Leonardbyskov3794
However, the mean differences were minute to notice clinically. Age difference did not have any effect on the treatment changes.
RPFM revealed treatment outcome with more protruded upper lip than RTB.
RPFM revealed treatment outcome with more protruded upper lip than RTB.
The aim of this study was to evaluate the protective effect of using four different fluoride bioactive enamel sealers against an acidic erosion challenge.
A sample of 50 freshly extracted sound upper premolars had their buccal surface bonded to 50 orthodontic brackets using Transbond PLUS color change adhesive; the first four groups had four compositions of fluoride bioactive glasses based on 37 mol% SiO
, 43.9-53.9 mol% CaO, 6.1 mol% P
O
and CaF
, and 0-10 mol% of Na
O applied to their surfaces and the fifth group served as control (which was not treated by any bioactive sealer). All specimens were challenged by 1% citric acid for 18 minutes which was stirred by a magnetic stirrer. The enamel surfaces next to the orthodontic brackets were examined by SEM. The Wilcoxon signed-rank test was used to compare the area covered by the fluoride bioactive pastes before/after erosion (
< 0.05). Samples from the layer formed on top of the examined teeth were tested before/after erosion to be examined by the attenuated total reflectance Fourier-transform infrared spectroscopy (FTIR/ATR).
The FTIR/ATR test showed that fluoride bioactive pastes' applications resulted in the formation of a hydroxyapatite-rich layer; the SEM analysis showed that the aforementioned layer significantly resisted erosion challenge when compared to the control group (
< 0.05).
Fluoride bioactive pastes can efficiently protect the enamel surfaces next to orthodontic brackets from acidic erosion challenges.
Fluoride bioactive pastes can efficiently protect the enamel surfaces next to orthodontic brackets from acidic erosion challenges.
Recent studies suggest a correlation between the reduced Sirt-1 expression with Alzheimer's diseases (AD) and depression, respectively, suggesting a possible pathogenic role of the altered Sirt-1 expression in neuronal degenerative diseases, such as AD and depression. However, the molecular mechanisms underlying how Sirt-1 reduction impairs neuronal functions remain unknown.
We used the SK-N-SH neuroblastoma cells to study the role of Sirt-1 expression on physiological roles in neuronal cells. this website Gain of Sirt-1 was achieved by transiently transfecting Sirt-1 expression plasmid. Sirt-1-specific shRNA was used to elucidate the role of Sirt-1 loss of function. CCK-8 (Cell Counting Kit-8) assay and flow cytometry were used to evaluate cell proliferation. Semiquantitative western blotting was used to detect relative protein levels. A further luciferase reporter gene assay was employed to examine the effect of Sirt-1 expression on the transcriptional activity of p53. RT-qPCR was used to determine the mRNA levels oN-SH cells, which protects them from oxidative stress-induced cell death, potentially via suppressing the transcriptional activity of p53. These results provide a molecular explanation underlying how the reduced Sirt-1 potentially causes the AD and depression-related diseases, supporting the idea that Sirt-1 can possibly be used as a diagnostic biomarker and/or therapeutic drug target for the AD and depression-related diseases.
Oxidative stress induces Sirt-1 in neuron cells, and Sirt-1 promotes proliferation in SK-N-SH cells, which protects them from oxidative stress-induced cell death, potentially via suppressing the transcriptional activity of p53. These results provide a molecular explanation underlying how the reduced Sirt-1 potentially causes the AD and depression-related diseases, supporting the idea that Sirt-1 can possibly be used as a diagnostic biomarker and/or therapeutic drug target for the AD and depression-related diseases.EPHA2 is a member of the ephrin receptor tyrosine kinase family and is closely related to the malignant tumor progression. The effect of EPHA2 on OSCC is not clear. This study explored the role of EPHA2 and AKT/mTOR signaling pathways in Cal-27 cell invasion and migration. The expression of EPHA2 and EPHA4 in human OSCC and normal oral tissue was detected by immunohistochemistry. EPHA2-overexpressing and EPHA2-knockdown Cal-27 cells were established, and the cells were treated with an AKT inhibitor (MK2206) and mTOR inhibitor (RAD001). The expression of EPHA2 was detected by qRT-PCR, cell proliferation was evaluated by MTT assay, cell migration and invasion were examined by scratch and Transwell assay, and cell morphology and apoptosis were assessed by Hoechst 33258 staining. Western blot was performed to detect the expression of proteins related to AKT/mTOR signaling, cell cycle, and pseudopod invasion. EPHA2 and EPHA4 were highly expressed in clinical human OSCC. Overexpression of EPHA2 promoted the proliferation, migration, and invasion of Cal-27 cells, inhibited cell cycle blockage and apoptosis, and enhanced the activity of the AKT/mTOR signaling pathway. MK2206 (AKT inhibitor) and RAD001 (mTOR inhibitor) reversed the effect of EPHA2 overexpression on the biological behavior of Cal-27 cells. EPHA2 promotes the invasion and migration of Cal-27 human OSCC cells by enhancing the AKT/mTOR signaling pathway.In the field of biology and medicine, one hears often about stem cells and their potential. The dental implant new surfaces, subjected to specific treatments, perform better and allow for quicker healing times and better clinical performance. The purpose of this study is to evaluate from a biological point of view the interaction and cytotoxicity between stem cells derived from dental pulp (DPSCs) and titanium surfaces. Through the creation of complex cells/implant, this study is aimed at analyzing the cytotoxicity of dental implant surfaces (Myth (Maipek Manufacturer Industrial Care, Naples, Italy)) and the adhesion capacity of cells on them and at considering the essential factors for implant healing such as osteoinduction and vasculogenesis. These parameters are pointed out through histology (3D cell culture), immunofluorescence, proliferation assays, scanning electron microscopy, and PCR investigations. The results of the dental implant surface and its interaction with the DPSCs are encouraging, obtaining results increasing the mineralization of the tissues.
