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Objective: To analyze the stress distribution in all-ceramic crowns when it was subjected to load., Methods: A 3D numerical model of the all-ceramic crown of the right mandibular first molar was generated from scanned CT images. Finite element analysis (FEA) was used to evaluate the stress distribution in the all-ceramic crown when it was subjected to 5 load conditions., Results: Stress distributions under 5 loading conditions were obtained. Stress concentrations were generally found near the loading areas at the veneer and at the lower surface of the core beneath the loading areas. In the 5 loading conditions, it was found that when the crown was loaded with vertical concentrated load, the tensile stresses around the shoulder areas were uniform, while stress concentration with maximum of 32.25 MPa was found at the shoulder areas in lingual-buccal direction when loads were applied at an angle of 10 degrees with the tooth axis on the buccal side. The masticatory load which was applied at 20 degrees with the tooth axis on the buccal side would cause stress concentration at the shoulder in mesial-distal direction. The maximum value could reach 11.29 MPa., Conclusions: The occlusal surface of the all-ceramic crown must be trimmed to increase multiple contact zones with the opposite surfaces in antagonist teeth to avoid excessive concentrated stress that may cause crown failure.

The purpose of this study was to explore the mechanism of CAG regimen eliminating T-cell acute lymphoblastic leukemia (T-ALL) A3 cell line and evaluate the role of G-CSF/G-CSFR system in this process. The expression levels of G-CSFR on the A3 cell membrane were detected by flow cytometry. Cell cycle changes of A3 cells treated with different concentrations of G-CSF for 48 hours were examined by propidium iodide staining method. The inhibition and apoptosis rates of A3 cells treated with various combinations of G-CSF, cytarabine (Ara-C), aclarubicin (ACR) were analyzed by Cell Counting Kit and AnnexinV Kit, respectively. The results indicated that the expression level of G-CSFR on A3 cells was 94.2%. The proportion of A3 cells in S-phase rose concomitantly with the increasing of G-CSF concentrations within 0-20 ng/ml. After incubation with Ara-C and G-CSF for 48 hours, A3 cells were inhibited more obviously compared with incubation with Ara-C alone (p<0.05, Ara-C 10(-5) mol/L and 10(-6) mol/L). After incubation with Ara-C, ACR and G-CSF for 48 hours, the apoptotic rate of A3 cells was much more than that after incubation with Ara-C and ACR. It is concluded that the expression level of G-CSFR on A3 cells is high, G-CSF/G-CSFR system has a synergetic effect on eliminating A3 cells when administrated simultaneously with chemical agents. This effect is caused through driving more cells from G0 phase into S phase, increasing sensitivity of A3 cells to chemical drugs and inducing cell apoptosis which may be one of the mechanisms of CAG regimen eliminating A3 cells.