Добірка наукової літератури з теми "Cellules CD34+hématopoïétiques"
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Статті в журналах з теми "Cellules CD34+hématopoïétiques":
Ivanovic, Z., P. Duchez, J. Chevaleyre, M. Vlaski, P. Brunet de la Grange, and G. Wouters. "Cryoconservation de cellules souches et progénitrices hématopoïétiques amplifiées ex vivo à partir de cellules CD34+ de sang placentaire." Transfusion Clinique et Biologique 20, no. 3 (June 2013): 343. http://dx.doi.org/10.1016/j.tracli.2013.03.183.
Duchez, Pascale, Laura Rodriguez, Philippe Brunet De La Grange, and Zoran Ivanovic. "Cryoconservation de cellules souches et de progéniteurs hématopoïétiques amplifiés ex vivo à partir de cellules CD34+ de sang placentaire." Transfusion Clinique et Biologique 24, no. 3 (September 2017): 377. http://dx.doi.org/10.1016/j.tracli.2017.06.300.
Corlu, A., B. Drenou, Y. Desille, O. Fardel, R. Lorho, C. Camus, A. Guillygomarc’h, K. Boudjema, and D. Guyader. "C04 - Le nombre de cellules souches hématopoïétiques circulantes CD34+ augmente tardivement au cours des hépatites aiguës graves." Gastroentérologie Clinique et Biologique 29, no. 8-9 (August 2005): 885. http://dx.doi.org/10.1016/s0399-8320(05)86369-9.
Astrugue, C., S. Dieterlé, and S. Lucas-Samuel. "Proportion de faibles rendements en CD34+ des greffons de cellules souches hématopoïétiques autologues après décongélation en France." Revue d'Épidémiologie et de Santé Publique 71 (March 2023): 101498. http://dx.doi.org/10.1016/j.respe.2023.101498.
Duchez, P., J. Chevaleyre, M. Vlaski, P. Brunet de la Grange, and Z. Ivanovic. "Stabilité fonctionnelle à +4°C des cellules souches et progénitrices hématopoïétiques amplifiées ex vivo à partir de cellules CD34+ de sang placentaire." Transfusion Clinique et Biologique 20, no. 3 (June 2013): 343–44. http://dx.doi.org/10.1016/j.tracli.2013.03.185.
Drouet, M., F. Mourcin, N. Grenier, J. F. Mayol, V. Leroux, J. J. Sotto, and F. Hérodin. "Effet des rayonnements ionisants sur les cellules souches et progéniteurs hématopoïétiques: place de l'apoptose et intérêt thérapeutique potentiel des traitements antiapoptotiques." Canadian Journal of Physiology and Pharmacology 80, no. 7 (July 1, 2002): 700–709. http://dx.doi.org/10.1139/y02-071.
Sellami, F., V. Chamfly, A. Leon, C. Mathiot, T. Palangié, J. Dumont, J. Michon, and M. Lopez. "P3-12 Contrôle de qualité des cellules souches hématopoïétiques pour autogreffe: faut-il privilégier un test quantitatif (énumération des cellules CD34) ou un test fonctionnel (culture des CFU-GM) pour évaluer la capacité hématopoïétique des greffons?" Transfusion Clinique et Biologique 5 (April 1998): 69s—70s. http://dx.doi.org/10.1016/s1246-7820(98)80052-9.
Ben Nasr, M., and F. Jenhani. "Contribution à l’étude de l’apoptose par la cytométrie en flux des cellules souches hématopoïétiques CD34+ avant et après le processus de congélation." Transfusion Clinique et Biologique 15, no. 3 (June 2008): 91–97. http://dx.doi.org/10.1016/j.tracli.2008.03.009.
Brignier, Anne, Virginie Ader, Katia Bellegarde, Christine Giraud, Marie-Agnès Guerout-Verite, Fati Hamzy, Thi Ngoc Phuong Huynh, et al. "Modalités de mobilisation des cellules souches hématopoïétiques autologues et objectifs cellulaires en cellules CD34 + : recommandations de la Société francophone de greffe de mœlle et de thérapie cellulaire (SFGM-TC)." Bulletin du Cancer 107, no. 1 (January 2020): S44—S51. http://dx.doi.org/10.1016/j.bulcan.2019.08.007.
Olivero, S., T. Alario, P. Ladaique, M. Haccoun, M. Mouren, G. Novakovitch, D. Blaise, and C. Chabannon. "P3-13 Étude comparative de la numération des cellules hématopoïétiques CD34+ aux moyens de deux trousses diagnostiques et d'une méthode interne à l'Institut Paoli-Calmettes." Transfusion Clinique et Biologique 5 (April 1998): 70s—71s. http://dx.doi.org/10.1016/s1246-7820(98)80053-0.
Дисертації з теми "Cellules CD34+hématopoïétiques":
Saeland, Sem. "Caractérisation et physiologie in vitro des cellules hématopoïétiques humaines exprimant l'antigène CD34." Lyon 1, 1992. http://www.theses.fr/1992LYO1H053.
Li, Na. "Expansion des cellules souches hématopoïétiques dans les systèmes de cocultures des cellules endothéliales et des cellules stromales." Nancy 1, 2005. http://www.theses.fr/2005NAN11320.
Croisille, Laure. "Caractérisation d'une population de progéniteurs hématopoïétiques humains primitifs CD34++CD38-, et étude de leur régulation par le microenvironnement médullaire." Paris 7, 1997. http://www.theses.fr/1997PA077350.
Traore, Yves. "Divers aspects de polymorphisme de la molécule CD34 : antigène des cellules souches hématopoïétiques humaines." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX22010.
Zebian, Abir. "Etude du facteur de réparation de l’ADN, Xeroderma pigmentosum du groupe C (XPC), dans les cellules souches hématopoïétiques." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0223/document.
DNA damage may accumulate in hematopoietic stem cells (HSC) due to external ormetabolic stresses, leading to perturbation in their function and/or maintenance. Nucleotide excisionrepair (NER), initiated in the DNA by the stop of transcription (TCR) or by the recognition of distortionsin transcribed regions (GGR), is necessary for long-term hematopoiesis. XPC, a key factor in GGR, isimplicated in oxidative stress. The laboratory has demonstrated that XPC loss leads to theaccumulation of mutations, metabolic stress and carcinogenesis. Our objective is to evaluate XPCexpression and its role in HSC maintenance and differentiation. Results showed that XPC is highlyexpressed in immature CD34+ cells compared to mature CD34- cells. In addition, XPC appeared withthree different molecular weights, certainly linked to post-translational modifications. XPC silencing byshRNA did not affect the proliferation or the progenitor ability of CD34+ cells in vitro. However, deficientcells transplanted in immunodeficient mice disappeared progressively, suggesting the loss of HSCs ortheir differentiation capacity. Postulating that mutations accumulate with time, we have studiedhematopoiesis in young and aged XPC deficient mice. Differences described in young and agedhematopoiesis systems were found but, surprisingly, no difference was observed between wild typeand mutant mice at any age or genotoxic stress. Data from human cells demonstrate a potential rolefor XPC in HSC but new investigations are necessary to better understand the mechanisms implicatedand if XPC may participate in leukemogenesis
Aveni-Piney, Maud D'. "Le rôle immunomodulateur dans la réponse allo-immune de cellules hématopoïétiques mobilisées par du G-CSF." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T021.
Allogeneic Hematopoietic Stem Cell Transplantation (Allo-HSCT) is the most effective immunotherapy for acute leukemia, due to the development of graft-versus-leukemia (GVL) effect mediated by alloreactive donor T cells. However, donor T cells specific for recipient alloantigens are also responsible for graft-versus-host disease (GVHD), a life-threatening complication that frequently occurs after allo-HSCT. The administration of Granulocyte colony stimulating factor (G-CSF) is routinely performed to collect Peripheral Blood Stem Cells (PBSC) from healthy donors for allo-HSCT. Few studies identified that G-CSF can induce myeloid suppressive cells in mice (CD11b+ Gr1+) with no human counterpart. We demonstrated in our study that G-CSF can induce a new population named CD34+Monocyte. The cumulative incidence of acute grade II to IV GVHD following allo-HSCT was lower in patients receiving grafts containing CD34+ monocyte frequencies above 12% of the CD34+ population. In mice, we demonstrated that G-CSF mobilized a highly conserved CD34+ monocyte population. CD34+Monocytes require T cell-mediated IFN-γ to produce Nitric Oxide that inhibits T cell activation and proliferation. In vivo, we report that CD34+ monocyte-derived NO regulates the alloreactive response by inducing T cell apoptosis and subsequently, the induction of regulatory T cells. In fact, uptake of apoptotic T cells by macrophages triggers them to produce high levels of TGF-β that drives the expansion of Tregs and induces immune tolerance. Such tolerogenic monocytes could represent a good candidate for the development of novel immunoregulatory and therapeutic cellular therapies
Golfier, François. "Greffe in utero de cellules souches hématopoïétiques foetales humaines : purification de cellules CD34+/++ de foie foetal et de moëlle osseuse foetale." Lyon 1, 2001. http://www.theses.fr/2001LYO1T007.
Refeyton, Alice. "La survie et les adaptations métaboliques des cellules primitives mésenchymateuses et hématopoïétiques en anoxie et anoxie/aglycémie." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0028.
Mesenchymal stromal cells (MStroC) comprise multipotent stem cells (SC) capable of regenerating tissues damaged by ischemic insults. However, high mortality of MStroC after transplantation is highlighted during their engraftment. Therefore, exploring strategies to improve the viability of cell grafts constitutes the challenge of cell therapy. To this end, we performed functional and metabolic analyzes on two different types of populations containing somatic SC: MStroC and a population of hematopoietic niche partner cells, CD34+.MStroC or CD34+ cells were cultured under conditions of anoxia (absence of O2) and ischemic type (anoxia/aglycemia, absence of O2 and glucose, AA) or at 3% O2 corresponding to the physiological optimal concentration, then analyzed.Functional assays reveal that MStroC and CD34+ cells exhibit complete proliferation and differentiation properties in anoxia. Functional analyzes of single cells and gene expression revealed that MStroC and CD34+ are not only maintained in an AA state, but are those in which SC, having the highest proliferation and differentiation capacity, are the most enriched. Multiparametric metabolic analysis shows that survival in anoxia is mainly supported by glycolysis and lipid metabolism. On the other hand, the energy homeostasis of MStroC in the AA condition is partially ensured by anaerobic mitochondrial activity particularly involving mitochondrial complexes I, III and ubiquinone. Furthermore, a significant accumulation of succinate in this condition for both types of SC was demonstrated. This is due in part to an inversion of succinate dehydrogenase, which in turn is driven by fumarate spillover from purine nucleotide degradation and malate-aspartate shuttle activity. However, major pathways contributing to succinate accumulation include glycogen-induced glucose/pyruvate stimulation, as well as ketone body, amino acid, and propanoate metabolism which provide succinyl-CoA converted to succinate. Furthermore, MStroC ischemia survival is linked to sulfide metabolism and H2S consumption, as well as improved survival in the presence of H2S donors. SQR-mediated H2S oxidation results in reverse electron transport at mitochondrial complex I, using glutathione as an electron acceptor. The analysis of the use of energy substrates showed that CD34+ cells in anoxia seem to mainly use simple sugars in order to fuel the glycolytic pathway and a consequent reduction in mitochondrial metabolism compared to the 3% O2 condition. In contrast, in AA, Krebs cycle intermediates are used intensively to provide the coenzyme NAD/NADH.Our results reveal a great metabolic flexibility of MStroC and CD34+ populations based on the enrichment of somatic SC detected in anoxia or in the condition mimicking ischemia. Thus, unlike differentiated cells, somatic SC (mesenchymal and hematopoietic) have the capacity to survive in conditions of anoxia and aglycemia using the evolutionary conservative energy pathways existing in early eukaryotes living in anoxic zones enriched in sulfide . Exploiting this ex vivo conditioning under conditions mimicking ischemia could constitute a strategy to improve the survival of MStroC implanted in hypoxic/ischemic tissues
Jobin, Christine. "Expansion ex vivo des cellules CD34+ du sang adulte : étude du microenvironnement et caractérisation des cellules générées en condition d'hypoxie." Master's thesis, Université Laval, 2016. http://hdl.handle.net/20.500.11794/27068.
Moreau, Isabelle. "Étude du rôle des cellules stromales de moelle osseuse humaine dans le soutien de l'hématopoièse in vitro." Lyon 1, 1992. http://www.theses.fr/1993LYO1T001.