Improving Interfacial Stability for All-Solid-State Secondary Batteries with Precursor-Based Gradient Doping.

Recently, sulfide solid-state electrolytes with excellent ionic conductivity and facile electrode integration have gained prominence in the field of all-solid-state batteries (ASSBs). However, owing to their inherently high reactivity, sulfide electrolytes interact with the cathode, forming interfacial layers that adversely affect the electrochemical performance of all-solid-state cells. Unlike conventional cathode-coating methods that involve the formation of surface coatings from high-cost source materials, the proposed strategy involves the doping of precursors with low-cost oxides (Nb2O5, Ta2O5, and La2O3) prior to cathode fabrication. This novel approach aims to improve the stability of the cathode-sulfide electrolyte interface. Notably, doping significantly improved the discharge capacity, rate capability, and cyclic performance of cathodes while reducing their impedance resistance. Scanning electron microscopy, transmission electron microscopy (TEM), and X-ray photoelectron spectroscopy (XPS) indicated a gradient dopant-concentration profile (with a high level of dopant at the surface) in the doped cathodes. Cathode doping, particularly with Nb and Ta, caused a reduction in cation mixing owing to crystal-structure adjustments and ionic-conductivity enhancements. XPS and high-resolution TEM confirmed that gradient doping effectively minimized cathodic side reactions, possibly due to the formation of a coating-like protective layer in the cathode-electrolyte interface coupled with structural stabilization attributed to the doping process. The protective ability of the interfacial layer generated by gradient doping was confirmed to be comparable to that of conventional surface coatings. Therefore, this study could guide the future development of low-cost, high-performance ASSBs, opening new frontiers in sustainable energy storage.

Bromodomain-containing protein 4 silencing by microRNA-765 produces anti-ovarian cancer cell activity.

Bromodomain-containing protein 4 (BRD4) overexpression promotes ovarian cancer progression, and represents an important therapeutic oncotarget. This current study identified microRNA-765 (miR-765) as a novel BRD4-targeting miRNA. We showed that miR-765 directly associated with and silenced BRD4. In primary ovarian cancer cells and established cell lines (SKOV3 and CaOV3), ectopic overexpression of miR-765 inhibited cancer cell proliferation, migration and invasion, and induced apoptosis activation. In contrast, miR-765 inhibition by its anti-sense induced BRD4 upregulation to promote ovarian cancer cell proliferation, migration and invasion. Significantly, miR-765 overexpression-induced anti-ovarian cancer cell activity was largely attenuated by restoring BRD4 expression through an UTR-null BRD4 construct. Moreover, CRISPR/Cas9-induced BRD4 knockout (KO)inhibited proliferation and activated apoptosis in ovarian cancer cells. BRD4 KO in ovarian cancer cells abolished the functional impact of miR-765. miR-765 expression levels were downregulated in human ovarian cancer tissues and cells, correlating with the upregulation of BRD4 mRNA. Collectively, BRD4 silencing by miR-765produces significant anti-ovarian cancer cell activity. miR-765 could be further tested for its anti-ovarian cancer potential.