On-Site Cross-Linking of Polyacrylamide to Efficiently Bind the Silicon Anode of Lithium-Ion Batteries.

Silicon anode suffers from rapid capacity decay because of its irreversible volume changes during charging and discharging. As one of the important components of the electrode structure, the binder plays an irreplaceable role in buffering the volume changes of the silicon anode and ensuring close contact between various components of the electrode. Traditional PVDF binder is based on weak van der Waals forces and cannot effectively buffer the stress coming from silicon volume expansion, resulting in rapid decay of silicon anode capacity. In addition, most natural polysaccharide binders with a single force face the same problem due to poor toughness. Therefore, it is extremely important to develop a binder with good force and toughness between the silicon particles. Herein, polyacrylamide (PAM) polymer chains that are premixed homogeneously with various components are cross-linked on-site on the current collector via the condensation reaction with citric acid, forming a polar three-dimensional (3D) network with improved tensile properties and adhesion for both silicon particles and current collector. The silicon anode with the cross-linked PAM binder exhibits higher reversible capacity and enhanced long-term cycling stability; the capacity remains at 1280 mA h g-1 after 600 cycles at 2.1 A g-1 and 770.9 mA h g-1 after being subjected to 700 cycles at 4.2 A g-1. It also exhibits excellent cycle stability in silicon-carbon composite materials. This study provides a cost-effective binder engineering strategy, which significantly enhances the long-term cycle performance and stability of silicon anodes, paving the way for large-scale practical applications.

Activation of mGluR5 Attenuates Microglial Activation and Neuronal Apoptosis in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats.

Activation of metabotropic glutamate receptor 5 (mGluR5) provided neuroprotection in multiple central nervous system injury, but the roles of mGluR5 in subarachnoid hemorrhage (SAH) remain unclear. In present study, we aimed to evaluate whether activation of mGluR5 attenuates early brain injury (EBI) after experimental SAH in rats. We found that selective mGluR5 orthosteric agonist CHPG or positive allosteric modulator VU0360172 administration significantly improves neurological function and attenuates brain edema at 24 h after SAH. Furthermore, mGluR5 obviously expresses in activated microglia (ED-1 positive) after SAH. CHPG or VU0360172 administration significantly reduces the numbers of activated microglia and the protein and mRNA levels of pro-inflammatory cytokines IL-1ß, IL-6 and TNF-α at 24 h after SAH. Moreover, CHPG or VU0360172 administration obviously reduces the number of TUNEL-positive cells and active caspase-3/NeuN-positive neurons in cortex at 24 h after SAH. CHPG or VU0360172 administration significantly up-regulates the expression of Bcl-2, and down-regulates the expression of Bax and active caspase-3, which in turn increases the ratio of Bcl-2/Bax. Our results indicate that activation of mGluR5 attenuates microglial activation and neuronal apoptosis, and improves neurological function in EBI after SAH.