Enabling Quasi-Zero-Strain Behavior of Layered Oxide Cathodes via Multiple-cations Induced Order-to-Disorder Transition.

The chemically pre-intercalated lattice engineering is widely applied to elevate the electronic conductivity, expand the interlayer spacing, and improve the structural stability of layered oxide cathodes. However, the mainstream unitary metal ion pre-intercalation generally produces the cation/vacancy ordered superstructure, which astricts the further improvement of lattice respiration and charge-carrier ion storage and diffusion. Herein, a multiple metal ions pre-intercalation lattice engineering is proposed to break the cation/vacancy ordered superstructure. Taking the bilayer V2O5 as an example, Ni, Co, and Zn ternary ions are simultaneously pre-intercalated into its interlayer space (NiCoZnVO). It is revealed that the Ni─Co neighboring characteristic caused by Ni(3d)-O(2p)-Co(3d) orbital coupling and the Co-Zn/Ni-Zn repulsion effect due to chemical bond incompatibility, endow the NiCoZnVO sample with the cation/vacancy disordered structure. This not only reduces the Li+ diffusion barrier, but also increases the diffusion dimension of Li+ (from one-dimension to two-dimension). Particularly, Ni, Co, and Zn ions co-pre-intercalation causes a prestress, which realizes a quasi-zero-strain structure at high-voltage window upon charging/discharging process. The functions of Ni ion stabilizing the lattice structure and Co or Zn ions activating more Li+ reversible storage reaction of V5+/V4+ are further revealed. The cation/vacancy disordered structure significantly enhances Li+ storage properties of NiCoZnVO cathode.

Association between functional variants in BIRC5/survivin gene 3' untranslated region and mRNA expression in lymphoblastoid cell lines.

Baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5)/survivin genetic microRNA (miRNA) binding site variants in the 3' untranslated region (3'UTR) are known to be significantly associated with cancer risk. However, the roles of genetic variants in BIRC5/survivin gene 3'UTRs and post-transcriptional regulation have not been elucidated. In the present study, we revealed that rs1042489, rs1042542, rs17882360, rs2239680, rs2661694 and rs4789560 in the BIRC5/survivin 3'UTR have potential miRNA binding sites using bioinformatics analysis. However, only rs1042489 was significantly associated with BIRC5/survivin mRNA expression in lymphoblastoid cell lines (P=0.030); rs1042489 may be a putative variant mediating the post-transcriptional regulation of the target BIRC5/survivin gene. An in-depth understanding of how 3'UTR variants regulate BIRC5/survivin activity is expected to pave the way to targeting the BIRC5/survivin pathway in cancer therapy.