ABSTRACT
Objective @#To compare the 2-year survival rate of anterior implants with delayed or immediate loading and to explore the risk factors associated with immediate loading implantation@*Methods @# A total of 126 patients were assessed from July 2012 to July 2015, including 210 implants. The patients were followed for more than 2 years. Univariate and multivariate survival analyses were performed using logrank tests and Cox regression analysis to identify risk factors for dental implant failure with the immediate loading or conventional loading of anterior teeth. @*Results @#The 2-year survival rates of anterior implants with delayed and immediate loading were 96.3% and 89.0%, respectively. The difference between the two groups was statistically significant(P < 0.05). The 2-year survival rate with delayed loading of implants was higher than that of the immediate loading of implants. Survival analysis indicated that the risk factors for implant failure were smoking and maxillary implantation in both the immediate loading and conventional loading groups@*Conclusion@#There is high risk associated with the immediate loading of anterior implants. The immediate loading of maxillary anterior implants and smoking in association with implantation may cause implant failure.
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Objective@# To assess the expression of miR-21, miR-221, and miR-222 in exosomes of CAL27 tongue squamous cell carcinoma cells.@*Methods @# CAL27 tongue squamous cell carcinoma cells and normal human oral keratinocytes (HOKs) were cultured, and then, the cultured supernatant was collected to separate the exosomes. Exosomes were detected by electron microscopy, and the expression levels of miR-21, miR-221, and miR-222 in the exosomes of tongue cancer cells were measured by qRT-PCR. @*Results@#Exosomes existed in the cultured supernatants of CAL27 cells and HOKs. Additionally, the expression levels of miR-21, miR-221, and miR-222 in the exosomes of CAL27 cells were significantly enhanced compared with those in the HOK exosomes (P < 0.05). @*Conclusion @#The expression levels of miR-21, miR-221, and miR-222 were markedly enhanced in the exosomes of CAL27 tongue squamous cell carcinoma cells.
ABSTRACT
Objective To evaluate the significance of human interleukin-31(IL-31)in the pathogenesis of atopic dermatitis and its correlation with pruritus in patients with atopic dermatitis(AD).Methods Twenty-two children with mild to severe atopic dermatitis and 22 age-matched healthy controls were included in this study.Patients and controls were randomly and equally assigned into stimulation and non-stimulation groups.Venous blood samples were obtained from all participants,peripheral blood mononuclear cells were isolated from these samples and cultured with(stimulation groups)or without(non-stimulation groups)staphylococcal enterotoxin B(SEB)for 24 hours.Then,the mRNA expression of IL-31 on PBMCs was assessed via real-time reverse transcription-PCR.ELISA was used to detect the total serum IgE level in these objects.The severity of AD in patients was rated according to scoring atopic dermatitis(SCORAD).The relationship between the mRNA expression of IL-31 and the level of serum total IgE.severity of atopic dermatitis,and degree of pruritus.was evaluated.Results The expression of IL-31 mRNA on non-stimulated PBMCs from patients was 23.2 folds as high as that from the healthy controls(P＜0.01).The stimulation with SEB upregulated the mRNA expression of IL-31 on PBMCs.and the increase on PBMCs from patients was 20.44 times of that from the controls.The total serum IgE level was 260.05 IU/mL(5.9-1131.01 IU/mL)and 17.7 IU/mL(5-140.7 IU/mL)in the Patients and controls respectively(P＜0.01).There was no significant correlation between the mRNA expression of IL-31 and disease severity or total serum IgE level(r=0.07.0.22respectively.both P＞0.05)in patients witll AD.Condusions IL.3 1 is involved in t11e pathogenesis of AD,which is unlikely to be IgE-dependent.SEB can induce the rapid expression of IL-31 on PBMCs of healthy human,and is an important modulator for the production of IL-31.