Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Nadira Ruzehaji"'
Autor:
Nadira Ruzehaji, Jerome Avouac, Muriel Elhai, Maxime Frechet, Camelia Frantz, Barbara Ruiz, Joerg H. Distler, Yannick Allanore
Publikováno v:
Arthritis Research & Therapy, Vol 25, Iss 1, Pp 1-1 (2023)
This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s13075-023-03211-7.
Externí odkaz:
https://doaj.org/article/6a9b2cdeaf4941408b675b954ca5d1c0
Autor:
Christophe Desterke, Christophe Martinaud, Nadira Ruzehaji, Marie-Caroline Le Bousse-Kerdilès
Publikováno v:
Mediators of Inflammation, Vol 2015 (2015)
Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm where severity as well as treatment complexity is mainly attributed to a long lasting disease and presence of bone marrow stroma alterations as evidenced by myelofibrosis, neoangioge
Externí odkaz:
https://doaj.org/article/e13fefbf39e44dbd91dcab0ad005e9e7
Autor:
Sonia Pezet, Thomas Guilbert, Nadira Ruzehaji, Yannick Allanore, Matthieu Ponsoye, Jean-Louis Junien, Jérôme Avouac, Pierre Broqua, Jean-Michel Luccarini, Camelia Frantz
Publikováno v:
Annals of the Rheumatic Diseases
Background The pathogenesis of systemic sclerosis (SSc) involves a distinctive triad of autoimmune, vascular and inflammatory alterations resulting in fibrosis. Evidence suggests that peroxisome proliferator-activated receptors (PPARs) play an import
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9e97c8b03f49e0f243a19c8aa8664e66
https://doi.org/10.1136/annrheumdis-2015-208029
https://doi.org/10.1136/annrheumdis-2015-208029
Autor:
Michal Tomcik, Jérôme Avouac, Holm Schneider, Oliver Distler, Katrin Palumbo-Zerr, Yannick Allanore, Georg Schett, Pawel Zerr, Jörg H W Distler, Clara Dees, Christian Beyer, Nadira Ruzehaji, Alfiya Distler
Publikováno v:
Arthritis & Rheumatology. 66:3140-3150
Objective Nuclear receptors regulate cell growth, differentiation, and homeostasis. Selective nuclear receptors promote fibroblast activation, which leads to tissue fibrosis, the hallmark of systemic sclerosis (SSc). This study was undertaken to inve
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::e967d7392a268a09c9a3e693fd622e0b
https://doi.org/10.1002/art.38819
https://doi.org/10.1002/art.38819
Publikováno v:
ResearcherID
A 72-year-old female with venous insufficiency presented to a hospital based multidisciplinary wound clinic after 20 years of recurrent episodes of venous leg ulcers. Examination showed bilateral leg ulcers with no evidence of arterial insufficiency,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fc672029180aced78c00e8fc5e742915
https://doi.org/10.12968/jowc.2013.22.sup10.s27
https://doi.org/10.12968/jowc.2013.22.sup10.s27
Autor:
Nadira Ruzehaji, Zlatko Kopecki, Allison J. Cowin, Detlef Zillikens, Christopher T. Turner, Dedee F. Murrell, Hioraki Iwata, Ralf Ludwig
Publikováno v:
Journal of Investigative Dermatology. 133(4):1008-1016
Epidermolysis bullosa (EB) is a chronic inheritable disease that leads to severe blistering and fibrosis. Previous studies have shown that the actin cytoskeletal protein flightless I (Flii) impairs wound healing associated with EB. Using a mouse mode
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dbd75553bfffc617736d999d3a2d48a9
Autor:
Ruth M. Arkell, Elizabeth Melville, Robert Fitridge, Nadira Ruzehaji, Stuart J. Mills, Allison J. Cowin
Publikováno v:
BioMed Research International
BioMed Research International, Vol 2013 (2013)
BioMed Research International, Vol 2013 (2013)
Impaired wound healing and ulceration represent a serious complication of both type 1 and type 2 diabetes. Cytoskeletal protein Flightless I (Flii) is an important inhibitor of wound repair, and reduced Flii gene expression in fibroblasts increased m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::76bae4e26cd25f547b118e33322e5ec2
https://doi.org/10.1155/2013/389792
https://doi.org/10.1155/2013/389792
Autor:
Maxime Fréchet, Øyvind Molberg, Hisaya Akiba, Yannick Allanore, Arun Subramaniam, Barbara Ruiz, André Kahan, Jérémy Sadoine, Hassina Brahiti, Carole Nicco, Muriel Elhai, Thomas Guilbert, Olivia Amiar, Anne Burgevin, Gilles Chiocchia, Sonia Pezet, Matthieu Ponsoye, Anna Maria Hoffmann-Vold, Jérôme Avouac, Nadira Ruzehaji, Robert Resnick, Vigo Heissmeyer
Publikováno v:
Proc. Natl. Acad. Sci. U.S.A. 113, E3901-E3910 (2016)
Treatment for fibrosis represents a critical unmet need, because fibrosis is the leading cause of death in industrialized countries, and there is no effective therapy to counteract the fibrotic process. The development of fibrosis relates to the inte
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a4d2cba5550fd31c09db79beed5181c3
https://doi.org/10.1073/pnas.1523512113
https://doi.org/10.1073/pnas.1523512113
Autor:
Nazi Lei, Carolin Offenhäuser, Zlatko Kopecki, Rachael Z. Murray, Nadira Ruzehaji, Linda Franken, Allison J. Cowin
Publikováno v:
Communicative & Integrative Biology
Intracellular Flightless I (Flii), a gelsolin family member, has been found to have roles modulating actin regulation, transcriptional regulation and inflammation. In vivo Flii can regulate wound healing responses. We have recently shown that a pool
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b5e99e96c0007fd73e5346861840f718
https://doi.org/10.4161/cib.21928
https://doi.org/10.4161/cib.21928
Autor:
Damian H. Adams, Nadira Ruzehaji, Hugh Campbell, John E. Greenwood, Ruth Arkell, Allison J. Cowin, Xanthe L. Strudwick
Publikováno v:
British Journal of Dermatology. 161:326-336
Background: The pathophysiological mechanisms involved in burn injury repair are still not fully understood but include processes involving cellular proliferation, migration and adhesion. The actin cytoskeleton is intricately involved in these key wo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6ca5e9d3e3049e71cd1a1a37610cac31
https://doi.org/10.1111/j.1365-2133.2009.09296.x
https://doi.org/10.1111/j.1365-2133.2009.09296.x