Um estudo comparativo entre os principais modelos empíricos e semi-empíricos de predição de nível de sinal para comunicações móveis celulares é descrito neste trabalho. Medidas de cobertura outdoor em ambiente urbano foram comparadas com os resultados simulados a partir dos modelos de Okumura-Hata e Lee, lkegami, Walfisch-Bertoni e Walfisch-Ikegami. As medidas de potência de sinal recebido foram realizadas na cidade de Conceição das Alagoas, MG, a partir da única estação rádio-base (ERB) da cidade, operando na banda A com tecnologia AMPS/TDMA. Foi utilizada como portadora de teste o canal de controle analógico 328. As informações foram coletadas em algumas ruas da cidade, por meio de equipamento instalado em veículo, em diferentes posicionamentos em relação a ERB, de forma a se obter amostras de cobertura em diferentes cenários, seja em visada direta, em obstrução parcial ou total. O modelo de Ikegami se mostrou apropriado para predição de níveis de sinal recebido no ambiente estudado, apresentando desvio médio 5,81 dB em relação às medidas realizadas. / A comparative study among the main empiric and semi-empiric models of prediction of signal leveI for cellular mobile communications is described in this work. Measurements of covering outdoor in an urban environment were compared to the simulated results from the models of Okumura-Hata, Lee, Ikegami, Walfisch-Bertoni and Walfisch-Ikegami. The measurements of received signal level were accomplished in some streets of the city of Conceição das Alagoas, MG, starting from the only radio base station of the city, operating in the A band with AMPS/TDMA technology. The 328-analog control channel was used as test carrier. The measurements were carried out using some equipment installed in a vehicle, in different positions in relation to the radio base station, in order to obtain covering profile in different circunstances such as line-of-sight, non line-of-sight, and partial obstruction. The model of Ikegami was shown appropriate for prediction of the received signal levels in the studied environment, exhibiting an average deviation of 5,81 dB in relation to the accomplished measurements.

Récemment, le concept monofonctionnel de la protéine Tau en tant que protéine stabilisatrice des microtubules a été remis en cause. Ces nouvelles fonctions sont liées à de nouvelles localisations comme le noyau, la membrane, la synapse ou encore les vésicules. La localisation extracellulaire est particulièrement intéressante car elle pourrait intervenir dans la sécrétion de Tau et expliquer l’évolution hiérarchisée de certaines tauopathies sporadiques dont fait partie la maladie d’Alzheimer. La pathologie Tau peut être induite chez l’animal par injection intracrânienne d’espèces pathologiques et semble se transmettre d’un neurone à un autre et d’une région à une autre. Ce phénomène suit des voies neuroanatomiques et suggère une propagation active des assemblages toxiques des protéines Tau. Des études in vitro ont mis en évidence que les protéines Tau sont capables de se déplacer d’une cellule à une autre propageant ainsi la pathologie par un mécanisme de recrutement des espèces saines. L’existence d’une progression hiérarchisée de la pathologie Tau combinée à sa localisation extracellulaire permet de formuler une nouvelle hypothèse. La protéine Tau serait une protéine de type prion et se comporterait comme telle pour propager la pathologie.Cette caractéristique implique l’existence de mécanismes cellulaires de transports actifs pour transférer les protéines pathologiques. Plusieurs travaux ont montré que la protéine Tau est libérée dans le milieu extracellulaire ou enfermée dans des vésicules extracellulaires lors de son transport entre les cellules. Parallèlement aux mécanismes de sécrétion/capture, des ponts membranaires établissant un contact direct entre deux cellules pourraient être impliquer dans la propagation de Tau. Les TNTs constituent une piste sérieuse de part leur rôle déjà établi dans le transfert de pathogènes et de protéines mal repliées impliqués dans différentes maladies neurodégénératives. Notre objectif a donc été d’étudier l’implication de ces structures dans le transfert interneuronal des assemblages de protéines Tau.Dans ce travail de thèse, nous démontrons que les espèces pathologiques de Tau empruntent les TNTs pour leur transfert interneuronal. Nous apportons les preuves, par vidéo-microscopie, de l’existence d’un transfert de protéines Tau pathologiques d’un neurone primaire à un neurone secondaire et donc d’une implication potentielle des TNTs dans la propagation de la pathologie Tau et la transmission de la maladie. Fait remarquable, la présence des fibres Tau au niveau extracellulaire active la formation des TNTs et facilite leur transfert. Ce résultat place les TNTs au coeur du processus pathologique de la propagation et de son cycle infernal (transfert de Tau dans les cellules naïves par les TNTs – seeding - mort neuronal - libération de Tau dans le milieu extracellulaire - augmentation du nombre des TNTs…). Nous avons aussi apporté une caractérisation des TNTs dans les neurones primaires. Ce résultat est d’autant plus important qu’il est difficile d’identifier des TNTs dans les neurones et c’est dans ce contexte que nous avons réalisé une découverte étonnante, la protéine Tau endogène est présente de manière physiologique dans les TNTs de neurones primaires. Ces résultats révèlent, et pour la première fois, que la protéine Tau, comme l’actine, peut être considérée comme une composante constitutive des TNTs dans les neurones. Elle pourrait ainsi être utilisée comme un marqueur des TNTs. Ces résultats mettent également en lumière une nouvelle fonction de Tau appuyant une fois de plus le caractère multifonctionnel de cette protéine [...] / Over the past few years, the monofunctional concept of Tau protein as a microtubule-associated stabilizing protein has been challenged. These new functions are linked to new localizations: nucleus, membrane, synapse or vesicles. The extracellular localization is particularly interesting as it could play a role in the secretion of Tau and explain the hierarchical evolution of some sporadic tauopathies such as Alzheimer's disease. The Tau pathology can be induced in animals by intracranial injection of pathological species and seems to be transferred from one neuron to another and from one region to another. This phenomenon follows neuroanatomic pathways and suggests an active propagation of the toxic assemblies of Tau proteins. In vitro studies have shown that proteins are able to move from one cell to another and induce the same abnormal conformation of endogenous Tau proteins initiating a self-amplifying cascade. The existence of a hierarchical progression of the Tau pathology combined with its extracellular localization enables to express a new hypothesis. The Tau protein would be a prion-like protein and would behave like that to propagate the pathology.This characteristic implies the existence of cellular active transport mechanisms to transfer pathological proteins. Several studies have shown that the Tau protein, during transport between cells, is released in the extracellular medium or enclosed in extracellular vesicles. Simultaneously with secretion / capture mechanisms, membrane bridges, establishing direct contact between two cells, could be involved in Tau propagation. TNTs are a serious candidate with their already established role in the transfer of pathogens and misfolding proteins involved in various neurodegenerative diseases. Thus, our objective was to study the involvement of these structures in the interneuronal transfer of Tau protein assemblies.In this thesis, we demonstrate that Tau pathological species use TNTs for their interneuronal transfer. We bring evidences, by videomicroscopy, that pathological Tau proteins are transferred from a primary to a secondary neuron and that TNTs could be involved in the spreading of Tau pathology and the disease transmission. Furthermore, the presence of extracellular Tau fibers can activate the formation of TNTs and facilitate their transfer. This result places TNTs in a central place for propagation pathological process and its vicious cycle (transfer of Tau in naive cells by TNTs - seeding - neuronal death – release of Tau in the extracellular environment - increase in the number of TNTs…). We also made a characterization of the TNTs in primary neurons. This result is really important as it is really complex to identify TNTs in neurons. And in this context, we made a surprising discovery: the endogenous Tau protein is physiologically present in TNTs in primary neurons. These results reveal, for the first time, that the Tau protein, like actin, can be considered as a constitutive component of TNTs in neurons. Thus, it could be used as a marker for TNTs. All these results also highlight a new Tau function and reinforce the multifunctional characteristic of this protein.To confirm the importance of this new pathway in the pathological process, further studies should be considered by analyzing if the transfer of pathological Tau species induces a pathological phenotype in the recipient cell and by looking for the cellular mechanisms involved in the transfer of toxic Tau assemblies by TNTs. In vivo studies on integrated systems such as Caenorhabditis elegans would confirm the involvement of these dynamic structures in the pathological process and identify a new therapeutic target.

O crescente aumento da demanda de tráfego nas redes celulares vem aumentando a necessidade de uma melhor utilização dos recursos do sistema, já que sua expansão é custosa. Nas estações rádio base (ERB), a disponibilidade de largura de faixa de freqüências é limitada e desta maneira, em uma rede de comunicação móvel celular, o controle de admissão de chamadas exerce grande influência no desempenho do sistema, pois determina a utilização de banda das ERBs e se uma determinada quantidade de recursos (banda) será alocado ou não para uma determinada chamada. O desempenho da rede pode ser atrelado a determinados parâmetros, como a probabilidade de bloqueio de novas chamadas, probabilidade de bloqueio de chamadas handoff e a utilização de banda da rede. Este trabalho propõe um controle de admissão de chamadas que, no atendimento de uma chamada, faz o empréstimo de banda de chamadas em andamento na célula no caso de banda insuficiente. O sistema adota um mecanismo heurístico que determina a banda disponível para novas chamadas conforme os valores de certos parâmetros do sistema. O empréstimo de banda é realizado em chamadas em andamento nas células até níveis mínimos estabelecidos para cada tipo de chamada, que se diferenciam pelas necessidades de banda de cada uma. O algoritmo foi aplicado às bandas e características de uma rede de terceira geração (3G), que possui chamadas de voz, videoconferência, interação multimídia, e-mail, downloads e transferência de arquivos e a uma rede GSM/GPRS (global system for mobile communications/ general packet radio service), que possui chamadas de voz e de dados. Os resultados mostram melhorias na probabilidade de bloqueio de novas chamadas, probabilidade de bloqueio de handoff e na utilização de banda do sistema. / The recent growth in traffic loads in cellular networks has seen the need for a better use of system resources as its expansion is expensive. In the base transceiver station (BTS), the bandwidth availability is limited. Thus, in cellular networks the call admission control greatly influences the system performance because it determines the bandwidth use of the BTSs and if an amount of resources will or will not be allocated to a call. The network performance can be evaluated by parameters such as blocking probability of new calls, dropping probability of handoff calls and bandwidth use. This work proposes a call admission control that carries out the bandwidth borrowing when a call arrives and there is not enough bandwidth. The system makes use of a heuristic mechanism that determines the available bandwidth for the new calls according to some parameter values of the system. The bandwidth borrowing is applied to the cell ongoing calls until the minimum levels for each type are met. The algorithm was applied to the bandwidths and characteristics of a third generation cellular network, which supports voice calls, videoconference, multimedia interaction, e-mails, downloads and file transfers. It was also applied to a GSM/GPRS (global system for mobile communications/ general packet radio service), which supports voice and data calls. The results show improvements in the blocking probability of new calls, dropping probability of handoff calls and in the bandwidth use of the system.

Um estudo comparativo entre os principais modelos empíricos e semi-empíricos de predição de nível de sinal para comunicações móveis celulares é descrito neste trabalho. Medidas de cobertura outdoor em ambiente urbano foram comparadas com os resultados simulados a partir dos modelos de Okumura-Hata e Lee, lkegami, Walfisch-Bertoni e Walfisch-Ikegami. As medidas de potência de sinal recebido foram realizadas na cidade de Conceição das Alagoas, MG, a partir da única estação rádio-base (ERB) da cidade, operando na banda A com tecnologia AMPS/TDMA. Foi utilizada como portadora de teste o canal de controle analógico 328. As informações foram coletadas em algumas ruas da cidade, por meio de equipamento instalado em veículo, em diferentes posicionamentos em relação a ERB, de forma a se obter amostras de cobertura em diferentes cenários, seja em visada direta, em obstrução parcial ou total. O modelo de Ikegami se mostrou apropriado para predição de níveis de sinal recebido no ambiente estudado, apresentando desvio médio 5,81 dB em relação às medidas realizadas. / A comparative study among the main empiric and semi-empiric models of prediction of signal leveI for cellular mobile communications is described in this work. Measurements of covering outdoor in an urban environment were compared to the simulated results from the models of Okumura-Hata, Lee, Ikegami, Walfisch-Bertoni and Walfisch-Ikegami. The measurements of received signal level were accomplished in some streets of the city of Conceição das Alagoas, MG, starting from the only radio base station of the city, operating in the A band with AMPS/TDMA technology. The 328-analog control channel was used as test carrier. The measurements were carried out using some equipment installed in a vehicle, in different positions in relation to the radio base station, in order to obtain covering profile in different circunstances such as line-of-sight, non line-of-sight, and partial obstruction. The model of Ikegami was shown appropriate for prediction of the received signal levels in the studied environment, exhibiting an average deviation of 5,81 dB in relation to the accomplished measurements.

PFOS (pluorooctane sulfonic acid) and PCB 180 (2,2′,3,4,4′,5,5′-heptachlorobiphenyl) are endocrine-disrupting chemicals (EDCs) ubiquitously found throughout the environment, given their persistence and extreme long biological half-life. PFOS and PCB 180 are predicted to disrupt retinoic acid receptor (Rar) signaling, interfering with important events of brain development, including neural differentiation and proliferation. Despite accumulating reports on the adversities of these EDCs, studies on the underlying mechanism continue to be largely unknown. The aim of this study was to validate transcriptional markers predictive of Rar disruption and to assess whether the same effects are induced by PFOS and PCB 180 exposure. Murine neural progenitor C17.2 cells were employed to mimic the developing brain. The cells were exposed to increasing nanomolar concentrations (nM) of Rar (ant)agonist, PFOS, and PCB 180. Interestingly, of all the transcriptional markers investigated, Ccn2 (cellular communication network factor 2), Il18 (Interleukin -18), and Ntn1(Netrin 1) were significantly altered by the Rar agonist (P< 0.05). Likewise, the expression of Il18 and Ntn1 was also altered by developmental exposure to PFOS and PCB 180. Altogether, these findings indicate that Il18 and Ntn1 may be promising markers for studying developmental neurotoxicity induced by disruption of the retinoic acid pathway.