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Academic literature on the topic 'Altérations transcriptomiques'
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Journal articles on the topic "Altérations transcriptomiques"
Boyault, S., D. S. Rickman, A. De Reyniès, C. Balabaud, S. Rebouissou, E. Jeannot, A. Hérault, et al. "CA 8-La classification transcriptomique des CHC est correlée aux altérations génétiques somatiques et à des pathways qui sont de potentielles cibles thérapeutiques." Gastroentérologie Clinique et Biologique 30, no. 8-9 (August 2006): 1053. http://dx.doi.org/10.1016/s0399-8320(06)73418-2.
Full textDissertations / Theses on the topic "Altérations transcriptomiques"
Platel, Anne. "Approches génotoxiques et transcriptomiques In Vitro pour la détermination de seuils de produits induisants des lésions oxydatives à l'ADN." Paris 11, 2010. http://www.theses.fr/2010PA114812.
Full textIn the context of risk assessment, the existence of a thresholded-mechanism is suspected for some genotoxins inducing oxidative stress. Reactive oxygen species can generate oxidative DNA damage when cellular defence systems become overloaded. We worked in vitro on the human lymphoblastoid TK6 cell line with 3 oxidizing agents (potassium bromate, bleomycin, hydrogen peroxide). The 1st objective (genotoxic approach) was to investigate the dose-effect relationships to assess the existence of thresholds. Various NOELs were determined. The 2nd objective (transcriptomic approach) was to identify the mechanisms of action. The main signaling pathways depend on the dose and reflect the cellular response to DNA damage and cellular stress. Overall, this work shows the usefulness of a global analysis with the combination of standard genotoxicity assays and gene expression profiling technology
Turrel, Davin Fanny. "Apport de la transcriptomique dans la compréhension et la prise en charge des états septiques sévères." Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10058.
Full textSeptic syndromes remain a real public health issue. For 20 years, despite improvements in early management of patients and despite a number of clinical trials, the rate of mortality due to septic syndrome has remained broadly constant. After the initial phase of sepsis, patients rapidly exhibit profound immunodepression. Amplitude and duration of this state vary between patients and appear to be associated with increased risk of nosocomial infections and secondary deaths. One of the current challenges is to develop novel immunostimulant therapeutics for the most immunocompromised septic patients. Development of biomarkers will allow patient stratification and will undoubtedly contribute to the development of appropriately targeted and individualized therapies. The goal of our study was to evaluate the potential of gene expression level for clinical monitoring and for research in pathophysiology. We conducted translational research by combining experimental data with clinical studies (lymphopenia, apoptosis). We used endotoxin tolerance as a model to test different therapeutic options. Our data confirmed that expression levels of a panel of mRNAs, measured in the whole blood of patients, is a powerful tool for patient stratification and the monitoring of the effect of immunostimulant therapy on the immune system
Lecluze, Estelle. "Analyse par RNA-seq de la différenciation des gonades fœtales humaines et de son altération par des perturbateurs endocriniens." Thesis, Rennes 1, 2018. http://www.theses.fr/2018REN1B031/document.
Full textFetal life is a crucial period for sexual reproduction when bipotential gonads differentiate into either a testis or an ovary. Gaining insights into the complex molecular events underlying this process is central to a better understanding of disorders of sexual development. The present work intends to improve the knowledge on molecular pathways at play during gonad development in humans using RNA-sequencing. This project particularly seeks to identify early transcriptional events that may play critical role in the regulatory network driving human sexual differentiation. To address this issue, we defined the transcriptional landscape of fetal human gonads by sequencing total RNA extracted from testes and ovaries between 6 and 17 gestational weeks. The resulting paired-end reads were mapped on the human genome and then assembled into transcripts using the Tuxedo suite. We next defined a high-confidence set of transcripts showing differential expression across samples. Clusters of co-expressed genes were subjected to functional analysis. The analysis of this massive RNA-seq dataset has led to a high-confidence set of 35,194 assembled transcripts; among which 32,391 known and novel isoforms coding genes (mRNAs), 1,209 to long non-coding (lnc) RNAs and 318 to novel unannotated transcripts/genes (NUTs). The dynamic of transcriptional landscape occurring during human fetal gonads development has been described and new genes and interesting candidates, including new genes, have been highlighted as potential key genes governing this biological process. The second interest of this work was the study of the impact of two endocrine disruptors, ibuprofene and chlordecone, on human fetal testis using RNA-seq. The transcriptional alteration induced by these compound in the gonad allowed a deeper understanding of their mechanisms of action of endocrine disruption. The last part of this work was the development of a new version of the ReproGenomics Viewer (http://rgv.genouest.org), a web tool dedicated to the integration and accumulation of sequencing data from studies performed in the field of reproduction
Barbier, Emeline. "Étude des mécanismes physiopathologiques impliqués dans la toxicité des particules ultrafines chez un modèle murin : une approche multi-organes." Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS063.
Full textAlthough there has been a significant reduction in air pollution since the 1990s, it remains a major public health problem, responsible for over 4.2 million premature deaths worldwide every year. At present, experts' attention is focused on ultrafine particles (PM0.1 or UFP) because of their ability to translocate into the systemic circulation and reach peripheral organs, where they are likely to have a harmful impact. Nevertheless, the knowledge of the cellular and molecular mechanisms involved in the toxicity of these particles is still very patchy, and most often remains focused on their main target, the lung. Thus, the main objectives of this thesis project were to provide innovative insights into the toxicokinetics (i.e., distribution/persistence) and toxicodynamics (i.e., pathophysiological mechanisms, associated cell signaling pathways) of UFP collected in urban environments, on the one hand, and the organospecific effects of UFP and the use of circulating miRNA as indicators of chronic and/or cumulative exposure to UFP in a mouse model, on the other hand. To answer these questions, Balb/cJRj mice were exposed for 3 months to various doses of UFP collected in the urban area of Lille, then analyzed in various target organs richly vascularized, and therefore directly exposed to UFP during their translocation and systemic distribution phase. The results showed that, in all target organs, the intrinsic oxidative potential of UFP undeniably induced the production of oxidative oxygen species and the activation of antioxidant defenses in sufficient quantities to restore a state of redox homeostasis, but were unable to prevent the onset of an inflammatory response in the lungs, heart and brain. Transcriptomic approaches carried out in the lungs, the target organ with the most marked deleterious effects, have suggested the deregulation of numerous signaling pathways in relation to oxidative and inflammatory responses, which constitute the central mechanisms of UFP toxicity, but also with more original toxicity mechanisms such as mitochondrial dysfunction, epithelial-mesenchymal transition and tissue remodeling, whose modulation has also been validated from a functional point of view. These promising data could ultimately contribute to better decision-making on the reduction of UFP emissions, as well as to the updating of current regulatory standards
Rashka, Charif. "Rôle des altérations génomiques et épigénomiques dans les mécanismes moléculaires à l’origine des pathologies associées aux maladies rares du métabolisme de la vitamine B12." Thesis, Université de Lorraine, 2019. http://www.theses.fr/2019LORR0193.
Full textGenetic defects of vitamin B12 or cobalamin (cbl) metabolism lead to a decrease of methionine synthase activity that could result in a decrease of S-adenosyl methionine (SAM) synthesis and in the methylation index SAM / SAH that could be responsible for methylation alterations of various substrates. Patients with inherited disorders of cbl metabolism generally have a wide spectrum of pathologies suggesting that various cellular processes may be affected. However, the molecular mechanisms responsible for the development of these disorders are not well known. In order to better understand these mechanisms, we have used fibroblasts of patients with cblC and cblG genetic defects to characterize the modifications of their transcriptome, methylome and proteome. Our data show a modification in the expression of many genes involved in developmental, neurological, ophthalmologic and cardiovascular processes. These associations are consistent with the clinical presentation of the patients. We have also provided evidence of abnormal splicing of genes important for cytoskeleton organization, stress response, methylation and RNA binding. The study of differentially expressed or spliced genes has allowed us to identify various RNA binding proteins (RBP) such as HuR and HNRNPL that are involved in these modifications. The study of DNA methylation also revealed modifications in genes playing a role in developmental and neurological pathologies. No variation in methylation of histones or mRNA has been detected. The proteome study has confirmed that alternative splicing was affected and has suggested that mitochondrial metabolism was also altered. Our results contribute to a better understanding of the molecular mechanisms at the origin of the pathologies associated with the cblC and cblG defects and highlight the crucial role of RBP in these processes