UV radiation was presented as the cause of increased oxidative stress and oxidative damage and its consequences on the skin.
Cellular response at the molecular level as the adaptive stress response was presented as a method for increasing cellular defense and repair system.
In order to improve biocompatibility of titanium surfaces, the topography of titanium dioxide nanotubes (NTs) obtained by electrochemical anodization was considered. The absolute value of the (negative) zeta potential of NTs decreased with increasing salt concentration in the solution. Comparatively higher protein binding to NTs was found with 100 nm diameters than with 50 or 15 nm. A dose-dependent effect of serum amyloid A protein binding to NTs was shown. These results and theoretical calculations of total available surface area for binding of proteins indicate that the largest surface area (also considering the NT lengths) was available for 100 nm NTs.
Novel mesoporous TiO2@DNA nanohybrid electrodes, combining covalently encoded DNA with meso-porous TiO2 microbeads using dopamine as a linker, were prepared and characterised for application in supercapacitors. Detailed information about donor density, charge transfer resistance and chemical capacitance, which have an important role in the performance of an electrochemical device, were studied by electrochemical methods. The results indicated the improvement of electrochemical performance of the TiO2 nanohybrid electrode by DNA surface functionalisation. A supercapacitor was constructed from TiO2@DNA nanohybrids with PBS as the electrolyte. From the supercapacitor experiment, it was found that the addition of DNA played an important role in improving the specific capacitance of the TiO2 supercapacitor. The nanohybrid electrodes were shown to be stable over long-term cycling, retaining 95% of their initial specific capacitance after 1500 cycles.
Oxidative stress produced in response to infection or sterile injury activates the innate immune response. By considering various methods that detect cell response we found that extracellular vesicles act as an oxidative stress–induced endogenous danger signal that underlies the pervasive role of TLR4 in inflammation.