Literatura científica selecionada sobre o tema "Hidradénite suppurée"
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Artigos de revistas sobre o assunto "Hidradénite suppurée"
Guerlin, M. "Laser et hidradénite suppurée ?" Annales de Dermatologie et de Vénéréologie 131, n.º 8-9 (agosto de 2004): 855. http://dx.doi.org/10.1016/s0151-9638(04)93781-7.
Texto completo da fonteNassar, D., e J. Revuz. "Hidradénite suppurée ou maladie de Verneuil". EMC - Dermatologie 3, n.º 1 (janeiro de 2008): 1–8. http://dx.doi.org/10.1016/s0246-0319(08)48425-x.
Texto completo da fonteMachan, A., S. Oumakhir, M. Khalidi, I. Anouar, N. Hjira e M. Boui. "Hidradénite suppurée induite par le léflunomide". Annales de Dermatologie et de Vénéréologie 145, n.º 12 (dezembro de 2018): S229—S230. http://dx.doi.org/10.1016/j.annder.2018.09.347.
Texto completo da fonteFaye, O., F. Petit, F. Poli, T. Petit, J. Wechsler, G. Gabison, F. Pouget e J. Revuz. "Lymphœdème compliquant une hidradénite suppurée : trois observations". Annales de Dermatologie et de Vénéréologie 134, n.º 6-7 (junho de 2007): 567–69. http://dx.doi.org/10.1016/s0151-9638(07)89271-4.
Texto completo da fonteKonstantinou, M. P., M. Thomas, L. Legendre, C. Richet, J. Revuz, C. Paul e N. Meyer. "Hidradénite suppurée aggravée par un inhibiteur d’EGFR". Annales de Dermatologie et de Vénéréologie 141, n.º 12 (dezembro de 2014): S430. http://dx.doi.org/10.1016/j.annder.2014.09.453.
Texto completo da fonteLegrand, A., D. Heron-Mermin, A. Pham-Ledard, M. Beylot-Barry e O. Cogrel. "Lymphœdème ano-génital et hidradénite suppurée : 6 cas". Annales de Dermatologie et de Vénéréologie 146, n.º 12 (dezembro de 2019): A218—A219. http://dx.doi.org/10.1016/j.annder.2019.09.331.
Texto completo da fonteRichette, P., A. Molto, K. Dawidowicz, D. Wendling, G. Hayem, F. Lioté, F. Aubin, A. Nassif, M. Viguier e H. Bachelez. "Hidradénite suppurée et rhumatisme inflammatoire : étude prospective multicentrique". Annales de Dermatologie et de Vénéréologie 139, n.º 12 (dezembro de 2012): B78. http://dx.doi.org/10.1016/j.annder.2012.10.065.
Texto completo da fonteHotz, C., C. Ram-Wolff, N. Ortonne, M. Bagot, G. Quereux, F. Skowron, O. Cogrel, M. Beylot-Barry e S. Oro. "Mycosis fongoïde pilotrope et hidradénite suppurée : un piège diagnostique ?" Annales de Dermatologie et de Vénéréologie 145, n.º 12 (dezembro de 2018): S235. http://dx.doi.org/10.1016/j.annder.2018.09.358.
Texto completo da fonteRandriamiarana, T., E. Wierzbicka-Hainaut, C. Barbarin, R. Riviere, M. Masson Regnault e D. Boutin. "Un cas de maladie de Darier avec hidradénite suppurée". Annales de Dermatologie et de Vénéréologie - FMC 2, n.º 8 (novembro de 2022): A246. http://dx.doi.org/10.1016/j.fander.2022.10.065.
Texto completo da fonteBenhadou, Farida, Virginie Vlaeminck-Guillem, Agnès Duquesne, Dillon Mintoff e Philippe Guillem. "Association hidradénite suppurée et déficit en mévalonate kinase : deux cas". Annales de Dermatologie et de Vénéréologie - FMC 1, n.º 8 (dezembro de 2021): A276—A277. http://dx.doi.org/10.1016/j.fander.2021.09.282.
Texto completo da fonteTeses / dissertações sobre o assunto "Hidradénite suppurée"
Orvain, Cindy. "Implication des cellules souches du follicule pileux dans la physiopathologie de l'hidradénite suppurée". Electronic Thesis or Diss., Paris Est, 2019. http://www.theses.fr/2019PESC0038.
Texto completo da fonteRole of hair follicle stem cells in hidradenitis suppurativa physiopathologyHidradenitis suppurativa (HS) is a chronic inflammatory dermatosis which affects 1% of the French population. Lesions are painful and characterized by abcesses, fistulaes and malodorous discharges. They appear in hair rich skin areas like the armpits, the pubis and the buttock. HS causes a high extent of emotional and physical distress, as well as social embarrassment, isolation and depression, making it the common dermatosis which leads to the most severe impairment of quality of life. As most treatments have been unsatisfactory, and as there are many recurrences, HS remains difficult to cure.HS appears to be a primary abnormality in the pilosebaceous-apocrine unit, which leads to follicular occlusion, perifollicular cyst development which traps commensal microbes, and rupture into the dermis. Our team focused on hair follicle cells and especially Outer Root Sheath Cells (ORS). We previously showed that ORS isolated from hair follicle of HS patients (HS-ORS) spontaneously secrete IP10 (CXCL10) and RANTES (CCL5). The aim of my thesis is to characterize molecular and cellular mechanisms involved in this pro-inflammatory phenotype of HS-ORS. We hypothesized that cell cycle deregulation in the ORS leads to replication stress and accumulation of cytoplasmic ssDNA, inducing IFN synthesis involved in the establishment of chronic inflammation.First, we performed a transcriptomic analysis of HS-ORS, which revealed an interferon signature and an alteration of cell cycle pathways. Colony-forming efficiency assay of ORS showed a much higher colony-forming ability of HS-ORS compared to healthy donor (HD)-ORS. We highlighted the loss of quiescent hair follicle stem cell population described as CD200+ CD34- CD49f+ CytoK15high cells and an increased number of proliferating cells in HS patients. The increased number of proliferating ORS cells in HS patients led us to analyse their cell-cycle distribution. The percentage of ORS in S phase was increased in HS patients. We next asked whether this was due to increased replication stress, which is defined as a global perturbation of the DNA replication program altering the speed of replication forks and activating the ATR-CHK1 pathway. We observed that the progression of replication fork was severely altered in HS-ORS. Moreover, the ATR-CHK1 pathway was spontaneously activated in HS-ORS cells. Recent evidence indicates that micronuclei formation is increased upon DNA damage and their rupture exposes DNA to cytosolic nucleases and activates the STING pathway. We observed an accumulation of ssDNA and micronuclei in the cytoplasm of HS-ORS. Thus we analyzed STING pathway. In HS patients, ORS lacking STING expressed reduced levels of IFN-β transcripts compared to ORS transfected with a scramble siRNA. Lastly, we revealed that STING activation was mediated by the DNA binding protein IFI16.We report the first mechanistic analysis of the etiology of HS in the hair follicle stem cells (HF-SC) compartment. Our results suggested that modifications of HF-SC homeostasis are the primum movens to initiate an inflammatory loop. Replicative stress leads to genomic DNA damage triggering inflammatory response through IFI16-STING pathway. Inflammation could also contribute to the perturbation of HF-SC homeostasis which perpetuates the inflammatory circle. Future work will focus on mechanisms which lead to quiescence loss of HF-SC. During our study, we noticed two groups of HS patients: one with high replicative stress and DNA damage activation and another with moderate replicative stress and DNA damage activation. It would be of interest to define new biomarkers to distinguish these two groups of patients in order to propose personalized treatment
Livros sobre o assunto "Hidradénite suppurée"
Jemec, Gregor B. E., Jean Revuz e James J. Leyden. Hidradénite suppurée. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-72063-5.
Texto completo da fonteJEMEC, Gregor B. E., Jean REVUZ e James J. LEYDEN. Hidradénite Suppurée. Springer London, Limited, 2008.
Encontre o texto completo da fonteLeyden, James J., Jean Revuz e Gregor Jemec. Hidradénite suppurée (French Edition). Springer, 2007.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Hidradénite suppurée"
von der Werth, Jan, Pam Wood, Alan D. Irvine e W. H. Irwin McLean. "La génétique de l’hidradénite suppurée". In Hidradénite suppurée, 77–93. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-72063-5_10.
Texto completo da fonte