Background: Limited evidence exists regarding the effect of carbamide peroxide and casein phospho‐peptide amorphous calcium phosphate (CPP‐ACP) on composite‐enamel bonding. Microshear bond strengths, using either a total‐etch or self‐etching adhesive, to enamel treated with carbamide peroxide and/or CPP‐ACP were investigated. Materials and methods: Twenty‐six extracted human third molars were sectioned into four parts, each being allocated into one of the four groups (n=26): bleach (Polanight, 16% carbamide peroxide), CPP‐ACP (GC Tooth Mousse), bleach and then CPP‐ACP, or untreated (control). The surfaces were bonded with a total‐etch bonding system (Single Bond) or a self‐etching primer system (Clearfil SE Bond) and tested using a microshear test. Results: A significant difference in bond strength was found between bonding systems. SE Bond showed the highest bond strength to untreated enamel (p < 0.05). The microshear bond strength of SE Bond decreased when the enamel was treated with carbamide peroxide, CPP‐ACP or both (p < 0.05). Only combined use of carbamide peroxide and CPP‐ACP significantly affected microshear bond strength with Single Bond. Conclusion : These findings suggest the shear bond strength of resin to enamel using a self‐etching priming adhesive may be affected if the enamel is treated with a bleaching agent or CPP‐ACP.
Interest in electron transport on high-index GaAs surfaces is increasing, especially since the advent of patterned substrate regrowth, in which high index surfaces are revealed on (001) GaAs after etching. In this paper we observe anisotropic mobility in orthogonal directions in two-dimensional electron gases grown on (311)B GaAs substrates. The mobility in the (233) direction is found to be up to 50 in the (011) direction. The lower mobility is accompanied by a large anomalous negative magnetoresistance. These effects are studied as a function of temperature and carrier density. It is suggested that interface roughness scattering could be a cause for the large anisotropies in mobility and a simple calculation is performed to demonstrate this hypothesis.
The omega-6 fatty acid derivative 15-Deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2) is believed to play a role in cellular protection against oxidative stress in diverse cell systems. However, the cellular mechanisms by which protection is afforded by 15d-PGJ2 are not fully elucidated in vascular smooth muscle cells (VSMCs). In this study, we report the finding that 15d-PGJ2 elicited a time and concentration- dependent increase in aldose reductase (AR) expression. This induction was independent of the activation of peroxisome proliferator- activated receptor γ. Inhibition of phosphatidylinositol 3-kinase (PI3K) significantly suppressed the increase in expression and promoter activity of AR induced by 15d-PGJ2. Luciferase reporter assays demonstrated that 15d-PGJ2 targets the multiple stress response regions comprising the antioxidant response element in the promoter of the AR gene. 15d-PGJ2-mediated induction of AR promoter activity was potentiated in the presence of nuclear factor-erythroid 2-related factor 2 (Nrf2), but not in cells expressing dominant negative Nrf2. Cells treated with 15d-PGJ2 were resistant to oxidant-induced apoptotic cell death by inhibiting production of reactive oxygen species. These effects were significantly attenuated in the presence of an AR inhibitor or small interfering RNA against AR, indicating that AR plays a protective role against oxidative injury. Taken together, these findings demonstrate that activation of PI3K by 15d-PGJ2 increases the expression of AR through Nrf2, and increased AR activity may function as an important cellular response against oxidative injury.
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