Bi_(2)O_(2)Se has been proved to be a promising candidate for electronic and optoelectronic devices due to their unique physical properties.However,it is still a great challenge to construct the heterostructures with ...Bi_(2)O_(2)Se has been proved to be a promising candidate for electronic and optoelectronic devices due to their unique physical properties.However,it is still a great challenge to construct the heterostructures with direct epitaxy of hetero semiconductor materials on Bi_(2)O_(2)Se nanosheets.Here,a two-step chemical vapor deposition(CVD)route was used to directly grow the CsPbBr_(3)nanoplate-Bi_(2)O_(2)Se nanosheet hetero structures.The CsPbBr_(3)nanoplates were selectively grown on the Bi_(2)O_(2)Se nanosheet along the edges,where the dangling bonds provide the nucleation sites.The epitaxial relationships between CsPbBr3 and Bi_(2)O_(2)Se were determined as[200]_(Bi_(2)O_(2)Se)‖[110]_(CsPbBr_(3))and[110]_(Bi_(2)O_(2)Se)‖[200]_(CsPbBr_(3))by transmission electron microscopy characterization.The photoluminescence(PL)results reveal that the formation of heterostructures results in the remarkable PL quenching due to the type-Ⅰband arrangement at CsPbBr_(3)/Bi_(2)O_(2)Se interface,which was confirmed by ultraviolet photoelectron spectroscopy(UPS)and Kelvin probe measurements,and makes the photogenerated carriers transfer from CsPbBr_(3)to Bi_(2)O_(2)Se.Importantly,the photodetectors based on the heterostructures exhibit a 4-time increase in the responsivity compared to those based on the pristine Bi_(2)O_(2)Se sheets,and the fast rise and decay time in microsecond.These results indicate that the direct epitaxy of the CsPbBr_(3)plates on the Bi_(2)O_(2)Se sheet may improve the optoelectronic performance of Bi_(2)O_(2)Se based devices.展开更多
Dilated cardiomyopathy(DCM)is the leading cause of heart transplantation.By microRNA(miRNA)array,a Kaposi’s sarcoma-associated herpes virus(KSHV)-encoded miRNA,kshv-miR-K12-1-5p,was detected in patients with DCM.The ...Dilated cardiomyopathy(DCM)is the leading cause of heart transplantation.By microRNA(miRNA)array,a Kaposi’s sarcoma-associated herpes virus(KSHV)-encoded miRNA,kshv-miR-K12-1-5p,was detected in patients with DCM.The KSHV DNA load and kshv-miR-K12-1-5p level in plasma from 696 patients with DCM were measured and these patients were followed-up.展开更多
Although numerous miRNAs have been discovered,their functions in the different subcellular organelles have remained obscure.In this study,we found that miR-665 was enriched in the nucleus of cardiomyocytes,and then in...Although numerous miRNAs have been discovered,their functions in the different subcellular organelles have remained obscure.In this study,we found that miR-665 was enriched in the nucleus of cardiomyocytes,and then investigated the underlying role of nuclear miR-665 in heart failure.RNA fluorescence in situ hybridization assays in human heart tissue sections and primary cardiomyocytes showed that miR-665 was localized in the nucleus of cardiomyocytes.Increased expression of nuclear miR-665 was observed not only in the cardiomyocytes isolated from the heart of mice treated in vivo by transverse aortic constriction(TAC),but also in phenylephrine(PE)-treated cultured cardiomyocytes in vitro.To further explore the role of miR-665 in heart failure,a type 9 recombinant adeno-associated virus(rAAV)system was employed to manipulate the expression of miR-665 in mice.Overexpression of miR-665 aggravated TAC-induced cardiac dysfunction,while down-expression of miR-665 showed opposite effects.Bioinformatic prediction and biological validation confirmed that the PTEN(phosphatase and tensin homolog)gene was one of the targets of miR-665 in the nucleus.Furthermore,restoring PTEN expression significantly eliminated the destructive effects of miR-665 over-expression in TAC-induced cardiac dysfunction.Our data showed that nuclear miR-665 aggravates heart failure via inhibiting PTEN expression,which provided a therapeutic approach for heart failure.展开更多
基金the National Natural Science Foundation of China(Grant No.51772088)Hunan Provincial Innovation Foundation for Postgraduate,China(Grant No.CX20200422)。
文摘Bi_(2)O_(2)Se has been proved to be a promising candidate for electronic and optoelectronic devices due to their unique physical properties.However,it is still a great challenge to construct the heterostructures with direct epitaxy of hetero semiconductor materials on Bi_(2)O_(2)Se nanosheets.Here,a two-step chemical vapor deposition(CVD)route was used to directly grow the CsPbBr_(3)nanoplate-Bi_(2)O_(2)Se nanosheet hetero structures.The CsPbBr_(3)nanoplates were selectively grown on the Bi_(2)O_(2)Se nanosheet along the edges,where the dangling bonds provide the nucleation sites.The epitaxial relationships between CsPbBr3 and Bi_(2)O_(2)Se were determined as[200]_(Bi_(2)O_(2)Se)‖[110]_(CsPbBr_(3))and[110]_(Bi_(2)O_(2)Se)‖[200]_(CsPbBr_(3))by transmission electron microscopy characterization.The photoluminescence(PL)results reveal that the formation of heterostructures results in the remarkable PL quenching due to the type-Ⅰband arrangement at CsPbBr_(3)/Bi_(2)O_(2)Se interface,which was confirmed by ultraviolet photoelectron spectroscopy(UPS)and Kelvin probe measurements,and makes the photogenerated carriers transfer from CsPbBr_(3)to Bi_(2)O_(2)Se.Importantly,the photodetectors based on the heterostructures exhibit a 4-time increase in the responsivity compared to those based on the pristine Bi_(2)O_(2)Se sheets,and the fast rise and decay time in microsecond.These results indicate that the direct epitaxy of the CsPbBr_(3)plates on the Bi_(2)O_(2)Se sheet may improve the optoelectronic performance of Bi_(2)O_(2)Se based devices.
基金This work was supported by grants from the National Natural Science Foundation of China(nos.81822002,82270363,91839302,81630010,81790624,31771264,31800973,and 82000387)National Key R&D Program of China(no.2017YFC0909400)the Natural Science Foundation of Hubei Province(no.2020CFA016).The funders had no role in study design,data collection and analysis,manuscript preparation,or decision to publish.
文摘Dilated cardiomyopathy(DCM)is the leading cause of heart transplantation.By microRNA(miRNA)array,a Kaposi’s sarcoma-associated herpes virus(KSHV)-encoded miRNA,kshv-miR-K12-1-5p,was detected in patients with DCM.The KSHV DNA load and kshv-miR-K12-1-5p level in plasma from 696 patients with DCM were measured and these patients were followed-up.
基金supported by grant from the National Natural Science Foundation of China(81822002,81630010,81790624,91839302,31771264 and 31800973)。
文摘Although numerous miRNAs have been discovered,their functions in the different subcellular organelles have remained obscure.In this study,we found that miR-665 was enriched in the nucleus of cardiomyocytes,and then investigated the underlying role of nuclear miR-665 in heart failure.RNA fluorescence in situ hybridization assays in human heart tissue sections and primary cardiomyocytes showed that miR-665 was localized in the nucleus of cardiomyocytes.Increased expression of nuclear miR-665 was observed not only in the cardiomyocytes isolated from the heart of mice treated in vivo by transverse aortic constriction(TAC),but also in phenylephrine(PE)-treated cultured cardiomyocytes in vitro.To further explore the role of miR-665 in heart failure,a type 9 recombinant adeno-associated virus(rAAV)system was employed to manipulate the expression of miR-665 in mice.Overexpression of miR-665 aggravated TAC-induced cardiac dysfunction,while down-expression of miR-665 showed opposite effects.Bioinformatic prediction and biological validation confirmed that the PTEN(phosphatase and tensin homolog)gene was one of the targets of miR-665 in the nucleus.Furthermore,restoring PTEN expression significantly eliminated the destructive effects of miR-665 over-expression in TAC-induced cardiac dysfunction.Our data showed that nuclear miR-665 aggravates heart failure via inhibiting PTEN expression,which provided a therapeutic approach for heart failure.
