[Comparison of two-year stability between immediate implant action and delayed implantation for anterior teeth with periodontal disease].

PURPOSE: To investigate the feasibility of immediate implantation after extraction of anterior teeth in patients with periodontal disease and its clinical effect within 2 years. METHODS: Thirty patients (36 implants) who underwent anterior dental implant treatment for periodontal disease from 2016 to 2018 were randomly divided into immediate implantation group (17 implants) and delayed implantation group (19 implants). The patients were followed up for 2 years, the clinical parameters such as periodontal probing depth, pink esthetic score（PES）and implant neck bone resorption volume of implant neck were obtained. The data was statistically analyzed with SPSS 21.0 software package. RESULTS: During the 2-year follow-up period, no implant loss, and there was no significant difference in the depth of peri-implant probing between the two groups at each time point(P＞0.05). There was no significant difference in the volume of bone resorption at implant neck between the two groups(P>0.05). At 6, 12 and 24 months after completion of superstructure repair, there was no significant difference in pink esthetic score（PES）between the two groups (P＞0.05), but there was significant difference in pink esthetic score（PES) at the third month after restoration (P＜0.05). The immediate implantation group obtained more satisfactory soft tissue morphology around the implants. CONCLUSIONS: Under appropriate treatment conditions, there is no significant difference in implant success rate between immediate implantation and delayed implantation of anterior teeth in patients with periodontal disease. At the same time, it reduces the number of operations and shortens the course of treatment. In terms of soft tissue aesthetics, immediate implantation is slightly better than delayed implantation in the early stage after restoration, and can maintain a good soft tissue aesthetic effect.

Novel PI3K/Akt/mTOR signaling inhibitor, W922, prevents colorectal cancer growth via the regulation of autophagy.

W922, a novel PI3K/Akt/mTOR pathway inhibitor, exhibits efficient anti­tumor effects on HCT116, MCF­7 and A549 human cancer cells compared with other synthesized compounds. The present study aimed to investigate its anti­tumor effects on colorectal cancer cells. A total, of seven different colorectal cell lines were selected to test the anti­proliferation profile of W922, and HCT116 was found to be the most sensitive cell line to the drug treatment. W922 inhibited HCT116 cell viability and cell proliferation in vitro in concentration­ and time­dependent manners. Furthermore, W922 suppressed the tumor growth in a xenograft mouse model and exhibited low toxicity. The proteomic alterations in W922­treated HCT116 cells were found to be associated with cell cycle arrest, negative regulation of signal transduction and lysosome­related processes. W922 caused cell cycle arrest of HCT116 cells in G0­G1 phase, but only triggered slight apoptosis. In addition, the PI3K/Akt/mTOR signaling proteins were dephosphorylated upon W922 treatment. It has been reported that inhibition of mTOR is relevant to autophagy, and the present results also indicated that W922 was involved in autophagy induction. An autophagy inhibitor, chloroquine, was used to co­treat HCT116 cells with W922, and it was identified that the cell cycle arrest was impaired. Moreover, co­treatment of W922 and chloroquine led to a significant population of apoptotic cells, thus providing a promising therapeutic strategy for colorectal cancer.

Indirubin Treatment of Lipopolysaccharide-Induced Mastitis in a Mouse Model and Activity in Mouse Mammary Epithelial Cells.

Indirubin is a Chinese medicine extracted from indigo and known to be effective for treating chronic myelogenous leukemia, neoplasia, and inflammatory disease. This study evaluated the in vivo anti-inflammatory activity of indirubin in a lipopolysaccharide- (LPS-) induced mouse mastitis model. The indirubin mechanism and targets were evaluated in vitro in mouse mammary epithelial cells. In the mouse model, indirubin significantly attenuated the severity of inflammatory lesions, edema, inflammatory hyperemia, milk stasis and local tissue necrosis, and neutrophil infiltration. Indirubin significantly decreased myeloperoxidase activity and downregulated the production of tumor necrosis factor-α, interleukin-1ß (IL-1ß), and IL-6 caused by LPS. In vitro, indirubin inhibited LPS-stimulated expression of proinflammatory cytokines in a dose-dependent manner. It also downregulated LPS-induced toll-like receptor 4 (TLR4) expression and inhibited phosphorylation of LPS-induced nuclear transcription factor-kappa B (NF-κB) P65 protein and inhibitor of kappa B. In addition to its effect on the NF-κB signaling pathway, indirubin suppressed the mitogen-activated protein kinase (MAPK) signaling by inhibiting phosphorylation of extracellular signal-regulated kinase (ERK), P38, and c-jun NH2-terminal kinase (JNK). Indirubin improved LPS-induced mouse mastitis by suppressing TLR4 and downstream NF-κB and MAPK pathway inflammatory signals and might be a potential treatment of mastitis and other inflammatory diseases.