Joining characteristics of titanium-based orthodontic wires connected by laser and electrical welding methods.

This study investigated the possibility of electrical and laser welding to connect titanium-based alloy (beta-titanium and nickel-titanium) wires and stainless-steel or cobalt-chromium alloy wires for fabrication of combination arch-wires. Four kinds of straight orthodontic rectangular wires (0.017 × 0.025 inch) were used: stainless-steel (S-S), cobalt-chromium (Co-Cr), beta-titanium alloy (ß-Ti), and nickel-titanium (Ni-Ti). Homogeneous and heterogeneous end-to-end joints (15 mm long each) were made by electrical welding and laser welding. Non-welded wires (30 mm long) were also used as a control. Maximum loads at fracture (N) and elongation (%) were measured by conducting tensile test. The data (n = 10) were statistically analyzed using analysis of variance/Tukey test (P < 0.05).The S-S/S-S and Co-Cr/Co-Cr specimens showed significantly higher values of the maximum load (ML) at fracture and elongation (EL) than those of the Ni-Ti/Ni-Ti and ß-Ti/ß-Ti specimens for electrical welding and those of the S-S/S-S and Co-Cr/Co-Cr specimens welded by laser. On the other hand, the laser-welded Ni-Ti/Ni-Ti and ß-Ti/ß-Ti specimens exhibited higher values of the ML and EL compared to those of the corresponding specimens welded by electrical method. In the heterogeneously welded combinations, the electrically welded Ni-Ti/S-S, ß-Ti/S-S and ß-Ti/Co-Cr specimens showed significantly (P < 0.05) higher ML and EL than those of the corresponding specimens welded by laser. Electrical welding exhibited the higher values of maximum load at fracture and elongation for heterogeneously welded combinations than laser-welding.

miR-22 represses cancer progression by inducing cellular senescence.

Cellular senescence acts as a barrier to cancer progression, and microRNAs (miRNAs) are thought to be potential senescence regulators. However, whether senescence-associated miRNAs (SA-miRNAs) contribute to tumor suppression remains unknown. Here, we report that miR-22, a novel SA-miRNA, has an impact on tumorigenesis. miR-22 is up-regulated in human senescent fibroblasts and epithelial cells but down-regulated in various cancer cell lines. miR-22 overexpression induces growth suppression and acquisition of a senescent phenotype in human normal and cancer cells. miR-22 knockdown in presenescent fibroblasts decreased cell size, and cells became more compact. miR-22-induced senescence also decreases cell motility and inhibits cell invasion in vitro. Synthetic miR-22 delivery suppresses tumor growth and metastasis in vivo by inducing cellular senescence in a mouse model of breast carcinoma. We confirmed that CDK6, SIRT1, and Sp1, genes involved in the senescence program, are direct targets of miR-22. Our study provides the first evidence that miR-22 restores the cellular senescence program in cancer cells and acts as a tumor suppressor.