RESUMEN
The principal motivation for this paper is to reduce stray light and line roughness in concave holographic gratings (CHG). Compared with other previously reported line-smoothing grating techniques such as dynamic-exposure near-field holography, we successfully improve the line smoothing of CHG to approximately 10 nm from 2 nm. Our method uses optimization technologies and a combination of photoresist hot-melting (PHM) and oxygen-ion ashing (OIA), thereby improving the degree of stray light before and after optimization by one order of magnitude; the level processed by OIA, PHM, and OIA successively is ${7.85} \times {{10}^{ - 5}}$7.85×10-5. Combining the two technologies, we achieve lower stray light and straighter groove lines for the concave gratings, which is more effective, easy to implement, and incurs a low cost.
RESUMEN
DNA-damage regulated autophagy modulator 1 (DRAM1) is known as a target of TP53-mediated autophagy, and has been reported to promote the migration and invasion abilities of glioblastoma stem cells. However, the precise contribution of DRAM1 to cancer cell invasion and migration, and the underlying mechanisms remain unclear. In the present study, small interfering (si)RNA or short hairpin RNA mediated knockdown of DRAM1 was performed in hepatoblastoma cells and the migration and invasion abilities were detected in vitro and in vivo. To investigate the underlying mechanisms, western blotting and immunofluorescence were used to detect the expression of autophagy-associated proteins and epithelial-mesenchymal-transition (EMT)-associated markers. The results showed that DRAM1 knockdown by specific siRNA abrogated cell autophagy, as well as inhibited the migration and invasion of HepG2 cells in Transwell assays, which may be reversed by rapamycin treatment. In addition, DRAM1 knockdown increased the expression of E-Cadherin while decreased the expression of vimentin in HepG2 cells, which was also be reversed by rapamycin treatment. Taken together, these results suggest that DRAM1 is involved in the regulation of the migration and invasion of HepG2 cells via autophagy-EMT pathway.