Docteur CHARLES BURTIN

Livres & ouvrages

• 📕

  Biothérapies

  que savent les patients traités et leurs médecins généralistes respectifs ? : expérience d'un centre hospitalier non universitaire : rappel de l'intérêt de l'éducation thérapeutique du patient et de l'information de son médecin traitant pour un suivi optimal

  2014 · 314 p.

  avec Stéphane Martinon, Université Claude Bernard (Lyon).

Source : Google Books — filtre catégories médicales/santé/sciences.

Lieu de consultation

• CH ST JOSEPH ST LUC

  20 Quai CLAUDE BERNARD, 69365 Lyon 7e Arrondissement

  ☎ 0478618181Hospitalier🏥 Centre CH ↗🏥 Voir cet établissement

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

Prendre rendez-vous & contact

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Top publications · les plus citées

• 1

  Synthesis and biological evaluation of novel pyrazoles and indazoles as activators of the nitric oxide receptor, soluble guanylate cyclase

  Journal of medicinal chemistry · 2001

  📚 55 citations🎯 RCR 1.41
• 2

  MicroRNA-146a-deficient mice develop immune complex glomerulonephritis

  Scientific reports · 2019

  📚 8 citations🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  AbstractMicroRNAs (miRNAs) play an important role in the kidneys under physiological and pathological conditions, but their role in immune glomerulonephritis is unclear. miR-146a has been identified as a key player in innate immunity and inflammatory responses, and in the kidney, this miRNA is involved in the response of injured tubular cells. We studied the renal and immune phenotypes of miR-146a+/+ and miR-146a−/− mice at 12 months of age, and the results showed that miR-146a−/− mice developed autoimmunity during aging, as demonstrated by circulating antibodies targeting double-stranded DNA and an immune complex-mediated glomerulonephritis associated with a mild renal immune infiltrate. In addition, miR-146a−/− mice showed reduced expression of the transmembrane protein Kim1/Tim1, a key regulator of regulatory B cell (Breg) homeostasis, in the kidney and the immune cells. The numbers of memory B cells and plasmablasts were increased in miR-146a−/− mice compared with the numbers in wild-type mice, whereas Bregs were decreased in number and displayed an altered capacity to produce IL-10. Finally, we showed that miR-146a−/− mice develop an autoimmune syndrome with increasing age, and this syndrome includes immune complex glomerulonephritis, which might be due to altered B cell responses associated with Kim1/Tim1 deficiency. This study unravels a link between miR-146a and Kim1 and identifies miR-146a as a significant player in immune-mediated glomerulonephritis pathogenesis.

Publications scientifiques (2) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

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