The Dilemma and Practice Paths of Multi-entity Participation in the Rural Living Environment—A Case Study of District Y in Chongqing

The remediation of the rural living environment is not only an important aspect of comprehensively promoting rural revitalization but also directly influences the villagers’ sense of happiness and attainment. This paper, taking District Y in Chongqing as an example, explores the practice paths of multi-entity coordinated governance in the rural living environment. The paper affirms the leading role of the government, participation responsibilities of the market, social organizations, and villagers, thereby constructing a multi-entity coordinated governance mechanism to effectively address the prominent problems currently faced

Constraint Mechanism of Environmental Regulation on Carbon Emission of Heavy Industry in Chengdu-Chongqing Region of China

Regional differences and development heterogeneity lead to an unbalanced distribution of heavy industry in Chengdu-Chongqing region of China. Under the background of low-carbon development, clarifying the constraint mechanism of environmental regulations on carbon emissions of heavy industry becomes more important to solve prominent problems of resources and the environment. In this work, literature analysis, comparative analysis and statistical induction are carried out to illustrate a constraint mechanism of environmental regulation on carbon emission. Based on literature reports and government yearbook data, the impacts of environmental regulations on carbon emissions of heavy industry in Chengdu-Chongqing region are studied. Analysis and demonstration are carried out from four dimensions: corporate identity, technological progress, policy constraints, and government supervision. The predicament of environmental regulation affecting heavy industry carbon emission reduction is expounded and puts forward reasonable policy suggestions. The research results can enrich the theory of environmental regulation, and provide policy suggestions for optimizing the green transformation of heavy industry

Study on the Effect of Regional Water Pollution—Take Huaxi River in Chongqing as an Example

Water pollution management plays a crucial role in China’s ecological environment development. It has evolved from being solely the responsibility of the government to a collaborative effort involving multiple entities. This paper presents findings from a field survey conducted around the collaborative capacity and effectiveness of wastewater treatment in Huaxi River, Chongqing. The study collected 427 valid questionnaires and employed SPSS26.0 software and AMOS24.0 software, utilizing structural equation modelling and regression analysis to verify the relationship between the variables. The results highlight that synergy mechanism acts as a mediating variable between synergy capability and synergy governance effect, underscoring the role of mechanism in the relationship between capability and governance effect. The conclusion emphasizes the importance of enhancing synergistic capacity and synergistic mechanism to effectively promote synergistic governance effect in the water pollution management of Huaxi River in Chongqing. This can be achieved by improving the abilities of multiple stakeholders in managing water pollution, enhancing cooperation among parties, and encouraging participation of social organizations, the public, and enterprises in the management process to achieve sustainable development of ecological civilization

A particle-based cohesive crack model for brittle fracture problems

Numerical simulations of the fracture process are challenging, and the discrete element (DE) method is an effective means to model fracture problems. The DE model comprises the DE connective model and DE contact model, where the former is used for the representation of isotropic solids before cracks initiate, while the latter is employed to represent particulate materials after cracks propagate. In this paper, a DE particle-based cohesive crack model is developed to model the mixed-mode fracture process of brittle materials, aiming to simulate the material transition from a solid phase to a particulate phase. Because of the particle characteristics of the DE connective model, the cohesive crack model is constructed at inter-particle bonds in the connective stage of the model at a microscale. A potential formulation is adopted by the cohesive zone method, and a linear softening relation is employed by the traction-separation law upon fracture initiation. This particle-based cohesive crack model bridges the microscopic gap between the connective model and the contact model and, thus, is suitable to describe the material separation process from solids to particulates. The proposed model is validated by a number of standard fracture tests, and numerical results are found to be in good agreement with the analytical solutions. A notched concrete beam subjected to an impact loading is modeled, and the impact force obtained from the numerical modeling agrees better with the experimental result than that obtained from the finite element method

MicroRNA-141 Inhibits the Proliferation of Penile Cavernous Smooth Muscle Cells Associated with Down-Regulation of the Rhoa/Rho Kinase Signaling Pathway

Background/Aims: The role of the RhoA/Rho kinase signaling pathway in diabetes mellitus-induced erectile dysfunction has been partially understood. Methods: In the present study, we explored the changes of the RhoA/Rho associated kinase (ROCK) signaling pathway in diabetic erectile dysfunction in vivo and the effects of microRNA-141 on the RhoA/ROCK signaling pathway in vitro. Results: The mRNA and protein expressions of RhoA and ROCK2 were significantly increased while the expression of microRNA-141 was decreased in the penile cavernous smooth muscle cells of rats with diabetic erectile dysfunction. Moreover, increased expression of microRNA-141, decreased expressions of RhoA and ROCK2 (mRNA and protein), accelerated cell proliferation rate and reduced cell apoptosis were found in the microRNA-141 mimics group and the siRNA-Rho group. The microRNA-141 expression in the microRNA-141 inhibitors + siRNA-Rho group was significantly decreased. microRNA-141 specifically bound to Rho-3’-UTR and down-regulated the expression of Rho gene at the post transcriptional level. Conclusion: Decreased expression of miR-141 is associated with up-regulation of RhoA and ROCK2 in the RhoA/ROCK signaling pathway in rats with diabetic erectile dysfunction. miR-141 inhibits the growth of penile cavernous smooth muscle cells associated with down-regulation of the RhoA/ROCK signaling pathway in vitro

Efficacy of Probiotics Supplementation On Chronic Kidney Disease: a Systematic Review and Meta-Analysis

Background/Aims: Dysbiosis of the intestinal microbiota may accelerate the progression of chronic kidney disease (CKD) by increasing the levels of urea toxins. In recent years, probiotics have been recognized to maintain the physiological balance of the intestinal microbiota. In this study, we aim to assess the therapeutic effects of probiotics on CKD patients with and without dialysis via meta-analysis. Methods: We conducted a meta-analysis of randomized controlled trials (RCTs) by searching the databases of Pubmed, EMBASE and Cochrane Library (No. CRD42018093080). Studies on probiotics for treatment of CKD adults lasting for at least 4 weeks were selected. The primary outcomes were the levels of urea toxins, and the second outcomes were the levels of interleukin (IL)-6, C-reactive protein (CRP) and hemoglobin (Hb). The risk of bias was assessed by Cochrane Collaboration’ tool, and the quality of evidence was appraised with the Grading of Recommendation Assessment. Means and standard deviations were analyzed by random effects analysis. Stratified analysis was done and sensitivity analysis was performed when appropriate. Results: Totally, eight studies with 261 patients at CKD stage 3 to 5 with and without dialysis were included. We found a decrease of p-cresyl sulfate (PCS) of 3 studies with 125 subjects (P = 0.01, SMD -0.57, 95% CI, -0.99 to -0.14, I2 = 25%) and an increase of IL-6 in 3 studies with 134 subjects (P = 0.03, 95% CI, SMD 0.37, 0.03 to 0.72, I2 = 0%) in the probiotics groups. Analysis of serum creatinine (P = 0.47), blood urine nitrogen (P = 0.73), CRP (P = 0.55) and Hb (P = 0.49) yielded insignificant difference. Conclusion: Limited number of studies and small sample size are limitations of our study. Probiotics supplementation may reduce the levels of PCS and elevate the levels of IL-6 whereby protecting the intestinal epithelial barrier of patients with CKD

lncRNA AFAP1-AS1 Promotes Migration and Invasion of Non-Small Cell Lung Cancer via Up-Regulating IRF7 and the RIG-I-Like Receptor Signaling Pathway

Background/Aims: Accumulating evidence has highlighted the importance of long non-coding RNAs (lncRNAs) as competing endogenous RNAs (ceRNAs) in tumor biology. Among others, actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been associated with non-small cell lung cancer (NSCLC). However, it remains unclear how AFAP1-AS1 participates in the development and progression of NSCLC. Methods: The peripheral blood samples were collected from patients with NSCLC. White blood cell subsets were classified and levels of interleukin (IL)-10, IL-12 and IFN-γ in serum were measured. We then identified its target gene of AFAP1-AS1 via bioinformatics methods. NSCLC cell line with the highest expression of AFAP1-AS1, i.e. H1975 was selected for in vitro experiments. A series of inhibitor, vector and siRNA were employed to validate the regulatory mechanisms of AFAP1-AS1 in the development and progression of NSCLC. Cell proliferation was detected by MTT assay and EdU staining. Cell migration and invasion, and cell cycle and apoptosis were measured by transwell assay and flow cytometry, respectively. Results: A high expression of AFAP1-AS1 was identified in NSCLC, alongside with a reduced level of IL-12 and increased levels of IL-10 and interferon (IFN)-γ. Aberrant expressions of AFAP1-AS1 were associated with pathological grade, TNM staging and metastatic potential of NSCLC. AFAP1-AS1 could activate interferon regulatory factor (IRF)7, the retinoid-inducible protein (RIG)-I-like receptor signaling pathway and Bcl-2 in vitro. Over-expression of AFAP1-AS1 promoted NSCLC cell proliferation, invasion and migration while inhibiting cell apoptosis. Conclusion: lncRNA AFAP1-AS1 promotes migration and invasion of non-small cell lung cancer via up-regulating IRF7 and the RIG-I-like receptor signaling pathway

High glucose dialysate-induced peritoneal fibrosis: Pathophysiology, underlying mechanisms and potential therapeutic strategies

Peritoneal dialysis is an efficient renal replacement therapy for patients with end-stage kidney disease. However, continuous exposure of the peritoneal membrane to dialysate frequently leads to peritoneal fibrosis, which alters the function of the peritoneal membrane and results in withdrawal from peritoneal dialysis in patients. Among others, high glucose dialysate is considered as a predisposing factor for peritoneal fibrosis in patients on peritoneal dialysis. Glucose-induced inflammation, metabolism disturbance, activation of the renin–angiotensin–aldosterone system, angiogenesis and noninflammation-induced reactive oxygen species are implicated in the pathogenesis of high glucose dialysate-induced peritoneal fibrosis. Specifically, high glucose causes chronic inflammation and recurrent peritonitis, which could cause migration and polarization of inflammatory cells, as well as release of cytokines and fibrosis. High glucose also interferes with lipid metabolism and glycolysis by activating the sterol-regulatory element-binding protein-2/cleavage-activating protein pathway and increasing hypoxia inducible factor-1α expression, leading to angiogenesis and peritoneal fibrosis. Activation of the renin–angiotensin-aldosterone system and Ras-mitogen activated protein kinase signaling pathway is another contributing factor in high glucose dialysate-induced fibrosis. Ultimately, activation of the transforming growth factor-β1/Smad pathway is involved in mesothelial-mesenchymal transition or epithelial-mesenchymal transition, which leads to the development of fibrosis. Although possible intervention strategies for peritoneal dialysate-induced fibrosis by targeting the transforming growth factor-β1/Smad pathway have occasionally been proposed, lack of laboratory evidence renders clinical decision-making difficult. We therefore aim to revisit the upstream pathways of transforming growth factor-beta1/Smad and propose potential therapeutic targets for high glucose-induced peritoneal fibrosis

Angiotensin II Silencing Alleviates Erectile Dysfunction Through Down-Regulating the Rhoa/Rho Kinase Signaling Pathway in Rats with Diabetes Mellitus

Background/Aims: We aim to explore the role of angiotensin (Ang)II and the RhoA/Rho kinase signaling pathway in the pathogenesis of erectile dysfunction in diabetes mellitus (DM). Methods: Male Sprague-Dawley (SD) rats were used for experiments and short hairpin RNA (shRNA) was used to silence the AngII gene. The erectile function of rats was observed and intracavernous pressure and mean arterial pressure (ICP/MAP) were measured after electrical stimulation. Relaxation and contraction of smooth muscle in the corpus cavernosum were tested. Western blotting and quantitative RT-PCR were applied to measure the expressions of RhoA, Rho-associated kinase (ROCK)1 and ROCK2. Radioimmunoassay was applied to detect the levels of AngII. Results: Rats in the control group had the most erectile times, followed by AngII-silenced rats with DMED and rats with DMED. Rats with DMED had worse ICP and MAP than AngII-silenced rats. The contraction ability was markedly improved and relaxation ability was decreased in AngII-silenced rats with DMED as compared with rats with DMED. The levels of AngII were significantly increased in DMED rats while significantly decreased after AngII silencing. The mRNA and proteins of RhoA and ROCK2 were expressed in a similar way. Conclusion: AngII silencing improves erectile dysfunction via down-regulating the RhoA/Rho kinase signaling pathway