📇 Rhumatologue · VANNES CEDEX · (56) · Salarié
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2 raisons identifiées
Praticien-chercheur
5 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
141.3 rhumatos / 100 000 hab. — département bien doté
6 publications sur 5 ans
✨ Génération du profil synthétique IA en cours…
Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
Influence scientifique
5
5 articles ont été cités au moins 5fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.
h-index
Total citations reçues
167
Nombre de fois où d'autres équipes ont mentionné ses publications dans leurs propres travaux.
Publications totales
17
Articles, revues et chapitres référencés dans les bases académiques internationales.
Articles influents
4
Publications ayant marqué leur domaine — chacune citée au moins 10 fois par d'autres chercheurs.
i10-index
Thématiques principales
Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.
CHBA SITE DE VANNES
20 BD GENERAL MAURICE GUILLAUDOT BP 70555, 56017 VANNES CEDEX
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 endocrinology · 2012
ContextPapillary thyroid microcarcinomas (PMC) defined as tumors ≤10 mm in diameter (including pT1a and pT3 according to the latest pTNM classification) have good prognosis, although recurrence is possible. Clinicians are interested in using a scoring system for predicting recurrences.ObjectiveTo identify the prognostic factors for recurrence in patients with PMC and to develop a scoring system based on lymph node involvement, multifocality, and sex. To determine the impact of extrathyroidal invasion (ETI) and a threshold value for analyzing multifocality.MethodsSingle-center retrospective study of a cohort of 1669 patients with PMC managed from 1960 to 2007. The Kaplan–Meier survival rate and prognostic factors of events were analyzed using log-rank tests and uni- and multivariate Cox model-based analyses. A scoring system was proposed.ResultsSixty-eight recurrences were observed. Initial lymph node metastases (P=0.0001), multifocality (P=0.05), and male sex (P=0.01) were significantly associated with recurrence, although there was a period effect (after 1990). PMC size was not a significant variable. Our scoring system allows us to separate patients into three risk groups according to their recurrence-free probability. For PMC Nx patients, total foci size of multifocal tumors >20 mm was significantly associated with recurrence (P<0.0001). Radioiodine (RAI) ablation was associated with better outcome only in PMC with ETI.ConclusionOur scoring system classifies recurrence risk. In PMC Nx patients, multifocality is important in planning therapeutic strategies. Recurrence probability of pT3 PMC appears lower if RAI ablation is performed.
Cancer research · 2009
Abstract The cyclic AMP signaling pathway can be altered at multiple levels in endocrine tumors. Its central component is the protein kinase A (PKA). Carney complex (CNC) is a hereditary multiple neoplasia syndrome resulting from inactivating mutations of the gene encoding the PKA type I α regulatory subunit (PRKAR1A). Primary pigmented nodular adrenocortical disease is the most frequent endocrine tumor of CNC. Transforming growth factor β (TGFβ) regulates adrenal cortex physiology and signals through SMAD2/3. We used an interference approach to test the effects of PRKAR1A inactivation on PKA and TGFβ pathways and on apoptosis in adrenocortical cells. PRKAR1A silencing stimulates PKA activity and increases transcriptional activity of a PKA reporter construct and expression of the endogenous PKA target, NR4A2, under basal conditions or after forskolin stimulation. PRKAR1A inactivation also decreased SMAD3 mRNA and protein levels via PKA, altering the cellular response to TGFβ. SMAD3 expression was also inhibited by adrenocorticorticotropic hormone in the mouse adrenal gland and by forskolin in H295R cells. TGFβ stimulates apoptosis in H295R cells, and this effect was counteracted by PRKAR1A inactivation. PRKAR1A silencing decreased the percentage of apoptotic cells and the cleavage of apoptosis mediators [caspase-3, poly(ADP-ribose) polymerase, and lamin A/C]. Inactivating mutations of PRKAR1A observed in adrenocortical tumors alter SMAD3, leading to resistance to TGFβ-induced apoptosis. This cross-talk between the PKA and the TGFβ signaling pathways reveals a new mechanism of endocrine tumorigenesis. [Cancer Res 2009;69(18):7278–84]
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
European journal of endocrinology · 2012 · Evaluation Study
Buffet C, Golmard JL, Hoang C, Trésallet C, et al.
Cancer research · 2009 · Journal Article
Ragazzon B, Cazabat L, Rizk-Rabin M, Assie G, et al.
La Revue de medecine interne · 2008 · English Abstract
Rosales C, Fierrard H, Bertagna X, Raffin-Sanson ML
Diabetes research and clinical practice · 2008 · Journal Article
Jacobi D, Lavigne C, Halimi JM, Fierrard H, et al.
Clinical nuclear medicine · 2010 · Case Reports
Ruel IF, Fierrard H, Vercellino L, Bernard L, et al.