Literatura académica sobre el tema "ARN – Troubles du métabolisme"
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Artículos de revistas sobre el tema "ARN – Troubles du métabolisme"
Jabi, R. y M. Bouziane. "Phéochromocytome et les troubles du métabolisme glucidique". Journal de Chirurgie Viscérale 159, n.º 4 (septiembre de 2022): S100. http://dx.doi.org/10.1016/j.jchirv.2022.07.101.
Texto completoThauvin-Robinet, C. y E. Roze. "Troubles du métabolisme des cobalamines chez l’adulte". Revue Neurologique 163, n.º 10 (octubre de 2007): 911–18. http://dx.doi.org/10.1016/s0035-3787(07)92634-x.
Texto completoMarcelli, Christian. "Maladies génétiques avec troubles du métabolisme phosphocalcique". Revue du Rhumatisme Monographies 79, n.º 4 (septiembre de 2012): 262–68. http://dx.doi.org/10.1016/j.monrhu.2012.09.001.
Texto completoJabi, R. y M. Bouziane. "Phéochromocytome et les troubles du métabolisme glucidique". Journal de Chirurgie Viscérale 157, n.º 3 (septiembre de 2020): S171. http://dx.doi.org/10.1016/j.jchirv.2020.07.094.
Texto completoBauduer, F. "Anémies par troubles du métabolisme du fer". EMC - Hématologie 4, n.º 1 (enero de 2009): 1–11. http://dx.doi.org/10.1016/s1155-1984(09)50262-2.
Texto completoMilh, M., A. Cano, C. Halbert y B. Chabrol. "Déficit moteur aigu et troubles du métabolisme énergétique". Archives de Pédiatrie 18, n.º 5 (mayo de 2011): H136—H137. http://dx.doi.org/10.1016/s0929-693x(11)71005-3.
Texto completoTeboul, Michèle y Franck Delaunay. "Les oscillations harmoniques des rythmes circadiens sortent de l’ombre". médecine/sciences 39, n.º 6-7 (junio de 2023): 544–50. http://dx.doi.org/10.1051/medsci/2023079.
Texto completoCortet, Bernard. "Endocrinopathies avec troubles du métabolisme phosphocalcique (hors hyperparathyroïdies primitives)". Revue du Rhumatisme Monographies 79, n.º 4 (septiembre de 2012): 244–47. http://dx.doi.org/10.1016/j.monrhu.2012.03.003.
Texto completoAnosa, V. O. "Changements hématologique et biochimique dans la trypanosomose humaine et animale". Revue d’élevage et de médecine vétérinaire des pays tropicaux 41, n.º 2 (1 de febrero de 1988): 151–64. http://dx.doi.org/10.19182/remvt.8716.
Texto completoAnosa, V. O. "Changements hématologique et biochimique dans la trypanosomosc humaine et animale". Revue d’élevage et de médecine vétérinaire des pays tropicaux 41, n.º 1 (1 de enero de 1988): 65–78. http://dx.doi.org/10.19182/remvt.8732.
Texto completoTesis sobre el tema "ARN – Troubles du métabolisme"
Clapé, Cyrielle. "Contrôle du métabolisme et de la prolifération par les microARN et les acteurs du cycle cellulaire". Montpellier 1, 2009. http://www.theses.fr/2009MON1T008.
Texto completoParticipation of cell cycle regulators in metabolic processes represents a new link between cell proliferation and cell metabolism. External stimuli, like cold and fasting conditions, could induce a proliferative response, but also a metabolic response. Previously, we have shown that the cell cycle regulators, CDK4, pRB and E2F1 play a crucial role during adipogenesis and pancreatic function. Here we show that E2F1 could actively participate in regulation of mitochondrial biogenesis and function. E2FA represses the expression of Pgc-1 alpha, which is master regulator of energy homeostasy in brown adipose tissue and muscle. Interestingly mitochondrial genes in cdk4-/- mice seems to be inversely correlated with gene expression in e2fl-/- mice. Finally, CDK4 coould [i. E. Could] play a role in lipid metabolism. MicroRNAs are endogenous, non-coding and small RNAs, which negatively regulate gene expression and are implicated in many cellular processes. We showed that mir-143 expression is inversely correlated with advanced stages of prostate cancer. ERK5, a target of mir-143, is known to promote the proliferation and its expression is aberrant in prostate cancer. Mir-143 could be directly implicated in carcinogenesis througe [i. E. Through] ERK5. This suggest taht [i. E. That] mir-143 could be a tumor suppressor in prostate cancer. Our results show that metabolic and proliferative changes observed in cancer development are closely linked, but also regulated by cell cycle regulators and microRNAs
Marguet, Christophe. "Contribution à l'étude des pathologies du métabolisme phosphocalcique : étude de la sous-unité de la proteine G stimulatrice de l'adényl-cyclase (Gsα)". Rouen, 1998. http://www.theses.fr/1999ROUES035.
Texto completoLallemant, Louison. "Pathologie neuronale et gliale en lien avec les atteintes neurologiques de la dystrophie myotonique de type 1 (DM1)". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS404.pdf.
Texto completoMyotonic dystrophy type 1 (DM1) is a severe neuromuscular disease affecting many tissues and organs. The debilitating neurological manifestations vary from executive dysfunction in adults, to attention deficits and low processing speed in pediatric patients, to severe intellectual disability in congenital cases. DM1 neurological manifestations have a profound impact on the daily life of patients and their families, and there is currently no treatment for this disease. DM1 is caused by the abnormal expansion of a CTG repeat in DMPK gene. Expanded DMPK transcripts are toxic because they accumulate in the cell nucleus, disrupting the activity of important RNA-binding proteins. As a consequence, DM1 cells show abnormal RNA metabolism and processing of many downstream transcripts. Despite progress in the understanding of the muscle pathophysiology, the disease mechanisms remain unclear in the CNS. We still do not know which cell types and molecular pathways are primarily affected in the brain and how they contribute to DM1 neurological symptoms. In order to investigate this problem, our laboratory has developed a transgenic mouse model of DM1: DMSXL mice express expanded human DMPK transcripts in multiple tissues, notably in the brain, and display relevant behavioral, electrophysiological and neurochemical phenotypes. Using this mouse model, the objective of my thesis was to better understand the cellular and molecular mechanisms involved in the neuronal and non-neuronal impairment linked to the neurological damages of DM1. I first focused on the characterization of the different cell types in the DMSXL brain. A multi-omics study was carried out on DMSXL neurons, astrocytes and oligodendrocytes. Our results, which show that glial cells are more impacted by CTG repeats, have allowed us to better understand the cellular and molecular mechanisms of DM1 in the CNS, but above all to emphasize the importance of studying not only the neurons, but also astrocytes and oligodendrocytes in the pathological context of DM1. I then got involved in the study of astrocyte pathology in DM1. We thus demonstrated that DMSXL astrocytes exhibited reduced ramification and impaired cell adhesion, and had a strong negative impact on neuritogenesis. In the same time, I also participated in the study of oligodendroglia impairment in DM1. We found that the toxic CUG RNA disrupts the molecular program of oligodendrocyte (OL) differentiation, impairing the transcriptome changes occurring during the oligodendrocyte precursor cells (OPC)-OL transition and leading to transient hypomyelination in mice. I also studied the neuronal pathology in DMSXL mice. Our results demonstrated that the accumulation of toxic RNA foci in neurons perturbs mainly protein phosphorylation, which seems to lead to neuronal morphological defects associated with vesicle dynamics impairment and axonal transport defects. The three main cell types of the brain therefore present significant damage in the context of DM1, which could have an impact on crucial processes of cerebral functioning. Indeed, we have demonstrated an alteration in neurotransmission and synaptic plasticity in DMSXL mice. All together my work has provided novel insight into the cell-specific mechanisms operating in DM1, demonstrating the implication of astrocyte, oligodendrocyte and neuron defects in a DM1mouse model, and contributing towards an integrative understanding of brain pathology
Quessard, Laurent. "Déplétion en Adn mitochondrial chez l'enfant : à propos d'un cas d'encéphalomyopathie de révélation précoce". Bordeaux 2, 1996. http://www.theses.fr/1996BOR2M102.
Texto completoTartarin, Pauline. "Rôle de la voie de signalisation AMPK/mTOR dans la fonction de reproduction". Thesis, Tours, 2013. http://www.theses.fr/2013TOUR4009/document.
Texto completoIn mammals, the energy metabolism exerts a strong influence on fertility. In females as in males, either a drop or an excess of the nutritional supplies induce modulations of the hormonal synthesis as well as viable gametes production. Our objective was 1) to define the role of AMPK, the AMP-activated protein kinase, a cell sensor of the energy reserves, in male reproduction; 2) to study the involvement of mTORC1, the mammalian target of rapamycin complex 1, another indicator of metabolism, in the cells of the central nervous system that regulate fertility. We have shown a decrease of fertility, linked to a testicular hyperandrogenia and dysfunctional spermatozoa in α1AMPK deficient mice. Moreover, in utero exposure to an AMPK activator, the metformin, induced a decrease in testicular volume and testosterone concentration (17dpc). Finally, inactivation of mTORC1 by interferent RNA in the adjacents cells of the hypothalamus tends to increase litter size, linked to a rise of FSH and the terminal folliculogenesis. In conclusion, this study confirms the role of these two complexes, energetic sensors, on the functionality of the hypothalamo-pituitary-gonadal axis
Delvenne, Véronique. "Le métabolisme cérébral dans les troubles des conduites alimentaires". Doctoral thesis, Universite Libre de Bruxelles, 1995. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212471.
Texto completoShleifer, Michae͏̈l. "Troubles du métabolisme lipidique et athérosclérose-études et stratégies". Paris 5, 1997. http://www.theses.fr/1997PA05P124.
Texto completoLieber, Ari Leib. "Macro- et microcirculation au cours des troubles du métabolisme glucidique". Paris 7, 2012. http://www.theses.fr/2012PA077163.
Texto completoHigh blood pressure and glucose metabolism disorders share common comorbidities that originate from a common ground : the vessel and its annexes. Epidemiological analysis of predictors of cardiovascular risk is based on the analysis of the macrocirculation with arterial stiffness, wave reflections, pulse pressure, and of the microcirculation due to structural changes of arterioles with target organ damage. We observed in this work that arterial stiffness was present in hypertensive diabetics. Among diabetics, those on insulin had a lower augmentation index, perhaps due to the vasodilatory effects of insulin on a ground where the mitogenic effects of long-term hyperinsulinism have stiffened the arterial wall. The criterion of disorder of glucose metabolism is probably responsible for the arterial stiffness in patients with metabolic syndrome. This study found that patients receiving ACE inhibitors and insulin patients had a higher PWV and PP, probably because they had the most advanced disease. Finally the question of wave reflection was assessed by measuring its speed and magnitude and the hypothesis of increased pressure made us think that thewave reflection does not return faster, but sooner and this had been added to the systolic peak systolic because the reflection sites were closer due to the small size in women or the microcirculatory damage
Hilaire, Nathalie. "Métabolisme cellulaire des lipides neutres cytoplasmiques et myopathie à surcharge lipidique multisystémique". Toulouse 3, 1994. http://www.theses.fr/1994TOU30051.
Texto completoDujeancourt, Laurent. "Métabolisme et traduction des ARN mitochondriaux chez la levure S. pombe". Phd thesis, Université d'Evry-Val d'Essonne, 2012. http://tel.archives-ouvertes.fr/tel-00845328.
Texto completoLibros sobre el tema "ARN – Troubles du métabolisme"
Lamond, Angus I. Pre-mRNA processing. New York: Springer-Verlag, 1995.
Buscar texto completoLamond, Angus I. Pre-mRNA processing. Austin: R.G. Landes Co., 1995.
Buscar texto completoJ, Favus Murray y American Society for Bone and Mineral Research., eds. Primer on the metabolic bone diseases and disorders of mineral metabolism. 6a ed. Washington, DC: American Society for Bone and Mineral Research, 2006.
Buscar texto completoPerlemuter, Léon. Diabète et maladies métaboliques. 4a ed. Paris: Masson, 2003.
Buscar texto completo1944-, Grimaldi André, ed. Dyslipidémie et athérogenèse. Paris: Elsevier, 2004.
Buscar texto completoPerlemuter, Léon. Diabète et maladies métaboliques. Paris: Masson, 1987.
Buscar texto completoDisorders of lipid metabolism. New York: Plenum Press, 1990.
Buscar texto completo1955-, Gaudet Daniel, Université Laval. Centre de recherche sur les maladies lipidiques y Complexe hospitalier de la Sagamie. Clinique des maladies lipidiques, eds. Les dyslipoprotéinémies: L'approche clinique. 2a ed. Sainte-Foy: Centre de recherche sur les maladies lipidiques, Centre hospitalier universitaire de Québec, Pavillon CHUL, 1997.
Buscar texto completoMundy, Gregory R. Calcium homeostasis: Hypercalcemia and hypocalcemia. London: Dunitz, 1989.
Buscar texto completoCalcium homeostasis: Hypercalcemia and hypocalcemia. 2a ed. London: M. Dunitz, 1990.
Buscar texto completoCapítulos de libros sobre el tema "ARN – Troubles du métabolisme"
Bourrillon, A. "Métabolisme – Troubles nutritionnels". En Pédiatrie, 567–97. Elsevier, 2011. http://dx.doi.org/10.1016/b978-2-294-71375-0.50020-9.
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