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Artykuły w czasopismach na temat "Scoliose – Étiologie"
Ozturk, Cagatay, Mehmet Tezer, Omer Karatoprak i Azmi Hamzaoglu. "Une étiologie rare de scoliose neuromusculaire : la maladie d’Alexander". Revue du Rhumatisme 76, nr 3 (marzec 2009): 297–300. http://dx.doi.org/10.1016/j.rhum.2008.06.021.
Pełny tekst źródłaHuang, Kuo-Yuan, Ruey-Mo Lin, Jing-Jou Yan i Chii-Jeng Lin. "L'histiocytose à cellule de Langerhans: une étiologie à envisager devant une scoliose douloureuse". Revue du Rhumatisme 74, nr 7 (lipiec 2007): 696–700. http://dx.doi.org/10.1016/j.rhum.2006.11.023.
Pełny tekst źródłaBENBELLAL, Amina, Hanène BELABBASSI, Sarrah AIT ZIANE, Redha ALLOUTI i Houria KACED. "Clinical and etiological aspects of vertebral deviations secondary to osteochondrdysplasias". Batna Journal of Medical Sciences (BJMS) 5, nr 1 (25.12.2018): 68–73. http://dx.doi.org/10.48087/bjmsoa.2018.5116.
Pełny tekst źródłaGueye, ML, Y. Seye, ISS Sarr, PM Faye, M. Ndiaye, O. Thiam, AO Touré i in. "C45: Syndrome de Wilkie : A propos de 6 observations". African Journal of Oncology 2, nr 1 Supplement (1.03.2022): S19—S20. http://dx.doi.org/10.54266/ajo.2.1s.c45.xszo1bitxc.
Pełny tekst źródłaRozprawy doktorskie na temat "Scoliose – Étiologie"
Djebar, Morgane. "Contrôle neurologique de la maintenance d'un axe droit : comment des défauts ciliaires conduisent à l'émergence de la scoliose idiopathique ?" Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS185.pdf.
Pełny tekst źródłaIdiopathic scoliosis (IS) is a highly prevalent three-dimensional spine deformity which affects 3-4% of the population in the absence of obvious congenital abnormalities, whose etiology is poorly understood. Recent genetic studies in zebrafish have shown that loss of Reissner fiber (RF), a sco-spondin protein polymer secreted by the subcomissural organ (SCO) and present along the cavities of the central nervous system, triggers scoliosis in juveniles (the "adolescent-like" stage). Impairment of cilia motility in embryos, necessary for RF polymerization, also leads to axis curvature defects, that correlates with decreased urp2 neuropeptide gene expression in sco-spondin mutants. It is yet not clear whether this scenario of CSF flow defect causing RF loss and decreased URP signaling holds true in other zebrafish mutants that do not impair directly cilia motility or may be relevant to human IS. Two studies also pointed to the existence of a neuro-inflammatory signature, downstream of RF loss, which contributes to scoliosis severity and penetrance. We generated a zebrafish mutant for rpgrip1l, a gene encoding a ciliary transition zone protein, which displays no embryonic anomaly and develops scoliosis with nearly full penetrance in juveniles. The goal of my thesis was to decipher the cascade of events leading to scoliosis in rpgrip1l-/-. We took advantage of the asynchronous scoliosis development in rpgrip1l-/- to show that the straight mutants already presented ciliary defects at trunk level with increase number of immune cells within the brain and urp1 and urp2 upregulation. At scoliosis onset, rpgrip1l-/- mutants had lost the RF and specific multi-ciliated tufts just lateral to the SCO. Reintroduction of RPGRIP1L into motile ciliated cells and progenitor cells thanks to tissue-specific transgenesis prevents scoliosis onset. By reducing URP level in rpgrip1l-/- via genetic crosses, we demonstrated that alteration of URP signaling does not contribute to the curvature phenotype of rpgrip1l-/-. Moreover, long-term anti-inflammatory/anti-oxidant treatment reduced the severity and penetrance of scoliosis by 50%, suggesting that inflammatory and/or oxidative processes are involved in rpgrip1l scoliosis onset and evolution. Finally, thanks to a proteomic analysis and immunostaining, we revealed an astrogliosis response within the SCO and rhombencephalic ventricle that develops asynchronously in straight rpgrip1l-/- and persists in scoliotic fish. We propose that the astrogliosis at SCO level associated with inflammatory cells recruitment induces locally the loss of multi-ciliated tufts, impairing RF polymerization and eventually leading to scoliosis. We hope these studies will provide new insights into the understanding of molecular and cellular defects leading to IS in zebrafish and highlight brain astrogliosis as a potential defect leading to human IS