. By selecting tags that were detected more frequently in MCs than in other tissues, genes characteristic of MCs were enriched. Reverse transcription-PCR and the high-density oligonucleotide array hybridization confirmed the validity of our SAGE result. About 70% of the selected genes were previously uncharacterized. Northern blot analysis showed the MC-specific expression of selected genes. This inventory will be useful to identify novel genes with important functions in MCs

Increased amyloidogenic processing of transgenic human APP in X11-like deficient mouse brain

<p>Abstract</p> <p>Background</p> <p>X11-family proteins, including X11, X11-like (X11L) and X11-like 2 (X11L2), bind to the cytoplasmic domain of amyloid β-protein precursor (APP) and regulate APP metabolism. Both X11 and X11L are expressed specifically in brain, while X11L2 is expressed ubiquitously. X11L is predominantly expressed in excitatory neurons, in contrast to X11, which is strongly expressed in inhibitory neurons. <it>In vivo </it>gene-knockout studies targeting X11, X11L, or both, and studies of X11 or X11L transgenic mice have reported that X11-family proteins suppress the amyloidogenic processing of endogenous mouse APP and ectopic human APP with one exception: knockout of X11, X11L or X11L2 has been found to suppress amyloidogenic metabolism in transgenic mice overexpressing the human Swedish mutant APP (APPswe) and the mutant human PS1, which lacks exon 9 (PS1dE9). Therefore, the data on X11-family protein function in transgenic human APP metabolism <it>in vivo </it>are inconsistent.</p> <p>Results</p> <p>To confirm the interaction of X11L with human APP ectopically expressed in mouse brain, we examined the amyloidogenic metabolism of human APP in two lines of human APP transgenic mice generated to also lack X11L. In agreement with previous reports from our lab and others, we found that the amyloidogenic metabolism of human APP increased in the absence of X11L.</p> <p>Conclusion</p> <p>X11L appears to aid in the suppression of amyloidogenic processing of human APP in brain <it>in vivo</it>, as has been demonstrated by previous studies using several human APP transgenic lines with various genetic backgrounds. X11L appears to regulate human APP in a manner similar to that seen in endogenous mouse APP metabolism.</p

Decrease in p3-Alcb37 and p3-Alcb40, products of Alcadein b generated by g-secretase cleavages, in aged monkeys and patients with Alzheimer’s disease

Introduction Neuronal p3-Alcβ peptides are generated from the precursor protein Alcadein β (Alcβ) through cleavage by α- and γ-secretases of the amyloid β (Aβ) protein precursor (APP). To reveal whether p3-Alcβ is involved in Alzheimer\u27s disease (AD) contributes for the development of novel therapy and/or drug targets. Methods We developed new sandwich enzyme-linked immunosorbent assay (sELISA) systems to quantitate levels of p3-Alcβ in the cerebrospinal fluid (CSF). Results In monkeys, CSF p3-Alcβ decreases with age, and the aging is also accompanied by decreased brain expression of Alcβ. In humans, CSF p3-Alcβ levels decrease to a greater extent in those with AD than in age-matched controls. Subjects carrying presenilin gene mutations show a significantly lower CSF p3-Alcβ level. A cell study with an inverse modulator of γ-secretase remarkably reduces the generation of p3-Alcβ37 while increasing the production of Aβ42. Discussion Aging decreases the generation of p3-Alcβ, and further significant decrease of p3-Alcβ caused by aberrant γ-secretase activity may accelerate pathogenesis in AD

Decrease in p3-Alcb37 and p3-Alcb40, products of Alcadein b generated by g-secretase cleavages, in aged monkeys and patients with Alzheimer’s disease

Introduction Neuronal p3-Alcβ peptides are generated from the precursor protein Alcadein β (Alcβ) through cleavage by α- and γ-secretases of the amyloid β (Aβ) protein precursor (APP). To reveal whether p3-Alcβ is involved in Alzheimer\u27s disease (AD) contributes for the development of novel therapy and/or drug targets. Methods We developed new sandwich enzyme-linked immunosorbent assay (sELISA) systems to quantitate levels of p3-Alcβ in the cerebrospinal fluid (CSF). Results In monkeys, CSF p3-Alcβ decreases with age, and the aging is also accompanied by decreased brain expression of Alcβ. In humans, CSF p3-Alcβ levels decrease to a greater extent in those with AD than in age-matched controls. Subjects carrying presenilin gene mutations show a significantly lower CSF p3-Alcβ level. A cell study with an inverse modulator of γ-secretase remarkably reduces the generation of p3-Alcβ37 while increasing the production of Aβ42. Discussion Aging decreases the generation of p3-Alcβ, and further significant decrease of p3-Alcβ caused by aberrant γ-secretase activity may accelerate pathogenesis in AD