Academic literature on the topic 'Syndrome des plaquettes grises'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Syndrome des plaquettes grises.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Syndrome des plaquettes grises":
Benet, Blandine, Elodie Lainey, Odile Fenneteau, Véronique Baudouin, and Marie-Françoise Hurtaud-Roux. "ARC syndrome et observation de plaquettes grises: utilité diagnostique." Annales de biologie clinique 68, no. 4 (July 2010): 485–89. http://dx.doi.org/10.1684/abc.2010.0453.
Lapillonne, H. "Thrombopénie et plaquettes grises." Revue d'Oncologie Hématologie Pédiatrique 3, no. 1 (March 2015): 51–53. http://dx.doi.org/10.1016/j.oncohp.2014.12.003.
Bojalian, M. O., A. G. Akingba, J. C. Andersen, P. S. Swerdlow, P. G. Bove, O. W. Brown, and J. R. Rubin. "Syndrome des plaquettes collantes : Une forme inhabituelle d’ischémie artérielle." Annales de Chirurgie Vasculaire 24, no. 5 (July 2010): 755.e1–755.e6. http://dx.doi.org/10.1016/j.acvfr.2010.12.051.
Abid, H., S. Toumi, B. Fendri, R. Lahouimel, H. Chaker, I. Agrebi, N. Dammak, K. Kammoun, S. Yaich, and M. Ben Hmida. "MIA syndrome en hémodialyse : apport des rapports neutrophiles/lymphocytes et plaquettes/lymphocytes." Néphrologie & Thérapeutique 17, no. 5 (September 2021): 373. http://dx.doi.org/10.1016/j.nephro.2021.07.060.
Badre, A., M. Lehlimi, M. Chemsi, K. Maani, A. Habzi, and S. Benomar. "Syndrome de Kasabach-Merritt : quelle prise en charge en période néonatale ?" Périnatalité 13, no. 1 (March 2021): 43–45. http://dx.doi.org/10.3166/rmp-2021-0112.
Ben amou, A., M. S. Hamdi, S. Rekik, S. Rahmouni, K. Ines, Z. Khaoula, M. Abbes, et al. "Paramètres de l’inflammation au cours du syndrome Sjörgen primitif : rapports neutrophiles/lymphocytes et plaquettes/lymphocytes." La Revue de Médecine Interne 45 (June 2024): A144—A145. http://dx.doi.org/10.1016/j.revmed.2024.04.029.
Nesrine, G., A. Guiga, K. Dhouha, A. Bouker, A. Atig, and N. Ghannouchi. "Le volume moyen des plaquettes peut-il être un facteur prédictif de l’activité de la maladie dans le syndrome de Sjogren ?" La Revue de Médecine Interne 40 (June 2019): A129. http://dx.doi.org/10.1016/j.revmed.2019.03.148.
Fall Dieng, S., A. Ndiaye, EHD Niang, MLT Camara, K. Sarr, A. Dakono, A. Sall, and FSD Ndiaye. "C29: Aspects diagnostiques, pronostiques et évolutifs de la leucémie lymphoïde chronique au service d’Hématologie Clinique du CHN de Dalal Jamm de 2018 à 2020." African Journal of Oncology 2, no. 1 Supplement (March 1, 2022): S13. http://dx.doi.org/10.54266/ajo.2.1s.c29.bdqthuzpwy.
Pau, Alice K., Melanie A. Fisher, Wanda Maldonado, and Marc Lebel. "Severe Thrombocytopenia Associated with Once-Daily Rifampin Therapy." Drug Intelligence & Clinical Pharmacy 21, no. 11 (November 1987): 882–84. http://dx.doi.org/10.1177/106002808702101107.
Srivatsav, Varun, Ardyth Milne, Karen Hofeld, and Mariam Abbas. "Case Report on the Rare Diagnosis of Schnitzler’s Syndrome." Canadian Journal of General Internal Medicine 17, no. 4 (October 17, 2022). http://dx.doi.org/10.22374/cjgim.v17i4.620.
Dissertations / Theses on the topic "Syndrome des plaquettes grises":
Delage, Laure. "Des déficiences génétiques comme modèles naturels pour l'étude de la régulation des checkpoints immunitaires et la caractérisation des réponses auto-immunes." Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5190.
Recessive NBEAL2 mutations have been reported in patients with Gray Platelet Syndrome (GPS). This syndrome is characterized by a macro-thrombocytopenia, with platelets lacking alpha-granules, leading to bleeding disorders, often associated with splenomegaly. Thus, NBEAL2 plays a crucial role in the trafficking of alpha-granules in platelets. Moreover, our lab has also described NBEAL2 deficiencies in patients presenting clinical features of the autoimmune lymphoproliferative syndrome, suggesting a role of NBEAL2 in immune homeostasis and tolerance. A broader international cohort of GPS patients has been described, revealing immune system abnormalities (autoimmune diseases, autoantibodies, lymphopenia). If the role of NBEAL2 in the traffic of granules is often investigated, the exact mechanism leading to the development of autoimmune manifestations in GPS patients remains unknown. NBEAL2 belongs to a protein family involved in vesicular trafficking, all of which possess a conserved BEACH domain. Within this BEACH-domain containing proteins family, one of the closest members to NBEAL2 is LRBA. LRBA is involved in the recycling of CTLA-4, an inhibitory immune checkpoint. CTLA-4 plays a crucial role in the regulation of immune responses and tolerance. Recessive mutations of LRBA lead to similar clinical features as partial CTLA-4 deficiency: autoimmunity, lymphocytic infiltrations, and progressive B lymphopenia. Physiologically, LRBA prevents the lysosomal degradation of CTLA-4 and allows its recycling to the membrane. By analogy with LRBA, we investigated the importance of NBEAL2 in immune checkpoints intracellular trafficking and we brought new insights on its role in lymphocytes. Thus, NBEAL2 is a scaffold protein, binding LRBA, and involved in CTLA-4 trafficking as well as in vesicular trafficking in general. This work brings new knowledge to the regulation of CTLA-4 in activated T lymphocytes, a list of new partners for NBEAL2 protein and a new model of vesicular trafficking in which NBEAL2 is involved. Finally, a better understanding of the mechanisms leading to autoimmunity in patients with gray platelets syndrome could lead to better diagnosis and treatment management
Lauzière, Véronique. "Distribution subcellulaire de la protéine FMRP dans les plaquettes sanguines quiescentes et activées." Mémoire, Université de Sherbrooke, 2011. http://hdl.handle.net/11143/5549.
Touat, Ziad. "Anévrysmes des aortes ascendante et abdominale chez l'homme : rôle des plaquettes dans ces pathologies." Paris 7, 2007. http://www.theses.fr/2007PA077069.
Aneurysms are defined by a dilation of the artery which leads to a loss of parallelism of the vascular wall. The implication of the blood component was neglected a long time in these pathologies. My work during my PhD concentrated on the study of a bond between aortic aneurysms of the aorta and the blood components. The abdominal aortic aneurysms are accompanied by a nonocclusive thrombus which forms an active interface between blood and arterial wall. We showed the active role for this thrombus in the AAA. The thrombi form a tank of proteases which attack the wall and prevent the cicatrization of the thrombus. I also showed that the renewal of these thrombi is responsible for enrichment in PMI1 via the constant exposure of P-selectin by activated platelets. These results were validated in vivo on an experimental model of aneurisms. I then showed for the first time a state of platelet activation and a generation of thrombin in patient with thoracic ascending aortic aneurysm, by detection of biomarkers. The development of these aneurisms is not accompanied by the formation of a thrombus. These original results suggest ; role for platelet activation and of the prothrombin on the evolution of this disease. In conclusion, my work highlights for the 1st time, the role of the platelets and coagulation cascade in the aneurysmal diseases. My results lead to a better understanding of this pathology whose inescapable evolution is the rupture, allowing to consider new clinical applications, into therapeutic and functional imagery
Tariket, Sofiane. "Investigation de la pathogenèse du syndrome de détresse respiratoire aiguë post-transfusionnel (TRALI) dans un modèle murin." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSES059/document.
Blood transfusion saves lives and reduces morbidity for many diseases and clinical conditions, but it is not without complications. A transfusion-related adverse event, also known as the Adverse Reaction (AR), is an incident occurring in a patient during or after a blood transfusion. Among them, TRALI is considered as one of the most critical inflammatory reactions. This pathology usually occurs within 6 hours after transfusion. Two types are recognized: immune TRALI and non-immune TRALI. In France, the first is almost completely prevented by a blood product safety policy, while the frequency of the second increases. The pathophysiology of TRALI remains poorly understood. While some scientists give an important function of patient blood platelets, others consider them dispensable. The aim of this thesis was, first, to investigate the inflammatory potential of blood platelets stored in platelet concentrates and its impact on the general vascular endothelium. Next, the role of patient blood platelets, including their secretory products, in the pathogenesis of this transfusion complication will be evaluated. For it, an ALI (mimicking a TRALI) was triggered, in an in vivo model, by an injection of anti-MHC I antibody in mice previously stimulated with LPS. Our results confirm the inflammatory potential of blood platelets in platelet concentrates, which can probably assume the entire responsibility for triggering a non-immune TRALI, and a secondary role for patient blood platelets in the amplification of the severity of this pathology. This thesis is the continuity of studies conducted in the laboratory GIMAP-EA3064, investigating the function of blood platelets in inflammation, thus opening up new perspectives in transfusion safety
Macchi, Laurent. "Etude de la caractérisation des anticorps anti-plaquettes dans différentes circonstances pathologiques et thérapeutiques." Bordeaux 2, 1997. http://www.theses.fr/1997BOR28524.
Lessard, Mandy. "Dosage quantitatif de la protéine FMRP développement d'un nouvel outil diagnostique pour le syndrome du X fragile." Mémoire, Université de Sherbrooke, 2011. http://hdl.handle.net/11143/5560.
Bellio, Marie. "La plaquette sanguine : un nouvel acteur du syndrome hémorragique de Noonan et du développement des maladies métaboliques." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30010.
Blood platelets play a major role in the maintenance of vascular integrity. They are the first blood cells recruited after vessel injury to stop bleeding by thrombus formation. Platelet hyper-activation is also a critical element in thrombotic events associated to several pathologies such as metabolic syndrome, which makes them major pharmacologic targets. My thesis work was focused on two main axis: (i) analysis of platelet activation in Noonan syndrome (NS) and Noonan syndrome with multiple lentigines (NSML) and (ii) characterization of the role of platelets in non-alcoholic fatty liver disease (NAFLD). Firstly, motivated by the occurrence of bleeding anomalies frequently reported in NS, we focused on characterizing platelet activation in NS and NSML caused respectively by a gain or a loss of function of the protein tyrosine phosphatase SHP2. We observed that platelets from NS patients display a defective in vitro aggregation to low concentrations of collagen, a GPVI agonist, associated to a decrease in thrombus growth ex vivo on a collagen surface under arterial shear stress. The mouse model phenocopying NS also exhibit a significant reduction in in vitro platelet aggregation induced by low concentrations of GPVI agonists, which is associated to a deficiency in GPVI signalling. The thrombus formation ex vivo under arterial shear stress as well as in vivo following a local carotid injury was also significantly affected. Primary haemostasis is also defective in NS mice as shown by a significant increase in mouse tail bleeding time. In contrast, NSML mouse platelets exhibited an increased activation after GPVI stimulation and an enhanced platelet thrombotic phenotype on collagen matrix under arterial shear stress. Interestingly, this platelet hyper-activation is also observed in blood samples from NSML patients ex vivo in arterial shear rate and exacerbated in high shear rate condition. This study allows the discovery of two new thrombopathies linked to platelet signalling defects and provides important information for the medical care of patient with NS or NSML in risk of bleeding or thrombosis situations. Besides, this study brings new insights into the understanding of SHP2 function in platelet activation. Secondly, I studied the role of platelets in NAFLD development. Using mouse models fed with different hyperlipidic diets mimicking different step of the NAFLD, we showed a protective role for platelets in hepatic glucidic and lipidic metabolism by inhibition of lipid storage. Furthermore, platelets protect against hepatic inflammation and fibrosis by decreasing inflammatory cells recruitment and fibrosis development. This protective role is associated to the presence of platelet aggregates in liver sinusoids. Interestingly, we demonstrate that platelet Vps34 deletion allows to slow down NAFLD development. Thereby, these innovative results highlight a new protective role of platelet in NAFLD development and could allow the identification of potential pharmacologic targets for preventing or limiting the disease. In conclusion, my thesis work brings new data on the role of platelets in different physiopathologic conditions: NS, NSML and NAFLD
Chappey, Olivier. "Intérêt de l'étude de l'incorporation de la sérotonine marquée par les plaquettes sanguines dans l'exploration biologique du syndrome d'Hermansky-Pudlak." Paris 5, 1991. http://www.theses.fr/1991PA05P106.
Roussillon, Emmanuel. "Importance de la thrombopénie dans la prise en charge du Hellp syndrome : à propos de 62 cas." Bordeaux 2, 1999. http://www.theses.fr/1999BOR23104.
Pellerin, David. "Correction de l’hyperactivité de la voie ERK par la lovastatine chez des individus avec syndrome du X fragile : potentiel des cascades signalétiques plaquettaires comme nouvelles mesures de la réponse clinique dans les essais thérapeutiques." Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/11082.
Abstract: Background: Fragile X syndrome (FXS) results from loss of FMRP expression, which causes several signaling dysregulations, including the hyperactivation of the Mitogen-activated protein kinase (MAPK)/Extracellular signal-regulated kinase (ERK) pathway. Lovastatin, a drug used for the treatment of hypercholesterolemia, pleiotropically inhibits the MAPK/ERK cascade and has successfully corrected key pathological phenotypes in the FXS mouse model, underscoring its ‘disease-modifying’ potential. Thereby, we conducted in 2013 the first open-label clinical trial investigating the effect of a 12-week lovastatin regimen on cognitive and behavioral disabilities in FXS. Most individuals presented subtle positive cognitive changes as assessed by the Vineland-II Adaptive Behavior Scale (VABS-II) as well as behavior improvements using the widely used scale Aberrant Behavior Checklist-Community (ABC-C). The latter two scales are filled up by caregivers making them rater-dependent and prone to observer-expectancy effect. This might result in a placebo effect which is inherent to the open-label design of the trial. We therefore investigated whether blood platelets’ signaling cascades may be used as objective biomarkers to monitor treatment response. Methods: Blood samples were gathered from 15 FXS individuals during the trial in order to evaluate by quantitative Western Blotting the in vivo effect of lovastatin on ERK activity in blood platelets, and to correlate clinical and biological responses. The basal phosphorylation status of ERK was also assessed in platelets from a control cohort. Results: Our results showed a more than two-fold significant increase in FXS blood platelet basal ERK phosphorylation as compared to controls (p=0.002). Of note, we found that this hyperphosphorylation was normalized following the 12-week lovastatin trial (p=0.007) in 13 of the 15 FXS individuals enrolled in the trial. This represents the first evidence for a beneficial effect of lovastatin in human FXS. The extent of changes in ERK phosphorylation was also found to partly correlate with the clinical response scales’ scores, especially for the VABS-II. Indeed, the composite total score and the ‘daily living skills’ as well as the ‘socialization’ subscales scores of the VABS-II were correlated with the biological response (p=0.03). In comparison, no correlation was observed with the ABC-C scale. Conclusion: Broadly, these results suggest that platelets’ signaling cascades could be used as biomarkers to objectively assess treatment response during future clinical trials.