Abstract Although numerous perovskite oxides can enhance the electrochemical activity via exsolved metallic nanoparticles on the surface, most of them can only be applied as catalysts in a reducing atmosphere. These nanoparticles cause serious performance degradation in oxidizing conditions due to the formation of low‐conductive metal oxides. This poses a big challenge to the design of highly active catalysts of electrochemical devices, especially for symmetrical solid oxide cells. Herein, based on the strategy of exsolved metallic nanoparticles in A‐site deficient perovskite, a unique and simple method is demonstrated for the synthesis of Ru/RuO 2 nanoparticles on the surface of perovskite oxide via in situ growth. The electrode material (La 0.75 Sr 0.25 ) 0.9 Cr 0.5 Mn 0.45 Ru 0.05 O 3− δ (LSCMR) is designed through careful choice of composition and the core idea is to make use of the exsolved nanoparticles concept applied for the first time at both hydrogen electrode and oxygen electrode for symmetrical solid oxide cells. Inspired by exsolved Ru and RuO 2 , the surface‐decorated LSCMR exhibits significantly enhanced electrochemical activity for both H 2 and O 2 , respectively, accompanied by high redox long‐term stability. Moreover, simple, low‐cost, and environmental‐friendly synthesis of Ru/RuO 2 nanoparticles on the substrate of typical perovskites is realized with this in situ growth approach.
Epithelial carcinoma is a subtype of ovarian cancers, with the highest lethality among all ovarian cancer subtypes. Hitherto surgical excision combined with chemotherapy has been the most extensively employed method in clinical treatment. However, the disease relapses very frequently, calling for more effective therapies. Mangiferin, a natural xanthone glucoside, has displayed promising anti-cancer activities by in vitro studies, but its therapeutic value in epithelial ovarian cancer treatment, either by in vivo or in vitro studies, remained to be known. This study aimed to determine the suppressive activities of mangiferin on human epithelial ovarian cancer and elucidate the underlying molecular mechanisms. We employed the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the crystal violet assay to determine the half maximal inhibitory concentration (IC50) values of mangiferin with paclitaxel as a positive control and the inhibitory effects of mangiferin on the proliferation of two human epithelial ovarian cancer cell lines. Wound healing and Transwell assays were used to determine anti-metastastic activities of mangiferin. ES-2 xenograft nude mouse model was used for the in vivo experiments. Western blotting, enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC) assays were carried out for evaluating the expression level of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9). In the present study, we demonstrated by both in vitro and in vivo assays that mangiferin suppressed the progress of epithelial ovarian cancer in a dose-dependent manner. In the animals treated with mangiferin, the tumor volume and weight were reduced significantly. Analyses of involved molecular events demonstrated that mangiferin down-regulated the expression of metastasis-associated proteins MMP2 and MMP9. Mangiferin strongly inhibited the progression of human epithelial ovarian cancer by down-regulating MMP2 and MMP9.
In vitro experimental study.To establish an axial impact injury model of intervertebral disc (IVD) and to investigate if a single impact injury without endplate structural disruption could initiate intervertebral disc degeneration (IDD), and what is the roles of Piezo1 in this process.Although IDD process has been confirmed to be associated with structural failures such as endplate fractures, whether a single impact injury of the endplates without structural disruption could initiate IDD remains controversial. Previous studies reported that Piezo1 mediated inflammation participated in the progression of IDD induced by mechanical stretch; however, the roles of Piezo1 in IVD impact injury remain unknown.Rats spinal segments were randomly assigned into Control, Low, and High Impact groups, which were subjected to pure axial impact loading using a custom-made apparatus, and cultured for 14 days. The degenerative process was investigated by using histomorphology, real-time Polymerase Chain Reaction(PCR), western-blot, immunofluorescence, and energy metabolism of IVD cell. The effects of Piezo1 were investigated by using siRNA transfection, real-time PCR, western-blot, and immunofluorescence.The discs in both of the impact groups presented degenerative changes after 14 days, which showed significant up-regulation of Piezo1, NLRP3 inflammasome, the catabolic (MMP-9, MMP-13), and pro-inflammatory gene (IL-1β) expression than that of the control group (P < 0.05), accompanied by significantly increased release of ATP, lactate, nitric oxide (NO), and glucose consumption of IVD cells at first 7 days. Silencing Piezo1 reduced the activation of NLRP3 inflammasome and IL-1β expression in the nucleus pulposus induced by impact injury.It demonstrated that not only fracture of the endplate but also a single impact injury without structural impairment could also initiate IDD, which might be mediated by activation of Piezo1 induced inflammation and abnormal energy metabolism of IVD cells.Level of Evidence: N/A.
Cytisine is a naturally occurring bioactive compound, an alkaloid mainly isolated from legume plants. In recent years, various biological activities of cytisine have been explored, showing certain effects in smoking cessation, reducing drinking behavior, anti-tumor, cardiovascular protection, blood sugar regulation, neuroprotection, osteoporosis prevention and treatment, etc. At the same time, cytisine has the advantages of high efficiency, safety, and low cost, has broad development prospects, and is a drug of great application value. However, a summary of cytisine's biological activities is currently lacking. Therefore, this paper summarizes the pharmacological action, mechanism, and pharmacokinetics of cytisine by referring to numerous databases, and analyzes the new and core targets of cytisine with the help of computer simulation technology, to provide reference for doctors.
Solid oxide cell (SOC) is the energy conversion device with a series of advantages such as high efficiency, environmental friendliness and durability, making it a promising way to deal with environmental pollution and energy crisis appearing with the development of human society. Perovskite oxides with hetero-phases which were prepared by in-situ exsolution are widely used as fuel electrode in SOC. In this work, Ni-doped perovskites Ruddlesden–Popper oxides, (La , Sr) n Ti n O 3n-2 with n = 5, 8, and 12 (LSTNn), were synthesized to design novel exsolution materials as solid oxide fuel cell anodes and for electrochemical catalysis applications. Compared with pure LSTNn without Ni, a small A-site deficiency (10%) promoted the exsolution of Ni from the perovskite oxides of Ni-doped LSTNn. It is found that the morphology as well as electrochemical activity of LSTNn anodes can be successfully manipulated by the exsolution of Ni. Since more Ni nanoparticles are exsolved from the parent oxides, LSTN8 displays better electrochemical performance by providing more active sides during the hydrogen oxidation reaction and significantly lowering electrode polarization resistance. DRT analysis is conducted to study substeps of the whole electrode reaction, finding that in-situ precipitation improves rate-limiting steps much. The CO 2 reduction reaction performance of LSTN materials is also studied, finding that in-situ grown nanoparticles on surface of LSTN significantly increases the density of surface active sites and three phase boundaries (TPBs), which are beneficial for CO 2 adsorption and subsequent conversion. It is clear from these results that varying Ni-doping in Ruddlesden–Popper oxides is a key factor in controlling the electrochemical performance and catalytic activity for hydrogen oxidation reaction in solid oxide fuel cells.
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