RESUMEN
In this paper, a quasi-omnidirectional transmitter is proposed and demonstrated for underwater wireless optical communication (UWOC) using the photoluminescence of perovskite quantum dots (QDs). The proposed transmitter, without complex driving circuits, is compact and reliable thanks to the lens-free design. The system performance is tested in a 50-m swimming pool with a water attenuation coefficient of 0.38 dB/m. The maximum data rates of on-off-keying (OOK) signals over 10-m and 20-m transmission distances can reach 60 Mbps and 40 Mbps, respectively. When four clients are adopted in a code division multiple access (CDMA) based UWOC network, the maximum data rates of each client can reach 10 Mbps and 7.5 Mbps over 10-m and 20-m underwater channels, respectively. The system can meet the requirements of the last meter end-user access in the Internet of underwater things (IoUT) and underwater optical cellular network systems.
RESUMEN
BACKGROUND: Colorectal cancer (CRC) is one of the most common carcinomas throughout the world. Although the diagnostic and therapeutic strategies have made some progression in the treatment of CRC patients, the mortality of CRC remains relatively high. Hence, it is an urgency to find out the detailed mechanisms of how CRC occurs. METHODS: LncRNA Sox2ot expression was explored in CRC tissues and cell lines by using quantitative real-time PCR (qRT-PCR). Cell proliferation, migration and invasion ability was measured following downregulated expression of lncRNA Sox2ot by siRNA in CRC cells. Furthermore, western blot was used to detected the expression of Cyclin B1, Cdc 25C, N-cadherin, and E-cadherin in si-Sox2ot transfected CRC cells. RESULTS: We found that lncRNA Sox2ot was increased in CRC tissues and cell lines. High expression of Sox2ot was associated with the progression of CRC patients. Decreased Sox2ot expression inhibited the proliferation capacity and caused cell cycle arrested in G0/G1 phase in CRC cells. The key cell cycle regulators Cyclin B1 and Cdc 25C were consistently downregulated by knockdown of Sox2ot. Furthermore, knockdown of Sox2ot suppressed cell migration and invasion and decreased the expression of mesenchymal protein N-cadherin, while it increased the expression of epithelial protein E-cadherin in CRC cells. CONCLUSIONS: LncRNA Sox2ot could promoted CRC cell proliferation and motility and associated with the outcome of CRC patients, suggesting Sox2ot could serve as a potential therapeutic target in the treatment of CRC.