Short-Packet Downlink Transmission with Non-Orthogonal Multiple Access

This work introduces downlink non-orthogonal multiple access (NOMA) into short-packet communications. NOMA has great potential to improve fairness and spectral efficiency with respect to orthogonal multiple access (OMA) for low-latency downlink transmission, thus making it attractive for the emerging Internet of Things. We consider a two-user downlink NOMA system with finite blocklength constraints, in which the transmission rates and power allocation are optimized. To this end, we investigate the trade-off among the transmission rate, decoding error probability, and the transmission latency measured in blocklength. Then, a one-dimensional search algorithm is proposed to resolve the challenges mainly due to the achievable rate affected by the finite blocklength and the unguaranteed successive interference cancellation. We also analyze the performance of OMA as a benchmark to fully demonstrate the benefit of NOMA. Our simulation results show that NOMA significantly outperforms OMA in terms of achieving a higher effective throughput subject to the same finite blocklength constraint, or incurring a lower latency to achieve the same effective throughput target. Interestingly, we further find that with the finite blocklength, the advantage of NOMA relative to OMA is more prominent when the effective throughput targets at the two users become more comparable.Comment: 15 pages, 9 figures. This is a longer version of a paper to appear in IEEE Transactions on Wireless Communications. Citation Information: X. Sun, S. Yan, N. Yang, Z. Ding, C. Shen, and Z. Zhong, "Short-Packet Downlink Transmission with Non-Orthogonal Multiple Access," IEEE Trans. Wireless Commun., accepted to appear [Online] https://ieeexplore.ieee.org/document/8345745

Echinacoside attenuates lipopolysaccharide-induced acute lung injury in newborn mice via inactivation of NF- κB/NLRP3 signaling pathway

Purpose: To investigate the effect of echinacoside (ECH) on acute lung injury (ALI) and the underlying mechanism of action.Methods: The ALI model was established through intranasal instillation of lipopolysaccharide (LPS). Lung tissue damage was determined using hematoxylin and eosin (H&E) staining and lung wet-to-dry–weight ratio. Bronchoalveolar lavage fluid (BALF) protein concentration, cell count, and cytokine level were evaluated. Western blotting was used to determine protein expression level.Results: ECH attenuated lung tissue injury and lung wet-to-dry–weight ratio in the ALI model (p < 0.01). The total protein content and number of total cells, neutrophils, and macrophages increased in BALF of mice treated with LPS, but these increases were reversed by ECH treatment (p < 0.01). The levels of TNF-α and IL-1β increased in BALF and lung tissue of LPS-treated mice; however, ECH treatment decreased these changes (p < 0.01). In addition, ECH inhibited the activation of the nuclear factor-κB (NF-κB)/NLR family pyrin domain containing 3 (NLRP3) pathway in LPS-treated mice (p < 0.01).Conclusion: Echinacoside attenuates LPS-induced ALI via inactivation of the NF-κB/NLRP3 pathway, making echinacoside a potential drug for the treatment of ALI. Keywords: Echinacoside, Acute lung injury, Lipopolysaccharide, Nuclear factor-κB, NLR family pyrin domain containing