Fabrication of Graphene-Based TiO2@CeO2 and CeO2@TiO2 Core-Shell Heterostructures for Enhanced Photocatalytic Activity and Cytotoxicity.

Development of light-harvesting properties and inhibition of photogenerated charge carrier recombination are of paramount significance in the photocatalytic process. In the present work, we described the synthesis of core-shell heterostructures, which are composed of titanium oxide (TiO2) and cerium oxide (CeO2) deposited on a reduced graphene oxide (rGO) surface as a conductive substrate. Following the synthesis of ternary rGO-CeO2@TiO2 and rGO-TiO2@CeO2 nanostructures, their photocatalytic activity was investigated toward the degradation of rhodamine B dye as an organic pollutant under UV light irradiation. The obtained structures were characterized with high-resolution transmission electron microscopy, field-emission scanning electron microscopy, energy-dispersive X-ray spectroscopy, Fourier transform infrared spectroscopy, X-ray diffraction, Brunauer-Emmett-Teller, X-ray photoelectron spectroscopy surface analysis, and UV-Vis spectroscopy. Various parameters including pH, catalyst dosage, temperature, and contact time were studied for photocatalysis optimization. Heterostructures showed considerable advantages because of their high surface area and superior photocatalytic performance. In contrast, rGO-CeO2@TiO2 showed the highest photocatalytic activity, which is attributed to the more effective electron-hole separation and quick suppression of charge recombination at core-shell phases. A biological assay of the prepared heterostructure was performed to determine the cytotoxicity against breast cancer cells (MCF-7) and demonstrated a very low survival rate at 7.65% of cells at the 17.5 mg mL-1 concentration of applied photocatalyst.

What sequences on high-field MR best depict temporal resolution of experimental ICH and edema formation in mice?

BACKGROUND AND PURPOSE: Pilot study to examine the use of T1-, T2-, and T2*-weighted images for evaluating hematoma size and extent of edema in mouse brain at high field. METHODS: Following collagenase-induced intracerebral hemorrhage, nine mice were imaged at 4.7 T using T1-, T2-, and T2*-weighted images for hematoma and edema quantitation on days 1, 3, 10, and 21 after surgery. Values were compared with morphometric analysis of cryosections at the time of final MR imaging. RESULTS: For hematoma quantitation, the Spearman correlation coefficient (r) between T1 signal change and histology was 0.70 (P < 0.04) compared with r = 0.61 (P < 0.09) for T2*. The extent of perihematomal edema formation on cryosections was well reflected on T2 with r = 0.73 (P < 0.03). CONCLUSIONS: Within the limits of our pilot study, MR imaging on 4.7 T appears to approximate the temporal changes in hematoma and edema sizes in murine ICH well, thus laying the groundwork for longitudinal studies on hematoma resorption and edema formation.

Attenuation of morphine tolerance after antisense oligonucleotide knock-down of spinal mGluR1.

1. Chronic systemic treatment of rats with morphine leads to the development of opioid tolerance. This study was designed to examine the effects of intrathecal (i.t.) infusion of a metabotropic glutamate receptor 1 (mGluR1) antisense oligonucleotide, concomitant with chronic morphine treatment, on the development of tolerance to morphine's antinociceptive effects. 2. All rats received chronic (6 day) s.c. administration of morphine to induce opioid tolerance. Additionally, rats were treated with either mGluR1 antisense (AS), missense (MIS) or artificial cerebrospinal fluid (ACSF) by i.t. infusion via chronically implanted i.t. catheters connected to osmotic mini-pumps. The effects of acute i.t. or s.c. morphine on tail-flick latencies were assessed prior to and following chronic s.c. morphine treatment for all chronic i.t. infusion groups. mGluR1 protein level in the spinal cord was determined by Western blot analysis for all treatments, assessing the efficiency of knock-down with AS treatment. 3. Acute i.t. morphine dose-dependently produced antinociception in the tail-flick test in naïve rats. Systemic morphine-treated rats administered i.t. ACSF or MIS developed tolerance to i.t. morphine. Chronic i.t. infusion with mGluR1 AS significantly reduced the development of tolerance to i.t. morphine. 4. In contrast to i.t. morphine, tolerance developed to the antinociceptive effects of s.c. morphine, in all i.t. infusion groups, including the mGluR1 AS group. 5. The spinal mGluR1 protein level was dramatically decreased after mGluR1 AS infusion when compared to control animals (naïve and ACSF-treated animals). 6. These findings suggest that the spinal mGluR1 is involved in the development of tolerance to the antinociceptive effects of morphine. Selective blockade of mGluR1 may be beneficial in preventing the development of opioid analgesic tolerance.