Implementation of a Multi-Agent Carbon Emission Reduction Strategy under the Chinese Dual Governance System: An Evolutionary Game Theoretical Approach.

A central-local dual governance system is the basic system of environmental governance in China. Co-governance between the central environmental protection department (CEPD) and local environmental protection departments (LEPDs) is an important means to effectively promote China's carbon emission reduction strategy. Accordingly, this paper discusses their interactive decision-making and investigates how to optimize the strategic relationships between the CEPD, LEPDs, and carbon emission enterprises (CEEs) under the dual governance system by constructing a trilateral evolutionary game model and analyzing evolutionary stability strategies, achieving a numerical experiment simulation of evolution processes and determining the impacts of various factors using MATLAB, leading to several countermeasures and suggestions. The results indicate that the CEPD should rationally use the incentive mechanism for LEPDs, improve the carbon tax system, and further penalize the nepotistic relationship of LEPDs and CEEs. Furthermore, it is essential to reform the current LEPD performance evaluation system and reduce the cost of LEPD positive regulation through subsidies and financial transfer payments. Additionally, the CEE strategy is affected by carbon reduction tax rates, penalties, subsides, and emission reduction costs and revenues. This study reveals the consequences of interactions between CEPD, LEPDs, and CEEs and presents options for the redesign of incentive and regulatory mechanisms to improve carbon emission reduction performance in China.

Overcoming Barriers to Agriculture Green Technology Diffusion through Stakeholders in China: A Social Network Analysis.

It is crucial to actively encourage the development of agriculture green technology, which has been regarded as one of the most effective solutions to the environmental degradation caused by agricultural activities. However, agriculture green technology diffusion is indeed a challenging task and still faces numerous barriers. The stakeholders who can potentially deal with these barriers, however, have been overlooked by previous studies. To address these issues, social network analysis was performed to identify critical stakeholders and barriers. Their interactions in agriculture green technology diffusion were analyzed based on the literature, a questionnaire survey and expert judgments. A two-mode network and two one-mode networks were used to analyze the relationships among the identified 12 barriers and 14 stakeholders who can influence these 12 barriers identified. The results show that agricultural research institutes, universities, agribusiness, agencies of township promotion, the government and farmers' relatives are key stakeholders and that the limited market demand for green technology and the high cost of its diffusion are two main barriers. However, poor green technology operability and farmer families in distress are factors that are not as important as previously perceived. Finally, some recommendations and suggestions are provided to promote agriculture green technology diffusion in China.

C1q/TNF-Related Protein 9 Inhibits Coxsackievirus B3-Induced Injury in Cardiomyocytes through NF-κB and TGF-ß1/Smad2/3 by Modulating THBS1.

C1q/TNF-related protein 9 (CTRP9) is implicated in diverse cardiovascular diseases, but its role in viral myocarditis (VMC) is not well explored. This study is aimed at investigating the role and potential mechanism of CTRP9 in VMC. Herein, we found that the peripheral blood collected from children with VMC had lower CTRP9 levels than that from children who had recovered from VMC. H9c2 cardiomyocytes treated with coxsackievirus B3 (CVB3) were applied to establish a VMC model in vitro, and the expression of CTRP9 was significantly decreased in CVB3-induced H9c2 cells. The overexpression of CTRP9 attenuated CVB3-induced apoptosis, inflammation, and fibrosis reactions in H9c2 cells by promoting cell proliferation, reducing the cell apoptosis rate, and inhibiting inflammatory cytokine levels and fibrosis-related gene expression. Moreover, we found that thrombospondin 1 (THBS1) levels were increased in children with VMC, and CTRP9 negatively regulated THBS1 expression by interacting with THBS1. The downregulation of THBS1 inhibited CVB3-induced apoptosis, inflammation, and fibrosis in H9c2 cells. In addition, our mechanistic investigation indicated that the overexpression of THBS1 impaired the inhibitory effect of CTRP9 on CVB3-induced H9c2 cells. The results further revealed that the CVB3-induced NF-κB and TGF-ß1/Smad2/3 signaling pathways of H9c2 cells were blocked by CTRP9 yet activated by THBS1. In conclusion, CTRP9 protected H9c2 cells from CVB3-induced injury via the NF-κB and TGF-ß1/Smad2/3 signaling pathways by modulating THBS1.

Interleukin-37 alleviates airway inflammation and remodeling in asthma via inhibiting the activation of NF-κB and STAT3 signalings.

Asthma is a common respiratory inflammatory disorder disease of childhood, and airway smooth muscle cells (ASMCs) play an important role in this disease. Recently, studies have found that interleukin (IL)-37 inhibits allergic airway inflammation of asthmatic mouse models. The aim of this study was to investigate the exact mechanism of IL-37 in asthma. In this study, we found recombinant human IL-37 protein significantly reduced ovalbumin (OVA)-induced airway hyperresponsiveness, inflammatory cell infiltration, the epithelial-mesenchymal-transition (EMT) process, and levels of IL-4, IL-6 and IL-13, but increased interferon (IFN)-γ expression. Moreover, IL-37 treatment remarkably inhibited transforming growth factor (TGF)-ß1-induced cell proliferation, migration, EMT, and inflammatory response in ASMCs. IL-37 notably upregulated IκB expression and downregulated levels of NF-κB p65, phospho-NF-κB p65, STAT3 and phospho-STAT3 both in OVA-induced mice and in TGF-ß1-stimulated ASMCs. The effects of IL-37 on TGF-ß1-induced ASMCs were abrogated by STAT3 upregulation. Additionally, PDTC, a NF-κB inhibitor, showed the similar effects as IL-37 in ASMCs. In conclusion, IL-37 may alleviate airway inflammation and remodeling in asthma through suppressing the activation of NF-κB and STAT3.