RESUMEN
Polarization via strain engineering provides a facial way to functionalize materials. We investigate the origin of electronic polarization in the bent elemental semiconductor thinfilms by combining analytical modeling with quantum mechanical simulation. A bond orbital model reveals a polarity of covalent bonds induced by strain gradient such that polarization along the strain gradient dimension can be induced, giving rise to the flexoelectric effect. At strain gradient1/R=0.01 nm-1, the net charge differences between the two sides are5×10-4e,2.5×10-3eand7.2×10-3efor C, Si and Ge films respectively. On the other hand, due to the emergent bond polarity, the polarization can be effectively tuned by normal strain applied to the bent film, mimicking the piezoelectric effect. Simulations using the generalized Bloch theorem strongly support this revelation. Findings have important implications for delineating the formation of polarization and related phenomena in semiconductors.
RESUMEN
Previously, we have demonstrated a role for fibroblast growth factor (Fgf) in spinal cord regeneration in both zebrafish and mouse. We have shown that exogenous Fgf2 treatment attenuates astrocytic gliosis and induces glia cells to become progenitors that undergo neurogenesis as well as differentiating into bipolar astrocytes that support axonal regeneration (Goldshmit et al., 2012, 2014). One of the downstream signaling target genes of Fgf is spry4, which acts as a feedback inhibitor for Fgf signaling. In this study we examined the effects of increased endogenous Fgf signaling, in spry4-/- mice, on the early events that occur after spinal cord injury (SCI). We demonstrate that in spry4-/- mice inflammatory responses, such as tumor necrosis factor α (TNFα) secretion and macrophage/neutrophil invasion into the lesion site are reduced. In addition, astrocytic gliosis is attenuated and neuronal survival is increased. These results further support a pro-regenerative role of Fgf after SCI, and suggest that increased endogenous Fgf signaling after SCI may contribute to functional recovery and therefore presents this pathway as a target for new therapy development.