Physical Layer Security of Intelligent Reflective Surface Aided NOMA Networks

Intelligent reflective surface (IRS) technology is emerging as a promising performance enhancement technique for next-generation wireless networks. Hence, we investigate the physical layer security of the downlink in IRS-aided non-orthogonal multiple access networks in the presence of an eavesdropper, where an IRS is deployed for enhancing the quality by assisting the cell-edge user to communicate with the base station. To characterize the network's performance, the expected value of the new channel statistics is derived for the reflected links in the case of Nakagami-m fading. Furthermore, the performance of the proposed network is evaluated both in terms of the secrecy outage probability~(SOP) and the average secrecy capacity (ASC). The closed-form expressions of the SOP and the ASC are derived. We also study the impact of various network parameters on the overall performance of the network considered. To obtain further insights, the secrecy diversity orders and the high signal-to-noise ratio slopes are obtained. We finally show that: 1) the expectation of the channel gain in the reflected links is determined both by the number of IRSs and by the Nakagami- m fading parameters; 2)~The SOP of both receiver 1 and receiver 2 becomes unity, when the number of IRSs is sufficiently high; 3) The secrecy diversity orders are affected both by the number of IRSs and by the Nakagami-m fading parameters, whereas the high-SNR slopes are not affected by these parameters. Our Monte-Carlo simulations perfectly demonstrate the analytical results

Inhibitors of Phosphatidylinositol 3′-Kinases Promote Mitotic Cell Death in HeLa Cells

The phosphatidylinositol 3-kinase (PI3K) pathway plays an important role in many biological processes, including cell cycle progression, cell growth, survival, actin rearrangement and migration, and intracellular vesicular transport. However, the involvement of the PI3K pathway in the regulation of mitotic cell death remains unclear. In this study, we treated HeLa cells with the PI3K inhibitors, 3-methyladenine (3-MA, as well as a widely used autophagy inhibitor) and wortmannin to examine their effects on cell fates using live cell imaging. Treatment with 3-MA decreased cell viability in a time- and dose-dependent manner and was associated with caspase-3 activation. Interestingly, 3-MA-induced cell death was not affected by RNA interference-mediated knockdown (KD) of beclin1 (an essential protein for autophagy) in HeLa cells, or by deletion of atg5 (an essential autophagy gene) in mouse embryonic fibroblasts (MEFs). These data indicate that cell death induced by 3-MA occurs independently of its ability to inhibit autophagy. The results from live cell imaging studies showed that the inhibition of PI3Ks increased the occurrence of lagging chromosomes and cell cycle arrest and cell death in prometaphase. Furthermore, PI3K inhibitors promoted nocodazole-induced mitotic cell death and reduced mitotic slippage. Overexpression of Akt (the downstream target of PI3K) antagonized PI3K inhibitor-induced mitotic cell death and promoted nocodazole-induced mitotic slippage. These results suggest a novel role for the PI3K pathway in regulating mitotic progression and preventing mitotic cell death and provide justification for the use of PI3K inhibitors in combination with anti-mitotic drugs to combat cancer