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Your search keyword '"Zhao, Xue-shan"' showing total 9 results
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9 results on '"Zhao, Xue-shan"'

1. Confirming the spin parameter of the black hole in Cygnus X-1 using the Insight-HXMT

Author

Zhao, Xue-Shan, Dong, Yan-Ting, Gou, Li-Jun, Feng, Ye, Jia, Nan, Li, Yu-Feng, Liao, Zhen-Xuan, Liu, Ji-Ren, Zheng, Xue-Ying, Zhang, Shuang-Nan, Qu, Jin-Lu, Song, Li-Ming, Zhang, Shu, Bu, Qing-Cui, Cai, Ce, Cao, Xue-Lei, Chang, Zhi, Chen, Gang, Chen, Li, Chen, Tian-Xiang, Chen, Yi-Bao, Chen, Yong, Chen, Yu-Peng, Cui, Wei, Cui, Wei-Wei, Deng, Jing-Kang, Dong, Yong-Wei, Du, Yuan-Yuan, Fu, Min-Xue, Gao, Guan-Hua, Gao, He, Gao, Min, Ge, Ming-Yu, Gu, Yu-Dong, Guan, Ju, Guo, Cheng-Cheng, Han, Da-Wei, Huang, Yue, Huo, Jia, Jia, Shu-Mei, Jiang, Lu-Hua, Jiang, Wei-Chun, Jin, Jing, Jin, Yong-Jie, Kong, Ling-Da, Li, Bing, Li, Cheng-Kui, Li, Gang, Li, Mao-Shun, Li, Ti-Pei, Li, Wei, Li, Xian, Li, Xiao-Bo, Li, Xu-Fang, Li, Yan-Guo, Li, Zheng-Wei, Liang, Xiao-Hua, Liao, Jin-Yuan, Liu, Bai-Sheng, Liu, Cong-Zhan, Liu, Guo-Qing, Liu, He-Xin, Liu, Hong-Wei, Liu, Xiao-Jing, Liu, Yi-Nong, Lu, Bo, Lu, Fang-Jun, Lu, Xue-Feng, Luo, Qi, Luo, Tao, Ma, Xiang, Meng, Bin, Nang, Yi, Nie, Jian-Yin, Ou, Ge, Sai, Na, Shang, Ren-Cheng, Song, Xin-Ying, Sun, Liang, Tan, Ying, Tao, Lian, Tuo, You-Li, Wang, Chen, Wang, Guo-Feng, Wang, Juan, Wang, Wen-Shuai, Wang, Yu-Sa, Wen, Xiang-Yang, Wu, Bai-Yang, Wu, Bo-Bing, Wu, Mei, Xiao, Guang-Cheng, Xiao, Shuo, Xiong, Shao-Lin, Xu, Yu-Peng, Yang, Jia-Wei, Yang, Sheng, Yang, Yan-Ji, Yang, Yi-Rong, Yi, Qi-Bin, Yin, Qian-Qing, You, Yuan, Zhang, Ai-Mei, Zhang, Cheng-Mo, Zhang, Fan, Zhang, Hong-Mei, Zhang, Juan, Zhang, Tong, Zhang, Wan-Chang, Zhang, Wei, Zhang, Wen-Zhao, Zhang, Yi, Zhang, Yi-Fei, Zhang, Yong-Jie, Zhang, Yue, Zhang, Zhao, Zhang, Zhi, Zhang, Zi-Liang, Zhao, Hai-Sheng, Zhao, Xiao-Fan, Zheng, Shi-Jie, Zhou, Deng-Ke, Zhou, Jian-Feng, Zhu, Yu-Xuan, Yue-Zhu, and Zhuang, Ren-Lin

Published
2020
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6. Imbalanced cholesterol metabolism in Alzheimer's disease

Author

Zhao Xue-shan, Tang Zhi-han, Pan Li-hong, Wu Qi, Ren Zhong, Wang Gui-xue, Liu Lu-shan, Peng juan, and Jiang Zhi-sheng

Subjects
0301 basic medicine, Apolipoprotein E, medicine.medical_specialty, Clinical Biochemistry, Hypercholesterolemia, Disease, Biology, Bioinformatics, Biochemistry, Pathogenesis, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Alzheimer Disease, Risk Factors, Internal medicine, medicine, Animals, Humans, Cholesterol, Mechanism (biology), PCSK9, Biochemistry (medical), General Medicine, medicine.disease, LRP1, 030104 developmental biology, Endocrinology, chemistry, Blood-Brain Barrier, lipids (amino acids, peptides, and proteins), Alzheimer's disease, 030217 neurology & neurosurgery
Abstract

Alzheimer's disease (AD) is a complex and multifactorial neurodegenerative disease that is mainly caused by β-amyloid accumulation. A large number of studies have shown that elevated cholesterol levels may perform a function in AD pathology, and several cholesterol-related gene polymorphisms are associated with this disease. Although numerous studies have shown the important function of cholesterol in AD pathogenesis and development, the underlying mechanism remains unclear. To further elucidate cholesterol metabolism disorder and AD, we first, review metabolism and regulation of the cholesterol in the brain. Second, we summarize the literature stating that hypercholesterolemia is one of the risk factors of AD. Third, we discuss the main mechanisms of abnormal cholesterol metabolism that increase the risk of AD. Finally, the relationships between AD and apolipoprotein E, PCSK9, and LRP1 are discussed in this article.

Published
2015

8. Functional regulatory roles of microRNAs in atherosclerosis

Author

Gao, Ya, primary, Peng, Juan, additional, Ren, Zhong, additional, He, Ni-ya, additional, Li, Qing, additional, Zhao, Xue-shan, additional, Wang, Mei-mei, additional, Wen, Hong-yan, additional, Tang, Zhi-han, additional, Jiang, Zhi-sheng, additional, Wang, Gui-xue, additional, and Liu, Lu-shan, additional

Published
2016
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9. Hyperlipidemia-induced apoptosis of hippocampal neurons in apoE(-/-) mice may be associated with increased PCSK9 expression.

Author

Zhao XS, Wu Q, Peng J, Pan LH, Ren Z, Liu HT, Jiang ZS, Wang GX, Tang ZH, and Liu LS

Subjects
Amyloid Precursor Protein Secretases metabolism, Animals, Apolipoproteins E deficiency, Caspase 3 metabolism, Cholesterol blood, Diet, High-Fat, Hippocampus cytology, Hippocampus metabolism, Hyperlipidemias metabolism, Immunohistochemistry, Mice, Mice, Knockout, Neurons cytology, Proprotein Convertase 9 metabolism, Proto-Oncogene Proteins c-bcl-2 metabolism, Triglycerides blood, bcl-2-Associated X Protein metabolism, Apolipoproteins E genetics, Apoptosis genetics, Gene Expression Regulation, Hyperlipidemias physiopathology, Neurons metabolism, Proprotein Convertase 9 genetics
Abstract

Hyperlipidemia is a risk factor for Alzheimer's disease (AD) and other neurodegenerative diseases. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a lipid regulatory gene involved in cell apoptosis. However, the function and mechanism of PCSK9 in neuronal apoptosis following hyperlipidemia remains to be elucidated. The present study established a hyperlipidemic mouse model by feeding a high‑fat diet (HFD) to 6‑week‑old apoE(‑/‑) mice. Plasma lipid levels, hippocampal lipid accumulation, hippocampal histology, and hippocampal neuronal apoptosis were all monitored for changes. The expression levels of PCSK9, β‑secretase 1 (BACE1), B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), and caspase‑3 in hippocampal CA3 and CA1 neurons were also measured. Results demonstrated that a HFD increased the lipid accumulation in the CA3 hippocampus and the levels of plasma lipids, including triglycerides, total cholesterol, low‑density lipoprotein, and high‑density lipoprotein. In addition, CA3 neurons in the HFD group indicated apparent injuries and increased neuronal apoptosis, which are associated with the expression of Bcl‑2, Bax, and caspase‑3. A HFD also increased the expression levels of PCSK9 and BACE1. BACE1 promotes cleavage of amyloid precursor proteins to generate β‑amyloid peptide (Aβ), which induces neuronal apoptosis. Protein levels of Aβ are associated with the observation of amyloid plaques in the hippocampus of the HFD group. The results suggest that hyperlipidemia regulates neuronal apoptosis by increasing PCSK9 and BACE1 expression. Overall, the current study may elucidate the role of lipid metabolism disorder in AD pathogenesis.

Published
2017
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