EVALUATION OF TORQUE MOMENT IN ESTHETIC BRACKETS

Objectives: To examine the torque moment that occurs between esthetic brackets and bendable alloy (stainless steel [SS], titanium-molybdenum [Ti-Mo], and titanium-niobium [Ti-Nb]) wires. Materials and Methods: This study examined ceramic (CR), zirconium oxide (ZC), polycarbonate (PC), and conventional metallic brackets (MT) (upper, 0.018-inch and 0.022-inch slots) combined with SS, Ti-Mo, and Ti-Nb wires using elastic module ligation. The torque moments delivered by various wire and bracket combinations were measured using a torque gauge apparatus. The wire torque angles at 5–40° were examined. Results: The torque value increased in the order of CR, ZC, MT, and PC brackets for both 0.018-inch and 0.022-inch slots. The fracture points of the CR and ZC brackets combined with SS and Ti-Mo wires were approximately more than 30° and 35°, respectively. No fracture points were detected in the combination of ZC brackets and Ti-Nb wires. Conclusions: The current study identified the material characteristics of CR, ZR, and PC brackets during torque tooth movements. The present results demonstrate a characteristic combined effect between different esthetic brackets and bendable alloy wires

Elimination of Hepatitis C Virus from Hepatocytes by a Selective Activation of Therapeutic Molecules

To eliminate hepatitis C virus (HCV) from infected hepatocytes, we generated two therapeutic molecules specifically activated in cells infected with HCV. A dominant active mutant of interferon (IFN) regulatory factor 7 (IRF7) and a negative regulator of HCV replication, VAP-C (Vesicle-associated membrane protein-associated protein subtype C), were fused with the C-terminal region of IPS-1 (IFNβ promoter stimulator-1), which includes an HCV protease cleavage site that was modified to be localized on the ER membrane, and designated cIRF7 and cVAP-C, respectively. In cells expressing the HCV protease, cIRF7 was cleaved and the processed fragment was migrated into the nucleus, where it activated various IFN promoters, including promoters of IFNα6, IFNβ, and IFN stimulated response element. Activation of the IFN promoters and suppression of viral RNA replication were observed in the HCV replicon cells and in cells infected with the JFH1 strain of HCV (HCVcc) by expression of cIRF7. Suppression of viral RNA replication was observed even in the IFN-resistant replicon cells by the expression of cIRF7. Expression of the cVAP-C also resulted in suppression of HCV replication in both the replicon and HCVcc infected cells. These results suggest that delivery of the therapeutic molecules into the liver of hepatitis C patients, followed by selective activation of the molecules in HCV-infected hepatocytes, is a feasible method for eliminating HCV