Mitigating environmental impact by development of ambient-cured EAF slag and fly ash blended geopolymer via mix design optimization.

This article discusses the utilization of industrial by-products, namely, electric arc furnace slag (EAFS) and fly ash to produce cementless geopolymer binder. Taguchi-grey optimization is used for experimental design and for investigating the effects of mix design parameters. Fly ash, in the levels of 0-75% (by mass), partly replaced EAFS in the binary-blended composite system. Experiments were performed on the microstructural development, mechanical properties, and durability of ambient-cured EAFS-fly ash geopolymer paste (EFGP). The optimal mix with 75-25% composition of EAFS and fly ash produced ~ 39 MPa compressive strength accrediting to the co-existence of C-A-S-H and N-A-S-H gels. The initial and final setting times were 127 min and 581 min, respectively, owing to adequate alkali and amorphous contents in the matrix, and the flowability was 108% due to sufficient activator content and the spherical shape of fly ash particles. SEM, XRD, and FTIR results corroborated the mechanical test results.

Ecofriendly Microencapsulated Phase-Change Materials with Hybrid Core Materials for Thermal Energy Storage and Flame Retardancy.

Microencapsulated phase-change material (ME-PCM) employing octadecane as a core material has been practiced for thermal-energy-storage (TES) applications in buildings. However, octadecane as a hydrocarbon-based PCM is flammable. Herein, silica-shelled microcapsules (SiO2-MCs) and poly(urea-formaldehyde)-shelled microcapsules (PUF-MCs) were successfully prepared, loaded with octadecane/tributyl phosphate (TBP) as hybrid core materials, which not only exhibited good TES properties but also high-effective flame retardancy. SiO2-MC (ΔHm = 124.6 J g-1 and ΔHc = 124.1 J g-1) showed weaker TES capacity than PUF-MC (ΔHm = 186.8 J g-1, ΔHc = 188.5 J g-1) but better flame retardancy with a lower peak heat-release rate (HRRpeak) of 460.9 W g-1 (556.9 W g-1 for PUF-MCs). As compared with octadecane (38.7 kJ g-1), the reduction in total heat release (THR) for SiO2-MC was up to 22% (30.1 kJ g-1) with combustion time shortened by 1/6. SiO2-MC had a typical diameter of 150-210 µm, shell thickness of ∼6.5 µm, and a core fraction of 84 wt %. SiO2-MC showed better thermal stability with a higher initial evaporation/pyrolysis temperature than PUF-MC. The thermal decomposition of MCs with its mechanism of flame retardancy was significantly studied using thermogravimetric analysis/infrared spectrometry (TG-IR). The strategy presented in this study should inspire the development of microcapsules with PCMs/flame retardants as hybrid core materials for structural applications.

Review of leaching behavior of municipal solid waste incineration (MSWI) ash.

Incineration is widely adopted in modern waste management because it provides an effective way to minimize municipal solid waste that needs to be disposed of in landfills. The ash residue is often disposed by landfilling. Alternatively, the incineration ash may be recycled and reused for various applications. The crucial issues, however, are the leaching of harmful elements during the use and the end-of-life phases. This review summarizes extensive studies on leaching behavior of municipal solid waste incineration ash. Specifically, pollutants generated through leaching, factors governing leaching, methodologies to study leaching, leaching mechanisms, and treatments to reduce leaching. Many types of pollutants are generated through leaching from municipal solid waste incineration ash, in which heavy metals and organic contaminants are the most toxic and concerned. Ash properties, pH and liquid to solid ratio are the main factors governing municipal solid waste incineration ash leaching. Leaching behavior of municipal solid waste incineration ash is complicated and existing methods to evaluate leaching may not be able to represent the field conditions. Solubility and sorption are the two major leaching mechanisms. Many treatment methods have been proposed. However, not all methods are effective and some approaches are associated with high energy and high cost, which makes them less economically feasible and attractive.

Humic acid-induced formation of tobermorite upon hydrothermal treatment with municipal solid waste incineration bottom ash and its application for efficient removal of Cu(II) ions.

In this study, conversion of municipal solid waste incineration bottom ash (IBA) into highly efficient sorbents for Cu(II) removal was reported. The formation of tobermorite induced by humic acid (HA) and IBA under hydrothermal condition was explored and its potential application for efficient removal of Cu(II) ions was further investigated. After hydrothermal treatment, the morphology and microstructure of IBA remarkably changed from sheet-like to particle-like, thereby resulting in substantial increases of sorption capacity. The synthesized tobermorite exhibited a strongly enhanced sorption performance toward Cu(II), which was 270.3 mg g-1 and higher than other reported sorbents. The adsorption behaviors were subsequently examined by isotherm and kinetic studies. Langmuir model was found to describe the adsorption process well, suggesting that the adsorption was chemisorption in nature. Therefore, the hydrothermally synthesized tobermorite may be used as sorbents to remove Cu(II). Conversion of IBA into valuable minerals recovers waste into potential resources and alleviates the needs for ash disposal.

Controllable mullite bismuth ferrite micro/nanostructures with multifarious catalytic activities for switchable/hybrid catalytic degradation processes.

In this work, controllable preparation of micro/nanostructured bismuth ferrites (BFOs) were used to investigate multifarious heterogeneous catalyses, including Fenton/Fenton-like reaction, photocatalysis, photo-Fenton oxidation, and peroxymonosulfate (PMS) activation. Results showed that BFO can be used asa novel catalyst to activate switchable catalytic degradation of organic matters. Additionally, a novel catalytic system for degradation of organic pollutants, which integrating all-above heterogeneous catalyses is denoted as BFO/H2O2/PMS hybrid reaction, is introduced for the first time. BFO/H2O2/PMS system effectively degraded>99% for both methyl orange (MO) and sulfamethoxazole (SMX) within 60min, which shows better efficiency than above BFO-driven catalyses. The major SMX degradation pathway in BFO/H2O2/PMS system is proposed via detecting intermediates using LC/MS/MS. It was found that catalytic activities of BFOs are in the order of BFO-L (co-precipitation, micro/nanosize, single crystals exposing facet (001))>BFO-H (hydrothermal, nanocluster with a higher surface area than other BFOs)>BFO-C (fabricated using calcination process, microsize), which demonstrated that crystallographic orientation is more significant in heterogeneous catalyses than specific surface area at micro/nanoscale. Besides, the required H2O2 consumption for achieving 99% TOC removal was identified in BFO-driven photo-Fenton oxidation. The other effects on degradation efficiency, such as H2O2 dosage and pH, were investigated as well. In Fenton/Fenton-like reaction, reaction conditions suggested are ∼61.5mM H2O2 dosage and pH≥4.5 to avoid quenching of HO into HO2 by excessive H2O2 and Fe leaching.

Inducible nitric oxide synthase and estradiol exhibit complementary neuroprotective roles after ischemic brain injury.

Estradiol-17beta exerts profound neuroprotective actions following cerebral ischemia through multiple molecular mechanisms. To examine the putative anti-inflammatory mechanisms employed by estradiol during stroke, we explored the interactions between estradiol and inducible nitric oxide synthase (iNOS) in both wildtype and iNOS knockout (iNOSKO) female mice following permanent middle cerebral artery occlusion (MCAO). Female mice were ovariectomized and treated with estradiol. One week later, they were subjected to MCAO, and then killed 24 h later. Analysis of total, cortical and striatal infarct volumes confirmed that estradiol is neuroprotective in wildtype mice. Infarct volumes were also significantly smaller in female iNOSKO female mice, but estradiol did not further decrease injury. We found that one mechanism by which estradiol may act is by decreasing nitric oxide synthase 2 gene expression in the cortex and in the striatum of wildtype mice. These results show that the pro-inflammatory actions of iNOS exacerbate stroke-induced injury within the cortex and striatum, and that iNOS deletion is neuroprotective in ovariectomized and estrogen-replaced female mice.

Timing of estrogen therapy after ovariectomy dictates the efficacy of its neuroprotective and antiinflammatory actions.

Recent studies describing the seemingly contradictory actions of estrogens in ischemic stroke injury have led us to reevaluate the circumstances under which estrogen therapy (ET) provides benefits against cerebral stroke and decipher its mechanisms of action. One prominent feature that follows stroke injury is massive central and peripheral inflammatory responses. Evidence now suggests that postischemic inflammatory responses strongly contribute to the extent of brain injury, and 17beta-estradiol (E(2)) may protect the ischemic brain by exerting antiinflammatory actions. In an attempt to explain recently reported dichotomous effects of E(2) in stroke injury, we tested the hypothesis that an extended period of hypoestrogenicity both prevents E(2) from protecting the brain against ischemia and simultaneously suppresses its antiinflammatory actions. We report that E(2) exerts profound neuroprotective action when administered immediately upon ovariectomy, but not when administered after 10 weeks of hypoestrogenicity. Consistently, E(2) treatment given immediately at the time of ovariectomy attenuated central and peripheral production of proinflammatory cytokines after ischemic stroke. In contrast, E(2) did not suppress production of proinflammatory molecules when it was administered after 10 weeks postovariectomy. These results demonstrate that a prolonged period of hypoestrogenicity disrupts both neuroprotective and antiinflammatory actions of E(2). Our findings may help to explain the results of the Women's Health initiative that reported no beneficial effect of ET against stroke because the majority of the subjects initiated ET after an extended period of hypoestrogenicity.

Estradiol enhances neurogenesis following ischemic stroke through estrogen receptors alpha and beta.

Neurogenesis persists throughout life under normal and degenerative conditions. The adult subventricular zone (SVZ) generates neural stem cells capable of differentiating to neuroblasts and migrating to the site of injury in response to brain insults. In the present study, we investigated whether estradiol increases neurogenesis in the SVZ in an animal model of stroke to potentially promote the ability of the brain to undergo repair. Ovariectomized C57BL/6J mice were implanted with capsules containing either vehicle or 17beta-estradiol, and 1 week later they underwent experimental ischemia. We utilized double-label immunocytochemistry to identify the phenotype of newborn cells (5-bromo-2'-deoxyuridine-labeled) with various cellular markers; doublecortin and PSA-NCAM as the early neuronal marker, NeuN to identify mature neurons, and glial fibrillary acidic protein to identify astrocytes. We report that low physiological levels of estradiol treatment, which exert no effect in the uninjured state, significantly increase the number of newborn neurons in the SVZ following stroke injury. This effect of estradiol is limited to the dorsal region of the SVZ and is absent from the ventral SVZ. The proliferative actions of estradiol are confined to neuronal precursors and do not influence gliosis. Furthermore, we show that both estrogen receptors alpha and beta play pivotal functional roles, insofar as knocking out either of these receptors blocks the ability of estradiol to increase neurogenesis. These findings clearly demonstrate that estradiol stimulates neurogenesis in the adult SVZ, thus potentially facilitating the brain to remodel and repair after injury.