[Study on related factors and characteristics of multimorbidity of overweight and obesity-related diseases in children in Hunan Province].

From January 2019 to December 2021, overweight and obese children who visited in health outpatient Center of Hunan Children's Hospital were studied to explore and analyze the rate, related factors and patterns of multimorbidity of overweight and obesity-related diseases in children in Hunan Province. Univariate and multivariate logistic regression models were used to analyze the multimorbidity-related factors of overweight and obesity-related diseases in children. Association rules (apriori algorithm) were used to explore the multimorbidity patterns of overweight and obesity-related diseases in children. A total of 725 overweight and obese children were included in this study. The multimorbidity rate of overweight and obesity-related diseases in children was 46.07% (334/725). Age, waist circumference, the frequency of food consumption such as hamburgers and fries and adding meals before bedtime were multimorbidity-related factors of overweight and obesity-related diseases in children. The multimorbidity associated with nonalcoholic fatty liver disease (NAFLD) was relatively common. The patterns with the top three support degrees were "NAFLD+dyslipidemia","NAFLD+hypertension" and "NAFLD+hyperuricemia". The patterns with the top three confidence and elevation degrees were "Hypertension+dyslipidemia => NAFLD","Hyperuricemia => NAFLD" and "NAFLD+hypertension => dyslipidemia".

[Circular RNA circHIPK3 acts as the sponge of microRNA-124 to promote human oral squamous cell carcinoma cells proliferation].

Objective: To explore the expression and clinical significance of circular RNA circHIPK3 in oral squamous cell carcinoma (OSCC), analyze the effect of circHIPK3 on the proliferation of OSCC cells. Methods: The expression of circHIPK3 in OSCC tissues, adjacent non-cancerous tissues and OSCC cell lines were detected by quantitative real-time polymerase chain reaction (qPCR). The correlations between the expression of circHIPK3 in OSCC tissues and the clinicopathological features were analyzed as well. circHIPK3-specific siRNA si-circHIPK3 and negative control siRNA si-NC were designed and synthesised and used to transfect CAL27 and SCC15 cells respectively. The proliferation capacity of CAL27 and SCC15 cells after transfection with si-circHIPK3 was detected by CCK-8 assay. The expression of miR-124 in OSCC was detected by qPCR, and the correlation between expression of circHIPK3 and the expression of miR-124 was analyzed. Using qPCR to detect the expression of miR-124 in CAL27 and SCC15 cells after transfection with si-circHIPK3 and si-NC respectively. Furthermore, using CCK-8 assay to detect the proliferation capacity of CAL27 and SCC15 cells after transfection with si-NC, si-circHIPK3, miR-124 mimic, si-circHIPK3+miR-124 inhibitor. Results: The expression of circHIPK3 in OSCC tissues [2.23 (1.86, 3.00)] was significantly higher than that of the adjacent non-cancerous tissues [1.05 (0.85, 1.26)] (U=1 094, P=0.000). The expression of circHIPK3 in CAL27 (3.02±0.51) and SCC15 cells (3.16±0.75) was higher than those of human normal oral keratinocytes (hNOK) (1.26±0.30) (P=0.000). The expression of circHIPK3 was found to be closely associated with TNM stage (P<0.05) and tumor grades (P<0.05). Knockdown of circHIPK3 can inhibit proliferation of CAL27 and SCC15 cells (P<0.05). The expression of miR-124 in OSCC tissues (0.61±0.35) was significantly lower than that in adjacent non-cancerous tissues (1.13+0.39) (t=-5.36, P<0.05). Correlation analysis showed that the expression of circHIPK3 in OSCC was negatively correlated with the expression of miR-124 (r=-0.767, P<0.001). Moreover, down-regulation of miR-124 rescued the phenotype induced by knockdown of circHIPK3. Conclusions: The expression of circHIPK3 in OSCC was increased, and silencing of circHIPK3 expression can inhibit the proliferation of OSCC cells. Our results suggest that circHIPK3 may play a key role in the occurrence and development process of OSCC through the regulation of miR-124 expression.