18 research outputs found

    Biological responses in stented arteries

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    Vascular walls change their dimension and mechanical properties in response to injury such as balloon angioplasty and endovascular stent implantation. Placement of bare metal stents induces neointimal proliferation/restenosis which progresses through different phases of repair with time involving a cascade of cellular reactions. These phases just like wound healing comprise distinct steps consisting of thrombosis, inflammation, proliferation, and migration followed by remodelling. It is noteworthy that animals show a rapid progression of healing after stent deployment compared with man. During stenting, endothelial cells are partially to completely destroyed or crushed along with medial wall injury and stretching promoting activation of platelets, and thrombus formation accompanied by inflammatory reaction. Macrophages and platelets play a central role through the release of cytokines and growth factors that induce vascular smooth muscle cell accumulation within the intima. Smooth muscle cells undergo complex phenotypic changes including migration and proliferation from the media towards the intima, and transition from a contractile to a synthetic phenotype; the molecular mechanisms responsible for this change are highlighted in this review. Since studies in animals and man show that smooth muscle cells play a dominant role in restenosis, drugs like rapamycin and paclitaxel have been coated on stent with polymers to allow local slow release of drugs, which have resulted in dramatic reduction of restenosis that was once the Achilles' heel of interventional cardiologist

    Case Report: Tracheal infiltration with wheezing revealing Hodgkin's disease [version 2; peer review: 2 approved]

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    Hodgkin's disease with an initial tracheobronchial involvement is not common. The symptoms might be misleading, resulting in a diagnosis delay. We report the case of a 38-year-old woman with a one-month history of wheezing associated with a dry cough. The physical examination revealed a good general state of health, bilateral wheezing and supra-clavicular lymphadenopathy. The adenopathy biopsy's histopathology revealed Hodgkin lymphoma. The whole body FDG-PET scan was an important tool to assess the diagnosis as well as for the staging. The patient was treated with chemotherapy. Another unusual aspect is the tracheobronchial metastasis confirmed by a bronchial biopsy. Thus, our patient was put on a second-line chemotherapy. She died one year after the initial diagnosis. To conclude, it is an atypical clinical presentation of an Hodgkin lymphoma with a tracheobronchial relapse. It should be considered in the differential diagnosis of asthma or a tracheal tumor

    Energy self-sufficient embedded system for mobile communicating objects

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    Le nombre et la complexité croissante des applications qui sont intégrées dans des objets mobiles communicants sans fil (téléphone mobile, PDA, etc.) implique une augmentation de la consommation d'énergie. Afin de limiter l'impact de la pollution due aux déchets des batteries et des émissions de CO2, il est important de procéder à une optimisation de la consommation d'énergie de ces appareils communicants. Cette thèse porte sur l'efficacité énergétique dans les réseaux de capteurs. Dans cette étude, nous proposons de nouvelles approches pour gérer efficacement les objets communicants mobiles. Tout d’abord, nous proposons une architecture globale de réseau de capteurs et une nouvelle approche de gestion de la mobilité économe en énergie pour les appareils terminaux de type IEEE 802.15.4/ZigBee. Cette approche est basée sur l'indicateur de la qualité de lien (LQI) et met en œuvre un algorithme spéculatif pour déterminer le prochain coordinateur. Nous avons ainsi proposé et évalué deux algorithmes spéculatifs différents. Ensuite, nous étudions et évaluons l'efficacité énergétique lors de l'utilisation d'un algorithme d'adaptation de débit prenant en compte les conditions du canal de communication. Nous proposons d'abord une approche mixte combinant un nouvel algorithme d'adaptation de débit et notre approche de gestion de la mobilité. Ensuite, nous proposons et évaluons un algorithme d'adaptation de débit hybride qui repose sur une estimation plus précise du canal de liaison. Les différentes simulations effectuées tout au long de ce travail montrent l’efficacité énergétique des approches proposées ainsi que l’amélioration de la connectivité des nœuds.The increasing number and complexity of applications that are embedded into wireless mobile communicating devices (mobile phone, PDA, etc.) implies an increase of energy consumption. In order to limit the impact of pollution due to battery waste and CO2 emission, it is important to conduct an optimization of the energy consumption of these communicating end devices. This thesis focuses on energy efficiency in sensor networks. It proposes new approaches to handle mobile communicating objects. First, we propose a global sensor network architecture and a new energy-efficient mobility management approach for IEEE 802.15.4/ZigBee end devices. This new approach is based on the link quality estimator (LQI) and uses a speculative algorithm. We propose and evaluate two different speculative algorithms. Then, we study and evaluate the energy efficiency when using a rate adaptation algorithm that takes into account the communication channel conditions. We first propose a mobility-aware rate adaptation algorithm and evaluate its efficiency in our network architecture. Then, we propose and evaluate a hybrid rate adaptation algorithm that relies on more accurate link channel estimation. Simulations conducted all along this study show the energy-efficiency of our proposed approaches and the improvement of the nodes’ connectivity

    Système embarqué autonome en énergie pour objets mobiles communicants

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    The increasing number and complexity of applications that are embedded into wireless mobilecommunicating devices (mobile phone, PDA, etc.) implies an increase of energy consumption. In order tolimit the impact of pollution due to battery waste and CO2 emission, it is important to conduct an optimization ofthe energy consumption of these communicating end devices. This thesis focuses on energy efficiency in sensor networks. It proposes new approaches to handle mobile communicating objects. First, we propose a global sensor network architecture and a new energy-efficient mobility management approach for IEEE 802.15.4/ZigBee end devices. This new approach is based on the link quality estimator (LQI) and uses a speculative algorithm. We propose and evaluate two different speculative algorithms. Then, we study and evaluate the energy efficiency when using a rate adaptation algorithm that takes into account the communication channel conditions. We first propose a mobility-aware rate adaptation algorithm and evaluate its efficiency in our network architecture. Then, we propose and evaluate a hybrid rate adaptation algorithm that relies on more accurate link channel estimation. Simulations conducted all along this study show the energy-efficiency of our proposed approaches and the improvement of the nodes’ connectivity.Le nombre et la complexité croissante des applications qui sont intégrées dans des objets mobiles communicants sans fil (téléphone mobile, PDA, etc.) implique une augmentation de la consommation d'énergie. Afin de limiter l'impact de la pollution due aux déchets des batteries et des émissions de CO2, il est important de procéder à une optimisation de la consommation d'énergie de ces appareils communicants. Cette thèse porte sur l'efficacité énergétique dans les réseaux de capteurs. Dans cette étude, nous proposons de nouvelles approches pour gérer efficacement les objets communicants mobiles. Tout d’abord, nous proposons une architecture globale de réseau de capteurs et une nouvelle approche de gestion de la mobilité économe en énergie pour les appareils terminaux de type IEEE 802.15.4/ZigBee. Cette approche est basée sur l'indicateur de la qualité de lien (LQI) et met en oeuvre un algorithme spéculatif pour déterminer le prochain coordinateur. Nous avons ainsi proposé et évalué deux algorithmes spéculatifs différents. Ensuite, nous étudions et évaluons l'efficacité énergétique lors de l'utilisation d'un algorithme d'adaptation de débit prenant en compte les conditions du canal de communication. Nous proposons d'abord une approche mixte combinant un nouvel algorithme d'adaptation de débit et notre approche de gestion de la mobilité. Ensuite, nous proposons et évaluons un algorithme d'adaptation de débit hybride qui repose sur une estimation plus précise du canal de liaison. Les différentes simulations effectuées tout au long de ce travail montrent l’efficacité énergétique des approches proposées ainsi que l’amélioration de la connectivité des noeuds

    Smooth muscle cell phenotypic switch: implications for foam cell formation

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    It is well accepted that LDLs and its modified form oxidized-LDL (ox-LDL) play a major role in the development of atherosclerosis and foam cell formation. Whereas the majority of these cells have been demonstrated to be derived from macrophages, smooth muscle cells (SMCs) give rise to a significant number of foam cells as well. During atherosclerotic plaque formation, SMCs switch from a contractile to a synthetic phenotype. The contribution of this process to foam cell formation is still not well understood

    Extracellular S100A4 induces smooth muscle cell phenotypic transition mediated by RAGE

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    We identified S100A4 as a marker of rhomboid (R) smooth muscle cells (SMCs) in vitro (the synthetic phenotype, typical of intimal SMCs) in the porcine coronary artery and of intimal SMCs in vivo in both pigs and humans. S100A4 is an intracellular Ca(2+) signaling protein and can be secreted; it has extracellular functions via the receptor for advanced glycation end products (RAGE). Our objective was to explore the role of S100A4 in SMC phenotypic change, a phenomenon characteristic of atherosclerotic plaque formation. Transfection of a human S100A4-containing plasmid in spindle-shaped (S) SMCs (devoid of S100A4) led to approximately 10% of S100A4-overexpressing SMCs, S100A4 release, and a transition towards a R-phenotype of the whole SMC population. Furthermore treatment of S-SMCs with S100A4-rich conditioned medium collected from S100A4-transfected S-SMCs induced a transition towards a R-phenotype, which was associated with decreased SMC differentiation markers and increased proliferation and migration by activating the urokinase-type plasminogen activator (uPA), matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). It yielded NF-ÎşB activation in a RAGE-dependent manner. Blockade of extracellular S100A4 in R-SMCs with S100A4 neutralizing antibody induced a transition from R- to S-phenotype, decreased proliferative activity and upregulation of SMC differentiation markers. By contrast, silencing of S100A4 mRNA in R-SMCs did not change the level of extracellular S100A4 or SMC morphology in spite of decreased proliferative activity. Our results show that extracellular S100A4 plays a pivotal role in SMC phenotypic changes. It could be a new target to prevent SMC accumulation during atherosclerosis and restenosis. This article is part of a Special Issue entitled: 13th European Symposium on Calcium

    Biological responses in stented arteries

    No full text
    Vascular walls change their dimension and mechanical properties in response to injury such as balloon angioplasty and endovascular stent implantation. Placement of bare metal stents induces neointimal proliferation/restenosis which progresses through different phases of repair with time involving a cascade of cellular reactions. These phases just like wound healing comprise distinct steps consisting of thrombosis, inflammation, proliferation, and migration followed by remodelling. It is noteworthy that animals show a rapid progression of healing after stent deployment compared with man. During stenting, endothelial cells are partially to completely destroyed or crushed along with medial wall injury and stretching promoting activation of platelets, and thrombus formation accompanied by inflammatory reaction. Macrophages and platelets play a central role through the release of cytokines and growth factors that induce vascular smooth muscle cell accumulation within the intima. Smooth muscle cells undergo complex phenotypic changes including migration and proliferation from the media towards the intima, and transition from a contractile to a synthetic phenotype; the molecular mechanisms responsible for this change are highlighted in this review. Since studies in animals and man show that smooth muscle cells play a dominant role in restenosis, drugs like rapamycin and paclitaxel have been coated on stent with polymers to allow local slow release of drugs, which have resulted in dramatic reduction of restenosis that was once the Achilles' heel of interventional cardiologists
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