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Structure and magnetic properties of CrN thin films on La0.67Sr0.33MnO3
Zhongpo Zhou,Dingbo Zhang,Haiying Wang,Tianxing Wang,Zhansheng Lu,Zongxian Yang,Zhiwei Ai,Hao Wu,Chang Liu 한국물리학회 2018 Current Applied Physics Vol.18 No.11
High crystalline quality CrN thin films have been grown on La0.67Sr0.33MnO3 (LSMO) templates by molecular beam epitaxy. The structure and magnetic properties of CrN/LSMO heterojunctions are investigated combining with the experiments and the first-principles simulation. The Nėel temperature of the CrN/LSMO samples is found to be 281 K and the saturation magnetization of CrN/LSMO increases compared to that of LSMO templates. The magnetic property of CrN/LSMO heterostructures mainly comes from Cr atoms of (001) CrN and Mn atoms of (001) LSMO. The (001) LSMO induces and couples the spin of the CrN sublattice at CrN/LSMO interface.
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Du Yuanfeng,Yang Dingbo,Dong Xiaoqiao,Du Quan,Wang Ding,Shen Yongfeng,Yu Wenhua 한국유전학회 2021 Genes & Genomics Vol.43 No.12
Background Subarachnoid hemorrhage (SAH) is a severe neurological emergency, resulting in cognitive impairments and threatening human's health. Currently, SAH has no efective treatment. It is urgent to search for an efective therapy for SAH. Objective To explore the expression of Omi protein after subarachnoid hemorrhage in rats. Methods SAH rat model was established by injecting blood into the prechiasmatic cistern. Neurological defcit was assessed by detecting neurological defcit scores and brain tissue water contents. Apoptotic cells were evaluated by TUNEL staining and IHC staining. Omi and Cleaved caspase 3 expressions in nerve cells were determined by double staining using IF. Apoptosis-related proteins were measured by Western blotting assay. Results SAH rat model was successfully established, showing more apoptotic cells and high neurological defcit scores in SAH rat. In SAH rat model, Omi expression in nerve cells was elevated and the upregulation of Omi mainly occurred in cytoplasm, accompanied by the degradation of XIAP and the increased cleaved caspase 3/9 and cleaved PARP. Once treated with UCF-101, a specifc inhibitor of Omi, the increased cell apoptosis, left/right brain moisture contents and neurological defcits were notably reversed in SAH rat brain. Of note, SAH-induced the increases of apoptosis-related protein in nerve cells were also rescued by the administration of UCF-101. Conclusions UCF-101-mediated Omi inhibition decreased the degradation of XIAP and subsequently inhibited the activation of apoptosis-related proteins, decreased nerve cell apoptosis, leading to the improvement on early brain injury in SAH rat. UCF-101-based Omi inhibition may be used to treat SAH with great potential application.
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