Engineered NiCo-LDH nanosheets- and ZnFe_(2)O_(4) nanocubes-decorated carbon nanofiber bonded mats for high-rate asymmetric supercapacitors

In this work,we have prepared the hierarchically nanostructured core–shell NiCo layered double hydroxide(NiCo-LDH)nanosheets-and ZnFe_(2)O_(4) nanocubes-decorated polyacrylonitrile(PAN)/pitch-based carbon nanofibers(PPCNs)webs(NiCo-LDH@PPCNs as cathode and ZnFe_(2)O_(4)@PPCNs as anode materials)with the bonded network structure by a facile and scalable hydrothemal method.Herein,the low-cost pitch with lower softening point(~90℃)as co-precursor was utilized to produce the PAN/pitch-based carbon nanofibers(PPCNs)with enhanced electrical conductivity.The obtained PPCNs with pitch content of 30%(PP30CNs)electrode material delivered higher specific capacitance(~67 F g^(-1))than that(~48 F g^(-1))of the PAN-based carbon nanofibers(PCNs)at 1 A g^(-1),due to the increased electrical conductivity and lower interfacial charge transfer resistance(RCT)of~0.16 U.Further,the NiCo-LDH-decorated PP30CNs(NiCoLDH@PP30CNs)as cathode material showed superior specific capacitance of 1162 F g^(-1) at 1.0 A g^(-1) and ultra-high retention rate of 91.56%at 10 A g^(-1).The ZnFe_(2)O_(4)@PP30CNs as anode material also showed higher specific capacitance of 282 F g^(-1) at 1 A g^(-1) and good rate capability with capacitance retention of 56.73%at 10 A g^(-1).The as-fabricated asymmetric NiCo-LDH@PP30CNs//ZnFe_(2)O_(4)@PP30CNs hybrid supercapacitor device delivered a specific capacitance of~98 F g^(-1) at 1 A g^(-1) and excellent capacitance retention of~88%after 5000 charge–discharge cycles.

Inhibitory Effects of AURKB Gene on Apoptosis and Cancer Cell Growth in HCT 116 Cells

[Objectives]To explore the inhibitory effect of AURKB gene in apoptosis and cancer cell growth in HCT 116 cells.[Methods]The in vitro cytology studies were carried out to confirm the expression of the AURKB gene in HCT 116 cells and make clear its role in cell activity,cell cycle control and apoptosis,and investigate the effect of AURKB gene in colorectal cancer(CRC).Quantitative reverse transcription/polymerase chain reaction(PCR)analysis and immunofluorescence(IF)staining for markers of AURKB gene were used to examine the effect of AURKB on HCT 116.The AURKB gene target was examined using western blot analysis.In addition,inhibition of AURKB expression was examined using RNA interference(RNAi)on HCT 116 cells in vitro.[Results]HCT 116 cells infected with AURKB shRNA virus suppressed expression of AURKB in vitro.AURKB gene knockdown HCT 116 cells showed reducing cell apoptosis in vitro.Finally,it demonstrated that AURKB function can induce apoptosis of HCT cells.[Conclusions]AURKB is a key regulator of colorectal cancer.AURKs are potential novel molecular targets for the prevention of cancer cell proliferation.