Development of a Tongue Immobilization Device Using a 3D Printer for Intensity Modulated Radiation Therapy of Nasopharyngeal Cancer Patients / Journal of the Korean Cancer Association, 대한암학회지

Purpose@#This study aimed to reduce radiation doses to the tongue, a patient-specific semi-customized tongue immobilization device (SCTID) was developed using a 3D printer for helical tomotherapy (HT) of nasopharyngeal cancer (NPCa). Dosimetric characteristics and setup stability of the SCTID were compared with those of a standard mouthpiece (SMP). @*Materials and Methods@#For displacement and robust immobilization of the tongue, the SCTID consists of four parts: upper and lower tooth stoppers, tongue guider, tongue-tip position guide bar, and connectors. With the SCTID and SMP, two sets of planning computed tomography and HT plans were obtained for 10 NPCa patients. Dosimetric and geometric characteristics were compared. Position reproducibility of the tongue with SCTID was evaluated by comparing with planned dose and adaptive accumulated dose of the tongue and base of the tongue based on daily setup mega-voltage computed tomography. @*Results@#Using the SCTID, the tongue was effectively displaced from the planning target volume compared to the SMP. The median mucosa of the tongue (M-tongue) dose was significantly reduced (20.7 Gy vs. 27.8 Gy). The volumes of the M-tongue receiving a dose of 15 Gy, 30 Gy, and 45 Gy and the volumes of the mucosa of oral cavity and oropharynx (M-OC/OP) receiving a dose of 45 Gy and 60 Gy were significantly lower than using the SMP. No significant differences was observed between the planned dose and the accumulated adaptive dose in any dosimetric characteristics of the tongue and base of tongue. @*Conclusion@#SCTID can not only reduce the dose to the M-tongue and M-OC/OP dramatically, when compared to SMP, but also provide excellent reproducibility and easy visual verification.

Superoxide Dismutase 1 Inhibits Alpha-Melanocyte Stimulating Hormone and Ultraviolet B-Induced Melanogenesis in Murine Skin

BACKGROUND: Over the last decade, the incidence of ultraviolet B (UVB)-related skin problems has increased. Oxidative stress caused by UVB induces the secretion of melanocyte growth and activating factors from keratinocytes, which results in the formation of cutaneous hyperpigmentation. Therefore, increasing the antioxidant abilities of skin cells is thought to be a beneficial strategy for the development of sunscreen agents. Superoxide dismutase 1 (SOD1) is an antioxidant enzyme that is known to exhibit antioxidant properties. OBJECTIVE: The purpose of this study was to investigate the effect of SOD1 on alpha-melanocyte stimulating hormone (alpha-MSH) and UVB-induced melanogenesis in B16F10 melanoma cells and HRM-2 melanin-possessing hairless mice. METHODS: The inhibitory effect of SOD1 on tyrosinase activity was evaluated in a cell-free system. Additional experiments were performed using B16F10 melanoma cells to demonstrate the effects of SOD1 in vitro, and HRM-2 melanin-possessing hairless mice were used to evaluate the antimelanogenic effects of SOD1 in vivo. RESULTS: We found that SOD1 inhibited melanin production in a dose-dependent manner without causing cytotoxicity in B16F10 melanoma cells. SOD1 did not inhibit tyrosinase activity under cell-free conditions. The results indicate that SOD1 may reduce pigmentation by an indirect, nonenzymatic mechanism. We also found that SOD1 decreased UVB-induced melanogenesis in HRM-2 melanin-possessing hairless mice, as visualized through hematoxylin and eosin staining and Fontana-Masson staining. CONCLUSION: Our results indicate that SOD1 has an inhibitory effect on alpha-MSH and UVB-induced melanogenesis, indicating that SOD1 may be a promising sunscreen agent.

Experimental autoimmune myasthenia gravis and CD5+ B-lymphocyte expression

Myasthenia gravis is one of the typical organ specific autoimmune disease and the CD5+ B-lymphocytes are known to be associated with the secretion of autoimmune antibodies. The authors performed the study to establish an animal model of experimental autoimmune myasthenia gravis (EAMG) by immunizing the nicotinic acetylcholine receptor (AChR) and to understand CD5+ B-lymphocyte changes in peripheral blood of EAMGs. Lewis rats weighing 150-200 g were injected subcutaneously three times with 50 microg AChR purified from the electric organ of Torpedo marmorata and Freund's adjuvant. The EAMG induction was assessed by evaluating clinical manifestations. The CD5+ B-lymphocyte was double stained using monoclonal PE conjugated anti-CD5+ and FITC conjugated anti-rat CD45R antibodies and calculated using a fluorescence-activated cell sorter (FACS). In three out of ten Lewis rats injected with purified AChR, the EAMG models were established. The animals showed definite clinical weakness responded to neostigmine; they had difficulty in climbing the slope, or easily fell down from a vertical cage. The range of CD5+ B-lymphocytes of peripheral blood in the EAMG models was 10.2%-17.5%, which was higher than in controls. In conclusion, the EAMG models were successfully established and the CD5+ B-lymphocyte expression in peripheral blood increased in EAMGs. This provided indirect evidence of the autoimmune pathomechanism of human myasthenia gravis.