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Bladder cancer is one of the most malignant tumors closely associated with macrophages. Polyporus polysaccharide (PPS) has shown excellent efficacy in treating bladder cancer with minimal side effects. However, the molecular mechanisms underlying the effects of PPS in inhibiting bladder cancer remain unclear. In this study, we used macrophages cultured alone or with T24 human bladder cancer cell culture supernatant as study models. We found that PPS enhanced the activities of IFN-γ-stimulated RAW 264.7 macrophages, as shown by the release of inducible nitric oxide synthase (INOS), secretion of tumor necrosis factor (TNF)-α and interleukin (IL)-6, phagocytosis activity, as well as expression of M1 phenotype indicators, such as CD40, CD284 and CD86. PPS acted upstream in activation cascade of nuclear factor (NF)-κB signaling pathways by interfering with IκB phosphorylation. In addition, PPS regulated NF-κB (P65) signaling by interfering with Toll-like receptor (TLR)-4, INOS and cyclooxygenase (COX)-2. Our results indicate that PPS activates macrophages through TLR4/NF-κB signaling pathways.

Abstract:Crude oil, as one of the most important energy sources in the world, plays a crucial role in global economic events. An accurate prediction for crude oil price is an interesting and challenging task for enterprises, governments, investors, and researchers. To cope with this issue, in this paper, we proposed a method integrating ensemble empirical mode decomposition (EEMD), adaptive particle swarm optimization (APSO), and relevance vector machine (RVM)-namely, EEMD-APSO-RVM-to predict crude oil price based on the "decomposition and ensemble" framework. Specifically, the raw time series of crude oil price were firstly decomposed into several intrinsic mode functions (IMFs) and one residue by EEMD. Then, RVM with combined kernels was applied to predict target value for the residue and each IMF individually. To improve the prediction performance of each component, an extended particle swarm optimization (PSO) was utilized to simultaneously optimize the weights and parameters of single kernels for the combined kernel of RVM. Finally, simple addition was used to aggregate all the predicted results of components into an ensemble result as the final result. Extensive experiments were conducted on the crude oil spot price of the West Texas Intermediate (WTI) to illustrate and evaluate the proposed method. The experimental results are superior to those by several state-of-the-art benchmark methods in terms of root mean squared error (RMSE), mean absolute percent error (MAPE), and directional statistic (Dstat), showing that the proposed EEMD-APSO-RVM is promising for forecasting crude oil price.

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Background and Aims M2 phenotype macrophages are involved in the resolution of inflammation and intestinal repair. Exosomes are emerging as important mediators of intercellular communication in the mucosal microenvironment. Methods M2 macrophages were transfected with or without miR-590-3p. Exosomes derived from M2 macrophages were isolated and identified. Proliferation and wound healing were tested in vitro and compared between groups. The mechanism involving LATS1, and activation of YAP and β-catenin signalling was investigated by using plasmid transfection, western blotting, immunofluorescence, and luciferase reporter assays. The effect of exosomes in vivo was detected in DSS-induced murine colitis. Results First, we demonstrated that M2 macrophages promoted colonic epithelial cell proliferation in an exosome-dependent manner. Epithelial YAP mediated the effect of M2 macrophage-derived exosomes (M2-exos) in epithelial proliferation. Moreover, miR-590-3p, which was significantly enriched in M2-exos, could be transferred from macrophages into epithelial cells, resulting in the enhanced proliferation and wound healing of epithelial cells. Mechanistically, miR-590-3p suppressed the expression of LATS1 by binding to its coding sequence and subsequently activated the YAP/β-catenin-modulated transcription process to improve epithelial cell wound-healing ability. MiR-590-3p also inhibited the induction of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6. More importantly, repression miR-590-3p in M2-exos resulted with severer mucosal damage and impaired colon repair of mice compared with those in M2-exo-treated mice after DSS-induced colitis. Conclusion M2 macrophage-derived exosomal miR-590-3p reduces inflammatory signals and promotes epithelial regeneration by targeting LATS1 and subsequently activating YAP/β-catenin-regulated transcription, which could offer a new opportunity for clinical therapy for ulcerative colitis (UC).

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With the popularization of wireless communication and smart devices in the medical field, mobile medicine has attracted more and more attention because it can break through the limitations of time, space, and objects and provide more efficient and quality medical services. However, the characteristics of a mobile smart medical network make it more susceptible to security threats such as data integrity damage and privacy leakage than those of traditional wired networks. In recent years, many digital signature schemes have been proposed to alleviate some of these challenges. Unfortunately, traditional digital signatures cannot meet the diversity and privacy requirements of medical data applications. In response to this problem, this paper uses the unique security attributes of sanitizable signatures to carry out research on the security and privacy protection of medical data and proposes a data security and privacy protection scheme suitable for smart mobile medical scenarios. Security analysis and performance evaluation show that our new scheme effectively guarantees data security and user privacy while greatly reducing computation and communication costs, making it especially suitable for mobile smart medical application scenarios.

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