Evolutionary privacy-preserving learning strategies for edge-based IoT data sharing schemes

The fast proliferation of edge devices for the Internet of Things (IoT) has led to massive volumes of data explosion. The generated data is collected and shared using edge-based IoT structures at a considerably high frequency. Thus, the data-sharing privacy exposure issue is increasingly intimidating when IoT devices make malicious requests for filching sensitive information from a cloud storage system through edge nodes. To address the identified issue, we present evolutionary privacy preservation learning strategies for an edge computing-based IoT data sharing scheme. In particular, we introduce evolutionary game theory and construct a payoff matrix to symbolize intercommunication between IoT devices and edge nodes, where IoT devices and edge nodes are two parties of the game. IoT devices may make malicious requests to achieve their goals of stealing privacy. Accordingly, edge nodes should deny malicious IoT device requests to prevent IoT data from being disclosed. They dynamically adjust their own strategies according to the opponent's strategy and finally maximize the payoffs. Built upon a developed application framework to illustrate the concrete data sharing architecture, a novel algorithm is proposed that can derive the optimal evolutionary learning strategy. Furthermore, we numerically simulate evolutionarily stable strategies, and the final results experimentally verify the correctness of the IoT data sharing privacy preservation scheme. Therefore, the proposed model can effectively defeat malicious invasion and protect sensitive information from leaking when IoT data is shared

Construction and verification of a novel prognostic risk model for kidney renal clear cell carcinoma based on immunity-related genes

Background: Currently, there are no useful biomarkers or prognostic risk markers for the diagnosis of kidney renal clear cell carcinoma (KIRC), although recent research has shown that both, the onset and progression of KIRC, are substantially influenced by immune-associated genes (IAGs).Objective: This work aims to create and verify the prognostic value of an immune risk score signature (IRSS) based on IAGs for KIRC using bioinformatics and public databases.Methods: Differentially expressed genes (DEGs) related to the immune systems (IAGs) in KIRC tissues were identified from The Cancer Genome Atlas (TCGA) databases. The DEGs between the tumor and normal tissues were identified using gene ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analyses. Furthermore, a prognostic IRSS model was constructed and its prognostic and predictive performance was analyzed using survival analyses and nomograms. Kidney renal papillary cell carcinoma (KIRP) sets were utilized to further validate this model.Results: Six independent immunity-related genes (PAEP, PI3, SAA2, SAA1, IL20RB, and IFI30) correlated with prognosis were identified and used to construct an IRSS model. According to the Kaplan-Meier curve, patients in the high-risk group had significantly poorer prognoses than those of patients in the low-risk group in both, the verification set (p <0.049; HR = 1.84; 95% CI = 1.02–3.32) and the training set (p < 0.001; HR = 3.12, 95% CI = 2.23–4.37). The numbers of regulatory T cells (Tregs) were significantly positively correlated with the six immunity-related genes identified, with correlation coefficients were 0.385, 0.415, 0.399, 0.451, 0.485, and 0.333, respectively (p <0.001).Conclusion: This work investigated the association between immune infiltration, immunity-related gene expression, and severity of KIRC to construct and verify a prognostic risk model for KIRC and KIRP

Remnant cholesterol traits and risk of stroke: A multivariable mendelian randomization study

Observational epidemiological studies have reported a relationship between remnant cholesterol and stroke. However, the results are inconclusive, and causality remains unclear due to confounding or reverse causality. Our objective in this study was to investigate the causal relevance of remnant cholesterol and the risk of stroke and its subtypes using the Mendelian randomization (MR) approach. Genome-wide association studies (GWASs) including 115,082 European individuals (UK Biobank) were used to identify instruments for remnant cholesterol, including intermediate-density lipoprotein (IDL) cholesterol and very-low-density lipoprotein (VLDL) cholesterol. Summary-level data for total stroke, intracerebral hemorrhage, subarachnoid hemorrhage, ischemic stroke (IS), and IS subtypes were obtained from GWAS meta-analyses conducted by the MEGASTROKE consortium. Univariable and multivariable MR analyses were performed. The GWAS identified multiple single-nucleotide polymorphisms after clumping for remnant cholesterol (n = 52), IDL cholesterol (n = 62), and VLDL cholesterol (n = 67). Assessed individually using MR, remnant cholesterol (weighted median: odds ratio [OR] 1.32 per 1-SD higher trait; 95% CI: 1.04–1.67; P = 0.024) had effect estimates consistent with a higher risk of LAS-IS, driven by IDL cholesterol (OR 1.32; 95% CI: 1.04–1.68; P = 0.022). In multivariable MR, IDL cholesterol (OR 1.46; 95% CI: 1.10–1.93; P = 0.009) retained a robust effect on LAS-IS after controlling for VLDL cholesterol and high-density lipoprotein cholesterol. The MR analysis did not indicate causal associations between remnant cholesterol and other stroke subtypes. This study suggests that remnant cholesterol is causally associated with the risk of LAS-IS driven by IDL cholesterol