Ferroelectric polarization effect on the photocatalytic activity of Bi_(0.9)Ca_(0.1)FeO_(3)/CdS S-scheme nanocomposites

BiFeO_(3)(BFO),as a kind of narrow band-gap semiconductor material,has gradually emerged advantages in the application of photocatalysis.In this paper,Ca doped BFO nanoparticles Bi_(0.9)Ca_(0.1)FeO_(3)(BCFO)were prepared by sol-gel method.And BCFO and CdS nanocomposites with two morphologies were obtained by controlling the time of loading CdS under a low temperature liquid phase process.It is found that the band gap becomes narrower after doping Ca into BFO,which is conducive to the absorption of visible light.Among all the samples,the composite of CdS nanowires and BCFO nanoparticles obtained by reaction time of 10 min has the best photocatalytic performance.The degradation rate of Methyl Orange solutionwas 94%after 90min under visible light irradiation,whichwasmuch higher than that of pure BCFO and CdS.Furthermore,significant enhancement in the degradation rate(100%degradation in 60 min)can be achieved in poled samples after electric polarization process.The highest degradation rate is due to the promoted separation of photogenerated carriers induced by the internal polarization field and the formation of S-scheme heterostructure between BCFO and CdS.Such BCFO-CdS nanocomposites may bring new insights into designing highly efficient photocatalyst.

Long non-coding RNA MILNR1 retards colorectal cancer growth by inhibiting c-Myc

Dear Editor,Colorectal cancer(CRC)is a prevalent subtype of carcinoma which accounts for about 10%of all cancer diagnosis and is the third leading cause of cancer-related deaths globally[1].However,a great number of pathogenic factors associated with CRC development are still elusive and need further investigation.In the last several years,long non-coding RNAs(lncRNAs)were deemed to be a critical driving force for the progression of CRC[2-6],and c-Myc was discovered to be a functional partner of lncRNAs[7].Nucleoporin 88(NUP88)is a component of nucleoporins,which is upregulated in tumor tissues including CRC[8].It is reported that NUP88 interacts with vimentin and protects its serine residue(Ser83)from dephosphorylation,thereby promoting cell proliferation[9].Another form of vimentin phosphorylation,namely the phosphorylation at Ser39,results in the development of cell migration and tumor metastasis[10].Here we report a lncRNA MILNR1,which was found to be down-regulated in CRC cells,that could regulate NUP88 in cis by interacting with c-Myc and inhibit vimentin phosphorylation and CRC growth.