INFLUENCE OF MOLD MATERIALS AND HEAT TREATMENT ON TENSILE PROPERTIES OF Ni-Ti ALLOY CASTINGS

The influence of mold materials and heat treatment on the tensile properties and the transformation temperatures of Ni-Ti alloy castings was investigated by tensile test and differential scanning calorimetry (DSC) in order to apply the special properties of the alloy to dental field. The compositions of the two alloys examined were 49.0 and 49.2 at% Ti. A silica investment and a magnesia investment were used as the mold materials. Heat treatment at 440 °C for 1.8 ks was performed.Apparent proof strength decreased in both compositions, and residual strain increased in Ni-49.2Ti by the heat treatment. Elongation increased in N i-49.0Ti with use of the magnesia mold or by the heat treatment. The transformation temperatures of Ni-49.2Ti increased with use of the magnesia mold. The change by the heat treatment suggested a structural change. The development of a suitable method for the casting of the alloy is expected to bring about the development of new devices and therapy in dentistry

Suppression of arthritic bone destruction by adenovirus-mediated csk gene transfer to synoviocytes and osteoclasts

Rheumatoid arthritis (RA) is characterized by a chronic inflammation of the synovial joints resulting from hyperplasia of synovial fibroblasts and infiltration of lymphocytes, macrophages, and plasma cells, all of which manifest signs of activation. Recent studies have revealed the essential role of osteoclasts in joint destruction in RA. Src family tyrosine kinases are implicated in various intracellular signaling pathways, including mitogenic response to growth factors in fibroblasts, activation of lymphocytes, and osteoclastic bone resorption. Therefore, inhibiting Src activity can be a good therapeutic strategy to prevent joint inflammation and destruction in RA. We constructed an adenovirus vector carrying the csk gene, which negatively regulates Src family tyrosine kinases. Csk overexpression in cultured rheumatoid synoviocytes remarkably suppressed Src kinase activity and reduced their proliferation rate and IL-6 production. Bone-resorbing activity of osteoclasts was strongly inhibited by Csk overexpression. Furthermore, local injection of the virus into rat ankle joints with adjuvant arthritis not only ameliorated inflammation but suppressed bone destruction. In conclusion, adenovirus-mediated direct transfer of the csk gene is useful in repressing bone destruction and inflammatory reactions, suggesting the involvement of Src family tyrosine kinases in arthritic joint breakdown and demonstrating the feasibility of intervention in the kinases for gene therapy in RA. J. Clin. Invest. 104:137–146 (1999)