This Master´s thesis describes different methods of wireless transmitting of energy: electromagnetic induction, electrostatic induction, laser radiation, transfer of energy by microwaves. This thesis is focused on wireless transfer of energy by microwaves. The paper describes the individual parts of the rectenna. Comparison of different types of antennas for use in the rectenna was made. In this thesis is described set of requirements for design of rectenna. Was made design of the rectenna and its simulation.

This diploma thesis deals with the research of the effect of free surface flow forces on the rectifying element and consists of several parts. The first part processes and evaluates the measured values from a physical model. In the next part measurement is checked according to hydraulic laws. In the third part comparison of both methods is created.

L'amélioration de l'autonomie énergétique des systèmes communicants constitue aujourd'hui une des préoccupations majeures pour leur déploiement massif dans notre environnement. On souhaite rendre complètement autonome ces dispositifs électroniques (on pense entre autres aux capteurs et réseaux de capteurs) en s'affranchissant des sources d'énergie embarquées qui nécessitent des opérations de remplacement ou de recharge périodiques. Parmi les sources d'énergie disponibles qui peuvent être exploitées, on trouve les ondes électromagnétiques. Le dispositif qui permet de capter cette énergie et la convertir en puissance continue utile est dénommé Rectenna (Rectifying antenna) qui associe une antenne de captation à un circuit de rectification à base de diodes. Les rectennae ont fait l'objet d'un nombre important de communications dans la littérature ces dernières années avec pour fil conducteur, la recherche de performances optimales compte tenu de l'atténuation des ondes électromagnétiques et des faibles niveaux de champ récupérés. C'est dans ce contexte que s'est déroulé ce travail de thèse dont le financement a été assuré par un contrat ANR (REC-EM).Dans ce travail, on s'est attaché à développer, à concevoir et à caractériser expérimentalement des structures planaires qui présentent des propriétés intéressantes :- En terme de polarisations orthogonales, ceci de façon à s'affranchir de l'orientation arbitraire de l'onde incidente à la rectenna. Une rectenna à double polarisation circulaire à 2.45 GHz et à double accès sera réalisée pour, de plus, s'affranchir de la perte de 3 dB lorsque l'onde récupérée est à polarisation linéaire à orientation arbitraire.- En termes de résonances multiples, ceci pour augmenter le niveau de puissance récupérée par l'antenne et optimiser la puissance continue convertie. Une rectenna à double fréquence (1.8 et 2.45 GHz) et à accès unique sera conçue ainsi qu'une rectenna constituée d'un réseau de deux antennes double fréquence.- En terme de réduction de taille en s'affranchissant de l'utilisation du filtre HF entre l'antenne et le circuit de conversion ceci pour l'ensemble des structures rectennae développées dans ce travail. Dans tous les cas, il sera nécessaire de développer le circuit de rectification le plus adapté à la topologie de l'antenne de captation et évaluer la technique de recombinaison optimale coté DC pour s'affranchir au mieux des déséquilibres qui peuvent apparaître entre les voies d'accès de l'antenne. Pour contenir les dimensions de la structure globale, des circuits mono diode seront dimensionnés et réalisés pour chacune des structures. Enfin, on exploitera l'antenne à double polarisation circulaire double accès, dont on cherchera à diminuer les dimensions, pour alimenter un capteur de température à affichage LCD. Pour augmenter le niveau de tension nécessaire au fonctionnement du capteur, nous associerons entre la rectenna et le capteur un convertisseur DC-DC. Il s'agit, dans ce cas, d'un dispositif de gestion d'énergie adapté pour les faibles puissances. Deux convertisseurs seront employés dont celui développé par les laboratoires Ampère de l'Ecole Centrale de Lyon et SATIE à l'ENS Cachan. Ce convertisseur a fait l'objet d'une thèse également financée par l'ANR dans le cadre de ce contrat REC-EM / Improving energy autonomy of communication systems constitutes one of the major concerns for their massive deployment in our environment. We want to make these electronic devices (sensors and sensor networks) completely autonomous, avoiding the embedded energy sources that require replacement operations or periodic charging. Among the available energy sources that can be harvested, there are electromagnetic waves. The device that can capture this energy and convert it into useful DC power is called Rectenna (Rectifying antenna), combining antenna with diode-based rectifier. In recent few years, rectennas have reached a significant number of papers in the literature. The main challenge consists in improving performances in term of efficiency, in an attempt to overcome the electromagnetic wave attenuation and the low available field level. According to this context, this PhD work supported by the ANR project REC-EM has taken place. In this study, we have developed, designed and characterized planar structures that have interesting properties:- In term of orthogonal polarizations, so energy harvesting becomes feasable regardless the arbitrary orientation of the incident wave on the rectenna. A dual-circularly polarized rectenna at 2.45 GHz with dual-access will be set up to overcome the 3 dB power loss in the case of linearly-polarized incident wave with unknown orientation.- In term of multiple resonances, so the amount of total RF power collected by the antenna can be increased and consequently the converted DC power level can also be improved. A dual-frequency rectenna (1.8 and 2.45 GHz) with single access will be designed, as well as a rectenna based upon a dual-frequency antenna array.- In term of size compactness by avoiding the use of the HF filter between the antenna and the rectifier for all developed rectenna structures during this work. In all cases, it will be necessary to define the most suitable rectifier topology to each antenna and select, if it is appropriated, the optimum DC recombination technique to overcome the effects of RF power imbalance that may occur between the different antenna accesses. Besides, single-diode circuits will be designed and fulfilled for each structure. Finally, we will miniaturize the dual-circularly polarized dual-access antenna, and exploit it to power a LCD display temperature sensor. To enhance the DC voltage level required to activate the sensor, a DC-DC converter is inserted between the rectenna and the sensor. Such energy management device should be able to operate under low delivered DC power. Two converters will be used. The first one is developed by Ampere Lab at Ecole Centrale de Lyon and SATIE Lab at ENS Cachan. This converter was the subject of another dissertation also supported by the ANR under the REC-EM project

The main aim of this graduation theses was to characterize the bad debt and is then analyzed in the reporting entity. The most important part of this graduation theses is aplication of lawful rectifying item and amortization of debts in practice and after that resulting effect on tax base and income range. After a complete analysis and mapping of debts can be stated that the company has an overview of overdue debts, records all borrowers and applied hedge funds. Also accounting entity should not fear to make up rectifying items to overdue debts because if they will be in step with law No. 593/1992 Sb. about backlog for finding the base of income tax it can have the only the positive impact for the base tax and high of tax as well.

The main aim of this graduation theses was assessment of outstandings from accountant and tax point of view. To analyse outstandings in concrete accounting entity and find out the way of its security of debt and debt recovery after term of expiration. The most important part of this graduation theses is aplication of lawful rectifying item and amortization of debts in practice and after that resulting effect on tax base and income range.

L’agression de l'organisme par un agent physique, psychique ou émotionnel déclenche une réponse physiologique et comportementale qui permet à un individu de se prévenir du danger et de maintenir sa survie. Le système nerveux central a depuis longtemps été identifié comme un majeur acteur de cette réponse adaptative. Cependant, une exposition prolongée au stress conduit à des adaptations cellulaires et des réadaptations de circuits neuronaux qui contribuent à l'émergence de troubles neuropsychiatriques. L’interaction entre le système dopaminergique (DA) et sérotoninergique (5HT) a été impliquées dans ces réarrangements physiologiques et pathologiques qui influencent les comportements motivationnels de l'individu face à une menace. Fait intéressant, l'habenula latérale (Hbl), une région du cerveau très conservée entre les espèces, contrôle directement et indirectement les systèmes DA et 5HT, et son activité est modulée par des stimuli aversifs chez les humains et les animaux. De plus, l'activité de la Hbl est augmentée chez des modèles animaux de la dépression ou lors de l'induction d'un épisode dépressif chez des patients humains. Inversement, l’emploie de stratégies ayant pour cible la Hbl permettent d’améliorer certains symptômes dépressifs à la fois chez les modèles animaux de dépression et chez l’homme. Ainsi, la dérégulation de l’Hbl pourrait jouer un rôle dans l'apparition de symptômes dépressifs. Cependant, les changements moléculaires et cellulaires précoces qui occurrent au niveau de Hbl suite à l'exposition continue à un environnent aversifs restent peu connus. De plus, la plupart des modèles animaux utilisés pour interroger le rôle de Hbl dans l'état dépressif implique une exposition répétée de l’animal à des stimuli douloureux. Si la fonction de l’Hb est aberrante lors d’une exposition chronique à d’autre type de stress reste méconnu. Dans mon travail de thèse, je me suis intéressée aux adaptations cellulaires et moléculaires au niveau des neurones Hbl suite à l’exposition de différents types d'expériences aversives et leurs relatives importances pour l'expression de symptômes dépressifs. Plus précisément, je présente dans ce manuscrit, les résultats d'un premier travail qui vise à identifier les adaptations cellulaires et moléculaires de Hbl suite à l’exposition de souris à des chocs électriques et leurs rôles dans l'émergence de symptômes dépressifs. Cette étude montre que l’exposition à de brefs aléatoires chocs électriques entraine une diminution de l’expression de surface de récepteur métabotropiques gamma-aminobutyrate B (GABABRs), et par conséquent une diminution de leur fonction au niveau des neurones de l’Hbl. GABABR est un récepteur métabotropique couplé à la protéine Gi, il hyperpolarise les neurones de l’Hbl 4.par l'activation du canal potassique GIRK. La diminution de la signalisation GABABR-GIRK est accompagnée par une augmentation de l'activité de la protéine phosphatase 2 (PP2A), reconnue pour induire l’endocytose du complexe GABABR-GIRK. GABABR-GIRK contrôle étroitement l'activité Hbl, et par conséquent une diminution de leurs fonctions conduit à l’hyperexcitabilité des neurones de l’Hbl. En adoptant des stratégies visant à restaurer spécifiquement la signalisation GABABR-GIRK dans l’Hbl, telle que la surexpression GIRK, ou l'inhibition pharmacologique locale de l'activité PP2A, nous avons observé une amélioration de certains symptomes « dépressifs », établissant ainsi un lien causal entre l’aberrante diminution du signal GABABR et certain aspect de l’état dépressifs. / Prolonged exposure to aversive stimuli leads to cellular and circuit adaptations that contribute to the emergence of neuropsychiatric disorders such as depression. Interactions between the dopaminergic (DA) and the serotoninergic (5HT) systems have been implicated in these pathological adaptations ultimately influencing motivated behaviors. Interestingly, the lateral habenula (LHb), an ethologically well-conserved epithalamic region, directly and indirectly controls DA and 5HT systems, and its activity is modulated by aversive events in both humans and animals. Moreover, the activity of the LHb increases in animal models of depression and depressed human patients. Conversely, strategies that locally target the LHb have been shown to reverse depressive-like symptoms both in animal models and in humans. Altogether, this led to the hypothesis that LHb dysregulation could play a role in the emergence of depressive like symptoms. However, little is known about the early cellular and molecular adaptations that occur within the LHb after exposure to aversive events. Moreover, most of the animal models employed to interrogate the LHb role in depressive states used acute painful stimuli; whether LHb function becomes aberrant after chronic exposure to painless stressors remain elusive. In my thesis work, I explored the precise cellular and molecular adaptations of LHb neurons following exposure to different kind of unpredictable aversive experiences, and their importance for the expression of depressive like symptoms.More precisely, I will present the results of an initial work aiming to identify early cellular and molecular adaptations within the LHb following unpredictable stimuli and their importance for the emergence of depressive symptoms. This study shows that unpredictable foot-shocks lead to decreased surface expression and function of the gamma-aminobutyrate receptor (GABABR), a metabotropic receptor that hyperpolarizes LHb neurons through the activation of the G protein-coupled inwardly-rectifying potassium channels (GIRKs). This decrease of GABABR-GIRK signaling went along with an upregulation of the activity of the protein phosphatase 2 (PP2A), which is a well-known down-regulator of GABAB-GIRK complex surface expression. GABABR-GIRK signaling tightly controls LHb activity, and its downregulation consequently leads to aberrant hyperexcitability of LHb neurons. Using specific strategies to restore the GABABR-GIRK signaling within the LHb, such as GIRK overexpression, or local pharmacological inhibition of PP2A activity, we were able to ameliorate depressive like states following unpredictable foot-shocks. The second study allowed instead to establish the cellular adaptations within the LHb following a chronic non-painful aversive experience and during a critical developmental period. I showed that exposure to maternal separation in childhood (MS mice) also leads to depressive like symptoms together with a hyperexcitability of LHb neurons. This stress-driven increase in LHb activity was causally linked to a decrease of the GABABR-GIRK signaling. Moreover, using diverse reversal strategies such as chemogenetics or a therapeutically-relevant intervention such as Deep Brain Stimulation (DBS), we could selectively decrease LHb neuronal activity and consequently ameliorate the depressive like symptoms, suggesting a causal link between these two phenotypes.Altogether, the work presented in this thesis suggests that LHb neuronal hyperexcitability could represent a common substrate necessary for the expression of certain aspects of the depressive like state and further supports its relevance as a potential target in the treatment of this disorder.

No description available.

Functional hyperaemia is an important mechanism by which increased neuronal activity is matched by a rapid and regional increase in blood supply. This mechanism is facilitated by a process known as “neurovascular coupling” – the orchestrated communication system involving the cells that comprise the neurovascular unit (neurons, astrocytes and the smooth muscle and endothelial cells lining arterioles). Blood flow regulation and neurovascular coupling are altered in several pathological states including hypertension, diabetes, Alzheimer’s disease, cortical spreading depression and stroke. By adapting and extending other models found in the literature, we create, for the first time, a mathematical model of the entire neurovascular unit that is capable of simulating two separate neurovascular coupling mechanisms: a potassium- and EET-based and a NO-based mechanism. These models successfully account for several observations seen in experiment. The potassium/EET-based mechanism can achieve arteriolar dilations similar in magnitude (3%) to those observed during a 60-second neuronal activation (modelled as a release of potassium and glutamate into the synaptic cleft). This model also successfully emulates the paradoxical experimental finding that vasoconstriction follows vasodilation when the astrocytic calcium concentration (or perivascular potassium concentration) is increased further. We suggest that the interaction of the changing smooth muscle cell membrane potential and the changing potassium-dependent resting potential of the inwardly rectifying potassium channel are responsible for this effect. Furthermore, our simulations demonstrate that the arteriolar behaviour is profoundly affected by depolarization of the astrocytic cell membrane, and by changes in the rate of perivascular potassium clearance or the volume ratio between the perivascular space and astrocyte. In the modelled NO-based neurovascular coupling mechanism, NO exerts its vasodilatory effects via neuronal and endothelial cell sources. With both sources included, the model achieves a 1% dilation due to a 60-second neuronal activation. When the endothelial contribution to NO production is omitted, the arteriole is more constricted at baseline. Without the endothelial NO contribution, the arteriolar change in diameter during neuronal activity is greater (6%). We hypothesize that NO has a dual purpose in neurovascular coupling: 1) it dixxxvi rectly mediates neurovascular coupling through release by neuronal sources, and 2) it indirectly modulates the size of the neurovascular coupling response by determining the baseline tone. Our physiological models of neurovascular coupling have allowed us to replicate, and explain, some of the phenomena seen in both neurovascular coupling-oriented and clinicallyoriented experimental research. This project highlights the fact that physiological modelling can be used as a tool to understand biological processes in a way that physical experiment cannot always do, and most importantly, can help to elucidate the cellular processes that induce or accompany our most debilitating diseases.

Der Morbus Parkinson ist die häufigste Erkrankung der Basalganglien und wird durch einen Abbau der dopaminergen Neurone in der Substantia nigra des Mittelhirns verursacht. Um Wege zu finden, die Nebenwirkungen bisheriger Therapien dieser Erkrankung zu vermeiden, sollten neue Angriffspunkte für pharmakologische Interventionen gesucht werden. Prinzipiell ist dabei jeder Schritt einer Signaltransduktions-Kaskade zu prüfen. Dazu gehören präsynaptische Transmitterfreisetzung, G-Protein-gesteuerte Effektormechanismen oder Veränderungen prä- und postsynaptischer Potentiale, wie sie durch ein bestimmtes lokales Ionenkanalmuster festgelegt werden. Aufgrund ihrer enormen molekularen Vielfalt bei gleichzeitig weiter, aber spezifischer Verbreitung, stellen Kaliumkanäle interessante Angriffspunkte für neue therapeutische Strategien dar. Die vorliegende Arbeit untersucht die zelluläre und subzelluläre Verteilung aller Mitglieder der Kir2-Familie, einer Gruppe von Proteinen, die einwärts-gleichrichtende Kaliumkanäle bildet. Zu diesem Zweck wurden polyklonale, monospezifische, affinitätsgereinigte Antikörper gegen den wenig konservierten carboxyterminalen Anteil der Kir2.1-, Kir2.2-, Kir2.3- und Kir2.4-Proteine hergestellt. Alle Untereinheiten der Kir2-Familie wurden an den Somata und Dendriten der meisten striatalen Neurone nachgewiesen. Zwei dieser Kanäle zeigten jedoch ein inhomogenes Verteilungsmuster: Das "patch"-Kompartiment des Striatums wurde von der Expression des Kir2.3-Kanals ausgespart, und das Kir2.4-Protein wurde am stärksten auf den tonisch aktiven, cholinergen striatalen Interneuronen exprimiert. Diese beiden Strukturen stellen die Schlüsselstellen für die Kontrolle und Regulation der dopaminergen und cholinergen Transmission im Striatum dar, weswegen ihnen eine zentrale Rolle für die efferenten Projektionen der Basalganglien zukommt. Die nachgewiesene heterogene Lokalisation der Kir2.3- und Kir2.4-Untereinheit an diesen strategisch relevanten Strukturen macht diese Kanäle zu viel versprechenden Angriffspunkten für zukünftige Pharmakotherapien. / Parkinson’s disease is the most frequent movement disorder caused by loss of dopaminergic neurons in the midbrain. Intentions to avoid side effects of conventional therapy should aim to identify additional targets for potential pharmacological intervention. In principle, every step of a signal transduction cascade, such as presynaptic transmitter release, type and occupation of postsynaptic receptors, G protein-mediated effector mechanisms, and the alterations of pre- or postsynaptic potentials as determined by the local ion channel composition, have to be considered. Due to their diversity and their widespread but distinct localizations, potassium channels represent interesting candidates for new therapeutic strategies. As a first step, the present report aimed to study the cellular and subcellular distribution of the individual members of the Kir2 family in the striatum, a group of proteins forming inwardly rectifying potassium channels. For this purpose polyclonal, monospecific, affinity purified antibodies against the less conserved carboxyterminal sequences from the Kir2.1, Kir2.2, Kir2.3, and Kir2.4 proteins were prepared. All subunits of the Kir2 family were detected on somata and dendrites of most striatal neurons. However, the distribution of two of them was not homogeneous. Striatal patch areas were largely devoid of the Kir2.3 protein, and the Kir2.4 subunit was most prominently expressed on the tonically active, giant cholinergic interneurons of the striatum. These two structures are among the key players in regulating dopaminergic and cholinergic neurotransmission within the striatum, and therefore are of major importance for the output of the basal ganglia. The heterogeneous localization of the Kir2.3 and the Kir2.4 subunits with respect to these strategic structures pinpoints these channel proteins as promising targets for future pharmacological efforts.

Inwardly rectifying potassium (Kir) channels establish and regulate the resting membrane potential of excitable cells in the heart, brain and other peripheral tissues. Phosphatidylinositol- 4,5-bisphosphate (PIP2) is a key direct activator of ion channels, including Kir channels. Gasotransmitters, such as carbon monoxide (CO), have been reported to regulate the activity of Kir channels by altering channel-PIP2 interactions. We tested, in a model system, the effects and mechanism of action of another important gasotransmitter, hydrogen sulfide (H2S) thought to play a key role in cellular responses under ischemic conditions. Direct administration of sodium hydrogen sulfide (NaHS), as an exogenous H2S source, and expression of cystathionine γ-lyase (CSE), a key enzyme that produces endogenous H2S in specific brain tissues, resulted in comparable current inhibition of several Kir2 and Kir3 channels. A “tag switch” assay provided biochemical evidence for sulfhydration of Kir3.2 channels. The extent of H2S regulation depended on the strength of channel-PIP2 interactions: H2S regulation was attenuated when strengthening channel-PIP2 interactions and was increased when channel-PIP2 interactions were weakened by depleting PIP2 levels via different manipulations. These H2S effects took place through specific cytoplasmic cysteine residues in Kir3.2 channels, where atomic resolution structures with PIP2 gives us insight as to how they may alter channel-PIP2 interactions. Mutation of these residues abolished H2S inhibition, and reintroduction of specific cysteine residues into the background of the mutant lacking cytoplasmic cysteine residues, rescued H2S inhibition. Molecular dynamics simulation experiments provided mechanistic insights as to how sulfhydration of specific cysteine residues could lead to changes in channel-PIP2 interactions and channel gating.