RESUMEN
BACKGROUND: Nutrients related to serum vitamin D level were previously shown to be significantly associated with the risk of many chronic diseases. This study aimed to assess potential relationships between serum vitamin D level and otitis media (OM) risk. METHODS: PubMed, EMBASE, and Cochrane Library databases were searched till Aug 18, 2015 for studies of quantitative OM risk estimates in relation to serum vitamin D level. The odds ratio and weighted mean difference, with 95% confidence intervals (CIs), were used to measure the relationship between serum vitamin D level and OM risk. RESULTS: Of the 89 articles identified by database search, 5 studies reported data of 16,689 individuals were included in our meta-analysis. We noted participants with OM was associated with lower level of plasma vitamin D when compared with patients without OM (weighted mean difference -5.67; 95% CI -8.08 to -3.26, Pâ<â0.001). Furthermore, as compared with control group, serum vitamin D level was not associated with the risk of OM (odds ratio 0.80, 95% CI 0.47-1.38, Pâ=â0.425). Subgroup analyses suggested that participants with acute OM might associate with lower serum vitamin D level. CONCLUSIONS: Plasma vitamin D level might play an important role on the progression of acute OM, whereas no significant impact in patients with chronic OM.
Asunto(s)
Otitis Media/sangre , Otitis Media/etiología , Vitamina D/sangre , Enfermedad Aguda , Enfermedad Crónica , HumanosRESUMEN
Plasma miRNAs have been reported as biomarkers for various diseases. In this study, we investigated whether plasma concentrations of miR-126 may be useful as biomarkers for laryngeal squamous cell carcinoma (LSCC). We examined the function and mechanism of miR-126 in LSCC by using cell biology and molecular pathology techniques such as western blotting, quantitative PCR, IHC and IF. The expression of Camsap1 mRNA and protein is higher in cancer tissues compared to that in normal tissues. Both miR-126 and Camsap1 were related with the prognosis of LSCC patients. We found that miR-126 was able to inhibit LSCC partly by suppressing Camsap1 expression. In addition, Camsap1 expression induced microtubule formation and aggregation. This mechanism possibly explains why loss of miR-126 is frequently associated with tumor metastasis.