Preparation of Mullite-Silica Composites Using Silica-Rich Monophasic Precursor Obtained as a Byproduct of Mineral Carbonation of Blast-Furnace Slag

Previously, mineral carbonation of blast-furnace slag was carried out to sequestrate CO2 and attain pure CaCO3 crystals. In this process, amorphous silica-alumina nanoparticles were obtained as a byproduct. In this study, the crystallization of these nanoparticles on calcination at various temperatures in air was examined using TGA-DTA, XRD, MAS-NMR spectroscopy, and FT-IR spectroscopy. The precursor nanoparticles (Si:Al = 78:22 mol %) were prepared using the solution extracted from blast-furnace slag (BFS) with acetic acid at room temperature. The XRD analysis showed that the initial amorphous state was retained up to 800 °C, and decomposition to amorphous silica and mullite started after calcination at 950 °C. At temperatures between 1150 °C and 1250 °C, amorphous silica crystalized to cristobalite, which eventually melted to glassy silica at 1500 °C. The mullite crystals initially adopted a metastable tetragonal phase and transformed to a stable, needle-like orthorhombic phase at higher temperatures. 27Al MAS-NMR spectroscopy revealed that octahedrally coordinated Al was favored up to a temperature of 800 °C as a result of the dehydration process and transformed into tetrahedrally coordinated Al at higher temperatures. A microstructural examination revealed that the initially randomly-oriented mullite developed into stable, needle-like grains owing to anisotropic grain growth in the presence of a glass phase at high temperatures. This study suggests that the recycling of BFS can be exploited for the procurement of a mullite-type ceramic material

The Effect of Phases in Nanoparticles Produced by Electrical Wire Explosion on Arsenic(III) Removal

Nano-sized iron oxide particles were prepared by electrical wire explosion (EWE) for As(III) removal. The electrical explosion of Fe wire in Ar5%O 2 , Ar10%O 2 , and Ar30%O 2 produced a wide spectrum of ironoxide phases from wüstite to hematite depending on the oxygen partial pressure in the chamber. An increase in oxygen partial pressure tended to shift the iron oxides towards higher oxidation states. The major phase of the explosion product was verified as the magnetite (Fe 3 O 4 )maghemite (£-Fe 2 O 3 ) mixture through the step scan o

Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection

Histone deacetylase (HDAC) inhibitors are currently in human clinical trials as antitumor drugs because of their ability to induce cell dysfunction and death in cancer cells. The toxic effects of HDAC inhibitors are also apparent in cortical neurons in vitro, despite the ability of these agents to induce significant protection in the cells they do not kill. Here we demonstrate that pulse exposure of cortical neurons (2 h) in an in vitro model of oxidative stress results in durable neuroprotection without toxicity. Protection was associated with transcriptional upregulation of the cell cycle inhibitor, p21(waf1/cip1), both in this model and in an in vivo model of permanent ischemia. Transgenic overexpression of p21(waf1/cip1) in neurons can mimic the protective effect of HDAC inhibitors against oxidative stress-induced toxicity, including death induced by glutathione depletion or peroxide addition. The protective effect of p21(waf1/cip1) in the context of oxidative stress appears to be unrelated to its ability to act in the nucleus to inhibit cell cycle progression. However, although p21(waf1/cip1) is sufficient for neuroprotection, it is not necessary for HDAC inhibitor neuroprotection, because these agents can completely protect neurons cultured from p21(waf1/cip1)-null mice. Together these findings demonstrate (1) that pulse inhibition of HDACs in cortical neurons can induce neuroprotection without apparent toxicity; (2) that p21(waf1/cip1) is sufficient but not necessary to mimic the protective effects of HDAC inhibition; and (3) that oxidative stress in this model induces neuronal cell death via cell cycle-independent pathways that can be inhibited by a cytosolic, noncanonical action of p21(waf1/cip1)

Quantum-centric Supercomputing for Materials Science: A Perspective on Challenges and Future Directions

Computational models are an essential tool for the design, characterization, and discovery of novel materials. Hard computational tasks in materials science stretch the limits of existing high-performance supercomputing centers, consuming much of their simulation, analysis, and data resources. Quantum computing, on the other hand, is an emerging technology with the potential to accelerate many of the computational tasks needed for materials science. In order to do that, the quantum technology must interact with conventional high-performance computing in several ways: approximate results validation, identification of hard problems, and synergies in quantum-centric supercomputing. In this paper, we provide a perspective on how quantum-centric supercomputing can help address critical computational problems in materials science, the challenges to face in order to solve representative use cases, and new suggested directions