Literatura científica selecionada sobre o tema "Modèles murins du SD"
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Artigos de revistas sobre o assunto "Modèles murins du SD"
Lanza, F. "Modèles murins de pathologies plaquettaires". Transfusion Clinique et Biologique 14, n.º 1 (maio de 2007): 35–40. http://dx.doi.org/10.1016/j.tracli.2007.04.010.
Texto completo da fonteAbdelhak, Sonia. "Modèles murins de surdités génétiques". Annales de l'Institut Pasteur / Actualités 6, n.º 4 (janeiro de 1995): 275–81. http://dx.doi.org/10.1016/0924-4204(96)83384-1.
Texto completo da fonteKahn, A. "Modèles murins du SIDA : drapeau rouge". médecine/sciences 6, n.º 4 (1990): 400. http://dx.doi.org/10.4267/10608/4159.
Texto completo da fonteDesmarets, M., e F. Noizat-Pirenne. "Modèles murins en transfusion sanguine : allo-immunisation, hémolyses". Transfusion Clinique et Biologique 18, n.º 2 (abril de 2011): 115–23. http://dx.doi.org/10.1016/j.tracli.2011.01.006.
Texto completo da fonteRamanantsoa, N. "Syndrome d’Ondine : modèles génétiques murins et perspectives thérapeutiques". Revue des Maladies Respiratoires 23, n.º 2 (abril de 2006): 181. http://dx.doi.org/10.1016/s0761-8425(06)71498-x.
Texto completo da fonteGrazziotin-Soares, D., e J. P. Lotz. "Le rôle des modèles murins en immuno-oncologie". Oncologie 19, n.º 11-12 (novembro de 2017): 399–403. http://dx.doi.org/10.1007/s10269-017-2731-z.
Texto completo da fonteReininger, L., C. Laporte e S. Izui. "Génétique du lupus : apport des modèles expérimentaux murins". Revue Médicale Suisse -2, n.º 2380 (2002): 390–94. http://dx.doi.org/10.53738/revmed.2002.-2.2380.0390.
Texto completo da fonteRomagnolo, B., e C. Perret. "Modèles murins de léiomyomes utérins obtenus par oncogenèse ciblée". médecine/sciences 12, n.º 10 (1996): 1118. http://dx.doi.org/10.4267/10608/632.
Texto completo da fonteGilgenkrantz, Simone. "Trois surdités, deux modèles murins, un seul gène,TMC1". médecine/sciences 18, n.º 8-9 (agosto de 2002): 804–5. http://dx.doi.org/10.1051/medsci/20021889804.
Texto completo da fonteLongvert, Christine, Gwendoline Gros, Friedrich Beermann, Richard Marais, Véronique Delmas e Lionel Larue. "Modèles murins de mélanomes cutanés. Importance du fond génétique". Annales de Pathologie 31, n.º 5 (novembro de 2011): S70—S73. http://dx.doi.org/10.1016/j.annpat.2011.09.002.
Texto completo da fonteTeses / dissertações sobre o assunto "Modèles murins du SD"
Ahumada, Saavedra José Tomás. "Craniofacial analysis of Down syndrome rodent models". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ041.
Texto completo da fonteThe most frequent and distinctive alterations found in Down syndrome (DS) are learning disability and craniofacial (CF) dysmorphism. The CF phenotype includes reduced head dimensions, brachycephaly, reduced mediolateral orbital region, reduced bizygomatic breadth, small maxilla, small mandible, and increased individual variability. Until now, the cellular and molecular mechanisms underlying this CF phenotype remain unknown. This thesis, using a new panel of rats and mice models proposed new candidate genes for the DS-CF phenotype. We confirmed the role of Dyrk1a in neurocranium brachycephaly and identified the overdosage of the transcription factor Ripply3 for midface shortening through the downregulation of Tbx1, another transcription factor involved in similar phenotypes was found in Di George Syndrome. We defined new dosage-sensitive genes responsible for DS-CF malformations, and new models were proposed to rescue the DS-CF phenotype. This new knowledge may also lead to insights for specific brain and cardiovascular phenotypes observed in Tbx1 mutants and DS models
Leoni, Anne-Laure. "Modèles murins en rythmologie expérimentale". Nantes, 2006. http://archive.bu.univ-nantes.fr/pollux/show.action?id=538b454d-5553-4cc8-8af0-c8f22d052097.
Texto completo da fonteCardiac impulse originates from the sinus node and propagates through the cardiac conduction system to depolarise atrial and ventricular myocardium. The work exposed herein reveals the implications of two ion channel subunits in sinus node automaticity and in cardiac electrical conduction by the use of mouse models. The first model confirms the hypothesis implicating the calcium channel subunit Cav3. 1 in sinus node automaticity, and shows its implication in atrioventricular (AV) conduction. The second model shows that heterozygous invalidation of Nav1. 5 sodium channel subunit (Scn5a+/- mice) induces sinus node dysfunction, impaired AV conduction and delayed intramyocardial conduction. These cardiac abnormalities are similar to the phenotype observed in patients with SCN5A mutations. Moreover, Scn5a+/- mice showed phenotype heterogeneity, just as in patients, revealing the importance of modulator genes or environment in the phenotype of genetic disorders. Finally, as cardiac rhythm modulation is of major interest in cardiac therapeutics, we have shown that chronic inhibition of HCN channels induces a complex ionic remodelling in the sinus node, but has little impact on ion channel expression in the mouse ventricle
Royer, Moës Anne. "Canalopathies cardiaques et modèles murins". Nantes, 2004. http://www.theses.fr/2004NANTA001.
Texto completo da fonteCardiac channelopathies are inherited or acquired diseases linked to ionic channel dysfonction. This thesis is about two transgenic murine models. The interest of transgenese is that gene expression and function can be study in vivo. The first murine model overexpresses the human HERG channel in the mouse heart. Its study has shown for the first time antiarrhythmic effects of HERG expression in vivo. The second murine model is a knock-out of Scn5a gene. Heterozygous mice have a 50 % reduction in their cardiac myocytes Na+ current and exhibit cardiac conduction defects. These cardiac conduction defects worsen with age and are associated with fibrosis. Scn5a +/- mice are a convincing model for Lenègre's disease
Faugeroux, Julie. "Caractérisation de modèles murins du syndrome d'Ehlers-Danlos vasculaire". Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T032.
Texto completo da fonteVascular Ehlers-Danlos (vEDS) syndrome is a rare, inherited, autosomal dominant disease that results from mutations in the COL3A1 gene, encoding type III collagen. Patients are mostly affected by missense mutations probably acting through a dominant negative mechanism. A few patients present large deletions or nonsense mutations leading to a haploinsufficient mechanism. These mutations are supposed to lead to a defect in the synthesis and secretion of collagen type III, resulting in arterial wall fragility. Consequently, vEDS is mostly characterized by ruptures/dissections in arteries at a young age, which ultimately lead to premature death. While there is currently no surgical or therapeutic treatments available, a recent study reported the beneficial effect of the beta-blocker celiprolol, which prevents vascular complications in patients.To investigate the vascular phenotype of vEDS, a mouse model of this disease has been generated by the complete and ubiquitous inactivation of the COL3A1 gene. Col3a1-/- mice exhibit severe perinatal mortality and die prematurely from spontaneous vascular rupture. However, Col3a1+/- mice are viable and exhibit no obvious vascular phenotype. To determine the susceptibility of Col3a1+/- mice to develop vascular rupture/dissection, an experimental model of aneurysm induction was used, through the chronic infusion of Angiotensin II (Ang II). Our results showed that Ang II infusion led to severe premature mortality in Col3a1+/- compared to wild type. This fragility was characterized by the development of rupture/dissection in the ascending aorta. These lesions could be caused by the elevation of blood pressure and/or the activation of Ang II signaling pathways. We showed that treatment with a beta-blocker (propranolol) and an arterial vasodilator (hydralazine) reduced the mortality induced by Ang II in Col3a1+/- mice. These results suggest the beneficial effect of adding a preventive treatment inhibitor of Ang II to the beta-blocker treatment recommended in human pathology.Meanwhile, given that a majority of human vEDS cases is caused by missense mutations in the COL3A1 gene, we established a knock-in mouse model bearing a point mutation (Gly183Ser) found in vEDS patients. The preliminary characterization of this model showed that Col3a1+/G183S mice die spontaneously as early as 4 weeks of age from a dissection or rupture of the ascending aorta. However, these mice do not showed any changes of their hemodynamic parameters or aortic diameter. Furthermore, about 20 % of mouse Col3a1+/G183S display wounds in the back and legs. This new mouse model is currently the only that mimic more closely the human disease and could therefore be used to test different therapeutic strategies
Boucher, Jérémie. "Modèles murins d'obésité : implication des catécholamines et des adipocytokines". Toulouse 3, 2004. http://www.theses.fr/2004TOU30120.
Texto completo da fonteDysregulation of energetic balance results in modification of adipose tissue mass. A decrease in caloric intake leads to lipid mobilization whereas an increase results in energy storage mainly in existing adipocytes (hypertrophy) or newly differenciated ones (hyperplasia). Catecholamines are potent modulators of adipocyte activity (metabolic as well as trophic) through activation of adrenergic receptors (AR). There's no suitable animal model to study the role of catecholamines in adipose tissue metabolism or development. Indeed, the b3-AR is highly expressed in adipocytes of most of rodents whereas there's a few or no expression of a2-AR. The contrary is true for humans. Thus we created transgenic mice with " human like " adrenergic receptivity in adipocytes. In b3-AR knock-out mice, expression of human a2-AR was performed with injection of a large human genomic DNA fragment (>30 kb). This fragment contains the regulatory sequences before (11 kb) and after (18 kb) the coding sequence of the a2C10 gene coding the a2-AR. In transgenic mice, expression profile of a2-AR in adipose tissue is similar to that usually described in humans. Moreover, whereas there's no apparent phenotype on a chow diet, these transgenic mice become obese when fed a high fat diet. Excessive adipose tissue development in obese mice is mainly due to hyperplasia of adipose tissue rather than hypertrophy of fat cells. However, depite obesity, these mice don't develop obesity associated disorders such as type II diabetes or hypertension. .
Frugier, Tony. "Création et caractérisation de modèles murins de l'amyothérapie spinale". Paris 5, 2001. http://www.theses.fr/2001PA05N093.
Texto completo da fonteDeffert, Delbouille Christine. "Modèles murins déficients en NOX1 ou NOX2 : applications physiopathologiques". Université Joseph Fourier (Grenoble), 2009. http://www.theses.fr/2009GRE10335.
Texto completo da fonteReactive oxygen species (ROS) are molecules derived from oxygen. They are generated by professional NADPH oxidases (NOX). The NOX family is proteins that transfer electrons across biological membranes. In general, the electron acceptor is oxygen and the product of the electron transfer reaction is superoxide. Seven NOXs proteins has been described and all of them generate or ROS. Despite their similar structure and enzymatic function, NOX family enzymes differ in their mechanism of activation, their tissues, cellular and subcellular localizations and in consequence their physiological functions. Physiological and pathological roles of NOX enzymes are usually discovered in transgenic mouse models. The goal of this thesis was to determine two new roles of NOX1 in human diseases : hypertension and respiratory distress syndrome using Nox1-deficient mice. Secondly, we have evaluated the anti-inflammatory role of NOX2 using Nox2-deficient mice. NOX1 has been involved in angiotensin II-induced hypertension. In this study, it has been demonstrated that NOX1-generated ROS have also implicated in angiotensin II-induced aneurysms. They can regulate the metallo-protease activity and fibrosis. NOX1 is activated by angiotensin II receptor (AT1) engagement. We have demontrated that NOX1 also regulates the AT1 expression to the plasma membrane. NOX1 seems to be a possible therapeutical target in hypertension and aneurysm formation. The respiratory distress syndrome especially in premature babies is characterized by immature lung development. During respiratory distress syndrome treatment with mechanical ventilation and high oxygen concentration, the lungs are exposed to increased oxidative stress leadings to pulmonary injury. During this study, we have demonstrated that Nox1 but not Nox2 participates to hyperoxie-induced lung injury. In Nox1-deficient mice, decreased ROS generation reduce cell death in alveolar epithelial and endothelial cells. NOX1 seems also to be possible therapeutical target in respiratory distress syndrome. Chronic granulomatous disease (CGD) is an immunodeficiency syndrome due to mutations in gene gp91(phox) coding for NOX2 protein. In consequence, CGD patients suffer from severe and recurrent infections. Indeed, they present hyperinflammatory response which plays a role in the morbidity of the disease. During this study, we have demonstrated that a possible stimulus of this CGD inflammatory complication is the β-glycans, in Nox2-deficient mice. These glucose polymers induce inflammatory that cannot be resolved in absence of NOX2. Also, CGD hyperinflammation is characterized by important TNFα production. But the blockage of TNFα has not dampened CGD hyperinflammation. In the other hand, the blockage of the principal β-glycans receptor, dectin-1 pharmacologically or genetically, has reduced significantly CGD inflammation. These data constiture new therapeutical target in CGD inflammatory syndrome
Le, Quang Khai. "Troubles du rythme cardiaque dans les modèles murins transgéniques". Thèse, Nantes, 2010. https://archive.bu.univ-nantes.fr/pollux/show/show?id=77640043-d85a-4ffa-b817-17b1b0c76068.
Texto completo da fonteCardiovascular disease is the leading cause of death in the world each year. If no action is taken to improve cardiovascular health and current trends continue, WHO estimates that 25% more healthy life years will be lost to cardiovascular disease globally by 2020. Cardiac hypertrophy is the consequence of an excessive workload of the heart muscle leading to cardiac remodeling process. As the workload increases, the ventricular walls grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart. Furthermore, hypertrophied myocardium is not physiologically normal and may confer a predisposition to potentially fatal arrhythmias. Generally, the causal mechanism is ventricular fibrillation, a cardiac rhythm disorder which is irreversible but the pathophysiological mechanisms are complex and poorly understood. The functional consequences of mutations or ionic remodeling are relatively simple to study in vitro, but their role in the pathophysiology of arrhythmias in vivo is more difficult to grasp. Among the different animal models developed in cardiac arrhythmias research, the mouse is increasingly used because of our ability to mutate, knock-out or over-express genes of interest. The objective of my thesis was to study the role of ion channels in physiology as well as cardiac pathophysiology, particularly in the involvement of the occurrence of cardiac arrhythmias in vivo. This thesis will improve our understanding of the role of genetic abnormalities involving ionic remodeling in the pathogenesis of the heart and may also open new therapeutic perspectives in the treatment of cardiac remodeling as well as sudden cardiac death
Le, Quang Khai. "Troubles du rythme cardiaque dans les modèles murins transgéniques". Thèse, Nantes, 2010. http://hdl.handle.net/1866/4903.
Texto completo da fonteCardiovascular disease is the leading cause of death in the world each year. If no action is taken to improve cardiovascular health and current trends continue, WHO estimates that 25% more healthy life years will be lost to cardiovascular disease globally by 2020. Cardiac hypertrophy is the consequence of an excessive workload of the heart muscle leading to cardiac remodeling process. As the workload increases, the ventricular walls grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart. Furthermore, hypertrophied myocardium is not physiologically normal and may confer a predisposition to potentially fatal arrhythmias. Generally, the causal mechanism is ventricular fibrillation, a cardiac rhythm disorder which is irreversible but the pathophysiological mechanisms are complex and poorly understood. The functional consequences of mutations or ionic remodeling are relatively simple to study in vitro, but their role in the pathophysiology of arrhythmias in vivo is more difficult to grasp. Among the different animal models developed in cardiac arrhythmias research, the mouse is increasingly used because of our ability to mutate, knock-out or over-express genes of interest. The objective of my thesis was to study the role of ion channels in physiology as well as cardiac pathophysiology, particularly in the involvement of the occurrence of cardiac arrhythmias in vivo. This thesis will improve our understanding of the role of genetic abnormalities involving ionic remodeling in the pathogenesis of the heart and may also open new therapeutic perspectives in the treatment of cardiac remodeling as well as sudden cardiac death.
Thèse en cotutelle avec Université de Nantes - Pays de La Loire - France (2005-2010)
St-Amour, Isabelle. "Effet des IGIV dans des modèles murins de maladies neurodégénératives". Thesis, Université Laval, 2014. http://www.theses.ulaval.ca/2014/30473/30473.pdf.
Texto completo da fonteIn the search of therapeutic solutions to neurodegenerative diseases, active and passive immunization strategies have been proposed for the clearance of protein aggregates. Intravenous immunoglobulin (IVIg) is a pharmaceutical preparation of over 98% immunoglobulin G prepared from the plasma of thousands of healthy donors. Since natural autoantibodies against pathological proteins have been identified in IVIg, it has been proposed as an alternative to immunotherapy and clinical trials in Alzheimer’s disease (AD) patients are underway. The aim of my PhD project was to evaluate the efficacy, analyze the mechanisms of action of IVIg in animal models of AD and Parkinson’s disease (PD), and identify potential targets for the development of pharmacological alternatives. The bioavailability of IVIg and its ability to reach therapeutic targets in the brain are unknown. In the first part of the project, we quantified the passage of IVIg through the blood-brain barrier (BBB). Our results provide quantitative evidence of BBB transport and brain bioavailability of IVIg in the absence of permeabilization and in sufficient amount to interact with therapeutic targets. In a triple transgenic mouse model of AD (3xTg-AD) that reproduces amyloid and tau pathologies, IVIg injections have improved the cognitive performance and reduced anxiety-like behaviors of treated mice. Despite limited effects on tau pathology, IVIg modulated the central (IL-5/IL-10 ratio) and peripheral (CX3CR1 + and T cells), and reduced the ratio of soluble Aβ42/Aβ40 (-22%) and the concentration of 56 kDa oligomers of Aß (Aß*56) by over 60%. This effect of IVIg on cognition, immunity and Aß pathology suggests that Aβ oligomers, effector T cells and the fractalkine pathway are potential pharmacological targets of IVIg in AD. Finally, we studied the effect of an IVIg treatment in a mouse model of PD. In this model of MPTP intoxication, our results did not demonstrate neurorestorative effects of IVIg on the nigrostriatal system and even suggested adverse effects of IVIg on the dopaminergic system. These preclinical data highlighted the importance of proceeding cautiously in the initiation of clinical trials with IVIg to treat PD patients.