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Relaying is supposed to be a low energy consumption technique since the long distance transmission is divided into several short distance transmissions. When the power consumptions (PCs) other than that consumed by transmitting information bits is taken into account, however, relaying may not be energy efficient. In this article, we study the energy efficiencies (EEs) of one-way relay transmission (OWRT) and two-way relay transmission (TWRT) by comparing with direct transmission (DT). We consider a system where two source nodes transmit to each other with the assistance of a half-duplex amplify-and-forward relay node. We first find the maximum EEs of DT, OWRT, and TWRT by optimizing the transmission time and the transmit powers at each node. Then we compare the maximum EEs of the three strategies, and analyze the impact of circuit PCs and data amount. Analytical and simulation results show that relaying is not always more energy efficient than DT. Moreover, TWRT is not always more energy efficient than OWRT, despite that it is more spectral efficient. The EE of TWRT is higher than those of DT and OWRT in symmetric systems where the circuit PCs at each node are identical and the numbers of bits to be transmitted in two directions are equal. In asymmetric systems, however, OWRT may provide higher EE than TWRT when the numbers of bits in two directions differ significantly.

We studied the effect of riccardin D, a macrocyclic bisbibenzyl, which was isolated from the Chinese liverwort plant, on human leukemia cells and the underlying molecular mechanism. Riccardin D had a significant antiproliferative effect on human leukemia cell lines HL-60, K562 and its multidrug resistant (MDR) counterpart K562/A02 cells, but showed no effect on the topoisomerase-II-deficient HL-60/MX2 cells, as measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. The pBR322 DNA relaxation assay revealed that riccardin D selectively inhibited the activity of topoisomerase II (topo II). The suppression of topo II activity by riccardin D was stronger than that of etoposide, a known topo II inhibitor. After treatment with riccardin D, nuclear extracts of leukemia K562 and K562/A02 cells left the majority of pBR322 DNA in a supercoiled form. Further examination showed that riccardin D effectively induced HL-60, K562 and K562/A02 apoptosis as evidenced by externalization of phosphatidylserine and formation of DNA ladder fragments. The activation of cytochrome c, caspase-9, caspase-3 and cleaved poly ADP-ribose polymerase (PARP) was also enhanced, as estimated by Western blot analysis. By contrast, riccardin D was unable to induce apoptosis in the topoisomerase-II-deficient HL-60/MX2 cells, indicating that the induction of apoptosis by riccardin D was due to the inhibition of topo II activity. In addition, riccardin D was able to significantly decrease P-glycoprotein (P-gp) expression in K562/A02 cells. Taken together, our data demonstrate that riccardin D is a novel DNA topo II inhibitor which can induce apoptosis of human leukemia cells and that it has therapeutic potential for both regular and MDR strains of leukemia cells.

Apple ring rot caused by Botryosphaeria dothidea is an important disease in China, which leads to serious economic losses during storage. Plant activators are compounds that induce resistance against pathogen infection and are considered as a promising alternative strategy to traditional chemical treatment. In the present study, butylated hydroxytoluene (BHT), a potential plant activator, was evaluated for its induced resistance against B. dothidea in postharvest apple fruits. The physiological and molecular mechanisms involved in induced resistance were also explored. The results showed that BHT treatment could trigger strong resistance in apple fruits against B. dothidea, and the optimum concentration was 200 μmol L–1 by immersion of fruits. BHT treatment significantly increased the activities of four defensive enzymes and alleviated lipid peroxidation by increasing antioxidant enzyme activities. In addition, salicylic acid (SA) content was enhanced by BHT treatment as well as the expression of three SA biosynthesis-related genes (MdSID2, MdPAD4, and MdEDS1) and two defense genes (MdPR1 and MdPR5). Our results suggest that BHT-conferred resistance against B. dothidea might be mainly through increasing the activities of defense-related enzymes and activating SA signaling pathway, which may provide an alternative strategy to control apple ring rot in postharvest fruits.

Deep learning recommendation models (DLRMs) have been used across many business-critical services at Meta and are the single largest AI application in terms of infrastructure demand in its data-centers. In this paper, we present Neo, a software-hardware co-designed system for high-performance distributed training of large-scale DLRMs. Neo employs a novel 4D parallelism strategy that combines table-wise, row-wise, column-wise, and data parallelism for training massive embedding operators in DLRMs. In addition, Neo enables extremely high-performance and memoryefficient embedding computations using a variety of critical systems optimizations, including hybrid kernel fusion, software-managed caching, and quality-preserving compression. Finally, Neo is paired with ZionEX , a new hardware platform co-designed with Neo's 4D parallelism for optimizing communications for large-scale DLRM training. Our evaluation on 128 GPUs using 16 ZionEX nodes shows that Neo outperforms existing systems by up to 40× for training 12-trillion-parameter DLRM models deployed in production.

BACKGROUND Dihydromyricetin (DMY) is a natural dihydroflavonol with many bioactive effects. However, the physicochemical properties of DMY related to its bioavailability, especially its stability, are unclear. RESULTS The effects of pH, temperature, metal ions and ascorbic acid (AA) on the stability of DMY were studied using high‐performance liquid chromatography (HPLC). The bioavailability of DMY in the presence and absence of AA was compared. Dihydromyricetin was unstable in weak alkaline solutions, and the degradation was significantly accelerated in the presence of Cu2+ and Fe3+. The degradation process followed the first‐order kinetic model. The degradation rate constant (k) increased with increasing pH and temperature. The remaining DMY was only 49% of its initial concnentration after 4 h in simulated intestinal fluid (SIF) at 37 °C. However, by supplementing with AA, the degradation of DMY was rarely occured within 6 h. The solubility of DMY at pH 3–5 was about 750 μg mL−1, slightly increasing to 853 μg mL−1 at pH 6. Pharmacokinetic studies showed that the bioavailability of DMY increased from 0.122% to 0.341% by supplementing with AA (10% of DMY). CONCLUSION The degradation of DMY is one reason for its poor bioavailability. The presence of AA could significantly improve the stability of DMY, and further improve its bioavailability in rats. © 2020 Society of Chemical Industry

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