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F. PICARD  - - - 
Top co-authors See all
J. Simon

303 shared publications

J. Horvath

241 shared publications

E. Hirsch

226 shared publications

Margaret Pericak-Vance

225 shared publications

F. Picard

180 shared publications

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Distribution of Articles published per year 
(1963 - 2016)
Total number of journals
published in
 
27
 
Publications See all
Article 2 Reads 1 Citation Molecular changes in gelatin aging observed by NIR and fluorescence spectroscopy Anne Duconseille, Donato Andueza, Fabienne Picard, Véronique... Published: 01 December 2016
Food Hydrocolloids, doi: 10.1016/j.foodhyd.2016.06.007
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Highlights•Gelatin aging is highlighted by both Fluorescence and NIR spectroscopies.•Dityrosine bonds are highly suspected to be formed in gelatin during aging.•Amines and aldehydes are likely to form cross-links during gelatin aging.•Gelatin aging induces DOPA chemical and/or structural environment changes. AbstractThe pharmaceutical industry requires a narrow variability in gelatin properties during storage to meet strict quality standards for hard capsules. To test the properties of gelatin during shelf life, gelatin is aged in high temperature and high humidity conditions. These conditions induce the formation of cross-links in gelatin chains that impact its chemical composition and thereby the properties of the capsules. Non-aged and aged pig skin gelatins were analyzed in raw granule or powder forms by near-infrared and fluorescence spectroscopy to elucidate the mechanisms of cross-link formation during aging. Both near-infrared and fluorescence spectroscopy clearly separated non-aged from aged samples. Aging induced the formation of dityrosine and other cross-links involving amine and aldehyde functions. The presence of 3,4-dihydroxyphenylalanine (DOPA), a fluorescent product of tyrosine oxidation involved in cross-link formation, was evidenced in gelatin. Graphical abstract
Article 1 Read 0 Citations Choking fits during sleep related to epilepsy Periklis Makrythanasis, Charles Behr, Stéphanie Baulac, Edou... Published: 01 August 2016
The American Journal of Medicine, doi: 10.1016/j.amjmed.2016.04.010
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Article 0 Reads 0 Citations Platelet-Rich Plasma with Basic Fibroblast Growth Factor for Treatment of Wrinkles and Depressed Areas of the Skin B. Hersant, J. Niddam, F. PICARD, J. Bouhassira, S. LAPADULA... Published: 01 June 2016
Plastic and Reconstructive Surgery, doi: 10.1097/prs.0000000000002195
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Article 1 Read 14 Citations Involvement of GATOR complex genes in familial focal epilepsies and focal cortical dysplasia Sarah Weckhuysen, Elise Marsan, Virginie Lambrecq, Cécile Ma... Published: 13 May 2016
Epilepsia, doi: 10.1111/epi.13391
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ObjectiveThe discovery of mutations in DEPDC5 in familial focal epilepsies has introduced a novel pathomechanism to a field so far dominated by ion channelopathies. DEPDC5 is part of a complex named GAP activity toward RAGs (GATOR) complex 1 (GATOR1), together with the proteins NPRL2 and NPRL3, and acts to inhibit the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) pathway. GATOR1 is in turn inhibited by the GATOR2 complex. The mTORC1 pathway is a major signaling cascade regulating cell growth, proliferation, and migration. We aimed to study the contribution of GATOR complex genes to the etiology of focal epilepsies and to describe the associated phenotypical spectrum.MethodsWe performed targeted sequencing of the genes encoding the components of the GATOR1 (DEPDC5, NPRL2, and NPRL3) and GATOR2 (MIOS, SEC13, SEH1L, WDR24, and WDR59) complex in 93 European probands with focal epilepsy with or without focal cortical dysplasia. Phospho-S6 immunoreactivity was used as evidence of mTORC1 pathway activation in resected brain tissue of patients carrying pathogenic variants.ResultsWe identified four pathogenic variants in DEPDC5, two in NPRL2, and one in NPRL3. We showed hyperactivation of the mTORC1 pathway in brain tissue from patients with NPRL2 and NPRL3 mutations. Collectively, inactivating mutations in GATOR1 complex genes explained 11% of cases of focal epilepsy, whereas no pathogenic mutations were found in GATOR2 complex genes. GATOR1-related focal epilepsies differ clinically from focal epilepsies due to mutations in ion channel genes by their association with focal cortical dysplasia and seizures emerging from variable foci, and might confer an increased risk of sudden unexplained death in epilepsy (SUDEP).SignificanceGATOR1 complex gene mutations leading to mTORC1 pathway upregulation is an important cause of focal epilepsy with cortical malformations and represents a potential target for novel therapeutic approaches.
Article 1 Read 0 Citations Reply to Kamtchum-Tatuene and Fogang Nicolas Nicastro, Fabienne Picard Published: 01 May 2016
Epilepsy & Behavior, doi: 10.1016/j.yebeh.2016.02.028
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We thank Kamtchum-Tatuene and Fogang for their interest in our recent paper [1] covering the possible contribution of epilepsy in the life and events of Joan of Arc, which could have been a form of idiopathic partial epilepsy with auditory features.
Article 2 Reads 0 Citations Néphropathie induite par les produits de contraste : une mise à jour V. Spagnoli, L. Azzalini, V.X. Tadros, F. PICARD, H.Q. Ly Published: 01 April 2016
Annales de Cardiologie et d'Angéiologie, doi: 10.1016/j.ancard.2016.01.002
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Contrast-induced nephropathy (CIN) is common in hospitalized patients. Its occurrence is associated with an increased hospitalization stay and cost, morbidity and mortality. Thus, preventives strategies remain a major issue. Patients that are referred for cardiac catheterization are among the most vulnerable to develop CIN due to their comorbidities. Moreover, in some cases, such preventives measures cannot be introduced due to emergent clinical settings. After a summary regarding the properties of iodinated contrast medium, the aim of this work was to review the definition, pathophysiology, diagnosis and preventive strategies related to CIN.