Auswahl der wissenschaftlichen Literatur zum Thema „Modélisation des gènes“
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Zeitschriftenartikel zum Thema "Modélisation des gènes"
LE BIHAN-DUVAL, E., R. TALON, M. BROCHARD, J. GAUTRON, F. LEFÈVRE, C. LARZUL, E. BAÉZA und J. F. HOCQUETTE. „Le phénotypage de la qualité des produits animaux : enjeux et innovations.“ INRAE Productions Animales 27, Nr. 3 (28.08.2014): 223–34. http://dx.doi.org/10.20870/productions-animales.2014.27.3.3069.
Der volle Inhalt der QuelleFAVERDIN, P., und C. LEROUX. „Avant-propos“. INRAE Productions Animales 26, Nr. 2 (16.04.2013): 71–76. http://dx.doi.org/10.20870/productions-animales.2013.26.2.3137.
Der volle Inhalt der QuelleMORAND-FEHR, P. M., R. BAUMONT und D. SAUVANT. „Avant-propos : Un dossier sur l’élevage caprin : pourquoi ?“ INRAE Productions Animales 25, Nr. 3 (25.08.2012): 227–32. http://dx.doi.org/10.20870/productions-animales.2012.25.3.3210.
Der volle Inhalt der QuelleDUCROT, C., J. CHARLEY-POULAIN und J. M. AYNAUD. „Numéro hors série 2004 : Encéphalopathies spongiformes transmissibles animales -Sommaire et avant-propos“. INRAE Productions Animales 17, HS (18.12.2004). http://dx.doi.org/10.20870/productions-animales.2004.17.hs.3612.
Der volle Inhalt der QuelleDissertationen zum Thema "Modélisation des gènes"
Evlampiev, Kirill. „Modélisation de réseaux biologiques“. Paris 6, 2007. http://www.theses.fr/2007PA066200.
Der volle Inhalt der QuelleRefahi, Yassin. „Modélisation multiéchelle de perturbation de la phyllotaxie d'Arabidopsis thaliana“. Phd thesis, Université Montpellier II - Sciences et Techniques du Languedoc, 2011. http://tel.archives-ouvertes.fr/tel-00859869.
Der volle Inhalt der QuelleHerbach, Ulysse. „Modélisation stochastique de l'expression des gènes et inférence de réseaux de régulation“. Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1155/document.
Der volle Inhalt der QuelleGene expression in a cell has long been only observable through averaged quantities over cell populations. The recent development of single-cell transcriptomics has enabled gene expression to be measured in individual cells: it turns out that even in an isogenic population, the molecular variability can be very important. In particular, an averaged description is not sufficient to account for cell differentiation. In this thesis, we are interested in the emergence of such cell decision-making from underlying gene regulatory networks, which we would like to infer from data. The starting point is the construction of a stochastic gene network model that is able to explain the data using physical arguments. Genes are then seen as an interacting particle system that happens to be a piecewise-deterministic Markov process, and our aim is to derive a tractable statistical model from its stationary distribution. We present two approaches: the first one is a popular field approximation, for which we obtain a concentration result, and the second one is based on an analytically tractable particular case, which provides a hidden Markov random field with interesting properties
Champion, Magali. „Contribution à la modélisation et l'inférence de réseau de régulation de gènes“. Toulouse 3, 2014. http://thesesups.ups-tlse.fr/2613/.
Der volle Inhalt der QuelleThis manuscript intends to study a theoretical analysis and the use of statistical and optimization methods in the context of gene networks. Such networks are powerful tools to represent and analyse complex biological systems, and enable the modelling of functional relationships between elements of these systems. The first part is dedicated to the study of statistical learning methods to infer networks, from sparse linear regressions, in a high-dimensional setting, and particularly the L2-Boosting algorithms. From a theoretical point of view, some consistency results and support stability results were obtained, assuming conditions on the dimension of the problem. The second part deals with the use of L2-Boosting algorithms to learn Sobol indices in a sensitive analysis setting. The estimation of these indices is based on the decomposition of the model with functional ANOVA. The elements of this decomposition are estimated using a procedure of Hierarchical Orthogonalisation of Gram-Schmidt, devoted to build an approximation of the analytical basis, and then, a L 2 -Boosting algorithm, in order to obtain a sparse approximation of the signal. We show that the obtained estimator is consistant in a noisy setting on the approximation dictionary. The last part concerns the development of optimization methods to estimate relationships in networks. We show that the minimization of the log-likelihood can be written as an optimization problem with two components, which consists in finding the structure of the complete graph (order of variables of the nodes of the graph), and then, in making the graph sparse. We propose to use a Genetic Algorithm, adapted to the particular structure of our problem, to solve it
Audrain, Mickaël. „Modélisation des phases précoces de la maladie d’Alzheimer par transfert de gènes“. Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB010/document.
Der volle Inhalt der QuelleEvaluation of biomarkers and new innovative therapies for Alzheimer's disease (AD) suffers from a misunderstanding of early phases and lack of appropriate animal models close to the human physiopathology. Most available rodent models reproduce hallmarks of AD such as amyloid plaques and neurofibrillary tangles in a few months, while it takes many years to be achieved in human. My PhD work consisted to develop a new modelling strategy of AD early phases without major overexpression of transgenes. To do so, we used gene transfer of human APPSL and PS1M146L using viral vectors injection in the hippocampus of 8 weeks old mice and rats. We characterized these models and showed peptides production, such as betaCTF and abeta42 from APP processing, similar to what is observed in AD patients hippocampi. We also highlighted a hyperphosphorylation of Tau followed by a synaptic failure characterized by a decrease of PSD-95 and GLT-1 levels and by an increase of the tonic current mediated by glutamate. These changes have been finally associated with behavioral deficits. My results suggest that many events appear well before the formation of amyloid plaques or tangles and lead to the disruption of the synapse and the early onset of behavioral defects. Thus, we now have relevant tools to understand the early stages of AD, which will allow us to test new drug compounds on these models with a wide therapeutic window and discover new early biomarkers in plasma and cerebrospinal fluid
Malherbe, Godefroy. „Modélisation de la diffusion dans le noyau et application à l'activation cellulaire“. Paris 6, 2010. http://www.theses.fr/2010PA066481.
Der volle Inhalt der QuelleAvran, David. „Oncogenèse et modélisation des leucémies aigues lymphoblastiques T“. Paris 7, 2013. http://www.theses.fr/2013PA077254.
Der volle Inhalt der QuelleT-celé acute lymphoblastic leukemia (T-ALL) are malignancies derived from lymphoid thymic precursors arrested in their differentiation. We focused on the deletion of the long arm of chromosome 6 (del6q), the most common caryotypic abnormality in T-ALL, which target(s) are, to date, not known. By using both a whole set of integrative genomics and functional approaches, we identified the role of the combined haploinsufficiency of two contiguous genes at 6q14 (by mimicking in vivo an interstitial microdeletion we identified), namely SYNCRIP (encoding hnRNP-Q) and SNHG5 (a non-protein-coding gene that hosts snoRNAs), involved in mRNA maturation and protein translation. These genes are included in the common deleted region in a subtype of T-ALLs characterized by aberrant expression of the TAL1 transcription factor oncogene. In vivo knockdown models using Talr9/Lmolt9/Notch1-ICNtransduced mouse cells, and xenograft of patient's SIL-TAL, not 6q deleted leukemic cells, showed that the combined silencing of both genes was associated to a gain of malignancy. In a parallel work, we identified in T-ALL, recurrent aberrations of a gene usually involved in myeloid malignancies, TET2. Using microarray-based CGH to screen a cohort of T-ALL, we found a focal heterozygous deletion of this gene in one case belonging to the TAL-related oncogenic sub¬group. Moreover, we found mutations in cases belonging to other oncogenic sub-groups. This genetic study reveals that TET2 can play a role in T leukemogenesis, highlighting the ubiquitous nature of epigenetic alterations linked to TET2
Robert, Philippe A. „Modélisation mathématique de la différenciation précoce des lymphocytes T auxiliaires“. Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT002.
Der volle Inhalt der QuelleT helper cells are required to produce cytokines adapted to the type of infection. Several subsets have been defined, including pro-inflammatory Th1, Th2, Th17; and anti-inflammatory, Foxp3+ iTreg cells. The fate-determining decision of a naive T cell to differentiate into a defined subset was investigated here.Recent findings showed that metabolic constituents impact T cell differentiation, but so far the influence of glutamine on T cell differentiation has been neglected although being the main source of nitrogen. In this study, deprivation of glutamine induced an abnormal expression of Foxp3 under Th1 but not under Th2 condition, while impairing Th1 and Th17 differentiation. Thus, in poor metabolic micro-environments like solid tumours, a lack of glutamine would initiate a detrimental anti-inflammatory response.A mathematical modelling approach using Ordinary Differential Equations was chosen to capture the properties of T cell differentiation, first in normal conditions with glutamine. In order to train the model, kinetics of the master transcription factors and cytokines expression were measured under different T cell differentiation polarizing conditions. The in vitro data revealed major delays in transcription, translation and secretion of cytokines, which shaped the order of fate decision events. The model could successfully reproduce the dynamics of differentiation, confirming that the 'canonical' differentiation in vitro can be explained by a simple regulatory network. However, it only partially reproduced the plastic behaviour of T cells. The mathematical model will be utilized to compare different mechanistic hypotheses linking glutamine sensing to differentiation
Marot, Guillemette. „Modélisation statistique pour la recherche de gènes différentiellement exprimés: modèles de variance-covariance, analyse séquentielle et méta-analyse“. Phd thesis, AgroParisTech, 2009. http://tel.archives-ouvertes.fr/tel-00458988.
Der volle Inhalt der QuelleMarot-Briend, Guillemette. „Modélisation statistique pour la recherche de gènes différentiellement exprimés : modèles de variance-covariance, analyse séquentielle et méta-analyse“. Paris, AgroParisTech, 2009. http://pastel.paristech.org/5473/01/phDreportGMarot.pdf.
Der volle Inhalt der QuelleBuchteile zum Thema "Modélisation des gènes"
BONNAFFOUX, Arnaud. „Inférence de réseaux de régulation de gènes à partir de données dynamiques multi-échelles“. In Approches symboliques de la modélisation et de l’analyse des systèmes biologiques, 7–50. ISTE Group, 2022. http://dx.doi.org/10.51926/iste.9029.ch1.
Der volle Inhalt der QuelleBÉAL, Jonas, Élisabeth REMY und Laurence CALZONE. „Connecter les modèles logiques aux données omiques“. In Approches symboliques de la modélisation et de l’analyse des systèmes biologiques. ISTE Group, 2022. http://dx.doi.org/10.51926/iste.9029.ch4.
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