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BACKGROUND: The contribution of chronic kidney disease (CKD) to mortality in diabetic patients is unclear. This study aimed to explore the association between diabetics with CKD and mortality in middle-aged and elderly people of different ages. METHODS: Data were obtained from the China Health and Retirement Longitudinal Study, including 1,715 diabetic individuals, 13.1% of whom also had CKD. Diabetes and CKD were assessed by combining the physical measurements and self-reports. We fitted Cox proportional hazards regression models to examine the effect of diabetics with CKD on mortality in middle-aged and elderly people. The risk factors for death were further predicted based on age stratification. RESULTS: The mortality rate of diabetic patients with CKD (29.3%) was increased as compared to that of diabetic patients without CKD (12.4%). Diabetics with CKD were at a higher risk of all-cause mortality than those without CKD, with a hazard ratio of 1.921 (95% CI: 1.438, 2.566). Additionally, for participants 45 to 67 years of age, the hazard ratio was 2.530 (95% CI: 1.624, 3.943). CONCLUSIONS: Our findings suggested that, for diabetics, CKD was a chronic stressor that led to death in middle-aged and elderly people, especially among participants aged 45 to 67 years.
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BACKGROUND: Ovarian cancer is the leading lethal gynecological cancer and is generally diagnosed during late-stage presentation. In addition, patients with ovarian cancer still face a low 5-year survival rate. Thus, innovative molecular targeting agents are required to overcome this disease. The present study aimed to explore the function of miR-362-3p and the underlying molecular mechanisms influencing ovarian cancer progression. METHODS: The expression levels of miR-362-3p were determined using qRT-PCR. Gain-of-function and loss-of-function methods were used to detect the effects of miR-362-3p on cell proliferation, cell migration, and tumor metastasis in ovarian cancer. A luciferase reporter assay was performed to confirm the potential target of miR-362-3p, and a rescue experiment was employed to verify the effect of miR-362-3p on ovarian cancer by regulating its target gene. RESULTS: miR-362-3p was significantly downregulated in ovarian cancer tissues and cell lines. In vitro, our data showed that miR-362-3p suppressed cell proliferation and migration. In vivo, miR-362-3p inhibited ovarian cancer growth and metastasis. Mechanistically, SERBP1 was identified as a direct target and functional effector of miR-362-3p in ovarian cancer. Moreover, SERBP1 overexpression rescued the biological function of miR-362-3p. CONCLUSIONS: Our data reveal that miR-362-3p has an inhibitory effect on ovarian cancer. miR-362-3p inhibits the development and progression of ovarian cancer by directly binding its target gene SERBP1.
Assuntos
Genes Supressores de Tumor/fisiologia , MicroRNAs/metabolismo , Neoplasias Ovarianas/genética , Proteínas de Ligação a RNA/metabolismo , Ensaios Antitumorais Modelo de Xenoenxerto/métodos , Animais , Linhagem Celular Tumoral , Feminino , Humanos , Camundongos , TransfecçãoRESUMO
Background: Studies investigating the relationship between polymorphisms of the sex hormone-binding globulin (SHBG) gene and polycystic ovary syndrome (PCOS) have reported differing results. Therefore, the present meta-analysis was performed to clarify the effects of the SHBG rs6259 and rs727428 polymorphisms on PCOS risk. Materials and Methods: Published English language studies were selected through an extensive search of the Web of Science, PubMed, and EMBASE databases. Chinese studies were identified using Wan Fang, VIP, and the Chinese National Knowledge Infrastructure (CNKI) databases. The pooled odds ratio and 95% confidence interval were calculated using the random-effects model. Subgroup analyses and heterogeneity analyses were also performed. Results: A total of 1660 cases and 1312 controls were included in this meta-analysis. We found that the SHBG rs6259 polymorphism was not significantly associated with an increased risk of PCOS in any of the genetic models with significant heterogeneity; the results were consistent for all subgroups. A nonsignificant association between the rs727428 polymorphism and an increased risk of PCOS was also detected in all genetic models. Conclusions: The findings of this meta-analysis suggest that neither the SHBG rs6259 nor rs727428 polymorphism are associated with susceptibility to PCOS. However, because of the considerable heterogeneity and the small sample size, these pooled results should be interpreted with caution.