An evolutionary game-based simulation study of a multi-agent governance system for smart senior care services in China.

BACKGROUND: The competing interests of the government, smart senior care technology service providers, and older adults have led to a serious fragmentation of governance in China. This study aims to identify the collaboration mechanisms and evolutionary stabilization strategies for these agents. METHODS: An evolutionary game model is developed to analyze the strategic decisions made by the government, smart senior care technology service providers, and older adults. A sensitivity analysis is conducted using data from Anhui Province, China, to verify the effects of relevant parameters on the strategy decisions of each agent. RESULTS: The results of the simulation and sensitivity analysis indicated that, first, despite changes in the initial willingness values of the tripartite agents, the system eventually converges on 1. Second, the collaboration mechanism of the tripartite agents in the smart senior care system is related to government incentives, penalties, and subsidies, smart senior care service costs, and the additional benefits provided to smart senior care technology service providers. CONCLUSION: The strategy decisions of the government, providers, and older adults interact with each other. To promote collaboration among the tripartite agents and improve governance effectiveness, the government should strengthen the regulations for providers, increase penalties for providers that engage in a breach of trust, provide moderate incentives and subsidies, and control smart senior care service costs.

Synergistic effect of zero-valent iron and static magnetic field on wastewater purification and bioelectricity generation in electroactive constructed wetlands.

This study investigated the enhancement effect of zero-valent iron and static magnetic field on the pollutant removal and power generation of electroactive constructed wetland. As demonstration, a conventional wetland was systematically modified by introducing zero-valent iron and then a static magnetic field, leading to progressive increases in pollutant (namely NH4+-N and chemical oxygen demand) removal efficiencies. By introducing both zero-valent iron and a static magnetic field, the power density increased four-fold to 9.2 mW/m2 and the internal resistance decreased by 26.7% to 467.4 Ω. Notably, static magnetic field decreased the relative abundance of electrochemically active bacteria (such as Romboutsia), while significantly enhancing species diversity. The permeability of the microbial cell membrane was improved, leading to a reduction in activation loss and internal resistance, thereby enhancing power generation capacity. Results showed that the addition of zero-valent iron and the applied magnetic field were beneficial to the pollutants removal and bioelectricity generation.

Fur Represses Vibrio cholerae Biofilm Formation via Direct Regulation of vieSAB, cdgD, vpsU, and vpsA-K Transcription.

Attached Vibrio cholerae biofilms are essential for environmental persistence and infectivity. The vps loci (vpsU, vpsA-K, and vpsL-Q) are required for mature biofilm formation and are responsible for the synthesis of exopolysaccharide. Transcription of vps genes is activated by the signaling molecule bis-(3'-5')-cyclic di-GMP (c-di-GMP), whose metabolism is controlled by the proteins containing the GGDEF and/or EAL domains. The ferric uptake regulator (Fur) plays key roles in the transcription of many genes involved in iron metabolism and non-iron functions. However, roles for Fur in Vibrio biofilm production have not been documented. In this study, phenotypic assays demonstrated that Fur, independent of iron, decreases in vivo c-di-GMP levels and inhibits in vitro biofilm formation by Vibrio cholerae. The Fur box-like sequences were detected within the promoter-proximal DNA regions of vpsU, vpsA-K, vieSAB, and cdgD, suggesting that transcription of these genes may be under the direct control of Fur. Indeed, the results of luminescence, quantitative PCR (qPCR), electrophoretic mobility shift assay (EMSA), and DNase I footprinting assays demonstrated Fur to bind to the promoter-proximal DNA regions of vpsU, vpsA-K, and cdgD to repress their transcription. In contrast, Fur activates the transcription of vieSAB in a direct manner. The cdgD and vieSAB encode proteins with GGDEF and EAL domains, respectively. Thus, data presented here highlight a new physiological role for Fur wherein it acts as a repressor of V. cholerae biofilm formation mediated by decreasing the production of exopolysaccharide and the intracellular levels of c-di-GMP.

Direct Binding and Regulation by Fur and HapR of the Intermediate Regulator and Virulence Factor Genes Within the ToxR Virulence Regulon in Vibrio cholerae.

Cholera toxin (CT) and toxin coregulated pilus (TCP, TcpA is the major subunit) are two major virulence factors of Vibrio cholerae, both of which play critical roles in developing severe diarrhea in human. Expression of CT and TCP is under the tight control of the regulatory cascade known as the ToxR virulence regulon, which is composed of three regulators ToxR, TcpP, and ToxT. Besides, their expression is also regulated by the quorum sensing (QS) master regulator HapR and the regulatory protein Fur. Though transcription of tcpP, toxT, and/or tcpA are reported to be regulated by HapR and Fur, to date there are no studies to verify their direct regulations. In the present study, we showed that HapR directly repress the transcription of tcpP and tcpA by binding to their promoter regions, and possibly repress toxT transcription in an indirect manner. Fur directly activated the transcription of tcpP, toxT, and tcpA by binding to their promoters. Taking account of the sequential expression of hapR, fur, tcpP, toxT, and tcpA in the different growth phases of V. cholerae, we deduce that at the early mid-logarithmic growth phase, Fur binds to the promoters of tcpP, toxT, and tcpA to activate their transcription; while at the later mid-logarithmic growth phase, HapR can bind to the promoters of tcpP and tcpA to repress their transcription. Our study reveals the new recognition in the virulence regulatory pathways in V. cholerae and suggests the complicated and subtle regulation network with the growth density dependence.

Expression of Hemolysin Is Regulated Under the Collective Actions of HapR, Fur, and HlyU in Vibrio cholerae El Tor Serogroup O1.

The biotype El Tor of serogroup O1 and most of the non-O1/non-O139 strains of Vibrio cholerae can produce an extracellular pore-forming toxin known as cholera hemolysin (HlyA). Expression of HlyA has been previously reported to be regulated by the quorum sensing (QS) and the regulatory proteins HlyU and Fur, but lacks the direct evidence for their binding to the promoter of hlyA. In the present work, we showed that the QS regulator HapR, along with Fur and HlyU, regulates the transcription of hlyA in V. cholerae El Tor biotype. At the late mid-logarithmic growth phase, HapR binds to the three promoters of fur, hlyU, and hlyA to repress their transcription. At the early mid-logarithmic growth phase, Fur binds to the promoters of hlyU and hlyA to repress their transcription; meanwhile, HlyU binds to the promoter of hlyA to activate its transcription, but it manifests direct inhibition of its own gene. The highest transcriptional level of hlyA occurs at an OD600 value of around 0.6-0.7, which may be due to the subtle regulation of HapR, Fur, and HlyU. The complex regulation of HapR, Fur, and HlyU on hlyA would be beneficial to the invasion and pathogenesis of V. cholerae during the different infection stages.