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- 저자 : Xiao Junting (검색결과 4 건)
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Emission properties of sequentially deposited ultrathin CH3NH3PbI3/MoS2 heterostructures
Shao Ziyi,Xiao Junting,Guo Xiao,You Siwen,Zhang Yangyang,Li Mingjun,Song Fei,Zhou Conghua,Xie Haipeng,Gao Yongli,Sun Jiatao,Huang Han 한국물리학회 2022 Current Applied Physics Vol.36 No.-
Hybrid organic-inorganic perovskite materials have obtained considerable attention due to their exotic optoelectronic properties and extraordinarily high performance in photovoltaic devices. Herein, we successively converted the ultrathin PbI2/MoS2 into the CH3NH3PbI3/MoS2 heterostructures via CH3NH3I vapor processing. Atomic force microscopy (AFM)、Scanning electron microscopy (SEM) and X-ray photoemission spectroscopy (XPS) measurements prove the high-quality of the converted CH3NH3PbI3/MoS2. Both MoS2 and CH3NH3PbI3 related photoluminescence (PL) intensity quenching in CH3NH3PbI3/MoS2 implies a Type-II energy level alignment at the interface. Temperature-dependent PL measurements show that the emission peak position shifting trend of CH3NH3PbI3 is opposite to that of MoS2 (traditional semiconductors) due to the thermal expansion and electron-phonon coupling effects. The CH3NH3PbI3/TMDC heterostructures are useful in fabricating innovative devices for wider optoelectronic applications.
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Epitaxial growth of <010>-oriented MoO2 nanorods on m-sapphire
Jinxin Liu,Jiao Shi,Di Wu,Xiaoming Zheng,Fengming Chen,Junting Xiao,Youzhen Li,Fei Song,Yongli Gao,Han Huang 한국물리학회 2020 Current Applied Physics Vol.20 No.10
Molybdenum dioxide (MoO2) materials have attracted considerable interests due to their superduper properties and potential applications, relating to the growth directions and exposed surfaces. Here, we reported as the substrate changes from c-to m-sapphire, the growth direction of epitaxial MoO2 nanorods via an atmospheric pressure chemical vapor deposition approach changes along from <001> to <010> of bulk monoclinic MoO2 accompanied by exposing different surfaces. Optical microscopy (OM), Raman spectroscopy, X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), cross-sectional scanning electron microscopy (SEM), highresolution transmission electron microscopy (HRTEM) and selected area electron diffraction (SAED) measurements reveal these MoO2 nanorods are epitaxially grown on m-sapphire substrates with the orientation of MoO2 (101)//sapphire (1010) and MoO2 <010> in line with sapphire <0001>. The electrical conductivity significantly depends on the crystallographic direction of MoO2 nanorods. The method to control the growth directions of 1D MoO2 nanorods has potential applications in nanoelectronic devices.
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Zongze He,Longyi Chen,Qi Wang,Cheng Yin,Junting Hu,Xiao Hu,Fan Fei,Jian Tang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.3
Pituitary tumors are usually benign but can occasionally exhibit hormonal and proliferative behaviors. Dysregulation of the G1/S restriction point largely contributes to the over-proliferation of pituitary tumor cells. F-box protein S-phase kinase-interacting protein-2 (SKP2) reportedly targets and inhibits the expression of p27Kip1, a well-known negative regulator of G1 cell cycle progression. In this study, SKP2 expression was found to be upregulated while p27Kip1 expression was determined to be downregulated in rat and human pituitary tumor cells. Furthermore, SKP2 knockdown induced upregulation of p27Kip1 and cell growth inhibition in rat and human pituitary tumor cells, while SKP2overexpression elicited opposite effects on p27Kip1 expression and cell growth. The expression of microRNA-186 (miR-186) was reported to be reduced in pituitary tumors. Online tools predicted SKP2 to be a direct downstream target of miR-186, which was further confirmed by luciferase reporter gene assays. Moreover, miR-186 could modulate the cell proliferation and p27Kip1-mediated cell cycle alternation of rat and human pituitary tumor cells through SKP2. As further confirmation of these findings, miR-186 and p27Kip1 expression were downregulated, while SKP2 expression was upregulated in human pituitary tumor tissue samples; thus, SKP2 expression negatively correlated with miR-186 and p27Kip1 expression. In contrast, miR-186 expression positively associated with p27Kip1 expression. Taken together, we discovered a novel mechanism by which miR-186/SKP2 axis modulates pituitary tumor cell proliferation through p27Kip1-mediated cell cycle alternation.
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He, Zongze,Chen, Longyi,Wang, Qi,Yin, Cheng,Hu, Junting,Hu, Xiao,Fei, Fan,Tang, Jian The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.3
Pituitary tumors are usually benign but can occasionally exhibit hormonal and proliferative behaviors. Dysregulation of the G1/S restriction point largely contributes to the over-proliferation of pituitary tumor cells. F-box protein S-phase kinase-interacting protein-2 (SKP2) reportedly targets and inhibits the expression of $p27^{Kip1}$, a well-known negative regulator of G1 cell cycle progression. In this study, SKP2 expression was found to be upregulated while $p27^{Kip1}$ expression was determined to be downregulated in rat and human pituitary tumor cells. Furthermore, SKP2 knockdown induced upregulation of $p27^{Kip1}$ and cell growth inhibition in rat and human pituitary tumor cells, while SKP2overexpression elicited opposite effects on $p27^{Kip1}$ expression and cell growth. The expression of microRNA-186 (miR-186) was reported to be reduced in pituitary tumors. Online tools predicted SKP2 to be a direct downstream target of miR-186, which was further confirmed by luciferase reporter gene assays. Moreover, miR-186 could modulate the cell proliferation and $p27^{Kip1}$-mediated cell cycle alternation of rat and human pituitary tumor cells through SKP2. As further confirmation of these findings, miR-186 and $p27^{Kip1}$ expression were downregulated, while SKP2 expression was upregulated in human pituitary tumor tissue samples; thus, SKP2 expression negatively correlated with miR-186 and $p27^{Kip1}$ expression. In contrast, miR-186 expression positively associated with $p27^{Kip1}$ expression. Taken together, we discovered a novel mechanism by which miR-186/SKP2 axis modulates pituitary tumor cell proliferation through $p27^{Kip1}$-mediated cell cycle alternation.
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