Combinaison de puissance hyperfréquence à faibles pertes et compacte

This PhD thesis deals with planar architecture design development of low loss and compact power combiner for solid-state high power amplification in X-band. The design is based on the study of innovative multilayer air dielectric stripline transmission structures. A reliable printed circuit process allows to obtain low loss, compact and replicable stripline structures. Electromagnetic FEM and thermal studies are proposed to evaluate transmission structures performances in X-band. Two compact and scalable structures were developed and may be integrated into complex multilayer systems. Finally a cooling system with periodic ceramic contacts is developed to improve the power handling capability of these stripline structures up to 50 W. The study, development and benchmark of these stripline structures demonstrated their compactness and low loss behaviour. Ultimately, these attributes make them excellent candidates for high power solid-state emitters.Ces travaux de thèse concernent le développement de combineur de puissance faibles pertes et compact selon une architecture planaire pour des applications amplificateur de forte puissance à état solide en bande X. La conception du combineur de puissance s’appuie sur l’étude de structures multicouches faibles pertes et compactes en triplaque à air suspendu. Une étude électromagnétique et thermique est proposée pour déterminer les performances de ces structures de transmission dans la bande X. Un système de refroidissement est également mis en place pour permettre aux structures de transmission de tenir des puissances moyenne de l’ordre de 50 W. La réalisation et la caractérisation de ces structures triplaques à air ont permis de démontrer les caractéristiques de faibles pertes et de compacité de ces circuits imprimés. Cette technologie triplaque à air suspendue est alors compatible pour des applications de forte puissance comme les émetteurs à état solide

Development of a Smart Application for Police Crash Reports

Gaining a significant amount of time to help police work Developing a User Friendly Interface Optimizing the GPS Gaining a significant amount of time to help police work Developing a User Friendly Interface Optimizing the bar code scan technology Application for MC 75 mobile technolog

Flooding dynamics within an Amazonian floodplain: water circulation patterns and inundation duration

Hydrodynamic

Physico-chemical qualities and potentials for biochar agro- environmental valorization

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Characterization of biochars by nuclear magnetic resonance

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MicroRNA-138 and microRNA-25 down-regulate mitochondrial calcium uniporter, causing the pulmonary arterial hypertension cancer phenotype

Rationale: Pulmonary arterial hypertension (PAH) is an obstructive vasculopathy characterized by excessive pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and apoptosis resistance. This cancer-like phenotype is promoted by increased cytosolic calcium ([Ca2+]cyto), aerobic glycolysis, and mitochondrial fission. Objectives: To determine how changes in mitochondrial calcium uniporter (MCU) complex (MCUC) function influence mitochondrial dynamics and contribute to PAH’s cancer-like phenotype. Methods: PASMCs were isolated from patients with PAH and healthy control subjects and assessed for expression of MCUC subunits. Manipulation of the pore-forming subunit, MCU, in PASMCs was achieved through small interfering RNA knockdown or MCU plasmid-mediated up-regulation, as well as through modulation of the upstream microRNAs (miRs) miR-138 and miR-25. In vivo, nebulized anti-miRs were administered to rats with monocrotaline-induced PAH. Measurements and Main Results: Impaired MCUC function, resulting from down-regulation of MCU and up-regulation of an inhibitory subunit, mitochondrial calcium uptake protein 1, is central to PAH’s pathogenesis. MCUC dysfunction decreases intramitochondrial calcium ([Ca2+]mito), inhibiting pyruvate dehydrogenase activity and glucose oxidation, while increasing [Ca2+]cyto, promoting proliferation, migration, and fission. In PAH PASMCs, increasing MCU decreases cell migration, proliferation, and apoptosis resistance by lowering [Ca2+]cyto, raising [Ca2+]mito, and inhibiting fission. In normal PASMCs, MCUC inhibition recapitulates the PAH phenotype. In PAH, elevated miRs (notably miR-138) down-regulate MCU directly and also by decreasing MCU’s transcriptional regulator cAMP response element–binding protein 1. Nebulized anti-miRs against miR-25 and miR-138 restore MCU expression, reduce cell proliferation, and regress established PAH in the monocrotaline model. Conclusions: These results highlight miR-mediated MCUC dysfunction as a unifying mechanism in PAH that can be therapeutically targeted