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The redox reactions occurring in the Li-S battery positive electrode conceal various and critical electrocatalytic processes, which strongly influence the performances of this electrochemical energy storage system. Here, we report the development of a single-dispersed molecular cluster catalyst composite comprising of a polyoxometalate framework ([Co 4 (PW 9 O 34 ) 2 ] 10− ) and multilayer reduced graphene oxide. Due to the interfacial charge transfer and exposure of unsaturated cobalt sites, the composite demonstrates efficient polysulfides adsorption and reduced activation energy for polysulfides conversion, thus serving as a bifunctional electrocatalyst. When tested in full Li-S coin cell configuration, the composite allows for a long-term Li-S battery cycling with a capacity fading of 0.015% per cycle after 1000 cycles at 2 C (i.e., 3.36 A g −1 ). An areal capacity of 4.55 mAh cm −2 is also achieved with a sulfur loading of 5.6 mg cm − 2 and E/S ratio of 4.5 μL mg −1 . Moreover, Li-S single-electrode pouch cells tested with the bifunctional electrocatalyst demonstrate a specific capacity of about 800 mAh g −1 at a sulfur loading of 3.6 mg cm −2 for 100 cycles at 0.2 C (i.e., 336 mA g −1 ) with E/S ratio of 5 μL mg −1 . Efficient electrochemical energy storage in Li-S batteries is hindered by sluggish sulfur redox reactions. Here, the authors propose a polyoxometalate/multilayer graphene composite as a bifunctional electrocatalyst for battery performance improvement.

Dendrite growth of alkali metal anodes limited their lifetime for charge/discharge cycling. Here, we report near-perfect anodes of lithium, sodium, and potassium metals achieved by electrochemical polishing, which removes microscopic defects and creates ultra-smooth ultra-thin solid-electrolyte interphase layers at metal surfaces for providing a homogeneous environment. Precise characterizations by AFM force probing with corroborative in-depth XPS profile analysis reveal that the ultra-smooth ultra-thin solid-electrolyte interphase can be designed to have alternating inorganic-rich and organic-rich/mixed multi-layered structure, which offers mechanical property of coupled rigidity and elasticity. The polished metal anodes exhibit significantly enhanced cycling stability, specifically the lithium anodes can cycle for over 200 times at a real current density of 2 mA cm –2 with 100% depth of discharge. Our work illustrates that an ultra-smooth ultra-thin solid-electrolyte interphase may be robust enough to suppress dendrite growth and thus serve as an initial layer for further improved protection of alkali metal anodes. The dendrite growth of alkali metal anodes leads to charge/discharge cycling instability. Here, the authors show that electrochemical polishing can yield near-perfect anodes of three alkali metals by constructing smooth and thin solid-electrolyte interphase layers.

Sodium metal anodes combine low redox potential (−2.71 V versus SHE) and high theoretical capacity (1165 mAh g−1), becoming a promising anode material for sodium‐ion batteries. Due to the infinite volume change, unstable SEI films, and Na dendrite growth, it is arduous to achieve a long lifespan. Herein, an oxygen‐doped carbon foam (OCF) derived from starch is reported. Heteroatom doping can significantly reduce the nucleation resistance of sodium metal; combined with its rich pore structure and large specific surface area, OCF provides abundant nucleation sites to effectively guide the nucleation and subsequent growth of sodium metal, and the nature of this foam can accommodate the deposited sodium. Furthermore, a more uniform, robust, and stable SEI layer is observed on the surface of OCF electrode, so it can maintain ultra‐high reversibility and excellent integrity for a long time without dendritic growth. As a result, when the current density is 10 mA cm−2, the electrode can maintain stable 2000 cycles and the coulombic efficiency can reach to 99.83%. Na@OCF||Na3V2(PO4)3 full cell also has extremely high capacity retention of about 97.53% over 150 cycles. These results provide a simple but effective method for achieving the safety and commercialization of sodium metal anode. An O‐doped carbon foam with a sodiophilic surface is constructed and applied to the sodium metal anode. The excellent sodiophilic property, abundant porous structure, and large specific surface make the material stable during multiple plating/stripping processes, and no sodium dendrites are formed. Consequently, the sodium metal battery exhibits excellent electrochemical performance.

Ti-substituted LiMn2O4 (LiMn2-x Ti x O4, x=,0.1,0.3,0.4,0.60, and 0.75) has been synthesized using solid-state reactions. Their crystal and electronic structures were investigated using X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), and ultraviolet photoelectron spectroscopy (UPS). XRD data suggested that the lattice parameters of LiMn2-x Ti x O4 increase due to the replacement of Mn by Ti ions. XPS results indicated that the substituted Ti ions were in +4 oxidation state; consequently, the normal oxidation state of Mn ions has been detected by measuring the binding energy splitting of Mn 3s states, which decreases with the content of substituted Ti. The valence band spectra suggested that the intensity of e g level of Mn 3d orbitals increased due to the increase of the Mn/Mn ratio.

Ti-substituted LiMn 2 O 4 (LiMn 2− x Ti x O 4 , x =0, 0.15, 0.30, 0.45, 0.60, and 0.75) has been synthesized using solid-state reactions. Their crystal and electronic structures were investigated using X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), and ultraviolet photoelectron spectroscopy (UPS). XRD data suggested that the lattice parameters of LiMn 2− x Ti x O 4 increase due to the replacement of Mn by Ti ions. XPS results indicated that the substituted Ti ions were in +4 oxidation state; consequently, the normal oxidation state of Mn ions has been detected by measuring the binding energy splitting of Mn 3s states, which decreases with the content of substituted Ti. The valence band spectra suggested that the intensity of e g level of Mn 3d orbitals increased due to the increase of the Mn 3+ /Mn 4+ ratio.

Traumatic brain injury （TBI） is a major cause of disability and death in patients who experience a traumatic injury. Mitochondrial dysfunction is one of the main factors contributing to secondary injury in TBI-associated brain damage. Evidence of compromised mitochondrial function after TBI has been, but the molecular mechanisms underlying the pathogenesis of TBI are not well understood Silent information regulator family protein 1 （SlRT1）, a member of the NAD~-dependent protein deacetylases, has been shown to exhibit neuroprotective activities in animal models of various pathologies, including ischemic brain injury, subarachnoid hemorrhage and several neurodegenerative diseases. In this study, we investigated whether SIRT1 also exert neuroprotective effect post-TBI, and further explored the possible regulatory mechanisms involved in TBI pathogenesi6. A lateral fluid-percussion （LFP） brain injury model was established in rats to mimic the insults of TBI. The expression levels of SIRT1, p-p38, cleaved caspase-9 and cleaved easpase-3 were all markedly increased and reached a maximum at 12 h post-TBI. In addition, mitochondrial function was impaired, evidenced by the presence of swollen and irregularly shaped mitochondria with disrupted and poorly defined cristae, a relative increase of the percentage of neurons with low ALPm, the opening of mPTP, and a decrease in neuronal ATP content, especially at 12 h post- TBI. Pretreatment with the SIRT1 inhibitor sirtinol （10 mg/kg, ip） induced p-p38 activation, exacerbated mitochondrial damage, and promoted the activation of the mitochondrial apoptosis pathway. In contrast, pretreatment with the p38 inhibitor SB203580 （200 pg/kg, ip） significantly attenuated post-TBI-induced expression of both cleaved caspase-9 and cleaved caspase-3 and rnitochondrial damage, whereas it had no effects on SlRT1 expression. Together, these results reveal that the 12 h after TBI may be a crucial time at which secondary damage occurs; the activation of SIRT1 expression and inhibition of the p38 MAPK pathway may play a neuroprotective role in preventing secondary damage post-TBI. For this reason, both SIRT1 and p38 are likely to be important targets to prevent secondary damage post-TBI.