Architecting the Microenvironment Skeleton of Active Materials in High-Capacity Electrodes by Self-Assembled Nano-Building Blocks.

In analogy to the cell microenvironment in biology, understanding and controlling the active-material microenvironment (ME@AM) microstructures in battery electrodes is essential to the successes of energy storage devices. However, this is extremely difficult for especially high-capacity active materials (AMs) like sulfur, due to the poor controlling on the electrode microstructures. To conquer this challenge, here, a semi-dry strategy based on self-assembled nano-building blocks is reported to construct nest-like robust ME@AM skeleton in a solvent-and-stress-less way. To do that, poly(vinylidene difluoride) nanoparticle binder is coated onto carbon-nanofibers (NB@CNF) via the nanostorm technology developed in the lab, to form self-assembled nano-building blocks in the dry slurry. After compressed into an electrode prototype, the self-assembled dry-slurry is then bonded by in-situ nanobinder solvation. With this strategy, mechanically strong thick sulfur electrodes are successfully fabricated without cracking and exhibit high capacity and good C-rate performance even at a high AM loading (25.0 mg cm-2 by 90 wt% in the whole electrode). This study may not only bring a promising solution to dry manufacturing of batteries, but also uncover the ME@AM structuring mechanism with nano-binder for guiding the design and control on electrode microstructures.

LncRNA CRNDE facilitates epigenetic suppression of CELF2 and LATS2 to promote proliferation, migration and chemoresistance in hepatocellular carcinoma.

Our study aimed to investigate the expression, functional significance, and related mechanism of long noncoding RNA CRNDE (colorectal neoplasia differentially expressed) in hepatocellular carcinoma (HCC) pathogenesis. The resulted revealed that CRNDE was significantly overexpressed in HCC tissues and cell lines, and was statistically correlated with poor clinical outcome. CRNDE knockdown markedly decreased HCC cell proliferation, migration, and chemoresistance. In addition, in vivo experiments confirmed the suppressive effect of CRNDE knockdown on HCC progression. Mechanically, CRNDE directly bound to EZH2 (enhancer of zeste homolog), SUZ12 (suppressor of zeste 12), SUV39H1, and mediated their inhibition of tumor suppressor genes, including CUGBP Elav-like family member 2 (CELF2) and large tumor suppressor 2 (LATS2). CELF2 exerted tumor suppressive effect in HCC and was involved in CRNDE-mediated oncogenic effect. In addition, the oncogenic effects of CRNDE on HCC proliferation, migration and tumorigenesis, as well as its inhibition of Hippo pathway were abolished by LATS2 overexpression. Together, our work demonstrated the importance of CRNDE in HCC progression and elucidated the underlying molecular mechanisms. These findings provided new insights into HCC pathogenesis and chemoresistance mediated by CRNDE.