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Rhumatologue

Docteur Charlotte LUCAS

📍 Quimper (29)HospitalierRPPS 10100981280
📊 Reconnaissance scientifique : 10/100📝 21 articles publiés📚 HAL (8)🏆 2 DU/DIU

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🏅 DU / DIU

  • DIU Pathologies osseuses médicales
  • DIU Etudes approfondies polyarthrites-maladies

🎓 Diplômes

  • DE Docteur en médecine

Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.

Activité de recherche & publications

Source : bases de données publiques (OpenAlex, PubMed).

h-index

10

h articles cités ≥ h fois chacun. Un h de 10 = 10 publications avec 10+ citations.

Citations

269

Publications

21

i10-index

11

Thématiques principales

  • Influenza Virus Research Studies ×13
  • SARS-CoV-2 and COVID-19 Research ×6
  • Animal Disease Management and Epidemiology ×6
  • Viral gastroenteritis research and epidemiology ×5
  • interferon and immune responses ×5

Affiliations FR : École Nationale Vétérinaire de Toulouse · Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement · Interactions hôtes-agents pathogènes

Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.

Bibliographie

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Lieu de consultation

  • CHIC QUIMPER

    14 Avenue YVES THEPOT, 29107 Quimper

    0298526060Hospitalier

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
    Tissue-Specific Immunopathology in Fatal COVID-19

    American journal of respiratory and critical care medicine · 2021

    📚 230 citations🎯 RCR 13.47Top 2% NIH🔓 Open Access
    Lire l'abstract Crossref ↓

    Abstract Rationale In life-threatening coronavirus disease (COVID-19), corticosteroids reduce mortality, suggesting that immune responses have a causal role in death. Whether this deleterious inflammation is primarily a direct reaction to the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or an independent immunopathologic process is unknown. Objectives To determine SARS-CoV-2 organotropism and organ-specific inflammatory responses and the relationships among viral presence, inflammation, and organ injury. Methods Tissue was acquired from 11 detailed postmortem examinations. SARS-CoV-2 organotropism was mapped by using multiplex PCR and sequencing, with cellular resolution achieved by in situ viral S (spike) protein detection. Histologic evidence of inflammation was quantified from 37 anatomic sites, and the pulmonary immune response was characterized by using multiplex immunofluorescence. Measurements and Main Results Multiple aberrant immune responses in fatal COVID-19 were found, principally involving the lung and reticuloendothelial system, and these were not clearly topologically associated with the virus. Inflammation and organ dysfunction did not map to the tissue and cellular distribution of SARS-CoV-2 RNA and protein between or within tissues. An arteritis was identified in the lung, which was further characterized as a monocyte/myeloid-rich vasculitis, and occurred together with an influx of macrophage/monocyte-lineage cells into the pulmonary parenchyma. In addition, stereotyped abnormal reticuloendothelial responses, including excessive reactive plasmacytosis and iron-laden macrophages, were present and dissociated from viral presence in lymphoid tissues. Conclusions Tissue-specific immunopathology occurs in COVID-19, implicating a significant component of the immune-mediated, virus-independent immunopathologic process as a primary mechanism in severe disease. Our data highlight novel immunopathologic mechanisms and validate ongoing and future efforts to therapeutically target aberrant macrophage and plasma-cell responses as well as promote pathogen tolerance in COVID-19.

  • 2
    Transforming growth factor beta 1 (TGF-beta 1) induced neutrophil recruitment to synovial tissues: implications for TGF-beta-driven synovial inflammation and hyperplasia

    The Journal of experimental medicine · 1991

    📚 192 citations🎯 RCR 4.51Top 9% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    We have studied the consequences of introducing human recombinant transforming growth factor beta 1 (hrTGF-beta 1) into synovial tissue of the rat, to begin to better understand the significance of the fact that biologically active TGF-beta is found in human arthritic synovial effusions. Within 4-6 h after the intra-articular injection of 1 microgram of hrTGF-beta 1 into rat knee joints, extensive recruitment of polymorphonuclear leukocytes (PMNs) was observed. Cytochemistry and high resolution histological techniques were used to quantitate the influx of PMNs, which peaked 6 h post-injection. In a Boyden chamber assay, hrTGF-beta 1 at 1-10 fg/ml elicited a chemotactic response from PMNs greater in magnitude than that evoked by FMLP, establishing that TGF-beta 1 is an effective chemotactic agent for PMNs in vitro as well as in vivo. That PMNs may represent an important source of TGF-beta in inflammatory infiltrates was strongly suggested by a demonstration that stored TGF-beta 1 was secreted during phorbol myristate acetate-stimulated degranulation in vitro. Acid/ethanol extracts of human PMNs assayed by ELISA contained an average of 355 ng of TGF/beta 1 per 10(9) cells potentially available for secretion during degranulation of PMNs. [3H]Thymidine incorporation in vivo and autoradiography of tissue sections revealed that widespread cell proliferation was triggered by TGF-beta 1 injection. Synovial lining cells and cells located deep within the subsynovial connective tissue were identified as sources of at least some of the new cells that contribute to TGF-beta 1-induced hyperplasia. Our results demonstrate that TGF-beta is capable of exerting pathogenic effects on synovial tissue and that PMNs may represent a significant source of the TGF-beta present in synovial effusions.

  • 3
    Risk factors for meniscal tears: a systematic review including meta-analysis

    The Journal of orthopaedic and sports physical therapy · 2013

    📚 139 citations🎯 RCR 6.77Top 5% NIH
    Lire l'abstract Crossref ↓

    Study Design Systematic review with meta-analysis. Objectives To review and critically appraise the literature for factors that increase the risk for meniscal tears. Background Meniscal tears are an important cause of disability and time lost from work, and are associated with a 4-fold increase in the long-term risk of knee osteoarthritis. Knowledge of the risk factors that lead to meniscal tears can help to correctly diagnose knee injuries and is important to the development of prevention strategies for knee osteoarthritis. Methods A search of the Cochrane Database of Systematic Reviews, MEDLINE, and Embase, from 1950 to January 2012, and a hand search of reference lists of all initially selected studies, without restriction on language or date of publication, were conducted. Prospective, retrospective, and case-control studies that included individuals over 16 years of age, who had no previous meniscal injuries or surgeries, were selected. A meta-analysis for 17 risk factors was performed. Where considerable heterogeneity among studies was present or the data did not provide sufficient information to perform a meta-analysis, a qualitative synthesis was conducted. Results Eleven studies, with a total of 7358 participants, were selected for systematic review. Data were available for meta-analysis for 10 of the 11 studies. Qualitative analysis was conducted using data from 3 of the 11 studies. Results showed strong evidence that age (older than 60 years), gender (male), work-related kneeling and squatting, and climbing stairs (greater than 30 flights) were risk factors for degenerative meniscal tears. We also found strong evidence that playing soccer and playing rugby were strong risk factors for acute meniscal tears. Waiting longer than 12 months between the anterior cruciate ligament injury and reconstructive surgery was a strong risk factor for a medial meniscal tear but not for a lateral meniscal tear. Conclusion The literature indicates a number of risk factors leading to either degenerative or acute meniscal tears, with some of these factors being potentially modifiable. Level of Evidence Prognosis, level 2a. J Orthop Sports Phys Ther 2013;43(6):352–367. Epub 29 April 2013. doi:10.2519/jospt.2013.4295

Publications scientifiques (29) — classées par pathologie

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

Transversal17

Génétique3

Revue / méta-analyse3

Revue générale3

Lupus2

Activité physique / Rééducation1

Biothérapies non-anti-TNF1

csDMARDs1

Essai clinique1

Recommandations1

Santé mentale / fatigue1

Vascularites des gros vaisseaux1

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