We describe a simple method to control the size of Pt nanoparticles with the use of an alcohol reduction. They then are assembled on the electrode by an electrophoretic deposition. The mean diameter of monodispersed Pt nanoparticles can be controlled from 19 to 33 Å in one-step reaction by changing the kind and/or the concentration of alcohol in water and the amount of protective polymer, poly(N-vinyl-2-pyrrolidone) (PVP). The monodispersed Pt nanoparticles of smaller diameter are obtained in the order of methanol > ethanol > 1-propanol, indicating that a faster reduction rate of [PtCl6]2- ions is an important factor to produce the smaller particles. The particle diameter decreases linearly with concentration of alcohol in water. Furthermore, increasing the amount of PVP makes the size of Pt nanoparticles smaller, the size distribution remaining quite narrow. By the combination of the one-step reaction with the stepwise growth reaction, Pt nanoparticles of arbitrary diameter in the range 19−50 Å can be obtained. The Pt nanoparticles obtained here have fcc structures such as bulk Pt. By using an electrophoretic deposition, more Pt nanoparticles move toward the anode with the increase of both the applied voltage and the electrophoretic time to form the Pt nanoparticle monolayer. Using the high concentration of Pt dispersion is effective to form the Pt nanoparticle monolayer.

Schizophrenia and other neuropsychiatric disorders await mechanism-associated interventions. Excess oxidative stress is increasingly appreciated to participate in the pathophysiology of brain disorders, and decreases in the major antioxidant, glutathione (GSH), have been reported in multiple studies. Technical cautions regarding the estimation of oxidative stress-related changes in the brain via imaging techniques have led investigators to explore peripheral GSH as a possible pathological signature of oxidative stress-associated brain changes. In a preclinical model of GSH deficiency, we found a correlation between whole brain and peripheral GSH levels. We found that the naturally occurring isothiocyanate sulforaphane increased blood GSH levels in healthy human subjects following 7 days of daily oral administration. In parallel, we explored the potential influence of sulforaphane on brain GSH levels in the anterior cingulate cortex, hippocampus, and thalamus via 7-T magnetic resonance spectroscopy. A significant positive correlation between blood and thalamic GSH post- and pre-sulforaphane treatment ratios was observed, in addition to a consistent increase in brain GSH levels in response to treatment. This clinical pilot study suggests the value of exploring relationships between peripheral GSH and clinical/neuropsychological measures, as well as the influences sulforaphane has on functional measures that are altered in neuropsychiatric disorders.

No abstract