[Predictive value of tooth loss risk with 2018 new classification of periodontitis:a literature review].

The occurrence, progression and treatment efficacy of periodontitis are affected by many factors. Development on accurate estimation of prognosis is essential for treatment plan determination. The application of the 2018 new classification of periodontitis is one of the most important advances in the prognosis and risk assessment of periodontitis. The predictive value of the new classification on tooth loss risk had been evaluated by several latest researches, however, consensus still lacks. This review focused on the predictive efficacy of the 2018 new classification of periodontitis on tooth loss risk in periodontitis patients, in order to provide scientific evidence for clinical application and further improvement of the new classification system.

MiR-217 inhibits apoptosis of atherosclerotic endothelial cells via the TLR4/PI3K/Akt/NF-κB pathway.

OBJECTIVE: To determine the effect of miR-217 on the apoptosis of atherosclerotic endothelial cells (AECs) through the Toll-like receptor (TLR) 4/PI3K/Akt/NF-κB pathway. MATERIALS AND METHODS: Oxidized low-density lipoprotein (ox-LDL) was used to construct an atherosclerotic endothelial cell model, and the expression of miR-217/TLR4/PI3K/Akt/NF-κB in the cells was regulated to explore their effects on the viability, apoptosis, inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10)], and endothelial-to-mesenchymal transformation (EndMT) of the endothelial cells. RESULTS: In AECs, miR-217 expression decreased, and the PI3K/Akt/NF-κB pathway was inhibited. The Dual-Luciferase reporter assay revealed that TLR4 was the target of miR-217, and it was up-regulated in AECs, and the further study revealed that up-regulation of miR-217 protected AECs, increased their activity, reduced their apoptosis, and inhibited inflammatory response and EndMT, while TLR4 acted contrary to miR-217. Besides, it was also found that miR-217 inhibited the PI3K/Akt/NF-κB pathway, thus weakening the influence of si-TLR4 on endothelial cells. Furthermore, miR-217 inhibited EndMT by inhibiting TLR4 from activating the PI3K/Akt/NF-κB signal pathway. CONCLUSIONS: In AECs, TLR4 expression increased, and miR-217 and the PI3K/Akt/NF-κB signaling pathway are inhibited. Additionally, miR-217 can increase the viability of AECs through the TLR4/PI3K/Akt/ NF-κB signal transduction pathway, and inhibit their apoptosis, inflammatory response, and EndMT.

Hypoglycemic effect and mechanism of a proteoglycan from ganoderma lucidum on streptozotocin-induced type 2 diabetic rats.

BACKGROUND AND OBJECTIVES: Diabetes mellitus inducing a leading cause of morbidity are widespread in the entire globe. The present study was to investigate the antidiabetic potency and mechanism of a proteoglycan extract, named FYGL (Fudan-Yueyang-G. lucidum), from the fruiting bodies of Ganoderma Lucidum as published recently, using streptozotocin-induced type 2 diabetic mellitus (T2DM) rats. MATERIAL AND METHODS: The T2DM model rats were treated with FYGL as well as metformin and rosiglitazone. The levels of plasma glucose and insulin were measured, and the expression and activity of the protein tyrosine phosphatase 1B (PTP1B) and the tyrosine phosphorylation level of the insulin receptor (IR) 3-subunit in the livers and skeletal muscles of the T2DM rats were analyzed by immunoprecipitation and Western blotting methods. In addition, the levels of free fatty acid and serum lipid profile were measured using commercial kits for those trailed rats. RESULTS: The decrease in fasting plasma glucose and the increase in insulin concentration dose- and time-dependently in the T2DM rats treated by FYGL, comparable with that by the clinical drugs, metformin and rosiglitazone. The levels of the PTP1B expression and activity were decreased, and the tyrosine phosphorylation level of the IR 1-subunit was increased in the skeletal muscles of the T2DM rats. Furthermore, FYGL significantly decreased the levels of free fatty acid, triglyceride, total cholesterol and low density lipoprotein-cholesterol as well as increased the level of high density lipoprotein-cholesterol. DISCUSSION: It is suggested that the hypoglycemic mechanisms of FYGL are caused by inhibition of the PTP1B expression and activity, consequently, regulation of the tyrosine phosphorylation level of the IR 13-subunit. As those results, FYGL also controlled the plasma biochemistry indexes relative to the type 2 diabetes-accompanied metabolic disorders. This is possibly the first report on the underlying mechanisms responsible for the antidiabetic effect of Ganoderma lucidum.

Comb-drive tracking and focusing lens actuators integrated on a silicon-on-insulator wafer.

This paper reports integrated tracking (horizontal) and focusing (vertical) actuators using microelectromechanical (MEMS) technology for optical storage. The design, fabrication and characterization of the integrated tracking and focusing actuators are demonstrated. The integrated tracking and focusing lens actuators that consist of springs, a lens holder and comb-drive actuators are implemented to obtain the two-dimensional tuning effect of an objective lens. A two-mask process is used to define the actuators on a silicon-on-insulator (SOI) wafer. The DC displacements and the frequency responses are characterized by applying voltage to the micro lens actuators. Displacements are experimentally characterized with ± 24.6µm in tracking direction and 5.7µm in focusing direction. Moreover, the influences of the cross-axis coupling are measured and evaluated. This MEMS device which has a small form factor provides an excellent response time and size reduction. The minimization and integration of the lens actuators can offer low costs in assembly and expand the application area of the optical head.

Detection of Fcgamma receptors on human endothelial cells stimulated with cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma).

This investigation was conducted to detect Fcgamma receptors (FcgammaR) on cytokine-stimulated human endothelial cells (EC) by measuring anti-FcgammaR MoAb binding with an ELISA. TNF-alpha and IFN-gamma significantly increased the expression of FcgammaR type II (FcgammaRII) and type III (FcgammaRIII) on aortic EC. Simultaneous treatment with both cytokines had a synergistic effect and pretreatment of EC with IFN-gamma augmented the effect of TNF-alpha. The greatest effect was the increase (up to four-to-six-fold) in expression of FcgammaRII found by the simultaneous treatment of aortic EC with both cytokines. The receptors were expressed on the cell surface and showed receptor capping after incubation at 37 degrees C. This study showed that the inflammatory cytokines TNF-alpha and IFN-gamma enhanced low-affinity FcgammaR expression on human EC in vitro. The expression of FcgammaR may contribute to the specific localization of circulating immune complexes on blood vessels in areas of vasculitis.