An rs13293512 polymorphism in the promoter of let-7 is associated with a reduced risk of ischemic stroke.

The expression of let-7 family members was differentiated in ischemic stroke (IS), functioning as an important regulating molecular in the pathophysiology of stroke. We hypothesized that genetic polymorphism in the promoters of let-7 family may be associated with the risk of IS. To test this hypothesis, we investigated the association of the rs10877887 and rs13293512 in the promoters of let-7 family with the susceptibility to IS. A hospital-based case-control study was performed. The rs10877887 genotype was determined by using a polymerase chain reaction-restriction fragment length polymorphism assay, and the rs13293512 genotype was determined by using a TaqMan assay. We found that the rs13293512CC genotype was associated with a reduced risk of IS (CC vs. TT: adjusted OR = 0.43, 95 % CI 0.26-0.71; dominant model: adjusted OR = 0.70, 95 % CI 0.49-0.98; recessive model: adjusted OR = 0.45, 95 % CI, 0.28-0.73). Stratification analysis showed that the rs10877887TT carriers had a higher level of total cholesterol compared to rs10877887TC/CC carriers (P = 0.03). Combined analysis showed that the rs10877887TC/CC and rs13293512TC/CC genotypes had a reduced risk of IS risk (adjusted OR = 0.58, 95 % CI 0.36-0.95). Our findings suggest that the rs13293512 polymorphism may be a protective factor for the development of IS.

Factors affecting the simple febrile seizures in COVID-19 children: a case-control study from China.

Objective: The over-age phenomenon of simple febrile seizures (SFS) was found during the epidemic in COVID-19, but there was no clear explanation, especially in China. This study aimed to analyze the clinical and auxiliary examination features of SFS in children infected with the coronavirus disease 2019 (COVID-19). Methods: In total, 78 patients with SFS in the Department of Pediatric and Neurology of Qujing First People's Hospital were enrolled and divided into the COVID-19-positive group (case group) and the COVID-19-negative group (control group). The clinical characteristics, auxiliary examinations, and risk factors were analyzed. Results: There were significant differences in age stratification between the two groups. The proportion of children aged over 5 years old in the case group (47.4%) was higher than that of the control group (5%) (p < 0.0001). In terms of sex distribution, the proportion of males in the case group was higher than that in the control group (71.1% vs. 50%), but the difference was not statistically significant (p = 0.0678). For blood cell analysis, the values of white blood cells (WBC), lymphocytes (LY), and monocytes (MN) in the case group were significantly lower than those in the control group (p < 0.01). Serum electrolyte analysis showed the greatest difference in blood sodium. The proportion of hyponatremia in the case group was higher than that in the control group (36.8% vs. 17.5%), but the difference did not reach statistical significance (p = 0.0745). A multivariate logistic regression analysis showed that the history of FS was a independent protective factors for SFS in children with COVID-19 (OR = 0.115, p = 0.009), and age was an independent risk factor for SFS in children with COVID-19 (OR = 1.042, p = 0.001). Conclusion: Age distribution, sex a previous history of FS and hyponatremia were different between children with and without COVID-19 in SFS. The history of FS was an independent protective factors for SFS in children with COVID-19.

Effects of miR-199a on autophagy by targeting glycogen synthase kinase 3ß to activate PTEN/AKT/mTOR signaling in an MPP+ in vitro model of Parkinson's disease.

Objectives: miR-199a can regulate autophagy, its underlying mechanisms remain unknown. The purpose of this study was to investigate the mechanisms of miR-199a involved in regulating autophagy in a 1-methyl-4-phenylpyridine (MPP+)-induced in vitro model of PD.Methods: PC12 cells were incubated in MPP+, and the expression levels of miR-199a were bidirectionally regulated via either transfection of an miR-199a mimic or incubation in miR-199a inhibitors. The experimental manipulations were divided into four groups, including the control group, MPP+ group, MPP+ + miR-199a mimic group, and MPP+ + miR-199a inhibitor group. MTT, CCK-8, qRT-PCR, Western blotting and linear correlation analysis were performed to evaluate various experimental indicators.Results: At increasing MPP+ concentrations, the following results were found: the expression levels of miR-199a, phosphorylated AKT and mTOR proteins expression decreased; the expression levels of phosphatase and tensin homologue (PTEN), GSK3ß, Beclin1, and LC3II increased; PC12 autophagy increased; and cellular viability and survival rates decreased. Transfection of an miR-199a mimic increased miR-199a expression and induced all of the following: the expression levels of PTEN, GSK3ß, Beclin1, and LC3II decreased; the expression levels of phosphorylated AKT and mTOR proteins expression increased; PC12 autophagy decreased; and cellular viability and survival rates increased.Discussion: In this in vitro study, we found that increasing miR-199a expression in PC12 cells reduced protein levels of Beclin1 and LC3II, decreased autophagy, enhanced cellular viability, increased survival rate, and ameliorated MPP+-induced parkinsonian-like cellular pathologies by targeting pro-autophagic pathways and GSK3ß to activate PTEN/AKT/mTOR signaling.