Distributed Cooperative Multicell Precoding Based on Local Channel State Information

Cooperative multicell precoding is an attractive way of improving the performance in multicell downlink scenarios especially for terminals at cell edges. Multiple base stations in a given area serve each terminal after precoding, which can coordinate the inter-cell interference and achieve higher performance. Most previous work in the area has focus on centralized precoding which requires gathering all transmitters’ channel state information (CSI) at central station (CS) through backhaul and then precoding at CS. However, the requirements on backhaul signaling and computational power scales rapidly in large and dense networks, which usually make such fully centralized approaches impractical. In this paper, we study two practical precoding strategies with only local CSI under a relatively realistic scenario. Performance is finally illustrated through numerical simulations

Chance-constrained approach for decentralized supply chain network under uncertain cost

A decentralized supply chain network under uncertain cost is studied to obtain the optimal decisions of the enterprises in a situation in which the cost is uncertain. The supply chain network members adopt a chance-constrained approach to make decisions. The second-order cone-constrained variational inequality problem is used to construct the chance-constrained supply chain network equilibrium model. Then, the existence and uniqueness properties of the proposed equilibrium model are discussed under some mild assumptions. For the discontinuous functions in the feasible region of the model, the proposed model is converted to a second-order cone complementarity problem. The numerical results show that the uncertainty and risk attitude of retailers and manufacturers have different effects on supply chain network members. When the risk attitude is high, a small change in the risk attitude will significantly change all decisions of supply chain members. If the supply chain member is affected by the uncertainty positively, its profit will increase as its risk attitude increases. Moreover, it is appropriate to adopt a chance-constrained approach when the supply chain members can estimate the distributions of the competitor's strategies

Function analysis of GhWRKY53 regulating cotton resistance to verticillium wilt by JA and SA signaling pathways

WRKY transcription factors (TFs) play an important role in regulating the mechanism of plant self-defense. However, the function of most WRKY TFs in upland cotton (Gossypium hirsutum) is still unknown. Hence, studying the molecular mechanism of WRKY TFs in the resistance of cotton to Verticillium dahliae is of great significance to enhancing cotton disease resistance and improving its fiber quality. In this study, Bioinformatics has been used to characterize the cotton WRKY53 gene family. we analyzed the GhWRKY53 expression patterns in different resistant upland cotton cultivars treated with salicylic acid (SA) and methyl jasmonate (MeJA). Additionally, GhWRKY53 was silenced using a virus-induced gene silencing (VIGS) to determine the contribution of GhWRKY53 to V. dahliae resistance in cotton. The result showed that GhWRKY53 mediated SA and MeJA signal transduction pathways. After VIGS of the GhWRKY53, the ability of cotton to resist V. dahliae decreased, indicating that the GhWRKY53 could be involved in the disease resistance mechanism of cotton. Studies on the levels of SA and jasmonic acid (JA) and their related pathway genes demonstrated that the silencing of GhWRKY53 inhibited the SA pathway and activated the JA pathway, thereby reducing the resistance of plants to V. dahliae. In conclusion, GhWRKY53 could change the tolerance of upland cotton to V. dahliae by regulating the expression of SA and JA pathway-related genes. However, the interaction mechanism between JA and SA signaling pathways in cotton in response to V. dahliae requires further study

New insights into the interplay between autophagy and cartilage degeneration in osteoarthritis

Autophagy is an intracellular degradation system that maintains the stable state of cell energy metabolism. Some recent findings have indicated that autophagy dysfunction is an important driving factor for the occurrence and development of osteoarthritis (OA). The decrease of autophagy leads to the accumulation of damaged organelles and macromolecules in chondrocytes, which affects the survival of chondrocytes and ultimately leads to OA. An appropriate level of autophagic activation may be a new method to prevent articular cartilage degeneration in OA. This minireview discussed the mechanism of autophagy and OA, key autophagy targets regulating OA progression, and evaluated therapeutic applications of drugs targeting autophagy in preclinical and clinical research. Some critical issues worth paying attention to were also raised to guide future research efforts

Gene editing in monogenic autism spectrum disorder: animal models and gene therapies

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disease, and its diagnosis is dependent on behavioral manifestation, such as impaired reciprocal social interactions, stereotyped repetitive behaviors, as well as restricted interests. However, ASD etiology has eluded researchers to date. In the past decades, based on strong genetic evidence including mutations in a single gene, gene editing technology has become an essential tool for exploring the pathogenetic mechanisms of ASD via constructing genetically modified animal models which validates the casual relationship between genetic risk factors and the development of ASD, thus contributing to developing ideal candidates for gene therapies. The present review discusses the progress in gene editing techniques and genetic research, animal models established by gene editing, as well as gene therapies in ASD. Future research should focus on improving the validity of animal models, and reliable DNA diagnostics and accurate prediction of the functional effects of the mutation will likely be equally crucial for the safe application of gene therapies

Preparation of biological sustained-release nanocapsules and explore on algae-killing properties

Introduction: Green algae seriously affect the quality and yield of Torreya grandis, it is important to explore new, environmentally friendly ways to control it. Objectives: The present study aimed at preparing sustained-release algae-killing nanocapsules without pollution to the environment. Methods: In this work, sodium carboxymethylcellulose (CMC), sodium alginate (SA), and chitosan (CTS) were used as raw materials in acylation reaction with the photosensitive catalytic material iron octaaminophthalocyanine (T) to generate the photoactive bio-based materials T-CMC, T-SA, and T-CMCS. Cinnamaldehyde and 2-aminobenzimidazole were combined using chemical grafting to produce a new algicide, and then formed nanocapsules by phase separation. The molecular structure of products was characterized by UV–Vis, FTIR, and NMR (1H NMR, 13C NMR). The particle size of the nanocapsules was determined by Zeta particle size analysis and TEM; DSC was used to investigate the thermal stability; The encapsulation efficiency and sustained-release performance were determined by HPLC. Then the phytotoxic of the new algicide was measured. Results: The bio-based nanocapsules was successfully synthesized, which had a particle size of 10–30 nm and was stable at 40 °C. The encapsulation efficiency of the nanocapsules was 48.77%, the cumulative release rate was 83%, and the new algicide killed the green algae in a dose-dependent way. Conclusions: The bio-based nano capsule is a new and valuable Sustained-release capsule, which is the method of green algae

An Integrative Analysis Reveals the Potential Mechanism between Herbal Medicine Yinchen and Immunoregulation in Hepatocellular Carcinoma

Aims. Abundant evidences in traditional Chinese medicine (TCM) supported the therapeutic value of herbal medicine Yinchen in hepatocellular carcinoma (HCC), but the underlying mechanism remains to be investigated. Main Methods. The intersection of immune gene set, module genes, HCC-associated genes, and target genes of Yinchen was employed for further analyses. The module genes were identified by weighted gene coexpression network analysis, and the other three gene sets were obtained from public databases. Subsequently, we further explored the clinical value and immunoregulation of the hub gene of intersection. The relevant pathways related to hub gene expression were investigated by gene set enrichment analysis. Finally, the interaction of active compounds and target genes was validated by molecular docking. Key Findings. Thirteen active compounds and 90 target genes of Yinchen were included. After constructing the network among Yinchen, target genes, and HCC, BIRC5 was identified as the hub gene. Significant difference was found between the high-expressed group and the low-expressed group in survival and stage. Different immune subtypes also presented significant difference in BIRC5 expression. Moreover, NK cell and T cell (CD4+ effector memory and CD4+ memory resting) were negatively correlated with BIRC5 expression, while CTLA4 and LAG3 were positively correlated. The results of molecular docking further validated a good binding activity of quercetin-BIRC5 interaction. Significance. In summary, our research identified for the first time a novel underlying association among herbal medicine Yinchen, BIRC5, immunotherapy, and HCC. We speculated that Yinchen may target the immune checkpoints (CTLA4 and LAG3) and activate the immune cells by suppressing BIRC5