Bimetallic cobalt-based spinel is sparking much interest, most notably for its excellent bifunctional performance.H owever,t he effect of Fe 3+ doping in Co 3 O 4 spinel remains poorly understood, mainly because the surface state of ac atalyst is difficult to characterize.H erein, ab ifunctional oxygen electrode composed of spinel Co 2 FeO 4 / (Co 0.72 Fe 0.28 ) Td (Co 1.28 Fe 0.72 ) Oct O 4 nanoparticles grown on Ndoped carbon nanotubes (NCNTs) is designed, which exhibits superior performance to state-of-the-art noble metal catalysts. Theoretical calculations and magnetic measurements reveal that the introduction of Fe 3+ ions into the Co 3 O 4 network causes delocalization of the Co 3d electrons and spin-state transition. Fe 3+ ions can effectively activate adjacent Co 3+ ions under the action of both spin and charge effect, resulting in the enhanced intrinsic oxygen catalytic activity of the hybrid spinel Co 2 FeO 4 .T his work provides not only ap romising bifunctional electrode for zinc-air batteries,b ut also offers an ew insight to understand the Co-Fes pinel oxides for oxygen electrocatalysis.Todayselectric vehicles are mostly powered by lithium-ion batteries,b ut safety issues and the high cost have long been criticized. Fortunately,z inc-air batteries can achieve almost the same energy density but are much safer,a nd so they are promising candidates with dual-cell configuration for automotive electrification. [1,2] Nevertheless,the long-term stability and intrinsic oxygen reduction reaction (ORR)/oxygen evolution reaction (OER) activities of the catalysts are the key to realize the reversible and durable operation of zinc-air batteries.T odate,Pt-and Ir-based compounds are recognized as the most efficient ORR and OER catalysts,but their largescale applications are hampered by the high cost and scarcity of noble metals. [3][4][5] Therefore,itisstill aformidable challenge to develop earth-abundant, stable,a nd efficient ORR/OER electrocatalysts.

In the hybrid spinel Co2FeO4 the Fe3+ ions can effectively activate the Co3+ ions through 3d electron delocalization and spin‐state transition. As Z.‐Q. Liu, T. Ma, and co‐workers report in their Communication on page 13291, a bifunctional electrode composed of these Co2FeO4 nanoparticles grown on N‐doped carbon nanotubes is a promising candidate for zinc–air batteries.

Herein, we highlight redox‐inert Zn2+ in spinel‐type oxide (ZnXNi1−XCo2O4) to synergistically optimize physical pore structure and increase the formation of active species on the catalyst surface. The presence of Zn2+ segregation has been identified experimentally and theoretically under oxygen‐evolving condition, the newly formed VZn−O−Co allows more suitable binding interaction between the active center Co and the oxygenated species, resulting in superior ORR performance. Moreover, a liquid flow Zn–air battery is constituted employing the structurally optimized Zn0.4Ni0.6Co2O4 nanoparticles supported on N‐doped carbon nanotube (ZNCO/NCNTs) as an efficient air cathode, which presents remarkable power density (109.1 mW cm−2), high open circuit potential (1.48 V vs. Zn), excellent durability, and high‐rate performance. This finding could elucidate the experimentally observed enhancement in the ORR activity of ZnXNi1−XCo2O4 oxides after the OER test.

Background Central nervous system damage is an essential clinical feature that occurs in the early or late stages of syphilis infection. The abnormal enhancement of microglial phagocytosis can cause damage to the nervous system. However, the contribution of abnormally enhanced microglial phagocytosis to the pathogenesis of Treponema pallidum subsp. pallidum (T. pallidum) infection remains unknown. Objectives In this study, we sought to determine the role of recombinant T. pallidum Tp47 in promoting microglia phagocytosis and its associated mechanisms. Methods Microglial HMC3 cells were used to investigate the effect of the Tp47 on phagocytosis and the roles of autophagy and endoplasmic reticulum stress in Tp47‐induced phagocytosis. Results HMC3 cells exhibited obvious phagocytosis when stimulated with Tp47. The levels of P62 degradation, Beclin1 expression and the LC3II/LC3I ratio were significantly elevated, and the fusion of autophagosomes and lysosomes was promoted in Tp47‐stimulated HMC3 cells. Treatment with the autophagy inhibitors 3‐MA and Baf A1 inhibited Tp47‐induced phagocytosis. Meanwhile, the endoplasmic reticulum stress markers PERK, IRE1α, GRP78, ATF4 and XBP1s were upregulated in Tp47‐stimulated HMC3 cells. In addition, we found that TUDCA could inhibit Tp47‐induced expression of IRE1α but not PERK or ATF4. 4‐PBA inhibited TP47‐induced PERK and ATF4 protein expression but did not inhibit IRE1α expression. Attenuation of endoplasmic reticulum stress by administration of TUDCA and 4‐PBA abrogated Tp47‐mediated autophagy. Conclusions These results suggested that Tp47 activated autophagy through two key pathways associated with endoplasmic reticulum stress, PERK/ATF4 and IRE1/XBP1, to promote phagocytosis in HMC3 cells. These findings provided a basis for the understanding of the pathophysiology of neurological disorders that occur during the course of syphilis.

Siva-1 is a well-known anti-apoptosis protein that serves a role in multiple types of cancer cells. However, whether Siva-1 affects multidrug resistance via the nF-κB pathway in gastric cancer is currently unknown. The present study aimed to determine the possible involvement of Siva-1 in gastric cancer anticancer drug resistance in vitro. a vincristine (Vcr)-resistant KaTo iii/Vcr gastric cancer cell line with stable Siva-1 overexpression was established. The protein expression levels of Siva-1, nF-κB, multidrug resistance 1 (Mdr1) and multidrug resistance protein 1 (MrP1) were detected via western blotting. The effect of Siva-1 overexpression on anticancer drug resistance was assessed by measuring the 50% inhibitory concentration of KATO III/VCR cells to VCR, 5-fluorouracil and doxorubicin. The rate of doxorubicin efflux and apoptosis were detected by flow cytometry. additionally, colony formation, wound healing and Transwell assays were used to detect the proliferation, migration and invasion of cells, respectively. The results of the current study revealed that the Siva-1-overexpressed KATO III/VCR gastric cancer cells exhibited a significantly decreased sensitivity to VCR, 5-fluorouracil and doxorubicin. The results of flow cytometry revealed that the percentage of apoptotic cells decreased following overexpression of Siva-1. The colony formation assay demonstrated that cell growth and proliferation were significantly promoted by Siva-1 overexpression. additionally, Siva-1 overexpression increased the migration and invasion of KaTo iii/Vcr cells in vitro. Western blot analysis determined that Siva-1 overexpression increased nF-κB, Mdr1 and MrP1 levels. The current study demonstrated that overexpression of Siva-1, which functions as a regulator of Mdr1 and MrP1 gene expression in gastric cancer cells via promotion of nF-κB expression, inhibited the sensitivity of gastric cancer cells to certain chemotherapies. These data provided novel insight into the molecular mechanisms of gastric cancer, and may be of significance for the clinical diagnosis and therapy of patients with gastric cancer.