• Restorative Dentistry and Endodontics
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• 제36권4호
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• pp.306-312
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• 2011

Objectives: This clinical study evaluated the effect of light activation on the whitening efficacy and safety of in-office bleaching system containing 15% hydrogen peroxide gel. Materials and Methods: Thirty-three volunteers were randomly treated with (n = 17, experimental group) or without light activation (n = 16, control group), using Zoom2 white gel (15% $H_2O_2$, Discus Dental) for a total treatment time of 45 min. Visual and instrumental color measurements were obtained using Vitapan Classical shade guide and Shadepilot (DeguDent) at screening test, after bleaching, and 1 month and 3 month after bleaching. Data were analyzed using t-test, repeated measure ANOVA, and chi-squared test. Results: Zoom2 white gel produced significant shade changes in both experimental and control group when pre-treatment shade was compared with that after bleaching. However, shade difference between two groups was not statistically significant (p > 0.05). Tooth shade relapse was not detected at 3 months after bleaching. The incidence of transient tooth sensitivity was 39.4%, with being no differences between two groups. Conclusions: The application of light activation with Zoom2 white gel system neither achieved additional whitening effects nor showed more detrimental influences.

• Radiation Oncology Journal
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• 제23권2호
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• pp.92-97
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• 2005

Purpose : Reports on the outcome of curative radiotherapy for the primary hepatocellular carcinoma (HCC) are rarely encountered in the literature. in this study, we report our experience of a clinical trial where fractionated stereotactic radiotherapy (SRT) was used in treating a primary HCC. Materials and Methods : A retrospective analysis was peformed on 20 patients who had been histologically diagnosed as HCC and treated by fractionated SRT. The long diameter of tumor measured by CT was $2\~6.5$ cm (average: 3.8 cm). A single dose of radiation used in fractionated SRT was S or 10 Gy: each dose was prescribed based on the planning target volume and normalized to $85\~99\%$ isocenter dose. Patients were treated $3\~5$ times per week for 2 weeks, with each receiving a total dose of 50 Gy (the median dose: 50 Gy). The follow up period was $\~55$ months (the median follow up period: 23 months). Results : The response rate was $50\%$ (12 patients), with 4 patients showing complete response ($20%$), 8 patients showing partial response ($40\%$), and 8 patients showing stable disease ($40\%$). The 1-year and 2-year survival rates were $70.0\%$ and $43.1\%$, respectively, and the median survival time was 20 months. The 1-year and 2-year disease free survival rates were $65\%$ and $32.5\%$, respectively, and the median disease-free survival rate was 19 months. Some acute complications of the treatment were noted as follows: dyspepsia in 12 patients ($60\%$), nausea/emesis in 8 patients ($40\%$), and transient liver function impairment in 6 patients ($30\%$). However, there was no treatment related death. Conclusion : The study indicates that fractionated SRT is a relatively safe and effective method for treating primary HCC. Thus, fractionated SRT may be suggested as a local treatment for HCC of small lesion and containing a single lesion, when the patients are inoperable or operation is refused by the patients. We thought that fractionated SRT is a challenging treatment modality for the HCC.

• Journal of Life Science
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• 제19권11호
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• pp.1529-1537
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• 2009

To elucidate further the antitumor effects of a natural L-arginine analogue, L-canavanine, the mechanism underlying apoptogenic activity of L-canavanine and its modulation by protein tyrosine kinase $p56^{lck}$ was investigated in human Jurkat T cells. When the cells were treated with 1.25 to 2.5 mM L-canavanine for 36 h, several apoptotic events including mitochondrial membrane potential (${\Delta\Psi}m$) loss, activation of caspase-9, -3, -8, and -7, poly (ADP-ribose) polymerase (PARP) degradation, and DNA fragmentation were induced without alteration in the levels of Fas or FasL. These apoptotic changes were more significant in $p56^{lck}$-deficient Jurkat clone JCaM1.6 than in $p56^{lck}$-positive Jurkat clone E6.1. The L-canavanine-induced apoptosis observed in $p56^{lck}$-deficient JCaM1.6 cells was significantly reduced by introducing $p56^{lck}$ gene into JCaM1.6 cells by stable transfection. Treatment of JCaM1.6/lck cells with L-canavanine caused a transient 1.6-fold increase in the kinase activity of $p56^{lck}$. Both FADD-positive wild-type Jurkat T cell clone A3 and FADD-deficient Jurkat T cell clone I2.1 exhibited a similar susceptibility to the cytotoxicity of L-canavanine, excluding involvement of Fas/FasL system in triggering L-canavanine-induced apoptosis. The L-canavanine-induced apoptotic sub-$G_1$ peak and activation of caspase-3, -8, and -7 were abrogated by pan-caspase inhibitor (z-VAD-fmk), whereas L-canavanine-induced activation of caspase-9 was not affected. These results demonstrated that L-canavanine caused apoptosis of Jurkat T cells via the loss of ${\Delta\Psi}m$, and the activation of caspase-9, -3, -8, and -7, leading to PARP degradation, and that the $p56^{lck}$ kinase attenuated the ${\Delta\Psi}m$ loss and activation of caspases, and thus contributed as a negative regulator to L-canavanine-induced apoptosis.