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Shuai Liu Xin Feng Xuelong Wang Xi Shen Enyuan Hu Ruijuan Xiao Richeng Yu Haitao Yang Ningning Song Zhaoxiang Wang Xiaoqing Yang Liquan Chen 《Liver Transplantation》2018,8(15)
The Li‐rich layer‐structured oxides are regarded one of the most promising candidates of cathode materials for high energy‐density Li‐ion batteries. However, the uninterrupted migration of the transition metal (TM) ions during cycling and the resultant continuous fading of their discharge potentials bring challenges to the battery design and impede their commercial applications. Various efforts have been taken to suppress the migration of the TM ions such as surface modification and elemental substitution, but no success has been achieved to date. Another strategy hereby is proposed to address these issues, in which the TM migration is promoted and the layered material is transformed to a rocksalt in the first few charge/discharge cycles by specially designing a novel Li‐rich layer‐structured Li1.2Mo0.6Fe0.2O2 on the basis of density functional theory calculations. With such, the continuous falling of the discharge potential is detoured due to enhanced completion of the cation mixing. In‐depth studies such as aberration‐corrected scanning transmission electron microscopy confirm the drastic structural change at the atomic scale, and in situ X‐ray absorption spectroscopy and Mössbauer spectroscopy clarify its charge compensation mechanism. This new strategy provides revelation for the development of the Li‐rich layered oxides with mitigated potential decay and a longer lifespan. 相似文献
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Addition of aluminum oxide microparticles to Trichoderma viride My preculture enhances cellulase production and influences fungal morphology
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Miaoyin Dong Shuyang Wang Fuqiang Xu Qiaoqiao Li Wenjian Li 《Engineering in Life Science》2018,18(6):353-358
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Review on Challenges and Recent Advances in the Electrochemical Performance of High Capacity Li‐ and Mn‐Rich Cathode Materials for Li‐Ion Batteries
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Prasant Kumar Nayak Evan M. Erickson Florian Schipper Tirupathi Rao Penki Nookala Munichandraiah Philipp Adelhelm Hadar Sclar Francis Amalraj Boris Markovsky Doron Aurbach 《Liver Transplantation》2018,8(8)
Li and Mn‐rich layered oxides, xLi2MnO3·(1–x)LiMO2 (M=Ni, Mn, Co), are promising cathode materials for Li‐ion batteries because of their high specific capacity that can exceed 250 mA h g?1. However, these materials suffer from high 1st cycle irreversible capacity, gradual capacity fading, low rate capability, a substantial charge‐discharge voltage hysteresis, and a large average discharge voltage decay during cycling. The latter detrimental phenomenon is ascribed to irreversible structural transformations upon cycling of these cathodes related to potentials ≥4.5 V required for their charging. Transition metal inactivation along with impedance increase and partial layered‐to‐spinel transformation during cycling are possible reasons for the detrimental voltage fade. Doping of Li, Mn‐rich materials by Na, Mg, Al, Fe, Co, Ru, etc. is useful for stabilizing capacity and mitigating the discharge‐voltage decay of xLi2MnO3·(1–x)LiMO2 electrodes. Surface modifications by thin coatings of Al2O3, V2O5, AlF3, AlPO4, etc. or by gas treatment (for instance, by NH3) can also enhance voltage and capacity stability during cycling. This paper describes the recent literature results and ongoing efforts from our groups to improve the performance of Li, Mn‐rich materials. Focus is also on preparation of cobalt‐free cathodes, which are integrated layered‐spinel materials with high reversible capacity and stable performance. 相似文献
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Aspartylglucosaminuria (AGU) is a lysosomal storage disorder caused by mutations in the gene for aspartylglucosaminidase (AGA). This enzyme participates in glycoprotein degradation in lysosomes. AGU results in progressive mental retardation, and no curative therapy is currently available. We have here characterized the consequences of AGA gene mutations in a compound heterozygous patient who exhibits a missense mutation producing a Ser72Pro substitution in one allele, and a nonsense mutation Trp168X in the other. Ser72 is not a catalytic residue, but is required for the stabilization of the active site conformation. Thus, Ser72Pro exchange impairs the autocatalytic activation of the AGA precursor, and results in a considerable reduction of the enzyme activity and in altered AGA precursor processing. Betaine, which can partially rescue the AGA activity in AGU patients carrying certain missense mutations, turned out to be ineffective in the case of Ser72Pro substitution. The Trp168X nonsense allele results in complete lack of AGA polypeptide due to nonsense-mediated decay (NMD) of the mRNA. Amlexanox, which inhibits NMD and causes a translational read-through, facilitated the synthesis of a full-length, functional AGA protein from the nonsense allele. This could be demonstrated as presence of the AGA polypeptide and increased enzyme activity upon Amlexanox treatment. Furthermore, in the Ser72Pro/Trp168X expressing cells, Amlexanox induced a synergistic increase in AGA activity and polypeptide processing due to enhanced processing of the Ser72Pro polypeptide. Our data show for the first time that Amlexanox might provide a valid therapy for AGU. 相似文献
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Rui Fu Myanna T. Olsen Kristofor Webb Eric J. Bennett Jens Lykke-Andersen 《RNA (New York, N.Y.)》2016,22(3):373-382
The zinc finger protein tristetraprolin (TTP) promotes translation repression and degradation of mRNAs containing AU-rich elements (AREs). Although much attention has been directed toward understanding the decay process and machinery involved, the translation repression role of TTP has remained poorly understood. Here we identify the cap-binding translation repression 4EHP-GYF2 complex as a cofactor of TTP. Immunoprecipitation and in vitro pull-down assays demonstrate that TTP associates with the 4EHP-GYF2 complex via direct interaction with GYF2, and mutational analyses show that this interaction occurs via conserved tetraproline motifs of TTP. Mutant TTP with diminished 4EHP-GYF2 binding is impaired in its ability to repress a luciferase reporter ARE-mRNA. 4EHP knockout mouse embryonic fibroblasts (MEFs) display increased induction and slower turnover of TTP-target mRNAs as compared to wild-type MEFs. Our work highlights the function of the conserved tetraproline motifs of TTP and identifies 4EHP-GYF2 as a cofactor in translational repression and mRNA decay by TTP. 相似文献