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RhumatologueMédecins généralistes et spécialistes👤 Libéral intégral

M. Docteur JEAN-FRANCOIS ANTOINE

📍 Agde (34)Libéral💶 Secteur 1RPPS 10003228342
📊 Reconnaissance scientifique : 12/100📝 60 articles publiés📚 HAL (8)

✨ Profil synthétique

IA · 29/04/2026

Le Dr Jean-François Antoine est un rhumatologue libéral à Agde. Il a publié 60 travaux de recherche et possède un h-index de 12 selon OpenAlex. Ses publications sur PubMed portent principalement sur les csDMARDs, le lupus, la pédiatrie et la maladie de Sjögren.

Expertises présumées

  • csDMARDs
  • Lupus
  • Pédiatrie
  • Sjögren
  • Rhumeumatisme pédiatrique
  • Thérapeutique biologique

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🎓 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

12

h articles cités ≥ h fois chacun. Un h de 12 = 12 publications avec 12+ citations.

Citations

630

Publications

60

i10-index

15

Thématiques principales

  • Manufacturing Process and Optimization ×11
  • Robotic Mechanisms and Dynamics ×9
  • Electric Motor Design and Analysis ×6
  • Magnetic Bearings and Levitation Dynamics ×6
  • Product Development and Customization ×6

Affiliations FR : Arts et Métiers · Laboratoire de Conception Fabrication Commande · HESAM Université

Voir sur OpenAlex ↗🆔 ORCID 0000-0003-2885-414X

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).

Localisation

Adresses géocodées via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.

Lieu de consultation

Tarifs & secteur de conventionnement

🟢 Secteur 1 — Tarif conventionnéSource CNAM (Annuaire santé Ameli)
💳 Carte VitaleLibéral intégral
📊 Comprendre le remboursement

Prendre rendez-vous & contact

🗓 Trouver sur Doctolib📇 Ajouter à mes contacts

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
    Inflammatory disease processes and interactions with nutrition

    The British journal of nutrition · 2009

    📚 355 citations🎯 RCR 11.31Top 2% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing as well as tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Various dietary components including long chain ω-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy. These components act through a variety of mechanisms including decreasing inflammatory mediator production through effects on cell signaling and gene expression (ω-3 fatty acids, vitamin E, plant flavonoids), reducing the production of damaging oxidants (vitamin E and other antioxidants), and promoting gut barrier function and anti-inflammatory responses (prebiotics and probiotics). However, in general really strong evidence of benefit to human health through anti-inflammatory actions is lacking for most of these dietary components. Thus, further studies addressing efficacy in humans linked to studies providing greater understanding of the mechanisms of action involved are required.

  • 2
    Clinical features and pathophysiological basis of sensory neuronopathies (ganglionopathies)

    Muscle & nerve · 2004

    📚 114 citations🎯 RCR 2.79Top 18% NIH
    Lire l'abstract Crossref ↓

    AbstractSensory ganglionopathies have a frequent association with neoplastic disorders (paraneoplastic subacute sensory neuronopathy, or SSN) or dysimmune disorders (Sjögren's syndrome, SS; Miller Fisher syndrome; and Bickerstaff's brainstem encephalitis, BBE), with drugs, such as cisplatin or pyridoxine, and with inherited disorders with degeneration of dorsal root ganglion cells. Unsteady gait and pseudoathetoid movements of the hand are the distinctive signs encountered in these disorders. The chronic disorders are characterized by non–length‐dependent abnormalities of sensory nerve action potentials (SNAPs) and differ from other sensory neuropathies in showing a global, rather than distal, decrease in SNAP amplitudes. This review focuses on recent advances in defining the mechanisms involved in sensory ganglionopathies. Specific topics include a summary of their clinical features, pathological findings, and immunopathology. In SSN, early diagnosis by the detection of anti‐Hu antibodies and early treatment of the cancer gives the best chance of stabilizing the disorder. In SS sensory ganglionitis, response to treatment has been disappointing, but immunomodulating treatments are emerging. The immunological profile common to BBE and Fisher syndrome supports a common pathogenesis. In toxic sensory neuronopathy, no treatment is available. The differential diagnosis involves separating sensory ganglionopathies from other ataxic polyneuropathies, such as infectious neuropathies, sensory neuropathies with various autoantibodies, and the neuropathies seen in celiac disease. Muscle Nerve 30:255–268, 2004

  • 3
    Carcinoma associated paraneoplastic peripheral neuropathies in patients with and without anti-onconeural antibodies

    Journal of neurology, neurosurgery, and psychiatry · 1999

    📚 94 citations🎯 RCR 3.37Top 14% NIH🔓 Open Access📄 PDF gratuit ↗

Publications scientifiques (20) — classées par pathologie

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

Transversal16

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csDMARDs1

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Lupus1

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Pédiatrie1

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Sjögren1

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