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Background The ultimate objective of rural health reform and development is to establish a mature healthcare service system that adapts to the socialist market economy and the developmental level of the Chinese economy and meets the health demands of the people. Reform of the payment system is one of the key elements. This article explores the effect of the system and the causes of benefit inequity, provides an objective evaluation of policy implementation and offers data support for policy adjustment. Methods A two-stage stratified random sampling data collection method comprising a survey in 2009 (the sample size was 3832 families) and a follow-up survey in 2015 (the sample size was 3992 families) was used. Qualitative data are presented as rates or ratios and the χ2 test was used for descriptive statistics. Quantitative data were analysed using a t test. A generalized linear model (GLM) with gamma distribution of the log connection function was adopted to analyse the factors of the compensation benefit inequity. The degree of the compensation benefit inequity contribution was analysed using the concentration index (CI) decomposition method and the Oaxaca decomposition method. Results Reimbursement refers to the reimbursement expense received by inpatients from the New Cooperative Medical System (NCMS). In the GLM, there were some positive factors for reimbursement in the NCMS, including economic level, level of health facility and deductibles. The CI decomposition analysis results show that the main factors that increased the compensation benefit inequity were economic levels and deductibles over the past 2 y. However, inpatient days (2009) and the actual reimbursement ratio (2015) decreased the inequity. The Oaxaca decomposition analysis results suggest that changes in compensation benefit inequity between 2009 and 2015 were more attributable to changes in economic status and variables related to policy compensation than to demographic variables. Conclusions: This study showed that inequity decreased from 2009 to 2015, which could be the result of adjustment of the compensation policy. However, we should remain vigilant lest the gap between the rich and the poor leads to an increase in inequity.

Objective. We aimed to explore the risk factors for coal workers’ pneumoconiosis and to further explore the significance of mitochondrial fission and fusion factors in CWP and verify the feasibility of mitochondrial fission and fusion factors as diagnostic and therapeutic targets. Methods. The data of 168 cases were collected, and they were divided into a healthy control group (40 cases), dust exposure control group (61 cases), and CWP group (67 cases) and entered into SPSS 24.0. The statistical data were analyzed by the chi-square test or Fisher’s exact probability method. The variables with statistically significant differences of the univariate analysis results were included in the generalized linear model. Test level was α = 0.05 . Blood samples were collected to detect the ROS content, MDA content, and SOD activity. The mRNA expression levels of OPA1, Drp1, MFN2, Fis1, Col I, Col III, and α-SMA were determined by q-PCR. The protein expression levels of OPA1, Drp1, MFN2, Fis1, Col I, Col III, and α-SMA were detected by western blot. Results. Generalized linear regression analysis showed that lower school education, no respiratory protective measures, the working age beyond 15 years, and the type of work like coal mine drillers were the risk factors for CWP. With the aggravation of CWP, the degree of fibrosis and inflammation increased oxidative damage, increased mitochondrion division, and decreased fusion, which were more sensitive in the second and third stages of CWP. Conclusion. The results in this found that mitochondria are injured by fission and fusion in the CWP patients. Detection of the mitochondria fission and fusion factors provides the application value to evaluate the injury degree and progress of CWP and the clues for finding the real and effective screening and diagnosis biomarkers.

Abstract(1) Objective: Greenhouse workers are considered a special occupational group who are exposed to more toxic and harmful substances than ordinary farmers. The health problem of this group is a public health problem that warrants attention. Taking greenhouse workers in Ningxia, China, as the research sample, this study analyzed the health risk to practitioners posed by the greenhouse working environment. (2) Method: To analyze the relationship between pesticide exposure and the health of greenhouse workers, the genetic matching method was used to exclude the influence of covariates on the results. (3) Results: The results showed a statistical significance regarding the prevalence of cardiovascular diseases (CVD), skeletal muscle system diseases (SMSD) and digestive diseases between the different exposure groups. Researching the disease symptoms found that different levels of exposure to pesticides in greenhouses could cause multisystem and multisymptom discomfort. In addition to some irritant symptoms such as eye itching, itching, and sneezing, there were also differences in terms of the frequency of discomfort such as back pain, a decline in sleep quality, memory loss, joint pain, swelling and weakness, upper abdominal pain and flatulence, in the different exposure groups. (4) Conclusion: Different levels of exposure to pesticides in greenhouses may be one of the risk factors for practitioners to suffer from various systemic diseases, affecting their health and work efficiency. This hazard is manifested not only in some acute irritant symptoms but also in chronic diseases due to long-term exposure.

Cyfluthrin is widely used in the field of sanitary pest control by its wide insecticidal spectrum, high efficiency and low toxicity, low residue, and good biodegradability. But, as a double‐edged sword, a large amount of cyfluthrin remains are still in the environment. The residual cyfluthrin is absorbed into the food chain through vegetation and then poses a risk to soil organisms and human health. Several studies have suggested that cyfluthrin is one of the main factors causing testicular damage, but the mechanism remains unclear. In this study, we established in vivo and in vitro models of testicular injury in rats and GC‐2 cells exposed to cyfluthrin to explore whether stimulator of interferon genes (STING) gene mediates the regulation of AMPK/mTOR/p70S6K autophagy pathway, which lays a foundation for further study of the mechanism of testicular injury induced by cyfluthrin. The results showed that the activity of super oxide dismutase in testis decreased and the activity of malonic dialdehyde increased with the increase of concentration in vivo and in vitro. At the same time, the levels of mitochondrial damage and inflammation in the testis also increased, which further activated autophagy. In this process, the increased level of inflammation is related to the increased expression of STING gene, and AMPK/mTOR/p70S6K autophagy pathway is also involved. To sum up, cyfluthrin has certain reproductive toxicity, and long‐term exposure can induce testicular cell damage. STING gene can participate in cyfluthrin‐induced testicular injury through AMPK/mTOR/P70S6K autophagy pathway.