Orientador: Dr. José L. Azcue Puma / Dissertação (mestrado) - Universidade Federal do ABC, Programa de Pós-Graduação em Engenharia Elétrica, 2016. / Este trabalho apresenta o estudo, modelagem e projeto de um sistema de conversão de energia para a conexão de um módulo fotovoltaico com a rede elétrica. Nesta pesquisa são abordados três conversores para adequar a energia gerada por um painel fotovoltaico e conectá-la à rede elétrica. O primeiro conversor é um Boost intercalado de dois níveis encarregado de implementar o MPPT (Maximum Power Point Tracking), o segundo conversor é um Ressonante LLC que realiza o isolamento galvânico e o terceiro conversor é um inversor em ponte completa que mantém a tensão de barramento em um valor determinado e realiza a conversão de corrente contínua para corrente alternada. Os três conversores são projetados, calculando os elementos passivos que os compõem e simulando os circuitos obtidos. Também, é realizada a modelagem dos conversores e o projeto dos controladores utilizando a análise de pequenos sinais. Os resultados de simulação são apresentados utilizando os softwares PSIM e MATLAB. Na parte experimental são verificados os dois primeiros conversores usando o kit High Voltage Isolated Solar MPPT fabricado pela Texas Instruments. / This work presents the study, modeling and design of a photovoltaic conversion system for the connection of a photovoltaic module with the grid. In this research three converters are approached to adequate the generated energy for a photovoltaic panel and to transfer the energy to the grid. The first converter is an interleaved two-level boost responsible for implementing the MPPT (Maximum Power Point Tracking) the second converter is a Resonant LLC that performs galvanic isolation and the third converter is a complete bridge inverter that keeps the bus voltage at a certain value and performs the conversion of continuos current to alternating current. The three converters are designed, calculating the passive elements that compose them and simulating the obtained circuits. Also, the modeling of the inverters and the design of the controllers are performed using small signal analysis. Simulation results are presented using the PSIM and MATLAB software. In the experimental part the first two inverters are verified using the High Voltage Isolated Solar MPPT kit manufactured by Texas Instruments.

Na lesão renal aguda, os mecanismos de defesa atuam como genes protetores, como a proteína heat shock 32 (HSP 32), também conhecida como heme oxigenase-1 (HO-1). A polimixina B (PmxB) é um antimicrobiano nefrotóxico. O objetivo deste estudo foi caracterizar a participação da enzima HO-1 na toxicidade da PmxB em células LLC-PK1. As células foram submetidas aos seguintes tratamentos: Controle (CTL- 0µM); Hemin (indutor de HO-1, 25µM); Hemin II (250M), Protoporfirina de zinco (ZnPP - inibidor de HO-1, 10M,); Nitro-L-arginina-metilester (L-NAME - inibidor de iNOS, 0,1mM); PmxB (375µM); PmxB + Hemin (25µM de Hemin uma hora antes da PmxB); PmxB + ZnPP (10M de ZnPP uma hora antes da PmxB); PmxB + Hemin + L-NAME (25M de Hemin e 0,1mM de L-NAME uma hora antes da PmxB). Os grupos foram avaliados em 24 e 72 horas. Foram analisados os seguintes parâmetros: desidrogenase láctica (DHL), peroxidação lipídica (MDA), expressão gênica da HO-1 por RT-PCR, síntese protéica da HO-1 por imunofluorescência, óxido nítrico (NO) pelo método de Griess e expressão protéica da HO-1 e da iNOS por western blotting. Os resultados mostraram que a PmxB elevou o DHL com aumento dos níveis de MDA. O Hemin e a ZnPP elevaram as variáveis DHL, MDA e óxido nítrico (NO). O indutor de HO-1 incrementou a expressão protéica da HO-1 e da iNOS. A PmxB se confirmou como citotóxica e a HO-1 intensificou a lesão por mecanismos oxidativos. O efeito da HO-1 na lesão celular parece ser mediado pelo NO / In the acute kidney injury, the mechanisms of defense act as protector genes, as the protein heat shock 32 (HSP 32), also known as heme oxygenase-1 (HO-1). The polymyxin B (PmxB) is a nephrotoxic antimicrobial. The aim of this study was to distinguish the role of the HO-1 enzyme in the PmxB toxicity in LLC-PK1 cells. The cells were submitted to the following treatments: Control (CTL- 0µM); Hemin (inhibitor of HO-1, 25µM); Hemin II (250M), Zinc protoporphyrin (ZnPP - inhibitor of HO-1, 10M,); NG-nitro-L-arginine methyl ester (L-NAME - inhibitor of iNOS, 0,1mM); PmxB (375µM); PmxB + Hemin (25µM of Hemin one hour before the PmxB); PmxB + ZnPP (10M of ZnPP one hour before the PmxB); PmxB + Hemin + L-NAME (25M of Hemin and 0,1mM of L-NAME one hour before the PmxB). All groups were evaluated in 24 and 72 hours. The following parameters were analysed: lactate dehydrogenase (LDH), lipid peroxidation (MDA), genic expression of HO-1 by RT-PCR, protein syntesis of HO-1 by immunofluorescence, nitric oxide (NO) by Griess method and protein expression of HO-1 and of iNOS by western blotting. The results showed that PmxB increased the LDH and the levels of MDA. Hemin and ZnPP also increased the LDH variables, MDA and nitric oxide (NO). The inducer of HO-1 improved the protein expression of HO-1 and of iNOS. The PmxB was confirmed as a cytotoxic and the HO-1 intensified the failure by oxidative mechanisms. The effect of HO-1 in the cell injury seemed to be mediated by NO

This thesis deals with the issue of switching power supply in terms of noise ratios in the output voltage. In the theoretical part analyzes the basic principle of classical and resonant topology switching power converters in terms of output voltage ripple and switching noise. There are also some possibilities of compensation to minimize switching noise and output ripple. The second part describes the custom design a low noise switching power supply, which is composed of an active power factor corrector, power converters and ripple limiter. The main power converter is designed as an LLC resonant converter. The last part deals with the actual construction of the proposed source, its measurement and presentation of the results.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

De nombreuses données expérimentales et cliniques ont montré l'importance des cellules Natural Killer (NK) dans l'immunosurveillance antitumorale. Les stratégies thérapeutiques basées sur les cellules NK pourraient donc être une alternative de choix dans le traitement de certains types de cancers. Nous avons focalisé notre étude sur deux types de cancer incurables malgré les récents progrès thérapeutiques : la leucémie lymphoïde chronique B (LLC-B) et le cancer de la prostate. Le but de notre étude est une meilleure compréhension des mécanismes mis en place par les cellules B leucémiques et les cellules tumorales prostatiques pour échapper à la réponse antitumorale des cellules NK. La connaissance de ces mécanismes d'échappement est un pré-requis indispensable à l'utilisation des cellules NK dans les thérapies antitumorales. Concernant la LLC-B, nos résultats suggèrent que les cellules NK de patients, fonctionnellement compétentes, ne peuvent pas initier une réaction immunitaire appropriée envers les cellules B leucémiques due au manque de reconnaissance de ces dernières. Concernant le cancer de la prostate, nos données préliminaires montrent que les cellules NK circulantes de patients sont également fonctionnellement compétentes, quelque soit le stade de la maladie, malgré la diminution significative de l'expression du récepteur NKp30. Ainsi, le degré d’immunogénicité des cellules B leucémiques et celui des cellules tumorales prostatiques devra être autant pris en compte que la fonctionnalité des cellules NK dans les stratégies visant à optimiser l'activité antitumorale de ces dernières. / Many experimental and clinical data have enlightened the importance of Natural Killer (NK) cells in tumor immunosurveillance. Therapeutic strategies based on NK cells could be an alternative in the treatment of certain cancers. We focused our study on two types of incurable cancers despite recent advances in treatment: B chronic lymphocytic leukemia (B-CLL) and prostate cancer. The aim of our study is a better understanding of the mechanisms set up by leukemic B cells and prostate cancer cells to escape from NK antitumor response. The knowledge of these escape mechanisms is an essential prerequisite to the use of NK cells in antitumor therapies. Regarding B-CLL, our results suggest that NK cells, although functionally competent, can not initiate an appropriate immune response against leukemic B cells due to a lack of recognition of the latter. Concerning the prostate cancer, our preliminary data show that circulating NK cells are functionally competent, whatever the stage of disease, despite the significant decrease in expression of the receptor NKp30. Thus, the degree of immunogenicity of leukemic B cells and of the prostate cancer cells must be taken into account as well as the functionality of NK cells in strategies aiming at improving NK antitumor activity.

Dans les cellules somatiques, les télomères s'érodent à chaque division cellulaire. Ce processus appelé « Sénescence Réplicative» est contrebalancé de manière basale chez la levure bourgeonnante S. cerevisiae par l'action de la télomérase qui, alors qu'elle est inactive dans les cellules somatiques des eucaryotes supérieures, est activée dans 85% des cancers. Un autre mécanisme impliqué dans les 15% des cas de cancer restants et est appelé Alternative Lengthening of Telomere (ALT). Dans ce processus, le maintien des télomères est assuré par des mécanismes de recombinaison télomérique induisant des échanges de séquences télomériques de chromatides sœurs (T-SCE).Nous avons évalué l'existence d'ALT dans la LLC-B connue pour rarement exprimer la télomérase. Nous avons montrer que 90% des patients LLC-B présentent une diminution de l'expression de TopoIIIα corrélée à une méthylation plus importante des îlots CpG de la région promotrice du gène suggérant que dans les LLC-B le maintien des télomères est défectueux.Nous avons étudié l'implication de la SUMOylation de TopoIIIα/Top3 dans les mécanismes de régulation du ALT. Nous avons montré que TopoIIIα était SUMOylée in vitro et in vivo au sein des cellules U2-OS ALT. Nous avons aussi observé chez S. cerevisiae que Top3 ne serait SUMOylée qu'en absence d'une activité télomérase. Nos résultats suggèrent que la SUMOylation de TopoIIIα augmenterait son activité in vitro et in vivo en diminuant son affinité pour les télomères une fois la recombinaison achevée et qu'elle serait requise pour son accumulation dans les APBs mais pas pour leur formation. / In somatic cells, telomeres erode with each cell division. This process named « Replicative Senescence » is basically counterbalanced in the budding yeast Saccharomyces cerevisiae by the action of telomerase which, while it is inactive in somatic cells of higher eukaryotes is activated in 85 % of cancer cases. Another process of telomere maintenance is involved in 15% of remaining cancer cases and is called Alternative Lengthening of Telomere (ALT). In this process, telomere maintenance is provided by telomeric recombination mechanisms inducing exchange of telomeric sister chromatid (T-SCE).We assessed the existence of an ALT mechanism in B-CLL known to rarely express telomerase. We have shown that 90% of B-CLL patients have a decreased expression of TopoIIIα correlated with largest methylation of CpG islands of the gene promoter region. Our results suggest that in B-CLL, telomere maintenance is defective either by telomerase or ALT mechanism.We investigated the involvement of post- SUMOylation of TopoIIIα/Top3 in mechanisms regulating ALT phenomenon. We have shown that TopoIIIα was SUMOylated in vitro and in vivo in U2-OS ALT cells. We also observed in S. cerevisiae that Top3p might be SUMOylated in absence of telomerase activity. Our results suggested that the SUMOylation of TopoIIIα increased its activity in vitro and in vivo by reducing its affinity for telomeres once recombination occurred and would be required for its accumulation in APBs but not for their formation.

An underlying issue which inheres in any taxation framework relates to the manner in which it operates and the actual distribution of its imposts or appropriations. In this respect, a tax system needs to confront two fundamental (and interrelated) questions – first, precisely how the tax or impost should be imposed and, secondly, who should bear the legal obligation or onus of payment. These issues can be conceptualised not only from a purely legal or positivist perspective, in terms of identifying who will incur the obligation to pay tax, but also in terms of a more economic and instrumental standpoint as to which entity or individual should effectively be paying the tax. These alternatives may not result in the same conclusions, particularly for the taxation of business forms. To provide one example, if the business form has separate legal entity status from its members, should the business form, as a legal person, be subject to tax separately from its members? From a legal standpoint the response to this question is that such a business form should bear the impost. However, from an economical perspective it may be preferable that the business income and/or losses are directly allocated to its members. Indeed, tax transparency (aggregate approach) has been argued as an economically superior model, although it is not without its critics...

In the past, hyperlipidemia (HL) has been shown to affect the pharmacokinetic and pharmacodynamic properties of lipophilic drugs extensively bound to lipoproteins, including halofantrine (HF). The present thesis examined the effect of HL on the biodistribution, metabolism and electrocardiographic (ECG) effects of HF in the poloxamer 407 rat model of HL. The HL state caused unexpected changes in the distribution of HF enantiomers. In contrast to plasma, concentrations of desbutyl-HF (DHF) were much higher in highly perfused tissues. Following in vitro incubation of racemic HF and DHF, HF and DHF enantiomers shifted from the lipoprotein deficient fraction to triglyceride-rich fractions in HL plasma. No significant differences were noted in HF metabolism between NL and HL liver microsomes. It appears that both reduced plasma unbound fraction and lipoprotein associated directed uptake of lipoprotein-bound drug by tissues play roles in enantiomer biodistribution. In everted gut metabolism, formation of DHF enantiomers was inversely proportional to bile concentration whereas addition of lipids in the presence of bile caused a significant decrease in DHF:HF ratio of (-)-enantiomers. Pre-treatment of rats with peanut oil had no significant effect on DHF formation in the incubated sacs or microsomal preparations, nor did it affect the expression of intestinal CYP450. The above results were consistent with previous in vivo evaluations showing that the DHF to HF ratio was decreased by the ingestion of a high fat meal. In the ECG study, HL by itself had no effect on the ECG. In HL rats, plasma but not heart concentrations of the HF enantiomers were significantly higher compared to NL rats. DHF did not impart significant ECG prolonging effects after HF administration. The unbound fraction of HF was the controlling factor for drug uptake by the heart. Despite the lack of difference in HF heart concentrations, the QT and QTc intervals were significantly higher in HL compared to NL rats, suggesting a greater vulnerability towards HF induced QT interval prolongation in the HL state. The HL serum resulted in decreased metabolism of HF enantiomers in the isolated primary rat hepatocytes. Studies with LLC PK1 and NRK 52E cells showed that HF is not a substrate of P-glycoprotein transporters. / Pharmaceutical Sciences

This work presents a new wireless Visible Light Communication lighting system targeted to future Smart Buildings. A digitally controlled LLC resonant dc-dc converter targeted to white LED luminaires is demonstrated. Visible Light Communication is implemented with minimal incremental cost, by operating the LLC converter in burst mode, without causing any visible disturbance. The converter operates with a regulated average LED current by adjusting the switching frequency, while the burst pulse timing is controlled to minimize the current disturbance and minimize the value of the output capacitor. Variable Pulse Position Modulation is used to modulate the data, while supporting a range of dimming settings. A digital demodulation scheme that supports variable frequency transmission is demonstrated. The 80 W, 400 V to 23 V converter experimental prototype has a peak efficiency of 93.8 %. The bit error rate of the complete system is fully characterized versus distance and angle.

No description available.