📇 Rhumatologue ·
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Praticien-chercheur
15 articles scientifiques publiés — formation continue solide
✨ Génération du profil synthétique IA en cours…
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Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
Articles déposés en accès libre sur l'archive ouverte des universités françaises (HAL) — gage d'activité de recherche en France.
Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).
Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).
Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
European journal of human genetics : EJHG · 1998
Arthritis and rheumatism · 2006
AbstractObjectiveThe IKK complex regulates NF‐κB activation, an important pathway implicated in the rheumatoid arthritis (RA) disease process. This study was undertaken to assess the efficacy of N‐(6‐chloro‐7‐methoxy‐9H‐β‐carbolin‐8‐yl)‐2‐methylnicotinamide (ML120B), a potent and selective small molecule inhibitor of IKKβ.MethodsPolyarthritis was induced in rats by injection of Freund's complete adjuvant into the hind footpad. ML120B was administered orally twice daily, either prophylactically or therapeutically. Paw volumes and body weights were measured every 2–3 days throughout the study. We assessed bone erosions by several methods: histologic evaluation, quantitative micro–computed tomography (micro‐CT) imaging analysis, and measurement of type I collagen fragments in the serum. Quantitative polymerase chain reaction was used to evaluate expression of messenger RNA for genes related to inflammation and to bone and cartilage integrity.ResultsOral administration of ML120B inhibited paw swelling in a dose‐dependent manner (median effective dosage 12 mg/kg twice daily) and offered significant protection against arthritis‐induced weight loss as well as cartilage and bone erosion. We were able to directly demonstrate that NF‐κB activity in arthritic joints was reduced after ML120B administration. Also, we observed that down‐regulation of the NF‐κB pathway via IKKβ inhibition dampened the chronic inflammatory process associated with rat adjuvant‐induced arthritis.ConclusionThe results of the present study suggest that IKKβ inhibition is an effective therapeutic approach to treat both the inflammation and the bone/cartilage destruction observed in RA. Methods for the determination of serum markers for bone and cartilage destruction, as well as micro‐CT analysis, may aid in predicting and evaluating the therapeutic efficacy of IKKβ inhibition therapy in humans.
eLife · 2022
Restoring damaged β-cells in diabetic patients by harnessing the plasticity of other pancreatic cells raises the questions of the efficiency of the process and of the functionality of the new Insulin -expressing cells. To overcome the weak regenerative capacity of mammals, we used regeneration-prone zebrafish to study β-cells arising following destruction. We show that most new in s ulin cells differ from the original β-cells as they coexpress Somatostatin and Insulin. These bihormonal cells are abundant, functional and able to normalize glycemia. Their formation in response to β-cell destruction is fast, efficient, and age-independent. Bihormonal cells are transcriptionally close to a subset of δ-cells that we identified in control islets and that are characterized by the expression of somatostatin 1.1 ( sst1.1 ) and by genes essential for glucose-induced Insulin secretion in β-cells such as pdx1 , s lc2a2 and gck . We observed in vivo the conversion of monohormonal sst1.1- expressing cells to sst1.1+ ins + bihormonal cells following β-cell destruction. Our findings support the conclusion that sst1.1 δ-cells possess a pro-β identity enabling them to contribute to the neogenesis of Insulin-producing cells during regeneration. This work unveils that abundant and functional bihormonal cells benefit to diabetes recovery in zebrafish.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Proceedings of the National Academy of Sciences of the United States of America · 2023 · Journal Article
Khatri D, Putoux A, Cologne A, Kaltenbach S, et al.
eLife · 2022 · Journal Article
Carril Pardo CA, Massoz L, Dupont MA, Bergemann D, et al.
Acta cardiologica · 2021 · Journal Article
Martens P, Ter Maaten JM, Vanhaen D, Heeren E, et al.
Biomedicines · 2021 · Journal Article
Massoz L, Dupont MA, Manfroid I
Human molecular genetics · 2019 · Journal Article
Dupont MA, Humbert C, Huber C, Siour Q, et al.
La Revue de medecine interne · 2013 · Case Reports
Kouassi Djaha JM, Jenvrin C, Dupont MP, Steiner J, et al.
Arthritis and rheumatism · 2006 · Journal Article
Schopf L, Savinainen A, Anderson K, Kujawa J, et al.
Revista iberoamericana de micologia · 2006 · Evaluation Study
Dupont J, Dennetière B, Jacquet C, Dupont MF
Cahiers d'anesthesiologie · 1987 · Journal Article
Dupont M, Alessandri C, Lebré P, Rastello C
Pathologie-biologie · 1984 · English Abstract
Dupont M, Jover B, Mialanes N, Mimran A
La Nouvelle presse medicale · 1977 · Case Reports
Guidet M, Gallinet E, Metzger JM, Dupont MJ, et al.
Annales chirurgiae et gynaecologiae Fenniae · 1968 · Journal Article
Dupont M, Vainio K
Acta orthopaedica Belgica · 1967 · Journal Article
Dupont M
Journal belge de rhumatologie et de medecine physique = Belgisch tijdschrift voor reumatologie en fysische geneeskunde · 1966 · Journal Article
Michotte L, Dupont M
European journal of human genetics : EJHG · 1998 · Journal Article
Dewalle M, Domingo C, Rozenbaum M, Ben-Chétrit E, et al.