The use of Torso Measurement Frame to create an Elongation Bending Derotation Brace in juvenile scoliosis during standing

2021 ◽  
Author(s):  
XC Liu ◽  
J Thometz ◽  
R Rizza
Keyword(s):  
Juvenile Scoliosis ◽  
Measurement Frame

Chylous Leak During Posterior Approach to Juvenile Scoliosis Surgery

2020 ◽  
Vol 10 (1) ◽  
pp. e0100-e0100
Author(s):  
Harsh A. Shah ◽  
Nicole Rynecki ◽  
Michael J. Vives ◽  
Daniel E. Choi ◽  
Justin T. Sambol ◽  
...  
Keyword(s):  
Posterior Approach ◽  
Scoliosis Surgery ◽  
Juvenile Scoliosis

scholarly journals Loss of the Reissner Fiber and increased URP neuropeptide signaling underlie scoliosis in a zebrafish ciliopathy mutant

2019 ◽  
Author(s):  
Christine Vesque ◽  
Isabelle Anselme ◽  
Guillaume Pezeron ◽  
Yasmine Cantaut-Belarif ◽  
Alexis Eschstruth ◽  
...  
Keyword(s):  
Receptor Gene ◽  
Urotensin Ii ◽  
Gene Encoding ◽  
Peptide Family ◽  
Juvenile Scoliosis ◽  
Genes Encoding ◽  
Juvenile Stages ◽  
Brain And Spinal Cord ◽  
The Brain ◽  
Axis Straightness

SUMMARYCilia-driven movements of the cerebrospinal fluid (CSF) are involved in zebrafish axis straightness, both in embryos and juveniles [1, 2]. In embryos, axis straightness requires cilia-dependent assembly of the Reissner fiber (RF), a SCO-spondin polymer running down the brain and spinal cord CSF-filled cavities [3]. Reduced expression levels of the urp1 and urp2 genes encoding neuropeptides of the Urotensin II family in CSF-contacting neurons (CSF-cNs) also underlie embryonic ventral curvature of several cilia motility mutants [4]. Moreover, mutants for scospondin and uts2r3 (a Urotensin II peptide family receptor gene) develop scoliosis at juvenile stages [3, 4]. However, whether RF maintenance and URP signaling are perturbed in juvenile scoliotic ciliary mutants and how these perturbations are linked to scoliosis is unknown. Here we produced mutants in the zebrafish ortholog of the human RPGRIP1L ciliopathy gene encoding a transition zone protein [5–7]. rpgrip1l-/- zebrafish had normal embryogenesis and developed 3D spine torsions in juveniles. Cilia lining the CNS cavities were normal in rpgrip1l-/- embryos but sparse and malformed in juveniles and adults. Hindbrain ventricle dilations were present at scoliosis onset, suggesting defects in CSF flow. Immunostaining showed a secondary loss of RF correlating with juvenile scoliosis. Surprisingly, transcriptome analysis of rgprip1l mutants at scoliosis onset uncovered increased levels of urp1 and urp2 expression. Overexpressing urp2 in foxj1-expressing cells triggered scoliosis in rpgrip1l heterozygotes. Thus, our results demonstrate that increased URP signaling drives scoliosis onset in a ciliopathy mutant. We propose that imbalanced levels of URP neuropeptides in CSF-cNs may be an initial trigger of scoliosis.

Effectiveness of serial EDF casting for children with infantile and juvenile scoliosis

2021 ◽  
Vol 72 (3) ◽  
Author(s):  
Federico CANAVESE ◽  
Flavia ALBERGHINA ◽  
Antonio ANDREACCHIO ◽  
Alain DIMEGLIO
Keyword(s):  
Juvenile Scoliosis
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