Nano ceramic fiber reinforced silicone maxillofacial prosthesis

Indiana University-Purdue University Indianapolis (IUPUI)The purpose of this study was to investigate the effect of nano ceramic fiber fillers on the physical properties of VST-50HD silicone maxillofacial prosthesis. Nano alumina fibers at 2 percent, 4-percent, and 6-percent wt were mixed into the VST-50HD silicone elastomer (Factor II Inc., Lakeside, AZ), a commercially-available poly(dimethylsiloxanes). Ten dumb-bell-shaped specimens were used to determine the tensile strength according to ISO 37:2005 and elongation at fracture. Ten trouser-shaped test pieces were used to determine the tear resistance according to ISO 34-1:2004. Shore A test method was used to measure the hardness of the material. The data collected from all quantitative studies of the modified silicones were analyzed using one-way ANOVA with concentration of nano ceramic fiber as the main variable. Specimens from VST- 50HD were also made and tested as control. Results: The mean values for tensile strength (MPa) of control group, 2-percent, 4-percent, and 6-percent reinforced nano ceramic fiber fillers were from 3.43 ± 0.12 to 5.48 ± 0.71. Tear strength (MPa) were from 2.34 ± 0.37 to 5.01 ± 0.39. Elongations at fracture were from 699.66 ± 43.69 to 793.51 ± 57.27. Shore A hardness were from 25.76 ± 2.18 to 38.76 ± 1.83. Conclusion: There was a significant difference (p < 0.001) in the mean tensile, tear and Shore A hardness strengths between the control group and 2-percent, 4-percent, and 6-percent percent reinforced nano ceramic fiber fillers; however, there was not a significant difference (p > 0.05) between 2-percent, 4-percent, and 6-percent reinforced nano ceramic fiber fillers. There was a significant difference (p < 0.001) in the mean elongation at fracture between the 2-percent and control group, 4-percent, and 6-percent reinforced nano ceramic fiber fillers; however, there was not a significant difference (p > 0.05) between control group, 4-percent, and 6-percent reinforced nano ceramic fiber fillers. The properties of the experiment were all lower than the control. Further research is needed to determine the appropriate material and amount of dispersing agent, coupling agent, and determination of the hydprophilicity of the nano ceramic fiber fillers with great emphasis on the dispersing agent

Caged-iron chelators - a novel approach towards protecting skin cells against UVA-induced necrotic cell death

Exposure of human skin cells to solar UVA radiation leads to an immediate dose-dependent increase of labile iron that subsequently promotes oxidative damage and necrotic cell death. Strong iron chelators have been shown to suppress cell damage and necrotic cell death by moderating the amount of labile iron pool (LIP), but chronic use would cause severe side effects owing to systemic iron depletion. Prodrugs that become activated in skin cells at physiologically relevant doses of UVA, such as “caged-iron chelators”, may provide dose- and context-dependent release. Herein, we describe prototypical iron chelator compounds derived from salicylaldehyde isonicotinoyl hydrazone and pyridoxal isonicotinoyl hydrazone and demonstrate that the intracellular LIP and subsequent necrotic cell death of human skin fibroblasts is significantly decreased upon exposure to a combination of the prototypical compounds and physiologically relevant UVA doses. Iron regulatory protein bandshift and calcein fluorescence assays reveal decreased intracellular LIP following irradiation of caged-chelator-treated cells, but not in control samples where either UVA light, or caged-chelator is absent. Furthermore, flow cytometry shows that these compounds have no significant toxicity in the skin fibroblasts. This novel light-activated prodrug strategy may therefore be used to protect skin cells against the deleterious effects of sunlight

Role of intracellular labile iron, ferritin, and antioxidant defence in resistance of chronically adapted Jurkat T cells to hydrogen peroxide

AbstractTo examine the role of intracellular labile iron pool (LIP), ferritin (Ft), and antioxidant defence in cellular resistance to oxidative stress on chronic adaptation, a new H2O2-resistant Jurkat T cell line “HJ16” was developed by gradual adaptation of parental “J16” cells to high concentrations of H2O2. Compared to J16 cells, HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death (up to 3mM) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin (FtMt) levels as well as higher glutathione-peroxidase (GPx) activity. In contrast, the level of the Ft H-subunit (FtH) in the H2O2-adapted cell line was found to be 7-fold lower than in the parental J16 cell line. While H2O2 concentrations higher than 0.1mM fully depleted the glutathione content of J16 cells, in HJ16 cells the same treatments decreased the cellular glutathione content to only half of the original value. In HJ16 cells, H2O2 concentrations higher than 0.1mM increased the level of FtMt up to 4-fold of their control values but had no effect on the FtMt levels in J16 cells. Furthermore, while the basal cytosolic level of LIP was similar in both cell lines, H2O2 treatment substantially increased the cytosolic LIP levels in J16 but not in HJ16 cells. H2O2 treatment also substantially decreased the FtH levels in J16 cells (up to 70% of the control value). In contrast in HJ16 cells, FtH levels were not affected by H2O2 treatment. These results indicate that chronic adaptation of J16 cells to high concentrations of H2O2 has provoked a series of novel and specific cellular adaptive responses that contribute to higher resistance of HJ16 cells to oxidative damage and cell death. These include increased cellular antioxidant defence in the form of higher glutathione and FtMt levels, higher GPx activity, and lower FtH levels. Further adaptive responses include the significantly reduced cellular response to oxidant-mediated glutathione depletion, FtH modulation, and labile iron release and a significant increase in FtMt levels following H2O2 treatment