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Sost down-regulation by mechanical strain in human osteoblastic cells involves PGE2 signaling via EP4Quantification of Alterations in Cortical Bone Geometry Using Site Specificity Software in Mouse models of Aging and the Responses to Ovariectomy and Altered LoadingProtein kinase Cα (PKCα) regulates bone architecture and osteoblast activity.Mechanical loading-related bone gain is enhanced by tamoxifen but unaffected by fulvestrant in female miceAge-related impairment of bones' adaptive response to loading in mice is associated with sex-related deficiencies in osteoblasts but no change in osteocytes.Risedronate does not reduce mechanical loading-related increases in cortical and trabecular bone mass in micePlanar cell polarity aligns osteoblast division in response to substrate strainWnt16 Is Associated with Age-Related Bone Loss and Estrogen Withdrawal in Murine Bone.Disuse rescues the age-impaired adaptive response to external loading in miceBones' adaptive response to mechanical loading is essentially linear between the low strains associated with disuse and the high strains associated with the lamellar/woven bone transition.Exercise does not enhance aged bone's impaired response to artificial loading in C57Bl/6 mice.Biomechanical coupling facilitates spinal neural tube closure in mouse embryos.The cyclooxygenase-2 selective inhibitor NS-398 does not influence trabecular or cortical bone gain resulting from repeated mechanical loading in female miceEstrogen receptor-α is required for the osteogenic response to mechanical loading in a ligand-independent manner involving its activation function 1 but not 2.Male mice housed in groups engage in frequent fighting and show a lower response to additional bone loading than females or individually housed males that do not fight.Estrogen receptor α mediates proliferation of osteoblastic cells stimulated by estrogen and mechanical strain, but their acute down-regulation of the Wnt antagonist Sost is mediated by estrogen receptor β.Estrogen receptors' roles in the control of mechanically adaptive bone (re)modelingSclerostin's role in bone's adaptive response to mechanical loading.Role of endocrine and paracrine factors in the adaptation of bone to mechanical loading.Neural tube closure: cellular, molecular and biomechanical mechanisms.Spina bifida-predisposing heterozygous mutations in Planar Cell Polarity genes and Zic2 reduce bone mass in young mice.Valproic acid disrupts the biomechanics of late spinal neural tube closure in mouse embryos.Vangl2 disruption alters the biomechanics of late spinal neurulation leading to spina bifida in mouse embryos.Spinal neural tube closure depends on regulation of surface ectoderm identity and biomechanics by Grhl2.Four-point bending protocols to study the effects of dynamic strain in osteoblastic cells in vitroNovel mouse model of encephalocele: post-neurulation origin and relationship to open neural tube defectsRefinement of inducible gene deletion in embryos of pregnant miceRho kinase-dependent apical constriction counteracts M-phase apical expansion to enable mouse neural tube closure
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description
researcher
@en
wetenschapper
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հետազոտող
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name
Gabriel L Galea
@ast
Gabriel L Galea
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Gabriel L Galea
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Gabriel L Galea
@nl
Gabriel L Galea
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type
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Gabriel L Galea
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Gabriel L Galea
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Gabriel L Galea
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Gabriel L Galea
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Gabriel L Galea
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prefLabel
Gabriel L Galea
@ast
Gabriel L Galea
@en
Gabriel L Galea
@es
Gabriel L Galea
@nl
Gabriel L Galea
@sl
P106
P21
P31
P496
0000-0003-2515-1342