Study on spatial distribution, regional differences and dynamic evolution of rural financial risk in China.

Based on panel data from 2009 to 2021, covering 30 provinces in China, we have been constructed the Rural Financial Risk Index using the objective entropy weighting method to study rural financial risk in China systematically from the perspective of spatial distribution. Specifically, we discuss the spatial distribution, regional differences and dynamic evolution of rural financial risk across Chinese four different regions divided into the Northeast, East, Central and West. It's found that Local government debt and Land transfer income are the two primary determinants influencing the level of rural financial risk in China. Furthermore, we conclude the ranking value of rural financial risk across four regions that the central exhibits the highest level, followed by the West, the East, and finally the Northeast, where the reasons for such ranking results as follows. Firstly, although the highest level of risk among provinces in the West is equivalent to that in the Central, there exists a smaller minimum rural financial risk in the former compared to the latter. Then, it should be noted that there's a low-low agglomeration of rural financial risk in the Northeast, while it demonstrates a high-high agglomeration in the Central according to the Moran Index test analysis. Again, there's a declining trend in rural financial risk disparity within the region and an upward trend is observed when comparing different regions (except the East vs West), especially increase largely between the Northeast and Central in past two years after analyzing the decomposition of Dagum Gini coefficient. Moreover, we study the absolute differences and dynamic evolution in different four regions through three-dimensional diagram of kernel density estimation, and it's found that the change of rural financial risk in four regions moved to the right as a whole, while the tail distribution remains inconspicuous. The absolute difference is diminishing in the Northeast, and the two-level differentiation characteristics tend to weaken as a whole in the Central, with a disordered wave peak height observed in both the East and West. Finally, the article presents pertinent policy implications but limitations according to the research findings.

Lack of IL-17 signaling decreases liver fibrosis in murine schistosomiasis japonica.

Accumulating evidence has identified the profibrogenic properties of IL-17A in organ fibrosis. However, the role of IL-17A signal in liver fibrosis induced by Schistosoma japonicum infection remains unclear. In this study, we investigated liver fibrosis in wild-type (WT) and IL-17RA(-/-) mice upon S. japonicum infection. Hepatic IL-17A, IL-17C, IL-17E (IL-25), IL-17F, IL-17RA, IL-17RB and IL-17RC transcript levels were determined by RT-PCR. IL-17A(+) cells were analyzed by flow cytometry and confocal microscopy among granuloma cells. Immunostaining of IL-17R was performed on liver sections. Collagen deposition was assessed by Van Gieson's staining. IL-17A, IL-17C, IL-17E, IL-17F, IL-17RA and IL-17RC mRNA levels were dramatically increased in fibrotic livers. Among granuloma cells, CD3(+) and CD3(-) lymphocytes, neutrophils and macrophages were found to express IL-17A. Compared to WT, IL-17RA(-/-) mice displayed attenuated granulomatous inflammation, liver fibrosis, improved liver function and high survival. Meanwhile, α-smooth muscle actin staining and the expression of fibrogenic genes (transforming growth factor ß, IL-13 and collagen-I) as well as IL-17A-induced proinflammatory mediators (IL-1ß, IL-6, tumor necrosis factor α, CXCL1 and CXCL2) and proteinases (MMP3 and TIMP1) involved in fibrosis were markedly reduced in IL-17RA(-/-) mice. In addition, Th2 cytokines IL-4 and IL-17E (IL-25) were also decreased in IL-17RA(-/-) mice. These results indicated that IL-17A signal contributes to the pathogenesis of liver fibrosis in murine schistosomiasis. This effect was induced possibly by activating hepatic stellate cells and stimulating the release of proinflammatory cytokines and chemokines. Furthermore, the Th2 response was also enhanced by IL-17A signals. Our data demonstrate that IL-17A may serve as a promising target for antifibrotic therapy.