38 research outputs found

    Tungsten Nanoparticles Accelerate Polysulfides Conversion: A Viable Route toward Stable Room-Temperature Sodium–Sulfur Batteries

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    Room-temperature sodium–sulfur (RT Na–S) batteries are arousing great interest in recent years. Their practical applications, however, are hindered by several intrinsic problems, such as the sluggish kinetic, shuttle effect, and the incomplete conversion of sodium polysulfides (NaPSs). Here a sulfur host material that is based on tungsten nanoparticles embedded in nitrogen-doped graphene is reported. The incorporation of tungsten nanoparticles significantly accelerates the polysulfides conversion (especially the reduction of Na2S4 to Na2S, which contributes to 75% of the full capacity) and completely suppresses the shuttle effect, en route to a fully reversible reaction of NaPSs. With a host weight ratio of only 9.1% (about 3–6 times lower than that in recent reports), the cathode shows unprecedented electrochemical performances even at high sulfur mass loadings. The experimental findings, which are corroborated by the first-principles calculations, highlight the so far unexplored role of tungsten nanoparticles in sulfur hosts, thus pointing to a viable route toward stable Na–S batteries at room temperatures

    Shrinkage mechanism of red clay based on changes in the thickness of bound water film

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    Objective The content and existence form of bound water have an important influence on the physical and mechanical properties of red clay, and macroscopic shrinkage of red clay leads to microstructure changes of soil particles, pores and bound water, which in turn may cause soil surface cracking, triggering infiltration, destabilization, and other engineering geological problems. Methods Thermogravimetric analysis tests, BET tests, scanning electron microscopy (SEM) and zeta potential tests were conducted to study the variation characteristics of bound water during the shrinkage of undisturbed red clay. The structural model of spherical and lamellar clay particles based on the uniform distribution of bound water film was established, and the formula for the calculation of bound water film thickness was derived. Results The results showed that most of the water in undisturbed red clay exists in the form of bound water and the loss of weakly-bounded water continues throughout the shrinkage process of red clay. During the process, the zeta potential, specific surface area and the thickness of the bound water film decreased continuously. Conclusion The results reveal the intrinsic mechanism of water loss and shrinkage of red clay, which can provide theoretical support for solving environmental engineering geological problems

    Mitochondrion-Targeted Peptide SS-31 Inhibited Oxidized Low-Density Lipoproteins-Induced Foam Cell Formation through both ROS Scavenging and Inhibition of Cholesterol Influx in RAW264.7 Cells

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    Foam cell formation as a result of imbalance of modified cholesterol influx and efflux by macrophages is a key to the occurrence and development of atherosclerosis. Oxidative stress is thought to be involved in the pathogenesis of atherosclerosis. SS-31 is a member of the Szeto-Schiller (SS) peptides shown to specifically target the inner mitochondrial membrane to scavenge reactive oxygen species. In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells. The results showed that SS-31 inhibited oxidized low-density lipoproteins (ox-LDL)-induced foam cell formation and cholesterol accumulation, demonstrated by intracellular oil red O staining and measurement of cholesterol content. The mechanism was revealed that SS-31 did not only significantly attenuated ox-LDL-induced generation of reactive oxygen species (ROS) and increased the activities of superoxide dismutases, but also dose-dependently inhibited the expression of CD36 and LOX-1, two scavenger receptors of ox-LDL, while the expression of ATP-binding cassette A1 and G1, playing a pivotal role in cholesterol efflux, was not affected. As a result, SS-31 decreased pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha, suggesting the prevention of inflammatory responses. In conclusion, our results demonstrate that SS-31 provides a beneficial effect on macrophages from foam cell formation, likely, through both ROS scavenging and inhibition of cholesterol influx. Therefore, SS-31 may potentially be of therapeutic relevance in prevention of human atherogenesis

    A Mitochondrion-Targeted Antioxidant Ameliorates Isoflurane-Induced Cognitive Deficits in Aging Mice.

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    Isoflurane possesses neurotoxicity and can induce cognitive deficits, particularly in aging mammals. Mitochondrial reactive oxygen species (mtROS) have been linked to the early pathogenesis of this disorder. However, the role of mtROS remains to be evaluated due to a lack of targeted method to treat mtROS. Here, we determined in aging mice the effects of the mitochondrion-targeted antioxidant SS-31, on cognitive deficits induced by isoflurane, a general inhalation anesthetic. We further investigated the possible mechanisms underlying the effects of SS-31 on hippocampal neuro-inflammation and apoptosis. The results showed that isoflurane induced hippocampus-dependent memory deficit, which was associated with mitochondrial dysfunction including reduced ATP contents, increased ROS levels, and mitochondrial swelling. Treatment with SS-31 significantly ameliorated isoflurane-induced cognitive deficits through the improvement of mitochondrial integrity and function. Mechanistically, SS-31 treatment suppressed pro-inflammatory responses by decreasing the levels of NF-κB, NLRP3, caspase 1, IL-1β, and TNF-α; and inhibited the apoptotic pathway by decreasing the Bax/Bcl-2 ratio, reducing the release of cytochrome C, and blocking the cleavage of caspase 3. Our results indicate that isoflurane-induced cognitive deficits may be attenuated by mitochondrion-targeted antioxidants, such as SS-31. Therefore, SS-31 may have therapeutic potentials in preventing injuries from oxidative stresses that contribute to anesthetic-induced neurotoxicity

    Dissecting Nucleosome Function with a Comprehensive Histone H2A and H2B Mutant Library

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    Using a comprehensive library of histone H2A and H2B mutants, we assessed the biological function of each amino acid residue involved in various stress conditions including exposure to different DNA damage-inducing reagents, different growth temperatures, and other chemicals. H2B N- and H2A C-termini were critical for maintaining nucleosome function and mutations in these regions led to pleiotropic phenotypes. Additionally, two screens were performed using this library, monitoring heterochromatin gene silencing and genome stability, to identify residues that could compromise normal function when mutated. Many distinctive regions within the nucleosome were revealed. Furthermore, we used the barcode sequencing (bar-seq) method to profile the mutant composition of many libraries in one high-throughput sequencing experiment, greatly reducing the labor and increasing the capacity. This study not only demonstrates the applications of the versatile histone library, but also reveals many previously unknown functions of histone H2A and H2B
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