3 research outputs found

    Moving forward : In search of synergy across diverse views on the role of physical movement in design for stem education

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    Inspired by the current embodiment turn in the cognitive sciences, researchers of STEM teaching and learning have been evaluating implications of this turn for educational theory and practice. But whereas design researchers have been developing domain-specific theories that implicate the role of physical movement in conceptual learning, the field has yet to agree on a conceptually coherent and empirically validated framework for leveraging and shaping students’ capacity for physical movement as a socio–cognitive educational resource. This symposium thus convenes to ask, “What is movement in relation to concepts such that we can design for learning?” To stimulate discussion, we highlight an emerging tension across a set of innovative technological designs with respect to the framing question of whether students should discover an activity’s targeted movement forms themselves or that these forms should be cued directly. Our content domains span mathematics (proportions, geometry), physics, chemistry, and ecological system dynamics (predator–prey, bees)

    Moving forward : In search of synergy across diverse views on the role of physical movement in design for stem education

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    Inspired by the current embodiment turn in the cognitive sciences, researchers of STEM teaching and learning have been evaluating implications of this turn for educational theory and practice. But whereas design researchers have been developing domain-specific theories that implicate the role of physical movement in conceptual learning, the field has yet to agree on a conceptually coherent and empirically validated framework for leveraging and shaping students’ capacity for physical movement as a socio–cognitive educational resource. This symposium thus convenes to ask, “What is movement in relation to concepts such that we can design for learning?” To stimulate discussion, we highlight an emerging tension across a set of innovative technological designs with respect to the framing question of whether students should discover an activity’s targeted movement forms themselves or that these forms should be cued directly. Our content domains span mathematics (proportions, geometry), physics, chemistry, and ecological system dynamics (predator–prey, bees)

    Involvement of Estrogen Receptor Variant ER-α36, Not GPR30, in Nongenomic Estrogen Signaling

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    Accumulating evidence suggested that an orphan G protein-coupled receptor (GPR)30, mediates nongenomic responses to estrogen. The present study was performed to investigate the molecular mechanisms underlying GPR30 function. We found that knockdown of GPR30 expression in breast cancer SK-BR-3 cells down-regulated the expression levels of estrogen receptor (ER)-α36, a variant of ER-α. Introduction of a GPR30 expression vector into GPR30 nonexpressing cells induced endogenous ER-α36 expression, and cotransfection assay demonstrated that GPR30 activated the promoter activity of ER-α36 via an activator protein 1 binding site. Both 17β-estradiol (E2) and G1, a compound reported to be a selective GPR30 agonist, increased the phosphorylation levels of the MAPK/ERK1/2 in SK-BR-3 cells, which could be blocked by an anti-ER-α36-specific antibody against its ligand-binding domain. G1 induced activities mediated by ER-α36, such as transcription activation activity of a VP16-ER-α36 fusion protein and activation of the MAPK/ERK1/2 in ER-α36-expressing cells. ER-α36-expressing cells, but not the nonexpressing cells, displayed high-affinity, specific E2 and G1 binding, and E2- and G1-induced intracellular Ca2+ mobilization only in ER-α36 expressing cells. Taken together, our results demonstrated that previously reported activities of GPR30 in response to estrogen were through its ability to induce ER-α36 expression. The selective G protein-coupled receptor (GPR)30 agonist G1 actually interacts with ER-α36. Thus, the ER-α variant ER-α36, not GPR30, is involved in nongenomic estrogen signaling
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