ABSTRACT
Urban agglomerations have gradually formed in different Chinese cities, exerting great pressure on the ecological environment. Ecosystem health is an important index for the evaluation of the sustainable development of cities, but it has rarely been used for urban agglomerations. In this study, the ecosystem health in the middle reaches of the Yangtze River Urban Agglomeration was assessed using the ecosystem vigor, organization, resilience, and services framework at the county scale. A GeoDetector was used to determine the effects of seven factors on ecosystem health. The results show that: (1) The spatial distribution of ecosystem health differs significantly. The ecosystem health in the centers of Wuhan Metropolis, Changsha-Zhuzhou-Xiangtan City Group, and Poyang Lake City Group is significantly lower than in surrounding areas. (2) Temporally, well-level research units improve gradually; research units with relatively weak levels remain relatively stable. (3) The land use degree is the main factor affecting ecosystem health, with interactions between the different factors. The effects of these factors on ecosystem health are enhanced or nonlinear; (4) The effect of the proportion of construction land on ecosystem health increases over time. The layout used in urban land use planning significantly affects ecosystem health.
Subject(s)
Ecosystem , Rivers , China , Cities , Conservation of Natural Resources , UrbanizationABSTRACT
BACKGROUND: Previous reports have revealed that down-regulation of miR-34a expression can promote colorectal cancer (CRC) cell growth by targeting cell cycle-related transcriptional factor E2F1. To date, the function of the single nucleotide polymorphism (SNP) located in the mature region of miR-34a has not been investigated. METHODS: We performed a case-control study including 685 CRC patients and 618 cancer-free controls. Genotyping, real-time PCR assay, cell transfection, and the dual luciferase reporter assay were used in our study. Cell proliferation and cell cycle analysis were measured in CRC cells including Hct-116 and SW480. The overall survival of different genotypes was also investigated. RESULTS: We found that the rs35301225 polymorphism in miR-34a was involved in the occurrence of CRC by acting as a tumor suppressor by down-regulation of tumor-promoting gene E2F1. C/A SNP of miR-34a could promote CRC cell proliferation by up-regulation of E2F1. Also, C/A genotype can change the cell cycle by increasing the S phase percentage. Moreover, the SNP in rs35301225 of miR-34a was associated with tumor size and tumor differentiation, as well as metastasis in CRC patients; C/A SNP was related to the significantly enhanced expression of E2F1 and shorter survival in post-surgery CRC patients. CONCLUSIONS: rs35301225 in miR-34a was highly associated with a decreased risk of CRC in a Chinese population and might serve as a novel biomarker for colon cancer.
ABSTRACT
BACKGROUND/AIMS: IGF-1 can act as an endocrine hormone and its signaling server as essential roles in regulating tumorigenesis. Polymorphisms in IGF-1 have been reported associated bad prognosis of with human cancer, but their association with the risk of human gastric cancer (GC) has not been found so far. In this study rs6218 located in the 3'UTR of IGF-1 was selected to evaluate its relationship with the risk of GC among Chinese population. METHODS: Questionnaire, SNaPshot genotype assay, real time PCR assay, cell transfection and the dual luciferase reporter assay were used in our study. RESULTS: SNP rs6218 in IGF-1 3'-UTR was involved in the occurrence of GC by acting as a tumor promotion factor while rs6128 acting as a risk factor. SNP rs6128 was also could be regulated by miR-603 which caused an up-regulation of IGF-1 in patients with UC and CC genotype. Furthermore, the carriers of UC and CC genotype presented a big tumor size as well as the high probability of metastasis. CONCLUSION: In conclusion, our findings have shown that the SNP rs6218 in IGF-1 3'-UTR, through disrupting the regulatory role of miR-603 in IGF-1 expression, rs16128 in IGF-1 might act as a promotion factor in the pathogenesis of GC.
