Breast cancer (BC) is a commonly diagnosed cancer in females. MicroRNA-660-5p (miR-660-5p) has been reported to be involved in the occurrence and development of BC. However, the regulatory network of miR-660-5p in BC has not been fully addressed. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the enrichment of miR-660-5p and tet-eleven translocation 2 (TET2) in BC tissues and cells. Cell counting kit-8 (CCK8), flow cytometry, and transwell migration and invasion assays were used to measure cell proliferation, apoptosis, migration, and invasion. The target relationship between miR-660-5p and TET2 was confirmed by dual luciferase reporter assay. Protein expression was measured by western blot. The expression of miR-660-5p was elevated in BC, and high expression of miR-660-5p was closely related to lymph node metastasis, advanced TNM stage, and vascular invasion of BC tumors. miR-660-5p silencing inhibited cell proliferation and metastasis, but induced apoptosis of BC cells. TET2 was identified as a direct target of miR-660-5p, and the interference of TET2 partly reversed the suppressive effects of miR-660-5p silencing on the malignant potential of BC cells. miR-660-5p promoted BC progression partly through modulating TET2 and PI3K/AKT/mTOR signaling. miR-660-5p/TET2 axis might be a promising target for BC treatment.The sympathetic nervous system (SNS) plays a fundamental role in the pathophysiology of cardiovascular diseases, including primary arterial hypertension. In this study, we aimed to investigate whether the expression of the rate-limiting enzyme in catecholamine synthesis, tyrosine hydroxylase (TH), and the β2-adrenergic receptor (β2-AR) in immune cells from peripheral blood, reflect central SNS activity in spontaneously hypertensive rats (SHR). TH expression in the lower brainstem and adrenal glands and β2-AR expression in the lower brainstem were analyzed by western blot analyses. https://www.selleckchem.com/products/pmsf-phenylmethylsulfonyl-fluoride.html In the leukocytes, TH and β2-AR expression was evaluated by flow cytometry before and after chronic treatment with the centrally-acting sympathoinhibitory drug clonidine. Western blot analyses showed increased TH and β2-AR expression in the lower brainstem and increased TH in adrenal glands from SHR compared to normotensive Wistar Kyoto rats (WKY). Lower brainstem from SHR treated with clonidine presented reduced TH and β2-AR levels, and adrenal glands had decreased TH expression compared to SHR treated with vehicle. Flow cytometry showed that the percentage of leukocytes that express β2-AR is higher in SHR than in WKY. However, the percentage of leukocytes that expressed TH was higher in WKY than in SHR. Moreover, chronic treatment with clonidine normalized the levels of TH and β2-AR in leukocytes from SHR to similar levels of those of WKY. Our study demonstrated that the percentage of leukocytes expressing TH and β2-AR was altered in arterial hypertension and can be modulated by central sympathetic inhibition with clonidine treatment.This study aimed to explore the association between serum non-high-density lipoprotein cholesterol (non-HDL-C) and cognitive dysfunction risk in patients with acute ischemic stroke (AIS). This cross-sectional study enrolled 583 AIS patients. Biochemical markers and lipid profile were collected after admission. AIS patients were classified into high group (non-HDL-C ≥3.4 mM) and normal group (non-HDL-C less then 3.4 mM). Mini-Mental State Examination scale (MMSE), Montreal Cognitive Assessment scale (MoCA), Activities of Daily Living (ADL) scale, Neuropsychiatric Inventory (NPI), and Hamilton Depression scale 21 version (HAMD-21) were applied on the third day after admission. Compared with the control group, patients of the high group had higher body mass index and higher frequency of intracranial artery stenosis, and exhibited higher levels of non-HDL-C, total cholesterol, triglycerides, low-density lipoprotein cholesterol, homocysteine, fasting blood glucose, and glycosylated hemoglobin (HbA1c), and lower levels of high-density lipoprotein cholesterol (all P less then 0.05). Compared with the control group, patients of the high group had significantly lower MMSE and MoCA scores (MMSE 26.01±4.17 vs 23.12±4.73, P less then 0.001; MoCA 22.28±5.28 vs 20.25±5.87, P less then 0.001) and higher scores on the NPI and HAMD-21 (both P less then 0.001). MMSE (r=-0.306, P less then 0.001) and MoCA scores (r=-0.251, P less then 0.001) were negatively associated with non-HDL-C level. Multivariate regression analysis revealed that non-HDL-C level (OR=1.361, 95%CI 1.059-1.729, P=0.016) was independently associated with the presence of cognitive dysfunction after adjusting for confounding factors. High serum non-HDL-C level might significantly increase the risk of cognitive dysfunction after AIS.The aim of this study was to evaluate the antimicrobial activity and toxicity of glass ionomer cement (GIC) modified with 5-methyl-2-(1-methylethyl)phenol (thymol) against Streptococcus mutans in silico and in vitro. The antimicrobial activity of thymol on GIC modified with concentrations of 2% (GIC-2) and 4% (GIC-4) was evaluated in a model of planktonic cell biofilm using agar diffusion test, minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), dynamic biofilm (continuous flow cell parallel), and bacterial kinetics. Conventional GIC (GIC-0) was used as a control. Thymol toxicity was evaluated in Artemia salina and in silico using Osiris® software. Differences between groups were estimated by analysis of variance, followed by Tukey post hoc test, with a 5% significance level. The results of the agar diffusion test between groups were not significantly different (P≥0.05). Thymol had potential bacteriostatic and bactericidal activity against Streptococcus mutans with respect to planktonic growth, with MIC of 100 µg/mL and MBC of 400 µg/mL. The groups GIC-0, GIC-2, and GIC-4 reduced the biofilm by approximately 10, 85, and 95%, respectively. Bacterial kinetics showed efficiency of the modified GICs for up to 96 h. GIC with thymol was effective against S. mutans, with significant inhibition of the biofilms. Analyses in silico and using Artemia salina resulted in no relevant toxicity, suggesting potential for use in humans. GIC-2 was effective against S. mutans biofilm, with decreased cell viability.