Literatura académica sobre el tema "Vieillissement prématuré"
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Artículos de revistas sobre el tema "Vieillissement prématuré"
C., M. "Contre le vieillissement prématuré, le sport". Revue Médicale Suisse 7, n.º 291 (2011): 879. http://dx.doi.org/10.53738/revmed.2011.7.291.0879.
Texto completoWallach, Isabelle. "L’expérience du vieillissement chez des femmes et des hommes vivant avec le VIH : un vécu à l’intersection du genre, de l’orientation sexuelle et du parcours relié au VIH". Recherche 25, n.º 1 (30 de agosto de 2013): 105–26. http://dx.doi.org/10.7202/1018233ar.
Texto completoHassler, P. y JM Brogard. "A propos d'un nouveau cas de syndrome de vieillissement prématuré". La Revue de Médecine Interne 14, n.º 10 (enero de 1993): 1174. http://dx.doi.org/10.1016/s0248-8663(05)80286-3.
Texto completoDereure, O., M. Marque y B. Guillot. "Syndromes avec vieillissement cutané prématuré : de l’expression phénotypique au gène". Annales de Dermatologie et de Vénéréologie 135, n.º 6-7 (junio de 2008): 466–78. http://dx.doi.org/10.1016/j.annder.2008.04.006.
Texto completoRauzy, O., E. Bousquet, A. Ghisolfi-Marque, D. Adoue y JL Albarède. "Le syndrome de Werner, un modèle de vieillissement prématuré: illustration à travers une observation". La Revue de Médecine Interne 18 (mayo de 1997): s244. http://dx.doi.org/10.1016/s0248-8663(97)80575-9.
Texto completoAmeisen, Jean-Claude. "Entre Charybde et Scylla : le vieillissement prématuré est-il un prix à payer pour la protection contre les cancers ?" médecine/sciences 18, n.º 4 (abril de 2002): 393–95. http://dx.doi.org/10.1051/medsci/2002184393.
Texto completoBoyer, L., C. Chouaid, E. Marcos, L. Margarit, A. Noroc, M. Sarni, P. Le Corvoisier et al. "Vieillissement prématuré lié à une destruction précoce du poumon chez les fumeurs et au cours de la broncho-pneumopathie chronique obstructive". Revue des Maladies Respiratoires 30 (enero de 2013): A10. http://dx.doi.org/10.1016/j.rmr.2012.10.037.
Texto completoCapeau, Jacqueline. "Le vieillissement prématuré des patients infectés par le virus de l’immunodéficience humaine (VIH) : mise en évidence, recherche des mécanismes physiopatholo-giques et prise en charge". Bulletin de l'Académie Nationale de Médecine 195, n.º 9 (diciembre de 2011): 2013–24. http://dx.doi.org/10.1016/s0001-4079(19)31893-x.
Texto completoCarette, Jean y Suzanne Lamont. "L’âge usé : une histoire de travail". Nouvelles pratiques sociales 2, n.º 2 (17 de enero de 2008): 59–69. http://dx.doi.org/10.7202/301048ar.
Texto completoJacobson, Jenna, Chang Z. Lin y Rhonda McEwen. "Aging with Technology: Seniors and Mobile Connections". Canadian Journal of Communication 42, n.º 2 (23 de mayo de 2017). http://dx.doi.org/10.22230/cjc.2017v42n2a3221.
Texto completoTesis sobre el tema "Vieillissement prématuré"
Pons, Alexandre. "Recherches sur l'arôme de vieillissement prématuré des vins". Bordeaux 2, 2006. http://www.theses.fr/2006BOR21393.
Texto completoDuring aging of wines, the flavour of certain white wines evolves quickly to honey and wax notes whereas red wines develop a nuance characteristic of the odor of prune. These aromas are associated with oxidations mecanisms. Among these flavours, sotolone is associated with oxydative ageing of white wines. Sotolon is a chiral compound, each enantiomer smelling curry with sensory thresholds being of o,8 µg/L and 89 µg/L for S and R forms respectively. We show the reaction of aldolization between α-ketobutyric acid and acetaldehyde, is responsible for the formation of sotolon in wines. Ascorbic acid, contrary to the glutathion can, in oxydative conditions support its formation. In red aromagrammes, we report two odorous zones induced by oxydative phenomena. While the second was identified as a nonalactone, the first one correspond to a still unknown carbonyl compound
Laurent, Gaëlle. "Rôle de junD dans le contrôle du stress oxydatif et du vieillissement prématuré". Paris 7, 2008. http://www.theses.fr/2008PA077187.
Texto completoThe AP-1 transcription factor is formed by the interaction between Jun (c-Jun, JunB et JunD) and Fos proteins (c-Fos, FosB, Frai et Fra2). A study in our lab has shown that JunD transcription factor regulates antioxidant defense genes leading to a constitutive oxidative stress. In junD ⁻/⁻ cells, the accumulation of Reactive Oxygen Species (ROS) leads to the constitutive activation of HIF-1α (Hypoxia Inducible Factor) which main target is VEGF-A, a pro-angiogenic factor. My project is based on the analysis of the consequences of junD deletion in vivo. JunD deficient mice display features of premature aging and a shortened lifespan. They also suffer from persistent hypoglycemia due to enhanced insulin secretion. Subsequently, the insulin/IGF-1-signaling pathways are constitutively stimulated leading to inactivation of FoxOl, a positive regulator of longevity. Hyperinsulinemia most likely results from enhanced β-islet vascularization owing to chronic pancreatic oxidative stress. Indeed, accumulation of free radicals in β-cells enhances VEGF-A transcription that, in turn, increases pancreatic angiogenesis and insulin secretion. Accordingly, long-term administration of anti-oxidant treatment rescues the phenotype o f junD⁻/⁻ mice. Indeed, dietary supplementation of anti-oxidant treatment turned out to be protective against pancreatic angiogenesis, hyperinsulinemia and subsequent activation of insulin signaling cascades in peripheral tissues. We then wonder if junD function was conserved from worms to mammals and then analyse jun mutants in C. Elegans. Jun regulates DAF-2 signaling pathway and plays a crucial role in oxidative stress resistance and longevity in worms. . Taken together, these data establish a pivotal role for oxidative stress in systemic regulation of insulin and define the JunD protein as a key player in longevity
Philipot, Didier. "Implication du miR-24 et du miR-199a-5p dans le vieillissement prématuré du chondrocyte au cours de l'arthrose". Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON1T015/document.
Texto completoOsteoarthritis (OA) is an age-related disease whose prevalence increases with late life. In osteoarthritic cartilage, chondrocytes presents age-specific changes such as a decrease in synthesis properties, a decrease in their response to growth and anabolic factors and an increase of cellular senescence. Senescent chondrocytes are characterized by an irreversible cell cycle arrest, DNA damage response activation (ATM/p53/p21), p16INK4a/pRb signaling pathway activation and the establishment of SAPS triggering to hypertrophy. The aim of my PhD project consisting to identify microRNAs involved in chondrocyte premature aging. microRNAs are small endogenous RNAs controlling several biological processes such as proliferation, differentiation and senescence. Two studies show that microRNAs have a preventive role in senescence and hypertrophy. During my PhD, we perform a cellular model based on OA chondrocytes placed in 3D and treated with IL-1β. We identified two miRs: miR-24 and miR-199a-5p. Repression of miR-24 leads to the induction of p16INK4a and MMP1, associated with chondrocyte hypertrophy. Moreover, preliminary datas suggests that miR-199a-5p is a potential regulator of anti-aging hormone Klotho which is deregulated in our model
Urli, Laureline. "Les cellules sénescentes sont-elles des caractéristiques communes à la maladie d'Alzheimer et à l'apnée du sommeil ?" Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS085.pdf.
Texto completoAlzheimer's disease (AD), a neurodegenerative, progressive and incurable diseaseleading to cognitive decline is characterized by extracellular Aβ plaques and intracellular neuronal tau-containing neurofibrillary tangles.Both of these lesions appear in the hippocampus and spread to other regions of the brain. Age is the primary risk factor, but other risk factors such as sleep disorders are also implicated in the development of AD. Obstructive sleep apnea syndrome (OSAS), characterized by sleep fragmentation and intermittent hypoxia (IH), is frequently found in AD patients, and people with OSAS are more prone to developing cognitive disorders and neurodegenerative pathologies. Experimentally, IH induces oxidative stress and neuroinflammation, specially, in the hippocampus, which may lead to and/or be a consequence of cellular senescence and premature aging.In this thesis work, we focused on chronic IH as a potential inducer of senescence in the hippocampus by analyzing senescence markers and the senescence-associated secretory phenotype (SASP) in mice subjected to chronic IH for six weeks. To determine the impact of IH-induced senescence on the development of AD, we also worked on cohorts of PS1Ki mice, AD models.We demonstrate detrimental effects of chronic IH exposure in adult mice by showing impairment in object recognition memory, induction of oxidative stress, and increased markers of cellular senescence and SASP in the hippocampus, particularly in the dentate gyrus and CA3. These effects are age-dependent and neuronal cells appear to be particularly affected by this state of senescence. In PS1Ki mice, alterations, already revealed under normoxic conditions, are exacerbated by chronic IH. Indeed, in addition to being present in the hippocampus, senescent cells accumulate in the entorhinal and prefrontal cortices depending on the age of the mice.Collectively, our results suggest that the process of cellular senescence may be a key factor in the transition from physiological brain ageing to neurodegenerative pathology. Senolytic treatment targeting senescent cells could be considered to improve current OSAS treatments and to prevent premature brain ageing, thereby accelerating the pathophysiology and symptoms of AD
Lefèvre, Chloé. "Sénescence prématurée et dysfonction endothéliale : implication des inhibiteurs de la protéase virale du VIH". Paris 6, 2011. http://www.theses.fr/2011PA066033.
Texto completoValdeolivas, Urbelz Alberto. "Approaches to explore multiplex biological networks and application to study premature aging diseases". Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0106.
Texto completoGenes and proteins do not act isolated in cells but rather interact to perform their functions in signaling pathways, molecular complexes, or, more generally, biological processes. These interactions can be represented as large networks in which nodes are genes or proteins and edges represent their interactions. Various graph-theory based approaches have been developed to extract the functional knowledge contained in biological networks. Nevertheless, these methods have been mainly applied to individual networks, ignoring the diversity of biological interactions. We state here that these different types of interactions can be represented as multiplex networks, i.e. collections of networks sharing the same nodes, leading to a more accurate description of biological systems. This thesis focuses on the extension from individual to multiplex networks of some of the state-of-the-art guilt-by-association methods in computational biology, and on their application to the study of human diseases. On the application side, we concentrate on premature aging diseases, a group of rare genetic disorders that resemble some aspects of physiological aging at an early age. In this framework, we applied our algorithms to detect the modules associated to more than 70 disorders annotated with at least one premature aging related phenotype. The results revealed the landscape of perturbed molecular processes in premature aging diseases, which can be paralleled with the hallmarks of physiological aging to help identifying common and specific features
Huyard, Fanny. "Impact du stress hyperoxique en période néonatale sur la structure vasculaire : implication des phénomènes de sénescence et rôle possible dans la programmation développementale de l'hypertension artérielle". Thèse, Université de Lorraine, 2013. http://hdl.handle.net/1866/12773.
Texto completoCe projet traite de la programmation développementale de l’hypertension artérielle (HTA) à travers des influences néonatales précoces pouvant moduler le développement vasculaire. Les bébés prématurés présentent des défenses antioxydantes diminuées comparés aux nouveau-nés à terme et sont exposés à la naissance à des concentrations élevées en oxygène (O2) engendrant la production d’espèces réactives de l’O2 (ERO). Les conséquences vasculaires à long terme de dommages liés aux ERO en période néonatale et les mécanismes impliqués sont très partiellement compris. Les précédents résultats du laboratoire ont montré qu’un stress hyperoxique néonatal conduit chez le rat adulte à de l’HTA, une dysfonction endothéliale et une rigidité artérielle, éléments de vieillissement vasculaire. Nous émettons l'hypothèse qu'un stress hyperoxique néonatale conduit à long terme à l'altération de la structure vasculaire et à un vieillissement vasculaire précoce. Nous avons démontré une diminution de la prolifération cellulaire, une capacité angiogénique altérée, des dommages à l’ADN et une augmentation de l’expression de protéines de sénescences (des indices de sénescence cellulaire) au-delà de la période néonatale suite à une exposition brève à l’O2 au niveau vasculaire dans un modèle animal (ratons Sprague-Dawley exposés à 80 % d’O2 du 3ème au 10ème jour de vie comparés à des ratons restés à l’air ambiant) et cellulaire (cellules musculaires lisses d'aortes thoraciques d'embryon de rat exposées à 40% O2 pendant 24h ou 48h, puis remises en normoxie pendant 96h). De plus, des altérations des composants de la structure vasculaire indiquant un remodelage vasculaire aortique ont été mises en évidence. Ces changements précèdent tous l’HTA et la dysfonction vasculaire observées dans le modèle animal à l’âge adulte et pourraient y contribuer. L’étude de jeunes adultes nés < 29 semaines comparés à des jeunes adultes nés à terme indique une augmentation de marqueurs de rigidité artérielle (indices d’un vieillissement vasculaire précoce) chez la population prématurée. L’ensemble des résultats démontre un vieillissement vasculaire précoce après une exposition néonatale transitoire à un stress hyperoxique permettant une meilleure compréhension des mécanismes physiopathologiques impliqués dans la survenue des troubles vasculaires retrouvés chez l’adulte et contribue à la mise en place de moyens de prévention chez des patients prématurés.
The scope of this thesis is developmental programming of arterial high blood pressure (HBP) hypertension through early neonatal stimuli that may alter vascular development. Premature newborns have decreased antioxidant defenses compared to term babies and are exposed upon birth to high oxygen (O2) concentration, causing reactive oxygen species (ROS) production. Long term vascular consequences of ROS related damage during the neonatal period and the mechanisms involved remain unknown. Recent data from the laboratory show that neonatal hyperoxic stress leads in adult rat to HBP, endothelial dysfunction and arterial rigidity, characteristic features of vascular aging. We hypothesize that a neonatal hyperoxic stress leads to long term vascular structure alteration explained by an early aging of the vascular system. We showed a decreased proliferation rate, an altered angiogenic capacity, as well as long term DNA damage and increased expression of senescence proteins at a vascular level following O2 exposure in the animal (male Sprague-Dawley pups kept at 80% O2 from postnatal days 3 to 10 vs. rats remained in room air) and cellular models (embryonic vascular smooth muscle cells from rat thoracic aorta exposed to 40% O2 for 24h or 48h followed by 96h recovery in control conditions). In addition, alterations of vascular structure components indicating vascular remodeling was shown before the onset of the HBP at adult age. Those changes precede the HBP and vascular dysfunction observed in our animal model at adult age and could contribute to them. Study of young adults born before 29 weeks vs. young adults born at term showed that young adults born preterm present indices of arterial stiffness vs. term controls. Results of the present thesis demonstrate a major role of premature vascular aging in the surge of vascular diseases in adulthood and contribute to a better understanding of the patho-physiological mechanisms involved and could put into practice new prevention strategies among preterm patients.
Métais, Sophie. "Étude de la perte prématurée de capacité d'accumulateurs au plomb : influence de la nature de l'alliage de la grille positive et du traitement de mûrissage de la plaque positive". Grenoble INPG, 1998. http://www.theses.fr/1998INPG0075.
Texto completoBaskara-Yhuellou, Indoumady. "Effet de l'exposition à la fumée de cigarette sur le profil oxydatif et la sénescence des différentes sous-populations lymphocytaires T CD4+". Thesis, Paris Est, 2013. http://www.theses.fr/2013PEST1064/document.
Texto completoThe Chronic obstructive pulmonary disease ( BPCO) is characterized by a destruction of the lung parenchyme, an obstruction of air traffics and an abnormal inflammatory answer in answer to an oxidizing stress chronicles smoking-related. The greater incidence of the disease at the elderly makes postulate(apply) that the cellular senescence could contribute to the pathogenesis of the disease
Voghel, Guillaume. "Vieillissement vasculaire chez des patients athérosclérotiques: Sénescence prématurée des cellules endothéliales?" Thèse, 2009. http://hdl.handle.net/1866/2847.
Texto completoVascular aging is associated with a decrease in endothelial dilatory and antithrombotic functions. This typical endothelial dysfunction, however, is also present in younger patients with cardiovascular diseases (CVD). At the cellular level, aging of healthy vascular endothelial cells (EC) leads to senescence, a state of permanent growth arrest. Senescence is characterized by specific changes in cell morphology and gene expression, which reduce EC function and thus are proposed to be pro-atherogenic. Age-associated telomere shortening leads to replicative senescence of human endothelial cells, but senescence can also be induced prematurely by oxidative stress (SIPS). Our aim was to characterize senescence of EC isolated from atherosclerotic patients and look at the influence of risk factors for CVD on the onset of senescence. To confirm the contribution of each of the two mains pathways triggering senescence, we then looked at the impact on senescence of a chronic treatment with an antioxidant combined or not with an overexpression of the catalytic subunit of telomerase (hTERT), a reverse transcriptase involved in telomere elongation. We used EC isolated from internal mammary arteries discarded during coronary bypass graft surgery. Depending on the study, EC were infected or not with a lentivirus overexpressing hTERT, and cells were cultured in vitro until senescence, in the presence or the absence of the antioxidant N-acetyl-L-cysteine (NAC). Different markers of the two main pathways of senescence (replicative ou SIS) were quantified. Senescence develops exponentially with time in culture and is associated with a decrease in cell viability and proliferation. In atherosclerotic patients, cellular aging displays an overlap between replicative and stress-induced senescence: short initial telomere length in vitro and a long exposure to risk factors for CVD in vivo predict the onset of a premature senescence. However, in smoking patients, premature senescence is exclusively induced by oxidative stress. Risk factors for CVD seem to accelerate the biological aging leading to EC dysfunction. When treated chronically with NAC, EC presenting initially lower levels of damage and a better endogenous antioxidant capacity develop a delayed senescence, probably due to a slight hTERT activation. When NAC is combined with an overexpression of hTERT, both pathways triggerring senescence are blocked and cellular immortalization is observed. In contrast, in EC presenting higher levels of damage undergone in vivo, NAC has no effect by itself on the onset of senescence, hTERT delays the onset of senescence in combination or not with NAC, but no cellular immortalization was observed in NAC-hTERT cells. In conclusion, our studies show that a chronic in vivo exposition to oxidative stress associated with risk factors for CVD accelerates the onset of vascular endothelial cells senescence that could potentially contribute to atherogenesis. EC having strong antioxidant defense capacity and DNA repair mechanisms may be rescued from replicative and stress-induced senescence unless EC have undergone an insurmountable cellular and molecular damage possibly due to uncontrolled free radical production associated with risk factors for CVD.