Interference Mitigation for FMCW Radar With Sparse and Low-Rank Hankel Matrix Decomposition

In this paper, the interference mitigation for Frequency Modulated Continuous Wave (FMCW) radar system with a dechirping receiver is investigated. After dechirping operation, the scattered signals from targets result in beat signals, i.e., the sum of complex exponentials while the interferences lead to chirp-like short pulses. Taking advantage of these different time and frequency features between the useful signals and the interferences, the interference mitigation is formulated as an optimization problem: a sparse and low-rank decomposition of a Hankel matrix constructed by lifting the measurements. Then, an iterative optimization algorithm is proposed to tackle it by exploiting the Alternating Direction of Multipliers (ADMM) scheme. Compared to the existing methods, the proposed approach does not need to detect the interference and also improves the estimation accuracy of the separated useful signals. Both numerical simulations with point-like targets and experiment results with distributed targets (i.e., raindrops) are presented to demonstrate and verify its performance. The results show that the proposed approach is generally applicable for interference mitigation in both stationary and moving target scenarios.Comment: 12 pages, 8 figure

The Application of Mobile Learning in College Experimental Teaching

First we analyzed the current forms of higher education and learning characteristics of the experimental courses, then we introduced mobile devices to the teaching process of experimental courses in colleges and universities. The introduction of mobile learning can meet the needs of higher education and to achieve the requirements of the reform. In this paper, we focuses on how to construct the learning platform in the integration of mobile learning and experimental courses. As well as the session framework for mobile learning activity design. Practice teaching proves that this method can better improve the efficiency of classroom teaching, and expand the depth and breadth of the students’ study. At the same time, it can also promote the improvement of students’ comprehensive ability

A New Stopping Criterion for BICM-ID System Based on Cross-Entropy

AbstractThis paper proposes a new stopping criterion for BICM-ID (bit-interleaved coded modulation with iterative decoding) system based on the CE (cross-entropy) stopping criterion. Unlike the conventional CE stopping criterion, the new scheme only computes and compares the cross-entropy value of the odd bits of the entire frame bits. We name the proposed new criterion as Partial-CE stopping criterion. The new criterion can reduce about 50% computation complexity of the BICM-ID receiver. Simulations comparing the new criterion with the original CE stopping criterion show that the proposed Partial-CE scheme can achieve similar performances in terms of BER and the average iteration numbers

Structure of human tryptophanyl-tRNA synthetase in complex with tRNA(Trp) reveals the molecular basis of tRNA recognition and specificity

Aminoacyl-tRNA synthetases (aaRSs) are a family of enzymes responsible for the covalent link of amino acids to their cognate tRNAs. The selectivity and species-specificity in the recognitions of both amino acid and tRNA by aaRSs play a vital role in maintaining the fidelity of protein synthesis. We report here the first crystal structure of human tryptophanyl-tRNA synthetase (hTrpRS) in complex with tRNA(Trp) and Trp which, together with biochemical data, reveals the molecular basis of a novel tRNA binding and recognition mechanism. hTrpRS recognizes the tRNA acceptor arm from the major groove; however, the 3′ end CCA of the tRNA makes a sharp turn to bind at the active site with a deformed conformation. The discriminator base A73 is specifically recognized by an α-helix of the unique N-terminal domain and the anticodon loop by an α-helix insertion of the C-terminal domain. The N-terminal domain appears to be involved in Trp activation, but not essential for tRNA binding and acylation. Structural and sequence comparisons suggest that this novel tRNA binding and recognition mechanism is very likely shared by other archaeal and eukaryotic TrpRSs, but not by bacterial TrpRSs. Our findings provide insights into the molecular basis of tRNA specificity and species-specificity

Dapagliflozin relieves renal injury in a diabetic nephropathy model by inducing autophagy through regulation of miR-30e-5p/AKT/mTOR pathway

Purpose: To investigate the mechanism of action of dapagliflozin on diabetic nephropathy. Methods: A rat model of diabetic nephropathy was established by injection of fructose-streptozotocin. Blood glucose and urinary protein levels were measured, while histopathological changes in kidney tissues were determined by hematoxylin & eosin staining (H & E). Serum levels of creatinine (Cr), blood urea nitrogen (BUN), malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), and lactate dehydrogenase (LDH) were evaluated by enzyme-linked immunosorbent assay (ELISA). Cell apoptosis and autophagy were investigated by evaluating apoptotic and autophagic protein expression by western blot. Results: Administration of fructose-streptozotocin increased the blood glucose level of the rats (p < 0.001) and induced pathological changes in the kidney tissues, including glomerulosclerosis, renal tubule dilation, and inflammatory cell infiltration of rats. However, long-term treatment with dapagliflozin attenuated the fructose-streptozotocin-induced increases in Cr, BUN, and urinary protein and reversed the fructose-streptozotocin-induced decrease in Bcl-2 expression and increases in Bax and cleaved PARP expression in diabetic rats. Dapagliflozin also reversed the increases in MDA and LDH and decreases in SOD and GSH in diabetic rats. The fructose-streptozotocin-induced increase in p62 expression and decreases in LC3 and Beclin 1 expression were reversed by dapagliflozin. It upregulated miR-30e-5p expression and downregulated phosphorylated AKT and mTOR expression in diabetic rats. MicroRNA-30e-5p targeted AKT and inhibition of miR-30e-5p attenuated the dapagliflozin-induced decrease in p-AKT and p-mTOR expression in diabetic rats. Conclusion: In fructose-streptozotocin-induced diabetic rats, dapagliflozin ameliorates kidney injury, suppresses cell apoptosis and oxidative stress, and promotes cell autophagy through upregulation of miR-30e-5p and inactivation of the AKT/mTOR pathway. Therefore, dapagliflozin is a potent therapeutic agent for the management of diabetic neuropathy