We have prepared three kinds of Co-Sn intermetallic compounds, i.e., Co 3 Sn 2 , CoSn, and CoSn 2 , by mechanical alloying followed by heat-treatment. The results of ex situ X-ray diffraction analysis and charge/discharge tests indicate that the electrochemical reaction of lithium with crystalline intermetallic CoSn 2 results in the formation of Li-rich tin phase ͑Li 4.4 Sn͒, whereas the crystalline Co 3 Sn 2 and CoSn alloys only partly form Li x Sn. All three alloys in the low-crystalline obtained by further mechanical milling show improved capacity. Co 3 Sn 2 shows the best cycling performance among the three alloys, but delivers small capacity. The cycling ability of CoSn 2 was also improved by partly introducing Co and C into the alloy.Lithium-ion batteries based on a carbon/graphite anode and a transition metal-oxide cathode have been commercially used in popular portable devices such as cell phones and laptop computers for ϳ15 years. One of the most interesting and challenging goals is to develop increased capacity electrode materials in order to increase the battery energy density. The conventional anode material, graphite, has a theoretical maximum capacity of 372 mAh/g, or a volumetric capacity of 818 Ah/L ͑the density of graphite is 2.2 g/cm 3 ͒. Metals and alloys present an attractive alternative to graphite as anode materials for lithium-ion batteries due in particular to the high capacity, an acceptable rate capability, and operating potentials well above the potential of metallic lithium. For example, Sn yields a maximum theoretical capacity of 990 mAh/g or 7200 Ah/L. One major problem preventing them from the commercial application is that they undergo large volume changes during cycling, which result in disintegration of the electrodes and subsequent rapid capacity fading.This problem has been solved by the tin oxide glass materials invented by the Fuji company. 1 The new Fuji anode was claimed to have both volumetric and gravimetric capacity advantages over graphite of four and two times, respectively. It was reported that the key reasons for the success of the Fuji materials are finely dispersed tin regions which are responsible for the reversible reaction with Li, and the Li 2 O and other oxides playing the role of a "matrix-glue" to hold the particles together. 2 However, the Sn oxide-based anode has a large irreversible capacity resulting from the Li, which reacts with the oxygen bonded to Sn to form Li 2 O. An interesting approach to overcoming these problems is the use of the intermetallic compound, MЈM, which consisting of an "inactive phase MЈ," which does not react with lithium, and "active phase M," which reacts with lithium, these intermetallic compounds include Cu 6 Sn 5 alloy, [3][4][5] Ni-Sn alloys, 6,7 Sn-Fe͑-C͒ system, 8 and Sn-Mn-C system. 9 For these alloys, lithium intercalation into alloy yields a lithium alloy ͑Li x MЈSn͒ or the mixed phase of lithium-tin alloys ͑Li 4.4 Sn͒ and nano-sized metal ͑MЈ͒ by controlling the discharge depth. The role of "inactive phase MЈ" is mainly...
Background Neuronal pyroptosis and neuroinflammation with excess microglial activation are widely involved in the early pathological process of ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS), as a non-invasive neuromodulatory technique, has recently been reported to be anti-inflammatory and regulate microglial function. However, few studies have elucidated the role and mechanism of rTMS underlying regulating neuronal pyroptosis and microglial polarization. Methods We evaluated the motor function in middle cerebral artery occlusion/reperfusion (MCAO/r) injury mice after 1-week intermittent theta-burst rTMS (iTBS) treatment in the early phase with or without depletion of microglia by colony-stimulating factor 1 receptor (CSF1R) inhibitor treatment, respectively. We further explored the morphological and molecular biological alterations associated with neuronal pyroptosis and microglial polarization via Nissl, EdU, TTC, TUNEL staining, electron microscopy, multiplex cytokine bioassays, western blot assays, immunofluorescence staining and RNA sequencing. Results ITBS significantly protected against cerebral ischemia/reperfusion (I/R) injury-induced locomotor deficits and neuronal damage, which probably relied on the regulation of innate immune and inflammatory responses, as evidenced by RNA sequencing analysis. The peak of pyroptosis was confirmed to be later than that of apoptosis during the early phase of stroke, and pyroptosis was mainly located and more severe in the peri-infarcted area compared with apoptosis. Multiplex cytokine bioassays showed that iTBS significantly ameliorated the high levels of IL-1β, IL-17A, TNF-α, IFN-γ in MCAO/r group and elevated the level of IL-10. ITBS inhibited the expression of neuronal pyroptosis-associated proteins (i.e., Caspase1, IL-1β, IL-18, ASC, GSDMD, NLRP1) in the peri-infarcted area rather than at the border of infarcted core. KEGG enrichment analysis and further studies demonstrated that iTBS significantly shifted the microglial M1/M2 phenotype balance by curbing proinflammatory M1 activation (Iba1+/CD86+) and enhancing the anti-inflammatory M2 activation (Iba1+/CD206+) in peri-infarcted area via inhibiting TLR4/NFκB/NLRP3 signaling pathway. Depletion of microglia using CSF1R inhibitor (PLX3397) eliminated the motor functional improvements after iTBS treatment. Conclusions rTMS could alleviate cerebral I/R injury induced locomotor deficits and neuronal pyroptosis by modulating the microglial polarization. It is expected that these data will provide novel insights into the mechanisms of rTMS protecting against cerebral I/R injury and potential targets underlying neuronal pyroptosis in the early phase of stroke.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.