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- 저자 : Wen-Cong Zhao (검색결과 5 건)
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Effects of Ca2+ ion substitution on the structure and magnetism of SrRuO3: Elusive magnetism
Zhang Wen-Ying,Yue Cai-Xia,Zhao De-Wei,Li Guo-Ke,Ma Li,Zhen Cong-Mian,Hou Deng-Lu 한국물리학회 2020 Current Applied Physics Vol.20 No.12
SrRuO3 is an orthogonally distorted perovskite (Pbnm) structure whose ferromagnetism is often viewed as an itinerant ferromagnet. Although SrRuO3 has been studied for more than half a century, its structure, magnetism and transport properties are still poorly understood. In this paper, the structure and magnetic evolution of SrRuO3 are discussed in depth through the substitution of Ca2+ for Sr2+ at A sites. The results show that as the Ca substitution increases, the lattice constant decreases, the orthogonal distortion becomes larger, and the saturation magnetization MS, Curie temperature TC and Weiss temperature θp decrease accordingly. Eventually, the ferromagnetic SrRuO3 changes to paramagnetic CaRuO3. The critical exponent β of samples with different substitution contents was obtained by fitting the experimental results, and the value for SrRuO3 (β = 0.55) was similar to that obtained by mean field theory. However, the value increases with the substitution x of Ca, which can’t be explained by any scaling theory. The results show that the increase in the value of β is related to the magnetic disorder caused by different magnetic interactions. Analysis using the Rhodes-Wohlfarth criterion indicates that Sr1-xCaxRuO3 has both itinerant-electron and localized-electron magnetism, which is consistent with the theoretical predictions.
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Hong-Qi Yang,Wen-Cong Zhao,Wei-Min Yang,Yong-Li Li,Zhi-Kun Sun,Shuai Chen,Wei Li,Jian-Jun Ma 대한신경과학회 2016 Journal of Clinical Neurology Vol.12 No.3
Background and PurposezzAcute disseminated encephalomyelitis (ADEM) is an infammatory demyelinating disorder that predominantly afects children. Previous studies have mostly involved children in Western developed countries. MethodszzTis study retrospectively reviewed the clinical profles of ADEM in adult Chinese patients. ResultszzADEM occurred during summer and autumn in about two-thirds of the 42 included patients. Prior infection was found in fve patients and no preimmunization was recorded. Te most frequent clinical presentations were alterations in consciousness (79%) and behavior changes (69%), followed by motor defcits (64%) and fever (50%). About one-quarter (26%) of the patients showed positive results for oligoclonal bands, and about half of them exhibited increases in the IgG index and 24-hour IgG synthesis rate. Magnetic resonance imaging showed white- and gray-matter lesions in 83% and 23% of the patients, respectively. Steroids were the main treatment, and full recovery occurred in 62% of the patients, with residual focal neurological defcits recorded in a few patients. Afer a mean follow-up period of 3.4 years, two patients exhibited recurrence and one patient exhibited a multiphasic course. One patient was diagnosed with multiple sclerosis (MS). ConclusionszzWith the exception of the seasonal distribution pattern and prior vaccine rate, the clinical profles of ADEM in adult Chinese patients are similar to those in pediatric populations. No specifc markers are available for distinguishing ADEM from MS at the initial presentation. Careful clinical evaluations, cerebrospinal fuid measurements, and neuroradiological examinations with long-term follow-up will aid the correct diagnosis of ADEM.
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Loss of MicroRNA-137 Impairs the Homeostasis of Potassium in Neurons via KCC2
Ting-Wei Mi,Xiao-Wen Sun,Zhi-Meng Wang,Ying-Ying Wang,Xuan-Cheng He,Cong Liu,Shuang-Feng Zhang,Hong-Zhen Du,Chang-Mei Liu,Zhao-Qian Teng 한국뇌신경과학회 2020 Experimental Neurobiology Vol.29 No.2
Neuropsychiatric disorders are the leading cause of mental and intellectual disabilities worldwide. Current therapies against neuropsychiatric disorders are very limited, and very little is known about the onset and development of these diseases, and their most effective treatments. MIR137 has been previously identified as a risk gene for the etiology of schizophrenia, bipolar disorder, and autism spectrum disorder. Here we generated a forebrain-specific MIR137 knockout mouse model, and provided evidence that loss of miR-137 resulted in impaired homeostasis of potassium in mouse hippocampal neurons. KCC2, a potassium-chloride co-transporter, was a direct downstream target of miR-137. The KCC2 specific antagonist VU0240551 could balance the current of potassium in miR-137 knockout neurons, and knockdown of KCC2 could ameliorate anxiety-like behavior in MIR137 cKO mice. These data suggest that KCC2 antagonists or knockdown might be beneficial to neuropsychiatric disorders due to the deficiency of miR-137.
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Neurotrophic Artemin Promotes Motility and Invasiveness of MIA PaCa-2 Pancreatic Cancer Cells
Meng, Ling-Xin,Chi, Yu-Hua,Wang, Xiang-Xu,Ding, Zhao-Jun,Fei, Li-Cong,Zhang, Hong,Mou, Ling,Cui, Wen,Xue, Ying-Jie Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.5
Objective: To analyze the capacity of neurotrophic artemin to promote the motility and invasiveness of MIA PaCa-2 pancreatic cancer cells. Methods: MIA PaCa-2 was cultured in vitro and studied using transwell chambers for motility and invasiveness on treatment with different concentrations of aArtemin or its receptor $GFR{\alpha}3$ were also determined. Expression of matrix metalloproteinase-2 (MMP-2) and epithelial cadherin (E-cadherin) was quantified using RT-PCR and Western blotting. Results: MIA PaCa-2 pancreatic cancer cell motility and invasiveness was significantly increased with artemin and its receptor $GFR{\alpha}3$ with dose dependence (P<0.01). MMP-2 production was also significantly increased (t = 6.35, t = 7.32), while E-cadherin was significantly lowered (t = 4.27, t = 5.61) (P <0.01). Conclusion: Artemin and its receptor $GFR{\alpha}3$ can promote pancreatic cancer cell motility and invasiveness and contribute to aggressive behavior. The mechanism may be related to increased expression of MMP-2 molecule and down-regulation of E-cadherin expression.
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