Cellulose membrane coated Mo-doped TiO2nanotube sheets for sustained oxidation of biomolecules.

Titanium dioxide nanotubes (TNT) are widely researched materials for the photocatalytic generation of free radicals, which are useful in wastewater treatment. We aimed to prepare Mo-doped TNT sheets, covered with a cellulose membrane to avoid TNT surface inactivation by protein adsorption. We studied the susceptibility of serum albumin (SA) bound to different molar ratios of palmitic acid (PA) to denaturation and fibrillation by this system, which is meant to mimic oxidative stress conditions such as non-alcoholic fatty liver disease. The results demonstrated that cellulose membrane-covered TNT successfully oxidized the SA, identified by structural changes to the protein. Increasing the molar ratio of PA to protein-enhanced thiol group oxidation while protecting the protein against structural changes. Finally, we propose that in this photocatalyzed oxidation system, the protein is oxidized by a non-adsorptive mechanism mediated by H2O2. Therefore, we suggest that this system could be used as a sustained oxidation system to oxidize biomolecules as well as potentially in wastewater treatment.

Dopamine effects on stress-induced working memory deficits.

The prefrontal cortex (PFC) plays a critical role in mediating executive functions and orchestrating the way in which we think, decide, and behave. Many studies have shown that PFC neurons not only play a major role in mediating behavioral responses to stress but are also sensitive to stress and undergo remodeling following stress exposure. Activation of the hypothalamic-pituitary-adrenal axis as a result of stress initiates a flood of alterations in prefrontal neurotransmitter release. Dopamine (DA) neurotransmission in the PFC is involved in the modulation of stress responsiveness. Compelling results show that stressful events are associated with increased DA concentrations in the medial PFC. Excessive DA-ergic activity in the medial prefrontal cortex following stress has a negative impact on working memory and executive functions in rodents, monkeys, and humans, making them unable to processing information selectively and impairing cognitive function. Therefore, an exact understanding of these mechanisms may provide important insights into the pathophysiology of executive dysfunction and novel treatment avenues. The present review provides a summary of the neuronal circuitry involved in alterations of PFC dopaminergic neurons under conditions of stress, and then addresses the interaction of PFC DA with glucocorticoids leading to impairment of working memory under conditions of stress.