Manipulating the Nanophase Separation of a Polymer-Salt Microfluid Generates an Advanced In Situ Separator for Component-Integrated Energy Storage Devices.

A polymer separator plays a pivotal role in battery safety, overall electrochemical performance, and cell assembly process. Traditional separators are separately produced from the electrodes and dominated by porous polyolefin thin films. In spite of their commercial success, today's separators are facing growing challenges with the increasing demand on the device safety and performance. As an attempt to address this urgent need, here, we propose a concept of in situ separator technology by manipulating the two-dimensional (2D) microfluid nanophase separation (2D-MFPS) of a poly(vinylidene difluoride)/lithium salt solution during drying. Particularly, nanophase separation is effectively regulated by low humidity, salt type, and compositions. For application studies, this 2D-MFPS is directly performed onto commercial electrodes under drying conditions with low humidity to fabricate a high-performance in situ separator with thickness and porous structures comparable to those of commercial Celgard separators. This in situ separator shows superior performance in high-temperature stability and wetting capability to a variety of liquid electrolytes. Finally, pouch cells with this in situ separator technology are successfully assembled with an extremely simplified separator-stacking-free process and demonstrate stable cycle performance due to the well-controlled porous structures and electrode-separator interface.

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.

Mass Production of Customizable Core-Shell Active Materials in Seconds by Nano-Vapor Deposition for Advancing Lithium Sulfur Battery.

Rational design and scalable production of core-shell sulfur-rich active materials is vital for not only the practical success of future metal-sulfur batteries but also for a deep insight into the core-shell design for sulfur-based electrochemistry. However, this is a big challenge mainly due to the lack of efficient strategy for realizing precisely controlled core-shell structures. Herein, by harnessing the frictional heating and dispersion capability of the nanostorm technology developed in the authors' laboratory, it is surprisingly found that sulfur-rich active particles can be coated with on-demand shell nanomaterials in seconds. To understand the process, a micro-adhesion guided nano-vapor deposition (MAG-NVD) working mechanism is proposed. Enabled by this technology, customizable nano-shell is realized in a super-efficient and solvent-free way. Further, the different roles of shell characteristics in affecting the sulfur-cathode electrochemical performance are discovered and clarified. Last, large-scale production of calendaring-compatible cathode with the optimized core-shell active materials is demonstrated, and a Li-S pouch-cell with 453 Wh kg-1 @0.65 Ah is also reported. The proposed nano-vapor deposition may provide an attractive alternative to the well-known physical and chemical vapor deposition technologies.

Knockdown of membrane-bound complement regulatory proteins suppresses colon cancer growth in mice through inducing tumor cell apoptosis.

CD46, CD55 and CD59 are membrane-bound complement regulatory proteins (mCRPs) and highly expressed in many tumor tissues. Our analysis by RNA sequencing and qRT-PCR revealed that the expression of mCRPs was significantly elevated in cancer tissues of 15 patients with colon cancer. To further investigate the role of mCRPs in the development of colon cancer, we suppressed the expression of mCRPs by CD46-shRNA, CD55-shRNA and CD59-shRNA in colon cancer cell lines, SW620 and HT-29 cells. The results indicated that CD46-shRNA, CD55-shRNA and CD59-shRNA effectively reduced the expression of mCRPs, accompanied with the increased LDH release and the percentage of Annexin V + 7-AAD- early phase of apoptotic cells. The similar cytotoxic effects were also observed in the cells treated with CD46 neutralizing antibody (aCD46), associated with the increased C5b-9 deposition, cleaved caspase-3 and Bax expression in the treated cells. The cytotoxic effects by mCRPs knock-down were potentiated in the cells co-treated with doxorubicin (Dox). In addition, STAT3, STAT6, and p38 MAPK inhibitors, including C188-9, AS1517499 and SB203580 effectively reduced the expression of CD46 in the treated colon cells, associated with increased cell apoptosis and LDH release. Further study with mouse model revealed that mCRPs knockdown by mCRPs-shRNA significantly reduced colon cancer growth, associated with increased expression of Bax, cleaved caspase-3 and C5b-9 deposition, but reduced expression of Bcl-2, IL-6 and IL-1beta in tumor tissues of nude mice transplanted with SW620 cells. Thereby, mCRPs expression in human colon cancer cells were upregulated by STAT3/STAT6/p38 MAPK signaling and mCRPs knockdown reduced colon cancer growth in mice through inducing tumor cell apoptosis.

Decreased expression and prognostic role of EHD2 in human breast carcinoma: correlation with E-cadherin.

Decreased expression of epithelial cadherin (E-cadherin) has been noted to associate with aggressiveness and metastasis of breast cancer. The aim of this study was to examine the effect of C-Terminal EH domain-containing protein 2 (EHD2) expression on E-cadherin and related mechanism in the metastasis of breast cancer. Immunohistochemical analysis was performed in 96 human breast carcinoma samples and the data were correlated with clinicopathologic characteristics. Furthermore, Western blot analysis was performed for EHD2 and E-cadherin in breast carcinoma samples and cell lines to evaluate their protein levels and molecular interaction. We found that the expression of EHD2 was positively related with E-cadherin expression (P < 0.01), moreover, EHD2 expression was significantly correlated with histologic grade (P < 0.01). Meanwhile, E-cadherin expression obtained similar results. Kaplan-Meier survival analysis showed that decreased expression of EHD2 and E-cadherin exhibited a significant correlation with poor prognosis in human breast cancer (P < 0.01). While in vitro, we employed siRNA technique to knock down EHD2 expressions and observed their effects on breast cancer cells growth. EHD2 depletion by siRNA promoted PCNA expression, and it was concurrent with the decreased expression of epithelial marker E-cadherin and the increased expression of N-cadherin by Western blot analysis. Consistent with these observations, the suppression of EHD2 in breast cancer cells remarkably promoted cellular proliferation and migration. On the basis of these results, we suggested that EHD2 can inhibit the metastasis of human breast cancer by regulating the EMT key markers E-cadherin and N-cadherin.