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Due to the small number of participants in realistic cases, the Nash equilibrium generated by an oligopolistic market is more appropriate for depicting the actual energy market than the competitive equilibrium generated by a competitive market. However, the market efficiency decreases when the Nash equilibrium is used rather than the competitive equilibrium because of the strategic behaviors of the participants. In this paper, we propose two new mechanisms (subsidization and punishment) for each generator, both of which drive the Nash equilibrium to the competitive equilibrium in heterogeneous oligopolistic energy markets with a uniform pricing mechanism. Under the two proposed mechanisms, the equivalence of the Nash equilibrium and the competitive equilibrium is strictly proven. Furthermore, we apply a distributed algorithm to numerically confirm that both mechanisms perfectly eliminate the market efficiency loss. Finally, these two mechanisms are applied to the energy market under three different stages of development. Simulation results illustrate that the additional costs caused by the mechanisms converge to a low value and that the subsidization mechanism slightly outperforms the punishment mechanism.

RAS/RAF/MAPK/p‐ERK signaling promotes the replication and oncolytic effect of M1 virus via inhibiting P21 and subsequent suppression of Cyclin‐dependent kinase 2 (CDK2). Inhibition of RAS/RAF/MAPK/p‐ERK signaling by sorafenib or U0126 suppresses the oncolytic effect of M1. Knockout of p21 enhances the effect of M1, while overexpression of p21 inhibits it. Inhibition of CDK2 by K03861 attenuates the efficacy of M1., Oncolytic viruses are potent anticancer agents that replicate within and kill cancer cells rather than normal cells, and their selectivity is largely determined by oncogenic mutations. M1, a novel oncolytic virus strain, has been shown to target cancer cells, but the relationship between its cancer selectivity and oncogenic signaling pathways is poorly understood. Here, we report that RAS mutation promotes the replication and oncolytic effect of M1 in cancer, and we further provide evidence that the inhibition of the RAS/RAF/MEK signaling axis suppresses M1 infection and the subsequent cytopathic effects. Transcriptome analysis revealed that the inhibition of RAS signaling upregulates the type I interferon antiviral response, and further RNA interference screen identified CDKN1A as a key downstream factor that inhibits viral infection. Gain‐ and loss‐of‐function experiments confirmed that CDKN1A inhibited the replication and oncolytic effect of M1 virus. Subsequent TCGA data mining and tissue microarray (TMA) analysis revealed that CDKN1A is commonly deficient in human cancers, suggesting extensive clinical application prospects for M1. Our report indicates that virotherapy is feasible for treating undruggable RAS‐driven cancers and provides reliable biomarkers for personalized cancer therapy.

Over the last decade, oncolytic virus (OV) therapy has shown its promising potential in tumor treatment. The fact that not every patient can benefit from it highlights the importance for defining biomarkers that help predict patients’ responses. As particular self-amplifying biotherapeutics, the anti-tumor effects of OVs are highly dependent on the host factors for viral infection and replication. By using weighted gene co-expression network analysis (WGCNA), we found matrix remodeling associated 8 (MXRA8) is positively correlated with the oncolysis induced by oncolytic virus M1 (OVM). Consistently, MXRA8 promotes the oncolytic efficacy of OVM in vitro and in vivo. Moreover, the interaction of MXRA8 and OVM studied by single-particle cryo-electron microscopy (cryo-EM) showed that MXRA8 directly binds to this virus. Therefore, MXRA8 acts as the entry receptor of OVM. Pan-cancer analysis showed that MXRA8 is abundant in most solid tumors and is highly expressed in tumor tissues compared with adjacent normal ones. Further study in cancer cell lines and patient-derived tumor tissues revealed that the tumor selectivity of OVM is predominantly determined by a combinational effect of the cell membrane receptor MXRA8 and the intracellular factor, zinc-finger antiviral protein (ZAP). Taken together, our study may provide a novel dual-biomarker for precision medicine in OVM therapy.

This paper investigates the efficiency loss in social cost caused by strategic bidding behavior of individual participants in a supply-demand balancing market, and proposes a mechanism to fully recover equilibrium social optimum via subsidization and taxation. We characterize the competition among supply-side firms to meet given inelastic demand, with linear supply function bidding and the proposed efficiency recovery mechanism. We show that the Nash equilibrium of such a game exists under mild conditions, and more importantly, it achieves the underlying efficient supply dispatch and the market clearing price that reflects the truthful system marginal production cost. Further, the mechanism can be tuned to guarantee self-sufficiency, i.e., taxes collected counterbalance subsidies needed. Extensive numerical case studies are run to validate the equilibrium analysis, and we employ individual net profit and a modified version of Lerner index as two metrics to evaluate the impact of the mechanism on market outcomes by varying its tuning parameter and firm heterogeneity.

Despite emerging advances in cancer treatment during the past decades, the increasing incidence of morbidity and mortality has made cancer the leading cause of death worldwide.

In the initial stage of electricity market construction, incentive-based demand response can effectively mitigate price spikes. Considering the overall equilibria of the market, it is of great significance to study the impact of incentive-based demand response on market clearing and participants’ behaviours. Firstly, this paper analyzes the compensation methods of incentive- based demand response and establishes an equilibrium model of day-ahead electricity market bidding that takes into account demand response. Secondly, considering the overall equilibrium conditions of the market, the overall equilibrium model of the market is established. Results show that the incentive-based demand response mechanism has a restraining effect on the generators’ bidding, and the load reduction effect is prominent when the network is congested.

Diabetes mellitus is a chronic metabolic health condition affecting the steady state of blood sugar level. The usual method of administration is subcutaneous injection of insulin. There are several ways to subcutaneously inject insulin, such as syringes, insulin pens, and insulin pumps. However, subcutaneous injections of insulin can lead to discomfort, pain and local infection. This review focuses on traditional methods of insulin administration, non-invasive approaches, and new insulin therapy technologies, and the advantages and disadvantages of these approaches, as well as future development prospects are also discussed.

As a major way to consume new energy, energy transmission across provinces and regions has increased rapidly in recent years. It is of great importance for the construction of the spot market to study the impact of different uncertainty of the outside power on the joint energy and reserve market. Firstly, this paper establishes a joint energy and reserve market equilibrium model that takes into account the uncertainty of the outside power which leads to additional reserve demand. Secondly, a game equilibrium algorithm is proposed to solve the market final equilibrium. The simulation results show that the uncertainty of the outside power will not only reduce market efficiency but also damage the interests of the outside new energy generator itself.