Modeling and analysis for group delay mismatch effect on wideband adaptive spatial interference cancellation

Abstract The adaptive interference cancellation technique has been widely utilized in radar, GPS, data link, etc., systems to address challenges from external interference, such as co-site and hostile interference. Since the anti-jamming performance of the adaptive interference cancellation technique is sensitive to group delay mismatch between channels, the group delay mismatch becomes one of the main factors that limit the system’s anti-jamming capability. However, the traditional adaptive interference cancellation system’s mathematical model cannot quantitatively characterize the group delay mismatch effect on the wideband interference cancellation performance. In this paper, the mathematical model of the wideband adaptive spatial interference cancellation (ASIC) system is established, which considers the group delay mismatch, to quantitatively analyze the impact of group delay mismatch on the hostile interference cancellation. The mathematical model utilizes the weighted multi-tone signals to fit the wideband interference, and then, delay differences are attached to each tone signal to simulate the group delay mismatch. Then, the analytic expressions of weight and interference cancellation ratio are derived, which consider the interference bandwidth and group delay mismatch, to quantitatively analyze the group delay mismatch effect on the anti-jamming performance of the wideband ASIC system. Simulation results indicate that the theoretical analysis based on the mathematical model of wideband ASIC system are accurate, which can achieve the quantitative analysis of the group delay mismatch effect on the WIC performance

MEG3 Activated by Vitamin D Inhibits Colorectal Cancer Cells Proliferation and Migration via Regulating Clusterin

The long non-coding RNA maternally expressed gene 3 (MEG3) is frequently dysregulated in human cancers; however, its roles in colorectal cancer (CRC) development are largely unknown. Here, we reported that MEG3 was down-regulated in CRC tissues and CRC patients with lower MEG3 showed poorer overall survival and disease-free survival than those with higher MEG3 level. MEG3 over-expression represses CRC cells proliferation and migration in vivo and in vitro, while MEG3 knockdown leads to the enhanced proliferation and metastasis of CRC cells. In CRC cells, MEG3 over-expression is related to decreased Clusterin mRNA and the corresponding protein levels, and it also directly binds to Clusterin protein through its 732–1174 region. In further, Clusterin over-expression rescues the compromised abilities of proliferation and metastasis induced by MEG3 over-expression, suggesting that MEG3 inhibits the CRC progression through regulating the Clusterin activities. Additionally, we found that 1α,25-(OH)2D and vitamin D receptor (VDR) stimulate MEG3 expression in CRC cells through directly binding to its promoter. These results suggested that MEG3 functions as a tumor suppressor in CRC via regulating the Clusterin activities and may underlie the anticancer activities of vitamin D on CRC cells. The VDR/MEG3/Clusterin signaling pathway may serve as potential therapeutic targets and prognosis biomarkers for CRC patients in future. Keywords: lncRNA, CRC, MEG3, Clusterin, Vitamin

Generation of pure GABAergic neurons by transcription factor programming

Approaches to differentiating pluripotent stem cells (PSCs) into neurons currently face two major challenges-(i) generated cells are immature, with limited functional properties; and (ii) cultures exhibit heterogeneous neuronal subtypes and maturation stages. Using lineage-determining transcription factors, we previously developed a single-step method to generate glutamatergic neurons from human PSCs. Here, we show that transient expression of the transcription factors Ascl1 and Dlx2 (AD) induces the generation of exclusively GABAergic neurons from human PSCs with a high degree of synaptic maturation. These AD-induced neuronal (iN) cells represent largely nonoverlapping populations of GABAergic neurons that express various subtype-specific markers. We further used AD-iN cells to establish that human collybistin, the loss of gene function of which causes severe encephalopathy, is required for inhibitory synaptic function. The generation of defined populations of functionally mature human GABAergic neurons represents an important step toward enabling the study of diseases affecting inhibitory synaptic transmission