RESUMEN
Potassium-ion batteries (PIBs) are recognized as promising alternatives for lithium-ion batteries as the next-generation energy storage systems. However, the larger radius of K+ hinders the K+ insertion into the conventional carbon electrode and results in sluggish potassiation kinetics and poor cycling stability. Here, nitrogen and fluorine dual doping of soft carbon nanotubes (NFSC) anode are synthesized in one pot, achieving extraordinary electrochemical performance for PIBs. It is demonstrated that NFSC with a doping dose of 5.6 at% nitrogen and 1.3 at% fluorine together exhibits the highest reversible capacity of 238 mAh g-1 at 0.2 A g-1 and cycling stability of 186 mAh g-1 after 1000 cycles at 1 A g-1 . The extraordinary electrochemical performance can be attributed to the hollow structure, expanded interlayer distance, nitrogen and fluorine dual doping, and the binding ability of abundant defect sites. Moreover, density functional theory shows that the extra fluorine modification can dramatically enhance the conventional nitrogen doping effect and reduces the formation energy which makes a great contribution to the improvement of electrical conduction and K-ions insert. This work may promote the development of low-cost and sustainable carbon-based materials for PIBs and other advanced energy storage devices.
RESUMEN
BACKGROUND: LncRNA PTCSC3 is a tumor suppressor in thyroid cancer, and its role in drug resistance of anaplastic thyroid cancer (ATC) to chemotherapy drug doxorubicin was investigated in this study. METHODS: Expression of RNA and protein was analyzed by qRT-PCR and western blot, respectively. Flow cytometry was used to analyze the expression rate of CD133+ cells. The endogenous expression of related genes was modulated by recombinant plasmids and cell transfection. Combination condition and interaction between PTCSC3 and STAT3 were determined by RIP and RNA pull-down assay, respectively. MTT assay was performed to detect cytotoxicity. Chromatin immunoprecipitation was conducted to identify interactions between STAT3 and DNA promoter of INO80. RESULTS: LncRNA PTCSC3 was low-expressed in ATC tissues and cells. Over-expressed PTCSC3 inhibited the drug resistance of ATC to doxorubicin. PTCSC3 negatively regulated STAT3, and STAT3 promoted expression of INO80. PTCSC3 regulated INO80 through STAT3. PTCSC3 suppressed stem cells properties and drug resistance of ATC to doxorubicin. CONCLUSION: LncRNA PTCSC3 inhibits INO80 expression by negatively regulating STAT3, and thereby attenuating drug resistance of ATC to chemotherapy drug doxorubicin.