The effect of orthodontic clinical use on the mechanical characteristics of nickel-titanium closed-coil springs.

OBJECTIVE: To examine the effect of clinical use on both force retention and the deactivation of closed-coil nickel-titanium (NiTi) springs in a 16-week trial. METHODS: The force-activation curves for NiTi springs were determined before and after clinical use. The rate of tooth movement and maximum force (MF), hysteresis between activation and deactivation, and mean force of the deactivation plateau (MDF) were examined and correlated as a function of 4, 8, 12 and 16 weeks of clinical use. To recover the force properties, the springs were heat treated at 100°C and the results were compared with the preceding data. RESULTS: A total of 36 springs were analysed. The MF loss after use was 60, 74, 55, and 48 g for the 4-, 8-, 12- and 16-week springs, respectively. Heat treating had little effect on the MF. Clinical use lowered hysteresis by a mean of 180 g*mm compared with the pre-clinical use data, and heat treating increased the hysteresis by a mean of 59 g*mm above the post clinic testing data. The MDF was nominally 100 g less than the MF. Teeth moved approximately 1 mm/month, independent of the force loss. CONCLUSIONS: The loss of MF and the lowering of the MDF was not time dependent. Heat treating can partially recover the mechanical properties of the used springs.

Ginsenoside Rh2 inhibiting HCT116 colon cancer cell proliferation through blocking PDZ-binding kinase/T-LAK cell-originated protein kinase.

BACKGROUND: Ginsenoside Rh2 (GRh2) is the main bioactive component in American ginseng, a commonly used herb, and its antitumor activity had been studied in previous studies. PDZ-binding kinase/T-LAK cell-originated protein kinase (PBK/TOPK), a serine/threonine protein kinase, is highly expressed in HCT116 colorectal cancer cells. METHODS: We examined the effect of GRh2 on HCT116 cells ex vivo. Next, we performed in vitro binding assay and in vitro kinase assay to search for the target of GRh2. Furthermore, we elucidated the underlying molecular mechanisms for the antitumor effect of GRh2 ex vivo and in vivo. RESULTS: The results of our in vitro studies indicated that GRh2 can directly bind with PBK/TOPK and GRh2 also can directly inhibit PBK/TOPK activity. Ex vivo studies showed that GRh2 significantly induced cell death in HCT116 colorectal cancer cells. Further mechanistic study demonstrated that these compounds inhibited the phosphorylation levels of the extracellular regulated protein kinases 1/2 (ERK1/2) and (H3) in HCT116 colorectal cancer cells. In vivo studies showed GRh2 inhibited the growth of xenograft tumors of HCT116 cells and inhibited the phosphorylation levels of the extracellular regulated protein kinases 1/2 and histone H3. CONCLUSION: The results indicate that GRh2 exerts promising antitumor effect that is specific to human HCT116 colorectal cancer cells through inhibiting the activity of PBK/TOPK.