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A river basin is a complex system of tributaries and a mainstream. It is vital to cooperatively manage the mainstream and the tributaries to alleviate water pollution and the ecological environment in the basin. On the other hand, existing research focuses primarily on upstream and downstream water pollution control mechanisms, ignoring coordinated control of the mainstream and tributaries, and does not consider the impacts of different environmental and economic conditions in each region on pollution control strategies. This study designed a differential game model for water pollution control in the Yellow River and two of its tributaries, taking regional differences into account and discussing the best pollution control strategies for each region under two scenarios: Nash noncooperative and cost-sharing mechanisms. Furthermore, the factors influencing regional differences in pollution control costs are analyzed, and their impacts on the cost-sharing mechanism of pollution control are discussed. The results show that: (1) The cost-sharing mechanism based on cooperative management can improve pollutant removal efficiency in the watershed and achieve Pareto improvement in environment and economy. (2) The greater the economic development pressure between the two tributaries, the fewer the effects of the cost-sharing mechanisms and the higher the proportion of pollution control costs paid by the mainstream government. (3) Industry water consumption, the proportion of the urban population to the total population at the end of the year, the value-added of secondary sectors as a percentage of regional GDP, the volume of industrial wastewater discharge, and granted patent applications all influence industrial wastewater pollution treatment investment. (4) The greater the coefficient of variation in pollution control costs between the two tributary areas, the less favorable the solution to water pollution management synergy. These findings can help governments in the basin regions negotiate cost-sharing arrangements.

Background: This study aimed to investigate potential factors, especially early-life exposures, associated with endometrioma (OMA) and/or deep infiltrating endometriosis (DIE) in Chinese women. Methods: This is a subgroup analyses of the FEELING study, which was a case–control study that investigated the clinical, lifestyle, and environmental factors associated with OMA and/or DIE in China, Russia, and France. In this subgroup analysis, the data for the Chinese participants were further analyzed using logistic regression model. Results: All women (N = 546) had fully completed the questionnaire. The mean age of the participants was 31.8 (range: 18-41) years. Univariable analysis showed that noncyclic chronic pelvic pain, dysmenorrhea intensity class, and whether breastfed during infancy were distributed differently between patients with OMA or DIE and those with no endometriosis (non-EM) or superficial peritoneal endometriosis (SUP; P < .05). Multivariable analysis revealed that not having been breastfed was a protective factor against OMA and DIE (odds ratio [OR] = 0.33, 95% confidence interval [CI]: 0.16-0.69). Further analysis indicated not having been breastfed was a protective factor for DIE compared with non-EM (OR = 0.13, 95% CI: 0.02-0.88) and with OMA + SUP (OR = 0.19, 95% CI: 0.04-0.85) but was not a protective factor for OMA compared with non-EM (OR = 0.66, 95% CI: 0.32-1.36) and with SUP (OR = 0.63, 95% CI: 0.31-1.30). Conclusion: This is the first study suggesting that not having been breastfed might protect against DIE in Chinese women.

AbstractAs a rare disease leading to male infertility, idiopathic hypogonadotropic hypogonadism (IHH) has strong heterogeneity of clinical phenotype and gene mutation. At present, there is no effective diagnosis and treatment method for this disease. This study is to explore the possible new pathogenic gene of idiopathic hypogonadotrophic hypogonadism and the pathological mechanism affecting its occurrence. We performed a whole-exome sequencing on 9 patients with normosmic idiopathic hypogonadotropic hypogonadism (nIHH), 19 varicocele patients with asthenospermia, oligospermia, or azoospermia, 5 patients with simple nonobstructive azoospermia, and 13 normal healthy adult males and carried out comparative analysis, channel analysis, etc. After preliminary sequencing screening, 309–431 genes harbouring variants, including SNPs and indels, were predicted to be harmful per single patient in each group. In genetic variations of nIHH patients' analysis, variants were detected in 10 loci and nine genes in nine patients. And in co-analysis of the three patient groups, nine nIHH patients, 19 VC patients, and five SN patients shared 116 variants, with 28 variant-harbouring genes detected in five or more patients. We found that the NEFH, CCDC177, and PCLO genes and the Gene Ontology pathways GO:0051301: cell division and GO:0090066: regulation of anatomical structure size may be key factors in the pathogenic mechanism of IHH. Our results suggest that the pathogenic mechanism of IHH is not limited to the central nervous system effects of GnRH but may involve other heterogeneous pathogenic genetic variants that affect peripheral organs.