MXene (2D titanium carbide) as the electrode material for supercapacitors has been studied extensively and deeply in recent years. In order to enhance the electrochemical performance of MXene, CoS2 nanoparticles grown on MXene surface are constructed by a simple one‐step solvent thermal method. CoS2 nanoparticles play a crucial part in increasing the active sites of metal ions on the surface of MXene. In three‐electrode system, the obtained MXene/CoS2 composite delivers high performance. Its specific capacitance can be up to 1320 F g−1 at a current density of 1 A g−1 and it shows remarkable cycle performance with 78.4% after 3000 cycles at 10 A g−1. Moreover, the asymmetric supercapacitors (ASCs) with reduced graphene oxide as the negative electrode and MXene/CoS2 composite as the positive electrode exhibit a wide potential window of 1.6 V and high energy density (28.8 Wh kg−1) at a power density of 800 W kg−1. After 5000 cycles, the ASCs maintain 98% of initial specific capacitance at 5 A g−1. These results can effectively promote the application in the supercapacitor materials.

The volume of the metallic lithium anode in allsolid-state Li metal batteries increases significantly due to the lithium dendrite formation during the battery cycling, and the rough surface of lithium metal also reduces Li-ion transport in Li/electrolyte interface. In this work, we developed a solid polymer composite by adding the lowcost Si 3 N 4 particles to protect the lithium anode in allsolid-state batteries. The Fourier transform infrared spectroscopy (FTIR) data show that the surface of 10 wt % Si 3 N 4 particles interacts with the polyethylene oxide (PEO) and lithium bis(trifluoromethanesulfonyl)imide (LiTFSI) salt; the interaction restricts the anion mobility and improves the ionic conductivity (1 9 10 -4 SÁcm -1 ) and lithium-ion transference number (0.28) of the composite electrolyte. The lithium metal anode is well protected by the composite electrolyte in all-solid-state cells, including symmetric and Li/LiFePO 4 cells. The lithium dendrite growth suppression by this composite electrolyte indicates the possible application of these low-cost composite electrolytes for lithium metal protection.

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This paper describes a new LC-MS method for the determination of phenazopyridine and the subsequent development of a pharmacokinetic model for phenazopyridine in vivo. Phenazopyridine hydrochloride is a strong analgesic used in the treatment of urinary tract infections. Although it has been used as a clinical treatment for a very long time, pharmacokinetic data and suitable methods for its determination in plasma are currently lacking. The study described in this paper used high performance liquid chromatography-mass spectrometry, HPLC-MS, to determine the plasma concentrations of phenazopyridine in human subjects after oral administration. After liquid-liquid extraction, the phenazopyridine in the plasma was analyzed on a C18 column under SIM mode. A double-peak phenomenon was observed in most of the concentration-time profiles of the subjects. Although some drugs are known to cause this phenomenon, phenazopyridine has not been reported to do so. Several possible causes were analyzed in order to obtain an explanation. We proposed a two-site absorption compartment model to fit the concentration data in vivo, which has one more absorption site than the classical one-compartment model. The model describes the concentration profiles in different dose groups well and could provide an explanation for the double-peak phenomenon. The three dose groups exhibited similar model parameters and a linear pharmacokinetic process over the dose range used.

Whereas it is appreciated that cancer cells rewire lipid metabolism to survive and propagate, the roles of lipid metabolism in metastasis remain largely unknown. In this study, using esophageal squamous cell carcinoma (ESCC) as a pulmonary metastasis model, we find that the enzyme fatty acid 2-hydroxylase (FA2H), which catalyzes the hydroxylation of free fatty acids (FAs), is enriched in a subpopulation of ESCC cells with high metastatic potential, and that FA2H knockdown markedly mitigates metastatic lesions. Moreover, increased FA2H expression is positively associated with poor survival in patients with ESCC. Lipidomics analysis identifies that two dihydroceramides—Cer(d18:0/24:0) and Cer(d18:0/24:1)—are increased in FA2H-depleted metastasizing ESCC cells. Upon administration, Cer(d18:0/24:0) and Cer(d18:0/24:1) impair the formation of overt metastases in a mouse experimental metastasis model. Then, forkhead box protein C2 (FOXC2) and FA2H are found to be co-upregulated in metastatic ESCC cell populations and ESCC specimens, and FA2H expression is further experimentally verified to be transcriptionally induced by FOXC2, which is boosted per se by tumour necrosis factor α (TNFα), a critical pro-metastasis cytokine in the tumour microenvironment, in metastasizing cells. Together, these results demonstrate that TNFα-FOXC2-FA2H is a novel signaling axis to promote metastasis, and its downstream dihydroceramide products could be promising drugs to intervene in metastasis.