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Low temperatures (< −20 °C) significantly diminish lithium‐ion battery performance due to freezing issues within commercial electrolytes and the high energy barrier for Li+ desolvation at the interface. Although high‐concentration electrolytes and localized high‐concentration electrolytes enhance Li+ desolvation kinetics featuring anion‐participated solvation structures, their high viscosity and propensity for Li salt precipitation render them unsuitable for low‐temperature environments. This study introduces an anion‐dominated conventional‐concentrations electrolyte (ACCE) created by incorporating Lithium difluorophosphate(LiPO2F2)into a 1 M Lithium bis((trifluoromethyl)sulfonyl)azanide(LiTFSI) Dimethyl carbonate(DMC)/Fluoroethylene carbonate(FEC)/Methyl acetate(MA) electrolyte solution. LiPO2F2, characterized by its poor solubility and strong binding with Li+, demonstrates a pronounced tendency to integrate into the primary solvation sheath of Li+. Moreover, the synergy between LiTFSI and LiPO2F2 establishes a dual anion configuration, unveiling a dual anion‐driven mechanism. This mechanism significantly diminishes the interaction between Li+ and solvent molecules, resulting in reduced desolvation energy under low temperatures. The ACCE exhibits high ionic conductivity of 1.3 mS cm−1 at −50 °C, enabling stable cycling of Li/NCM811 cells at −50 °C, and further allows 0.75 Ah graphite(Gr)/LiNi0.8Co0.1Mn0.1O2(NCM811) batteries dischargeable at −40 °C. This study presents a practical application potential for poorly soluble lithium salts and provides a new avenue for designing electrolytes suitable for low‐temperature applications. [ABSTRACT FROM AUTHOR]

Surgical resection is the preferred option for hepatocellular carcinoma (HCC), but surgical navigation technology using indocyanine green still has some drawbacks such as non‐specific imaging, thus it is very important to develop new fluorescence imaging technology. All‐cis hexaphenyl‐1,3‐butadiene derivative (ZZ‐HPB‐NC) with aggregation‐induced emission (AIE) feature has been reported to be quickly turned‐on fluorescent response in the intraoperative frozen‐section slides of HCC. However, the probe did not respond to normal liver tissue around HCC. In order to enhance the diagnostic rate and elucidate the response mechanism, all‐trans configuration EE‐HPB‐NC, was furtherly synthesized. Within two minutes, non‐cancer tissues could be fluorescently labeled by EE‐HPB‐NC by spraying, showing the same effect with ZZ‐HPB‐NC to HCC. The results indicated that the configuration‐induced cross‐identification fluorescence imaging strategy was achieved through the combination of ZZ‐ and EE‐HPB‐NC. Then the mechanism of HPB‐NC localization in HCC lesions was explored, and the binding of HPB‐NC with specific proteins in cells resulted in the AIE effect to label HCC cells. On this basis, the accuracy of specific fluorescence imaging for HCC was further verified on the mouse hepatic neoplasm models, indicating that it has clinical application potential for surgical fluorescence real‐time navigation. [ABSTRACT FROM AUTHOR]

The unstable interface between Li metal and ethylene carbonate (EC)‐based electrolytes triggers continuous side reactions and uncontrolled dendrite growth, significantly impacting the lifespan of Li metal batteries (LMBs). Herein, a bipolar polymeric protective layer (BPPL) is developed using cyanoethyl (−CH2CH2C≡N) and hydroxyl (−OH) polar groups, aiming to prevent EC‐induced corrosion and facilitating rapid, uniform Li+ ion transport. Hydrogen‐bonding interactions between −OH and EC facilitates the Li+ desolvation process and effectively traps free EC molecules, thereby eliminating parasitic reactions. Meanwhile, the −CH2CH2C≡N group anchors TFSI− anions through ion‐dipole interactions, enhancing Li+ transport and eliminating concentration polarization, ultimately suppressing the growth of Li dendrite. This BPPL enabling Li|Li cell stable cycling over 750 cycles at 10 mA cm−2 for 2 mAh cm−2. The Li|LiNi0.8Mn0.1Co0.1O2 and Li|LiFePO4 full cells display superior electrochemical performance. The BPPL provides a practical strategy to enhanced stability and performance in LMBs application. [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]

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]

A microwave absorbing patch (MAP) was prepared by compounding millable polyurethane elastomer (MPU) and carbonyl iron powder (CIP). Surfaces of CIP were modified using silane coupling agents (SCA). The effects of different types and amounts of SCA, the amount of vulcanizing agent and the amount of CIP on the microstructure and mechanical properties were investigated. SCA was found to improve the interface compatibility between MPU and CIP and also reinforced the mechanical properties of MAP. The KH550 was the best modifier, and the optimal dosage of KH550 was 2% of the mass of CIP based on a comparison of tensile properties. The optimal dosage of the vulcanizing agent DDPH was 3% of the mass of MPU. However, a large number of CIP could be filled into MPU. The maximum filling content of CIP increased with the increasing Mooney viscosity of MPU, and the maximum filling content of CIP was 1200% of the mass of MPU. The electromagnetic parameters and reflection loss of MPU absorbers and MPU filled with CIP absorbers were measured in the 1-18 GHz frequency range. The absorbers of MPU filled with CIP had excellent microwave absorbing properties compared with the absorbers of MPU. [ABSTRACT FROM AUTHOR]

The article discusses the design and synthesis of a new bismaleimide monomer, 2-((4-maleimidophenoxy)-methyl)-5-(4-maleimidophenyl)-1,3,4-oxiadazole (Mioxd). The monomer's chemical structure and thermal properties are confirmed and characterized. Mioxd as a reactive modifier was combined with epoxy resin based on bisphenol A diglycidyl ether (DGEBA) and using 4,4'-diaminodiphenyl sulfone (DDS) as hardener. The effect of the addition of Mioxd on the thermal properties and the cure behavior of the blend resins is evaluated.

The aim of this study was to elucidate the reproductive toxicity of the coadministration of diltiazem and cyclosporine A or tacrolimus. Testicular development, semen quality, sex hormones and testicular tissues were assessed in unilateral nephrectomised (UN) rats, including the control group, UN group, UN+CsA group, UN+FK506 group, UN+Rapa group, UN+CsA+Dil group and UN+FK506+Dil group. The testicular coefficient, the sperm number and the sperm motility were lower in the treatment groups (except UN+FK506) than in the control and UN groups (all p < 0.05). The lowest sperm number and motility were identified in the UN+CsA+Dil group, followed by the UN+CsA group. The proportion of abnormal sperm was higher in the UN+CsA and UN+CsA+Dil groups than in the control and UN groups, respectively (p < 0.05). The plasma concentrations of sex hormones were changed in the treatment groups. Dil can increase the blood concentrations of CsA and FK506 (◇p < 0.05, ◆p < 0.05). Therapeutic doses of these agents induced morphological changes in the testicular tissue and ultrastructural changes in the testosterone, mesenchymal cells and supporting cells. Our present study suggests that Dil can increase the testicular toxicity of CNIs (calcineurin inhibitors, including CsA and FK506) by enhancing the plasma concentrations of CNIs. [ABSTRACT FROM AUTHOR]