Combined Electrochemical, XPS, and STXM Study of Lithium Nitride as a Protective Coating for Lithium Metal and Lithium-Sulfur Batteries.

Li3N is an excellent protective coating material for lithium electrodes with very high lithium-ion conductivity and low electronic conductivity, but the formation of stable and homogeneous coatings is technically very difficult. Here, we show that protective Li3N coatings can be simply formed by the direct reaction of electrodeposited lithium electrodes with N2 gas, whereas using battery-grade lithium foil is problematic due to the presence of a native passivation layer that hampers that reaction. The protective Li3N coating is effective at preventing lithium dendrite formation, as found from unidirectional plating and plating-stripping measurements in Li-Li cells. The Li3N coating also efficiently suppresses the parasitic reactions of polysulfides and other electrolyte species with the lithium electrode, as demonstrated by scanning transmission X-ray microscopy, X-ray photoelectron spectroscopy, and optical microscopy. The protection of the lithium electrode against corrosion by polysulfides and other electrolyte species, as well as the promotion of smooth deposits without dendrites, makes the Li3N coating highly promising for applications in lithium metal batteries, such as lithium-sulfur batteries. The present findings show that the formation of Li3N can be achieved with lithium electrodes covered by a secondary electrolyte interface layer, which proves that the in situ formation of Li3N coatings inside the batteries is attainable.

LiFePO4 Battery Material for the Production of Lithium from Brines: Effect of Brine Composition and Benefits of Dilution.

Lithium battery materials can be advantageously used for the selective sequestration of lithium ions from natural resources, which contain other cations in high excess. However, for practical applications, this new approach for lithium production requires the battery host materials to be stable over many cycles while retaining the high lithium selectivity. Here, a nearly symmetrical cell design was employed to show that LiFePO4 shows good capacity retention with cycling in artificial lithium brines representative of brines from Chile, Bolivia and Argentina. A quantitative correlation was identified between brine viscosity and capacity degradation, and for the first time it was demonstrated that the dilution of viscous brines with water significantly enhanced capacity retention and rate capability. The electrochemical and X-ray diffraction characterisation of the cycled electrodes also showed that the high lithium selectivity was preserved with cycling. Raman spectra of the cycled electrodes showed no signs of degradation of the carbon coating of LiFePO4 , while scanning electron microscopy images showed signs of particle cracking, thus pointing towards interfacial reactions as the cause of capacity degradation.

Pressure-Tuneable Visible-Range Band Gap in the Ionic Spinel Tin Nitride.

The application of pressure allows systematic tuning of the charge density of a material cleanly, that is, without changes to the chemical composition via dopants, and exploratory high-pressure experiments can inform the design of bulk syntheses of materials that benefit from their properties under compression. The electronic and structural response of semiconducting tin nitride Sn3 N4 under compression is now reported. A continuous opening of the optical band gap was observed from 1.3 eV to 3.0 eV over a range of 100 GPa, a 540 nm blue-shift spanning the entire visible spectrum. The pressure-mediated band gap opening is general to this material across numerous high-density polymorphs, implicating the predominant ionic bonding in the material as the cause. The rate of decompression to ambient conditions permits access to recoverable metastable states with varying band gaps energies, opening the possibility of pressure-tuneable electronic properties for future applications.

Raf-1 activation stimulates proliferation and inhibits IGF-stimulated differentiation in L6A1 myoblasts.

Our previous work has demonstrated that the insulin-like growth factors (IGFs), acting through a single receptor, stimulate both proliferation and differentiation of L6A1 myoblasts. This unique model system has enabled us to closely examine the switch that regulates these two opposing responses. We have previously shown, using specific inhibitors of the IGF-I signal transduction pathway, that the mitogenic response is mediated by the Ras/Raf/MAP kinase pathway and the myogenic response by the PI 3-kinase/p70s6k pathway (Coolican SA, Samuel DS, Ewton DZ, McWade FJ, Florini JR, J Biol Chem 1997; 272: 6653-62). In that study we found that PD098059, an inhibitor of MEK activation, inhibited the proliferative response, but dramatically enhanced IGF-stimulated differentiation which was associated with elevation of p70s6k activity. Since there have been reports of elevation of Raf-1 activity in PD098059-treated L6 myoblasts, and stimulation of p70s6k activity in cells expressing an activated Raf-1, it was important to determine whether or not Raf-1 elevation plays a role in the myogenic response. To test this, we have transfected L6A1 myoblasts with delta Raf-1:ER, an estradiol-regulated form of oncogenic Raf-1. We found that activation of Raf-1 by estradiol resulted in increased phosphorylation of p42 and p44 MAP kinases and stimulation of proliferation. In contrast, Raf-1 activation inhibited all measured aspects of the myogenic response: myogenin expression, creatine kinase elevation, and fusion of myoblasts to form myotubes. In addition, we found no elevation of p70s6k activity upon Raf-1 activation. These results indicate the following: (1) stimulation of myogenic differentiation by PD098059 treatment is not simply due to the elevation of Raf-1, (2) Raf-1 has a positive role in the MAP kinase pathway and myoblast proliferation, and (3) Raf-1 activation inhibits myogenesis, possibly by forcing cells to remain in the proliferative state.

The mitogenic and myogenic actions of insulin-like growth factors utilize distinct signaling pathways.

It is well established that mitogens inhibit differentiation of skeletal muscle cells, but the insulin-like growth factors (IGFs), acting through a single receptor, stimulate both proliferation and differentiation of myoblasts. Although the IGF-I mitogenic signaling pathway has been extensively studied in other cell types, little is known about the signaling pathway leading to differentiation in skeletal muscle. By using specific inhibitors of the IGF signal transduction pathway, we have begun to define the signaling intermediates mediating the two responses to IGFs. We found that PD098059, an inhibitor of mitogen-activated protein (MAP) kinase kinase activation, inhibited IGF-stimulated proliferation of L6A1 myoblasts and the events associated with it, such as phosphorylation of the MAP kinases and elevation of c-fos mRNA and cyclin D protein. Surprisingly, PD098059 caused a dramatic enhancement of differentiation, evident both at a morphological (fusion of myoblasts into myotubes) and biochemical level (elevation of myogenin and p21 cyclin-dependent kinase inhibitor expression, as well as creatine kinase activity). In sharp contrast, LY294002, an inhibitor of phosphatidylinositol 3-kinase, and rapamycin, an inhibitor of the activation of p70 S6 kinase (p70(S6k)), completely abolished IGF stimulation of L6A1 differentiation. We found that p70(S6k) activity increased substantially during differentiation, and this increase was further enhanced by PD098059. Our results demonstrate that the MAP kinase pathway plays a primary role in the mitogenic response and is inhibitory to the myogenic response in L6A1 myoblasts, while activation of the phosphatidylinositol 3-kinase/p70(S6k) pathway is essential for IGF-stimulated differentiation. Thus, it appears that signaling from the IGF-I receptor utilizes two distinct pathways leading either to proliferation or differentiation.

Stimulation of myogenic differentiation by a neuregulin, glial growth factor 2. Are neuregulins the long-sought muscle trophic factors secreted by nerves?

It has long been known that nerves stimulate growth and maintenance of skeletal muscles in ways not dependent on physical contacts, but numerous attempts to identify and characterize the myotrophic agent(s) secreted by nerves have been unsuccessful. We here suggest that products of the neuregulin gene may be these agents. The neuregulins are a family of proteins made by alternative splicing of a single transcript to give as many as 15 protein products. One member of this family, glial growth factor 2 (rhGGF2) is a very potent stimulator of myogenesis in L6A1 myoblasts, giving a maximal stimulation of cell fusion and creatine kinase elevation at a concentration of 1 ng/ml (18 pM). The stimulation of myogenesis is not rapid, but it is prolonged, continuing over a period of at least 6 days. The effects of rhGGF2 are additive with those of insulin-like growth factor I (IGF-I) or its analog R3-IGF-I, suggesting that the actions of these two myotrophic agents differ in at least one rate-limiting step. We have observed one possible difference; unlike the IGFs, rhGGF2 does not induce elevation of the steady state level of myogenin mRNA.

Isolation of the rat F1-ATPase inhibitor gene and its pseudogenes.

Multiple mitochondrial ATPase inhibitor genes have been identified in the rat-genome. The sequences of two genomic clones indicate that one encodes the functional gene, and the other is a processed pseudogene. The ATPase inhibitor gene isolated is about 1.5 kb long and the coding region contains three exons and two introns. The presence of multiple pseudogenes in the rat is suggested by this study and this is unique since in the bovine genome only a single gene has been found, which is also confirmed here. The presence of multiple inhibitor transcripts in the rat suggests that the functional gene might have multiple transcriptional start sites.