Asunto(s)
Anafilaxia/inducido químicamente , Carboximetilcelulosa de Sodio/efectos adversos , Excipientes Farmacéuticos/efectos adversos , Dolor de Hombro/tratamiento farmacológico , Anciano , Anafilaxia/diagnóstico , Carboximetilcelulosa de Sodio/administración & dosificación , Femenino , Glucocorticoides/administración & dosificación , Humanos , Inyecciones Intraarticulares/efectos adversos , Excipientes Farmacéuticos/administración & dosificación , Pruebas Cutáneas , Triamcinolona Acetonida/administración & dosificaciónRESUMEN
[Purpose] To investigate the effects of core strength training on core stability with and without the Valsalva maneuver. [Participants and Methods] Twenty-four students were randomly assigned to the training and control groups. Students in the training group undertook a 4-week training program that included exercises for the transverse abdominis, multifidus, diaphragm, and pelvic floor muscles, whereas students in the control group performed their usual activities. Participants were required to perform four types of task with and without the Valsalva maneuver. Seated stabilometry was assessed according to the center of pressure (COP). [Results] In the training group, the rectus area in the quiet sitting position with the Valsalva maneuver was enlarged and the length of trajectory during a sudden perturbation task was decreased. No significant changes to the COP were seen in the control group. [Conclusion] Some parameters of core stability improved after participants completed a 4-week core strength training program.
RESUMEN
The hemangioblast is a progenitor cell with the capacity to give rise to both hematopoietic and endothelial progenitors. Currently, the regulatory mechanisms underlying hemangioblast formation are being elucidated, whereas those controllers for the selection of hematopoietic or endothelial fates still remain a mystery. To answer these questions, we screened for zebrafish mutants that have defects in the hemangioblast expression of Gata1, which is never expressed in endothelial progenitors. One of the isolated mutants, it627, showed not only down-regulation of hematopoietic genes but also up-regulation of endothelial genes. We identified the gene responsible for the it627 mutant as the zebrafish homolog of Lys-specific demethylase 1 (LSD1/KDM1A). Surprisingly, the hematopoietic defects in lsd1(it627) embryos were rescued by the gene knockdown of the Ets variant 2 gene (etv2), an essential regulator for vasculogenesis. Our results suggest that the LSD1-dependent shutdown of Etv2 gene expression may be a significant event required for hemangioblasts to initiate hematopoietic differentiation.