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      • Towards more thermally stable Li-ion battery electrolytes with salts and solvents sharing nitrile functionality

        Kerner, Manfred,Lim, Du-Hyun,Jeschke, Steffen,Rydholm, Tomas,Ahn, Jou-Hyeon,Scheers, Johan Elsevier 2016 Journal of Power Sources Vol.332 No.-

        <P><B>Abstract</B></P> <P>The overall safety of Li-ion batteries is compromised by the state-of-the-art electrolytes; the thermally unstable lithium salt, lithium hexafluorophosphate (LiPF<SUB>6</SUB>), and flammable carbonate solvent mixtures. The problem is best addressed by new electrolyte compositions with thermally robust salts in low flammability solvents. In this work we introduce electrolytes with either of two lithium nitrile salts, lithium 4,5-dicyano-1,2,3-triazolate (LiDCTA) or lithium 4,5-dicyano-2-trifluoromethylimidazolide (LiTDI), in solvent mixtures with high flashpoint adiponitrile (ADN), as the main component. With sulfolane (SL) and ethylene carbonate (EC) as co-solvents the liquid temperature range of the electrolytes are extended to lower temperatures without lowering the flashpoint, but at the expense of high viscosities and moderate ionic conductivities. The anodic stabilities of the electrolytes are sufficient for LiFePO<SUB>4</SUB> cathodes and can be charged/discharged for 20 cycles in Li/LiFePO<SUB>4</SUB> cells with coulombic efficiencies exceeding 99% at best. The excellent thermal stabilities of the electrolytes with the solvent combination ADN:SL are promising for future electrochemical investigations at elevated temperatures (> 60 °C) to compensate the moderate transport properties and rate capability. The electrolytes with EC as a co-solvent, however, release CO<SUB>2</SUB> by decomposition of EC in presence of a lithium salt, which potentially makes EC unsuitable for any application targeting higher operating temperatures.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Solvents and salts with nitrile groups are combined into novel electrolytes. </LI> <LI> Sulfolane in adiponitrile provides thermally stable, high flashpoint electrolytes. </LI> <LI> LiDCTA and LiTDI electrolytes have high oxidation stability (4.5 V vs Li+/Li°). </LI> <LI> Ethylene carbonate is decomposed into CO2 in the presence of lithium salt. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

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        Accumulation of myeloid lineage cells is mapping out liver fibrosis post injury: a targetable lesion using Ketanserin

        Saeid Amini-Nik,Ali-Reza Sadri,Li Diao,Cassandra Belo,Marc G. Jeschke 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-

        Liver fibrosis is problematic after persistent injury. However, little is known about its response to an acute insult. Accumulation of myeloid lineage cells contributes into the promotion and resolution of inflammation and fibrosis. Using Cre-transgenic mice that specifically mark myeloid lineage cells with EYFP and burn as a model of acute systemic injury, we investigated the role of myeloid lineage cells in the liver after acute injury. Our data show that thermal injury in mice (30% total body surface area) induces fibrosis predominantly around portal venules whereas myeloid cells are enriched throughout the liver. The fibrosis peaks around 1–2 weeks post injury and resolves by week 3. Ablating myeloid cells led to lower fibrosis. Through FACS sorting, we isolated myeloid lineage cells (EYFP +ve cells) from injured animals and from the control uninjured animals and subjected the extracted RNA from these cells to microarray analysis. Microarray analysis revealed an inflammatory signature for EYFP +ve cells isolated from injured animals in comparison with control cells. Moreover, it showed modulation of components of the serotonin (5-HT) pathway in myeloid cells. Antagonizing the 5HT2A/2C receptor decreased fibrosis in thermally injured mice by skewing macrophages away from their pro-fibrotic phenotype. Macrophages conditioned with Ketanserin showed a lower profibrotic phenotype in a co-culture system with mesenchymal cells. There is a spatiotemporal pattern in liver fibrosis post-thermal injury, which is associated with the influx of myeloid cells. Treating mice with a 5HT2A/2C receptor antagonist promotes an anti-fibrotic effect, through modulating the phenotype of macrophages.

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