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3 raisons identifiées
Plateau technique de référence
Assistance publique – Hôpitaux de Paris (APHP) — équipements et expertise pointus pour les cas complexes
Auteur de référence en rhumatologie
32 articles scientifiques publiés — un praticien à la pointe de la recherche
Délais de RDV courts dans la région
336.2 rhumatos / 100 000 hab. — département bien doté
✨ Génération du profil synthétique IA en cours…
Articles déposés en accès libre sur l'archive ouverte des universités françaises (HAL) — gage d'activité de recherche en France.
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
Essential role of smooth muscle Rac1 in severe asthma-associated airway remodelling
2021ArticleThorax
Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).
GHU APHP NUP SITE BICHAT C BERNARD
46 R HENRI HUCHARD, 75877 PARIS CEDEX 18
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).
American journal of respiratory and critical care medicine · 2003
Abstract To identify airway pathologic abnormalities selectively associated with severe asthma, we examined 10 control subjects, 10 patients with intermittent asthma, 15 patients with mild-to-moderate persistent asthma, 15 patients with severe persistent asthma, and 10 patients with chronic obstructive pulmonary disease. Bronchial biopsies were assessed for epithelial integrity; subepithelial basement membrane (SBM) thickness; collagen type III deposition; eosinophil, neutrophil, and fibroblast numbers; mucous gland and airway smooth muscle (ASM) areas; SBM-ASM distance; ASM hypertrophy (increased cell size); and the expression of the contractile proteins α-actin, smooth muscle myosin heavy-chain isoforms, myosin light-chain kinase, and the phosphorylated form of the regulatory light chain of myosin. Neither mucosal eosinophilia nor neutrophilia, epithelial damage, or SBM thickness reflected asthma severity. In contrast, higher numbers of fibroblasts (p < 0.001), an increase in collagen type III deposition (p < 0.020), larger mucous gland (p < 0.040) and ASM (p < 0.001) areas, augmented ASM cell size (p < 0.001), and myosin light-chain kinase expression (p < 0.005) distinguished patients with severe persistent asthma from patients with milder disease or with chronic obstructive pulmonary disease. Stepwise multivariate regression analysis established that fibroblast numbers and ASM cell size were negatively associated with prebronchodilator and postbronchodilator FEV1 values in patients with asthma. We conclude that fibroblast accumulation and ASM hypertrophy in proximal airways are selective determinants of severe persistent asthma.
The New England journal of medicine · 2007
American journal of respiratory and critical care medicine · 2010
Abstract Rationale Chronic obstructive pulmonary disease (COPD) is characterized by airway inflammation and remodeling. High-mobility group box 1 (HMGB1), a nuclear protein that is released during inflammation and repair, interacts with proinflammatory cytokines and with the receptor for advanced glycation end products (RAGE), which is highly expressed in the lung. Objectives To determine whether HMGB1 is augmented in COPD and is associated with IL-1β and RAGE. Methods HMGB1 was assessed in the bronchoalveolar lavage (BAL) of 20 never-smokers, 20 smokers, and 30 smokers with COPD and it was correlated with inflammatory and clinical parameters. In parallel, HMGB1 and RAGE immunolocalization was determined in bronchial and lung tissues. Last, binding of HMGB1 to IL-1β in human macrophages and in BAL fluid was examined. Measurements and Main Results BAL levels of HMGB1 were higher in smokers with COPD than in smokers and never-smokers (P < 0.0001 for both comparisons), and similar differences were observed in epithelial cells and alveolar macrophages. BAL HMGB1 correlated positively with IL-1β (rs = 0.438; P = 0.0006) and negatively with FEV1 (rs = −0.570; P < 0.0001) and transfer factor of the lung for carbon monoxide (rs = −0.382; P = 0.0026). HMGB1–IL-1β complexes were found in BAL supernatant and alveolar macrophages from smokers and patients with COPD, as well as in the human macrophage cell line, THP-1, where they enhanced the synthesis of tumor-necrosis factor-α. RAGE was overexpressed in the airway epithelium and smooth muscle of patients with COPD and it colocalized with HMGB1. Conclusions Elevated HMGB1 expression in COPD airways may sustain inflammation and remodeling through its interaction with IL-1β and RAGE.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
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The Journal of infectious diseases · 1987 · Case Reports
Saraux JL, Vigneron AM, Berthelot G, Dombret MC, et al.
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Naccache JM, Jouneau S, Didier M, Borie R, et al.
The open respiratory medicine journal · 2013 · Journal Article
Taillé C, Poulet C, Marchand-Adam S, Borie R, et al.
The journal of allergy and clinical immunology. In practice · 2014 · Case Reports
Justet A, Neukirch C, Poubeau P, Arrault X, et al.
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