Study of compressible turbulent flows in supersonic environment by large-eddy simulation

A Large-Eddy Simulation (LES) methodology adapted to the resolution of high Reynolds number turbulent flows in supersonic conditions was proposed and developed. A novel numerical scheme was designed, that switches from a low-dissipation central scheme for turbulence resolution to a flux difference splitting scheme in regions of discontinuities. Furthermore, a state-of-the-art closure model was extended in order to take compressibility effects and the action of shock / turbulence interaction into account. The proposed method was validated against fundamental studies of high speed flows and shock / turbulence interaction studies. This new LES approach was employed for the study of shock / turbulent shear layer interaction as a mixing-augmentation technique, and highlighted the efficiency in mixing improvement after the interaction, but also the limited spatial extent of this turbulent enhancement. A second practical study was conducted by simulating the injection of a sonic jet normally to a supersonic crossflow. The validity of the simulation was assessed by comparison with experimental data, and the dynamics of the interaction was examined. The sources of vortical structures were identified, with a particular emphasis on the impact of the flow speed onto the vortical evolution.Ph.D.Committee Chair: Menon, Suresh; Committee Member: Ruffin, Stephen; Committee Member: Sankar, Lakshmi; Committee Member: Seitzman, Jerry; Committee Member: Stoesser, Thorste

La gouvernance autochtone en milieu urbain: le cas de Montréal

Au fil des années, les Autochtones ont obtenu la reconnaissance par l’État canadien de certains droits inhérents, soit le droit à l’autodétermination et le droit à l’autonomie gouvernementale. Cependant, lors de la mise en places d’initiatives de gouvernance autochtone, les différents niveaux de gouvernement ont présumé que les groupes revendicateurs disposaient d’une assise territoriale pour réaliser ces objectifs, telles les communautés d’origine des Premières nations, Inuites ou métisses. Or, ces modèles sont inadéquats pour la majorité des Autochtones au pays qui vivent en milieu urbain, une population hétérogène, disparate, très mobile et surtout sans assise territoriale. Pour tenter de concilier l’exercice de l’autonomie gouvernementale avec l’urbanité, certains modèles théoriques de gouvernance ont été élaborés afin de permettre une meilleure représentation politique aux Autochtones en milieu urbain. En gardant à l’esprit la situation de Montréal, c’est-à-dire le problème de l’identité du titulaire du droit à l’autodétermination, le territoire et la nature des pouvoirs à exercer, nous tenterons au cours de ce mémoire de déterminer quel modèle de gouvernance autochtone serait le plus approprié pour les Autochtones de Montréal.In recent years, Aboriginals have obtained from the Canadian State recognition of certain inherent rights, including the right to self-determination and the right to self-government. However, when implementing Aboriginal governance initiatives, the various levels of government have operated on the assumption that Aboriginal groups all have a land base on which they can achieve their objectives, such as First Nations, Inuit and Métis home communities. These models are inadequate for the majority of Aboriginals who live in urban areas and who form a diverse and extremely mobile population without a land base. In order to reconcile the exercise of self-government and urbanity, new theoretical models of governance were developed to provide for better political representation of urban Aboriginals. By taking into account the issue of identifying who holds the right to self-determination, the nature of powers to be exercised and the area over which they would be exercised, we will attempt to determine in this thesis which Aboriginal governance model is best suited for Montreal’s Aboriginal population

A Ralstonia solanacearum type III effector directs the production of the plant signal metabolite trehalose-6-phosphate

The plant pathogen Ralstonia solanacearum possesses two genes encoding a trehalose-6-phosphate synthase (TPS), an enzyme of the trehalose biosynthetic pathway. One of these genes, named ripTPS, was found to encode a protein with an additional N-terminal domain which directs its translocation into host plant cells through the type 3 secretion system. RipTPS is a conserved effector in the R. solanacearum species complex, and homologues were also detected in other bacterial plant pathogens. Functional analysis of RipTPS demonstrated that this type 3 effector synthesizes trehalose-6-phosphate and identified residues essential for this enzymatic activity. Although trehalose-6-phosphate is a key signal molecule in plants that regulates sugar status and carbon assimilation, the disruption of ripTPS did not alter the virulence of R. solanacearum on plants. However, heterologous expression assays showed that this effector specifically elicits a hypersensitive-like response on tobacco that is independent of its enzymatic activity and is triggered by the C-terminal half of the protein. Recognition of this effector by the plant immune system is suggestive of a role during the infectious process.Ralstonia solanacearum, the causal agent of bacterial wilt disease, infects more than two hundred plant species, including economically important crops. The type III secretion system plays a major role in the pathogenicity of this bacterium, and approximately 70 effector proteins have been shown to be translocated into host plant cells. This study provides the first description of a type III effector endowed with a trehalose-6-phosphate synthase enzymatic activity and illustrates a new mechanism by which the bacteria may manipulate the plant metabolism upon infection. In recent years, trehalose-6-phosphate has emerged as an essential signal molecule in plants, connecting plant metabolism and development. The finding that a bacterial pathogen could induce the production of trehalose-6-phosphate in plant cells further highlights the importance of this metabolite in multiple aspects of the molecular physiology of plants

Sobre la corrosión de armaduras de hormigón en presencia de cloruros

The purpose of this study is to give a scientific justification to some empirical results, in steel corrosion field, from concrete containing chlorides. First, it appears that corrosion products on the steels, have different structures and natures in function of the chloride content would be inferior or superior to a characteristic value. Second, the penetration of the chlorides in the concrete can be described by a simple Fick's diffusion law in the most frecuent cases. When cement has a high proportion of tricalcium aluminates and the concrete a small porosity, Fick's law cannot be applied.Este estudio pretende dar a ciertos resultados empíricos, una justificación científica en el campo de la corrosión de los aceros, en un hormigón que contenga cloruros. En primer lugar, se pone de manifiesto que los productos de corrosión sobre los aceros tienen estructuras y naturalezas diferentes, en función de que el contenido de cloruro sea inferior o superior a un valor característico. En segundo lugar, se puede describir la penetración de los cloruros en el hormigón por una sencilla ley de difusión de Fick, en los casos más frecuentes. Cuando el cemento contiene una elevada proporción de aluminato tricálcico, y el hormigón poca porosidad, no se aplica la ley de Fick

Effects of copper sulfate-oxidized or myeloperoxidase- modified LDL on lipid loading and programmed cell death in macrophages under hypoxia

Atheromatous plaques contain heavily lipid-loaded macrophages that die, hence generating the necrotic core of these plaques. Since plaque instability and rupture is often correlated with a large necrotic core, it is important to understand the mechanisms underlying foam cell death. Furthermore, macrophages within the plaque are associated with hypoxic areas but little is known about the effect of low oxygen partial pressure on macrophage death. The aim of this work was to unravel macrophage death mechanisms induced by oxidized low-density lipoproteins (LDL) both under normoxia and hypoxia. Differentiated macrophages were incubated in the presence of native, copper sulfate-oxidized, or myeloperoxidase-modified LDL. The unfolded protein response, apoptosis, and autophagy were then investigated. The unfolded protein response and autophagy were triggered by myeloperoxidase-modified LDL and, to a larger extent, by copper sulfate-oxidized LDL. Electron microscopy observations showed that oxidized LDL induced excessive autophagy and apoptosis under normoxia, which were less marked under hypoxia. Myeloperoxidase-modified LDL were more toxic and induced a higher level of apoptosis. Hypoxia markedly decreased apoptosis and cell death, as marked by caspase activation. In conclusion, the cell death pathways induced by copper sulfate-oxidized and myeloperoxidase-modified LDL are different and are differentially modulated by hypoxia

Effects of copper sulfate-oxidized or myeloperoxidase-modified LDL on lipid loading and programmed cell death in macrophages under hypoxia

Atheromatous plaques contain heavily lipid-loaded macrophages that die, hence generating the necrotic core of these plaques. Since plaque instability and rupture is often correlated with a large necrotic core, it is important to understand the mechanisms underlying foam cell death. Furthermore, macrophages within the plaque are associated with hypoxic areas but little is known about the effect of low oxygen partial pressure on macrophage death. The aim of this work was to unravel macrophage death mechanisms induced by oxidized low-density lipoproteins (LDL) both under normoxia and hypoxia. Differentiated macrophages were incubated in the presence of native, copper sulfate-oxidized, or myeloperoxidase-modified LDL. The unfolded protein response, apoptosis, and autophagy were then investigated. The unfolded protein response and autophagy were triggered by myeloperoxidase-modified LDL and, to a larger extent, by copper sulfate-oxidized LDL. Electron microscopy observations showed that oxidized LDL induced excessive autophagy and apoptosis under normoxia, which were less marked under hypoxia. Myeloperoxidase-modified LDL were more toxic and induced a higher level of apoptosis. Hypoxia markedly decreased apoptosis and cell death, as marked by caspase activation. In conclusion, the cell death pathways induced by copper sulfate-oxidized and myeloperoxidase-modified LDL are different and are differentially modulated by hypoxia

Low Cognitive Awareness, but Not Complaint, is a Good Marker of Preclinical Alzheimer's Disease

Subjective cognitive decline (SCD) may result from many conditions, including Alzheimer's disease (AD)