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Stable Li metal anodes have become the driving factor for high-energy-density battery systems. However, uncontrolled growth of Li dendrite hinders the application of rechargeable Li metal batteries (LMBs). Here, a multifunctional electrolyte additive bisfluoroacetamide (BFA) was proposed to facilitate high-performance LMBs. The uniform and dense deposition of Li+ was achieved due to the reduced nucleation and plateau overpotential by the addition of BFA. Moreover, X-ray photoelectron spectroscopy (XPS) tests reveal a gradient solid electrolyte interface (SEI) structure on the Li metal surface. Cyclic voltammetry (CV) curves at different sweep speeds prove the formation of pseudocapacitance at the electrode-electrolyte interface, which accelerates the Li+ transport rate and protects the electrode structure. The low activation energy also indicates the ability of rapid Li+ transportation in electrolyte bulk. Therefore, the Li∥Li symmetric cells with 1.0 wt.% BFA electrolyte exhibit good cycling performance at 0.5 mA·cm−2 for over 2000 h, and Li∥LiNi0.6Co0.2Mn0.2O2 (NCM622) full cells maintain a high capacity for 200 cycles at 1 C rate. [ABSTRACT FROM AUTHOR]

Affected by many factors, the local wind environment on the bridge deck is complex and changeable, and it seriously threatens traffic safety. To accurately evaluate the wind field on the bridge deck, this paper develops a system to monitor the actual local wind environment and applies it to field measurement of the wind parameters at different positions of a complex truss girder bridge. The results show that the wind parameters on the bridge deck, including wind speed, gust factor, and turbulence intensity, are different from the bridge site due to the influence of the ancillary facilities. Also, the wind profile of the local wind field on the bridge deck is more in line with the polynomial distribution, which makes the equivalent height of the wind load much higher than the vehicle gravity. It should be noted that the measured power spectrum of the bridge deck is quite different from the wind spectrum applicable to the bridge site area, so it is not appropriate to use the wind spectrum of the bridge site area to carry out the analysis of the windmill bridge, and a more suitable wind spectrum for bridge deck wind field is proposed. [ABSTRACT FROM AUTHOR]

A new bismaleimide monomer, 2-((4-maleimidophenoxy)-methyl)-5-(4-maleimidopheny1maleimidophenyl)-1,3,4-oxadiazole (Mioxd), was designed and synthesized. The chemical structure of the monomer was confirmed by means of Fourier transform infrared (FTIR) spectroscopy, proton nuclear magnetic resonance (1H NMR) spectroscopy and elemental analysis, and its thermal properties were characterized using differential scanning calorimetry (DSC) and thermogravimetric analysis (TGA). Mioxd as a reactive modifier was blended with epoxy resin based on bisphenol A diglycidyl ether (DGEBA) in weight ratio of 5, 10, and 15%, using 4,4'-diaminodiphenyl sulfone (DDS) as hardener. The effect of Mioxd addition on the cure behavior and thermal properties of the blend resins was studied by DSC, TGA, and dynamic mechanical analysis (DMA). DSC investigations showed that the main exothermic peak temperature (T[T.sub.p]) of the blend systems did not obviously shift with increasing Mioxd content whereas a new shoulder appeared and gradually grew on the high temperature side of the exothermic peak. The results of DMA measurements exhibited the glassy storage modulus (G') and glass transition temperatures (T[T.sub.g]) increased as the Mioxd content was increased, the cured blends investigated were miscible and no phase separation occurred. Further, the thermal decomposition temperature first decreased and then increased, but the char yield at 600 ° C increased with an increase in Mioxd content. POLYM. ENG. SCI., 51:1599-1606, 2011. © 2011 Society of Plastics Engineers, INTRODUCTION Bismaleimides (BMIs) possess an advantageous combination of properties, such as favorable processability, good dielectric property, excellent chemical resistance, outstanding thermal stability, unexpectedly high strength, and high modulus (1). Therefore, [...]

Aim: To elucidates the mechanism that disulfiram/copper complex (DSF/Cu) treatment activates chloride channels and induces apoptosis in prostate cancer cells. Methods: Cellular membrane currents were measured by membrane clamp technique; western blot to detect protein expression; flow cytometry to detect apoptosis; immunofluorescence to detect target protein co‐localization, and further validated by a combination of protein‐protein interaction and mock protein molecular docking techniques. Results: DSF/Cu activated chloride channels and induced apoptosis in LNCaP (a type of androgen‐dependent prostate cancer cells) cells. The chloride currents activated by DSF/Cu were significantly reduced after knockdown of CLC3 with siRNA. In addition, DSF/Cu‐activated chloride currents were reduced to background current levels after perfusion with genistein, a highly specific tyrosine kinase inhibitor. Conversely, DSF/Cu failed to activate chloride currents in LNCaP cells after 30 minutes of pre‐incubation with genistein. When genistein was removed, and DSF/Cu was added, the activated currents were small and unstable, and gradually decreased. Immunofluorescence in LNCaP cells also showed co‐localization of the CLC3 protein with tyrosine kinase 2β (PTK2B). Conclusion: DSF/Cu can activate chloride channels and induce apoptosis in LNCaP cells with the involvement of tyrosine kinase. These results provide new insights into the target therapy of prostate cancer. [ABSTRACT FROM AUTHOR]

Aims: Bone morphogenetic proteins (BMPs) are a group of proteins related to bone morphogenesis. BMP‐binding endothelial regulator (BMPER), a secreted protein that interacts with BMPs, is known to be involved in ischemic injuries. Here, we explored the effects of BMPER on cerebral ischemia and its mechanism of action. Methods: A mouse model of brain ischemia was induced by middle cerebral artery occlusion (MCAO). An in vitro ischemic model was established by subjecting primary cultured neurons to oxygen‐glucose deprivation/reperfusion (OGD/R). Serum levels of BMPs/BMPER were measured in MCAO mice and in patients with acute ischemic stroke (AIS). Brain damages were compared between BMPER‐ and vehicle‐treated mice. Quantitative polymerase chain reaction (qPCR), immunohistochemistry, and immunofluorescence staining were performed to examine neuroinflammation and cell death. BMPER‐related pathways were assessed by Western blotting. Results: BMPER level was elevated in MCAO mice and AIS patients. BMPER administration reduced mortality, infarct size, brain edema, and neurological deficit after MCAO. Neuroinflammation and cell death after ischemia were alleviated by BMPER both in vivo and in vitro. BMPER activated the Smad3/Akt/Nrf2 pathway in OGD/R‐challenged neurons. Conclusion: BMPER is a neuroprotective hormone that alleviates ischemic brain injury via activating the Smad3/Akt/Nrf2 pathway. These findings may provide potential therapeutic strategies for stroke. [ABSTRACT FROM AUTHOR]