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6. Adenosine kinase inhibition protects mice from abdominal aortic aneurysm via epigenetic modulation of VSMC inflammation

Author

Xu, Jiean, primary, Liu, Zhiping, additional, Yang, Qiuhua, additional, Ma, Qian, additional, Zhou, Yaqi, additional, Cai, Yongfeng, additional, Zhao, Dingwei, additional, Zhao, Guizhen, additional, Lu, Tammy, additional, Ouyang, Kunfu, additional, Hong, Mei, additional, Kim, Ha Won, additional, Shi, Huidong, additional, Zhang, Jifeng, additional, Fulton, David, additional, Miller, Clint, additional, Malhotra, Rajeev, additional, Weintraub, Neal L, additional, and Huo, Yuqing, additional

Published
2024
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7. Comprehensive Similarity Algorithm and Molecular Dynamics Simulation-Assisted Terahertz Spectroscopy for Intelligent Matching Identification of Quorum Signal Molecules (N-Acyl-Homoserine Lactones)

Author

Zhang, Lintong, primary, Kong, Xiangzeng, additional, Qu, Fangfang, additional, Chen, Linjie, additional, Li, Jinglin, additional, Jiang, Yilun, additional, Wang, Chuxin, additional, Zhang, Wenqing, additional, Yang, Qiuhua, additional, and Ye, Dapeng, additional

Published
2024
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11. Regulation of endothelial intracellular adenosine via adenosine kinase epigenetically modulates vascular inflammation.

Author

Xu, Yiming, Wang, Yong, Yan, Siyuan, Yang, Qiuhua, Zhou, Yaqi, Zeng, Xianqiu, Liu, Zhiping, An, Xiaofei, Toque, Haroldo A, Dong, Zheng, Jiang, Xuejun, Fulton, David J, Weintraub, Neal L, Li, Qinkai, Bagi, Zsolt, Hong, Mei, Boison, Detlev, Wu, Chaodong, and Huo, Yuqing

Subjects
Blood Vessels, Cerebral Cortex, Endothelial Cells, Animals, Mice, Reperfusion Injury, Inflammation, Adenosylhomocysteinase, Adenosine Kinase, Adenosine, Gene Expression Regulation, Epigenesis, Genetic, Atherosclerosis, Gene Knockdown Techniques, Mice, Knockout, ApoE, Cardiovascular, 2.1 Biological and endogenous factors, Inflammatory and Immune System, Epigenesis, Genetic, Knockout, ApoE
Abstract

The molecular mechanisms underlying vascular inflammation and associated inflammatory vascular diseases are not well defined. Here we show that endothelial intracellular adenosine and its key regulator adenosine kinase (ADK) play important roles in vascular inflammation. Pro-inflammatory stimuli lead to endothelial inflammation by increasing endothelial ADK expression, reducing the level of intracellular adenosine in endothelial cells, and activating the transmethylation pathway through increasing the association of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH). Increasing intracellular adenosine by genetic ADK knockdown or exogenous adenosine reduces activation of the transmethylation pathway and attenuates the endothelial inflammatory response. In addition, loss of endothelial ADK in mice leads to reduced atherosclerosis and affords protection against ischemia/reperfusion injury of the cerebral cortex. Taken together, these results demonstrate that intracellular adenosine, which is controlled by the key molecular regulator ADK, influences endothelial inflammation and vascular inflammatory diseases.The molecular mechanisms underlying vascular inflammation are unclear. Here the authors show that pro-inflammatory stimuli lead to endothelial inflammation by increasing adenosine kinase expression, and that its knockdown in endothelial cells inhibits atherosclerosis and cerebral ischemic injury in mice.

Published
2017

12. Intracellular adenosine regulates epigenetic programming in endothelial cells to promote angiogenesis

Author

Xu, Yiming, Wang, Yong, Yan, Siyuan, Zhou, Yaqi, Yang, Qiuhua, Pan, Yue, Zeng, Xianqiu, An, Xiaofei, Liu, Zhiping, Wang, Lina, Xu, Jiean, Cao, Yapeng, Fulton, David J, Weintraub, Neal L, Bagi, Zsolt, Hoda, Nasrul, Wang, Xiaoling, Li, Qinkai, Hong, Mei, Jiang, Xuejun, Boison, Detlev, Weber, Christian, Wu, Chaodong, and Huo, Yuqing

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Adenosine, Adenosine Kinase, Animals, Aorta, DNA Methylation, Epigenesis, Genetic, Human Umbilical Vein Endothelial Cells, Humans, Mice, Neovascularization, Physiologic, Promoter Regions, Genetic, Vascular Endothelial Growth Factor Receptor-2, adenosine, adenosine kinase, angiogenesis, DNA methylation, endothelial cells, Medical and Health Sciences, Biochemistry and cell biology
Abstract

The nucleoside adenosine is a potent regulator of vascular homeostasis, but it remains unclear how expression or function of the adenosine-metabolizing enzyme adenosine kinase (ADK) and the intracellular adenosine levels influence angiogenesis. We show here that hypoxia lowered the expression of ADK and increased the levels of intracellular adenosine in human endothelial cells. Knockdown (KD) of ADK elevated intracellular adenosine, promoted proliferation, migration, and angiogenic sprouting in human endothelial cells. Additionally, mice deficient in endothelial ADK displayed increased angiogenesis as evidenced by the rapid development of the retinal and hindbrain vasculature, increased healing of skin wounds, and prompt recovery of arterial blood flow in the ischemic hindlimb. Mechanistically, hypomethylation of the promoters of a series of pro-angiogenic genes, especially for VEGFR2 in ADK KD cells, was demonstrated by the Infinium methylation assay. Methylation-specific PCR, bisulfite sequencing, and methylated DNA immunoprecipitation further confirmed hypomethylation in the promoter region of VEGFR2 in ADK-deficient endothelial cells. Accordingly, loss or inactivation of ADK increased VEGFR2 expression and signaling in endothelial cells. Based on these findings, we propose that ADK downregulation-induced elevation of intracellular adenosine levels in endothelial cells in the setting of hypoxia is one of the crucial intrinsic mechanisms that promote angiogenesis.

Published
2017

15. Transcriptome Analysis of Sea Cucumber (Apostichopus Japonicus) in Southern China Under Heat Stress

Author

Yang, Qiuhua, primary, Zhong, Yanfang, additional, Yang, Fuyuan, additional, Li, Huiyao, additional, Tran, Ngoc Tuan, additional, Zhang, Ming, additional, Wang, Lili, additional, He, Libin, additional, Zhang, Zhe, additional, Ge, Hui, additional, Wu, Jianshao, additional, Ai, Chunxiang, additional, Li, Shengkang, additional, and Lin, Qi, additional

Published
2024
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18. PFKFB3-mediated endothelial glycolysis promotes pulmonary hypertension

Author

Cao, Yapeng, Zhang, Xiaoyu, Wang, Lina, Yang, Qiuhua, Ma, Qian, Xu, Jiean, Wang, Jingjing, Kovacs, Laszlo, Ayon, Ramon J., Liu, Zhiping, Zhang, Min, Zhou, Yaqi, Zeng, Xianqiu, Xu, Yiming, Wang, Yong, Fulton, David J., Weintraub, Neal L., Lucas, Rudolf, Dong, Zheng, Yuan, Jason X.-J., Sullivan, Jennifer C., Meadows, Louise, Barman, Scott A., Wu, Chaodong, Quan, Junmin, Hong, Mei, Su, Yunchao, and Huo, Yuqing

Published
2019

21. Inactivation of adenosine receptor 2A suppresses endothelial-to-mesenchymal transition and inhibits subretinal fibrosis in mice.

Author

Yang, Qiuhua, Cai, Yongfeng, Ma, Qian, Xiong, Albert, Xu, Peishan, Zhang, Zhidan, Xu, Jiean, Zhou, Yaqi, Liu, Zhiping, Zhao, Dingwei, Asara, John, Li, Wei, Shi, Huidong, Caldwell, Ruth B., Sodhi, Akrit, and Huo, Yuqing

Subjects
MACULAR degeneration, ADENOSINES, ENDOTHELIAL growth factors, FIBROSIS, LIPOPROTEIN A, LIPOPROTEIN receptors, SUCCINATE dehydrogenase
Abstract

Anti–vascular endothelial growth factor therapy has had a substantial impact on the treatment of choroidal neovascularization (CNV) in patients with neovascular age-related macular degeneration (nAMD), the leading cause of vision loss in older adults. Despite treatment, many patients with nAMD still develop severe and irreversible visual impairment because of the development of subretinal fibrosis. We recently reported the anti-inflammatory and antiangiogenic effects of inhibiting the gene encoding adenosine receptor 2A (Adora2a), which has been implicated in cardiovascular disease. Here, using two mouse models of subretinal fibrosis (mice with laser injury–induced CNV or mice with a deficiency in the very low–density lipoprotein receptor), we found that deletion of Adora2a either globally or specifically in endothelial cells reduced subretinal fibrosis independently of angiogenesis. We showed that Adora2a-dependent endothelial-to-mesenchymal transition contributed to the development of subretinal fibrosis in mice with laser injury–induced CNV. Deficiency of Adora2a in cultured mouse and human choroidal endothelial cells suppressed induction of the endothelial-to-mesenchymal transition. A metabolomics analysis of cultured human choroidal endothelial cells showed that ADORA2A knockdown with an siRNA reversed the increase in succinate because of decreased succinate dehydrogenase B expression under fibrotic conditions. Pharmacological inhibition of ADORA2A with a small-molecule KW6002 in both mouse models recapitulated the reduction in subretinal fibrosis observed in mice with genetic deletion of Adora2a. ADORA2A inhibition may be a therapeutic approach to treat subretinal fibrosis associated with nAMD. Editor's summary: Retinal fibrosis reversal age-related macular degeneration (AMD) is driven by neovascularization and is associated with subretinal fibrosis. Working in mice with genetically induced AMD or with a laser-induced retinal injury, Yang et al. show that deleting the gene encoding adenosine receptor 2A (Adora2a) prevented subretinal fibrosis in both mouse models. Specifically, deleting Adora2a in endothelial cells was sufficient to reverse subretinal fibrosis by preventing endothelial-to-mesenchymal transition. In human choroidal endothelial cells, the authors showed that endothelial-to-mesenchymal transition was associated with succinate accumulation due to decreased succinate dehydrogenase subunit B expression. Treatment with an ADORA2A antagonist reversed subretinal fibrosis in both mouse models, suggesting that targeting ADORA2A in endothelial cells could be a therapeutic strategy to treat AMD. —Brandon Berry [ABSTRACT FROM AUTHOR]

Published
2024
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28. Structure-based virtual screening identifies small molecule inhibitors of O-fucosyltransferase SPINDLY

Author

Aizezi, Yalikunjiang, Zhao, Hongming, Zhang, Zhenzhen, Bi, Yang, Yang, Qiuhua, Guo, Guangshuo, Zhang, Hongliang, Guo, Hongwei, Jiang, Kai, and Wang, Zhi-Yong

Subjects
Article
Abstract

Protein O-glycosylation is a nutrient-signaling mechanism that plays essential roles in maintaining cellular homeostasis across different species. In plants, SPINDLY (SPY) and SECRET AGENT (SEC) catalyze posttranslational modifications of hundreds of intracellular proteins by O-fucose and O-linked N-acetylglucosamine, respectively. SPY and SEC play overlapping roles in cellular regulation and loss of both SPY and SEC causes embryo lethality in Arabidopsis. Using structure-based virtual screening of chemical libraries followed by in vitro and in planta assays, we identified a S PY O - f ucosyltransferase i nhibitor (SOFTI). Computational analyses predicted that SOFTI binds to the GDP-fucose-binding pocket of SPY and competitively inhibits GDP-fucose binding. In vitro assays confirmed that SOFTI interacts with SPY and inhibits its O-fucosyltransferase activity. Docking analysis identified additional SOFTI analogs that showed stronger inhibitory activities. SOFTI treatment of Arabidopsis seedlings decreased protein O-fucosylation and caused phenotypes similar to the spy mutants, including early seed germination, increased root hair density, and defect in sugar-dependent growth. By contrast, SOFTI had no visible effect on the spy mutant. Similarly, SOFTI inhibited sugar-dependent growth of tomato seedlings. These results demonstrate that SOFTI is a specific SPY O-fucosyltransferase inhibitor and a useful chemical tool for functional studies of O-fucosylation and potentially for agricultural management.

Published
2023

29. Purine synthesis suppression reduces the development and progression of pulmonary hypertension in rodent models

Author

Ma, Qian, primary, Yang, Qiuhua, additional, Xu, Jiean, additional, Sellers, Hunter G, additional, Brown, Zach L, additional, Liu, Zhiping, additional, Bordan, Zsuzsanna, additional, Shi, Xiaofan, additional, Zhao, Dingwei, additional, Cai, Yongfeng, additional, Pareek, Vidhi, additional, Zhang, Chunxiang, additional, Wu, Guangyu, additional, Dong, Zheng, additional, Verin, Alexander D, additional, Gan, Lin, additional, Du, Quansheng, additional, Benkovic, Stephen J, additional, Xu, Suowen, additional, Asara, John M, additional, Ben-Sahra, Issam, additional, Barman, Scott, additional, Su, Yunchao, additional, Fulton, David J R, additional, and Huo, Yuqing, additional

Published
2023
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30. High-Throughput Automatic Identification of Quorum Signaling Molecules (N-Acyl-Homoserine Lactones) Based on Terahertz Spectroscopy Combined with Molecular Dynamics Simulation and Spectral Similarity Calculation

Author

Zhang, lintong, primary, Qu, Fangfang, additional, Chen, Linjie, additional, Li, Jinglin, additional, Jiang, Yilun, additional, Wang, Chuxing, additional, Yang, Qiuhua, additional, Kong, Xiangzeng, additional, and Ye, Dapeng, additional

Published
2023
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33. Single-cell transcriptome analyses reveal microglia types associated with proliferative retinopathy

Author

Liu, Zhiping, primary, Shi, Huidong, additional, Xu, Jiean, additional, Yang, Qiuhua, additional, Ma, Qian, additional, Mao, Xiaoxiao, additional, Xu, Zhimin, additional, Zhou, Yaqi, additional, Da, Qingen, additional, Cai, Yongfeng, additional, Fulton, David J.R., additional, Dong, Zheng, additional, Sodhi, Akrit, additional, Caldwell, Ruth B., additional, and Huo, Yuqing, additional

Published
2022
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34. ATIC-Associated De Novo Purine Synthesis Is Critically Involved in Proliferative Arterial Disease

Author

Ma, Qian, primary, Yang, Qiuhua, additional, Xu, Jiean, additional, Zhang, Xiaoyu, additional, Kim, David, additional, Liu, Zhiping, additional, Da, Qingen, additional, Mao, Xiaoxiao, additional, Zhou, Yaqi, additional, Cai, Yongfeng, additional, Pareek, Vidhi, additional, Kim, Ha Won, additional, Wu, Guangyu, additional, Dong, Zheng, additional, Song, Wen-Liang, additional, Gan, Lin, additional, Zhang, Chunxiang, additional, Hong, Mei, additional, Benkovic, Stephen J., additional, Weintraub, Neal L., additional, Fulton, David, additional, Asara, John M., additional, Ben-Sahra, Issam, additional, and Huo, Yuqing, additional

Published
2022
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35. Suppression of myeloid PFKFB3‐driven glycolysis protects mice from choroidal neovascularization

Author

Liu, Zhiping, primary, Mao, Xiaoxiao, additional, Yang, Qiuhua, additional, Zhang, Xiaoyu, additional, Xu, Jiean, additional, Ma, Qian, additional, Zhou, Yaqi, additional, Da, Qingen, additional, Cai, Yongfeng, additional, Sopeyin, Anu, additional, Dong, Zheng, additional, Hong, Mei, additional, Caldwell, Ruth B., additional, Sodhi, Akrit, additional, and Huo, Yuqing, additional

Published
2022
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36. Gemstone: A New Stream Cipher Using Coupled Map Lattice

Author

Yin, Ruming, Yuan, Jian, Yang, Qiuhua, Shan, Xiuming, Wang, Xiqin, Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Bao, Feng, editor, Yung, Moti, editor, Lin, Dongdai, editor, and Jing, Jiwu, editor

Published
2010
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39. Identification and Validation of a Ferroptosis-Related Signature for Predicting Prognosis and Immune Microenvironment in Papillary Renal Cell Carcinoma

Author

Da, Qingen, Ren, Mingming, Huang, Lei, Qu, Jianhua, Yang, Qiuhua, Xu, Jiean, Ma, Qian, Mao, Xiaoxiao, Cai, Yongfeng, Zhao, Dingwei, Luo, Junhua, Yan, Zilong, Sun, Lu, Ouyang, Kunfu, Zhang, Xiaowei, Han, Zhen, Liu, Jikui, Wang, Tao, Da, Qingen, Ren, Mingming, Huang, Lei, Qu, Jianhua, Yang, Qiuhua, Xu, Jiean, Ma, Qian, Mao, Xiaoxiao, Cai, Yongfeng, Zhao, Dingwei, Luo, Junhua, Yan, Zilong, Sun, Lu, Ouyang, Kunfu, Zhang, Xiaowei, Han, Zhen, Liu, Jikui, and Wang, Tao

Abstract

Objective: We aimed to explore the prognostic patterns of ferroptosis-related genes in papillary renal cell carcinoma (PRCC) and investigate the relationship between ferroptosis-related genes and PRCC tumor immune microenvironment. Methods: We obtained the mRNA expression and corresponding clinical data of PRCC from the public tumor cancer genome atlas database (TCGA). The PRCC patients were randomly divided into two cohort, training cohort and verification cohort, respectively. Univariate Cox regression, LASSO Cox regression, multivariate Cox regression analysis were utilized to construct ferroptosis signature for PRCC patients. And then, risk prognostic model was established and verified. The correlation of ferroptosis-related signature with survival and immune microenvironment was systematically analyzed. Results: A 4-genes ferroptosis signature (CDKN1A, MIOX, PSAT1, and RRM2) was constructed. Multivariate Cox regression assay indicates that the risk score of ferroptosis signature was an independent prognostic indicator (HR=1.391, p<0.001). The survival curve shows that the high-risk group has a poorer prognosis than the low-risk group (p<0.001). The risk prognostic model was established based on prognostic factors of clinical-stage, hemoglobin, and risk score. The time-dependent receiver operating characteristic curve (ROC) analysis proves the predictive capacity of the ferroptosis signature, the 3 years area under the curve (AUC) is 0.890, and the 5 years AUC is 0.733. Further analysis suggested that cell cycle, pentose phosphate pathway, P53 signaling pathway were significantly enriched in the high-risk group. The significantly different fractions of dendritic cells resting, macrophage cells, and T cells follicular helper were observed in risk groups. Conclusion: This study implicates a ferroptosis signature which has a good predict capacity of the prognosis in PRCC patients. Ferroptosis-related genes may have a key role in the process of anti-tumor and serve

Published
2022

40. Identification and Validation of a Ferroptosis-Related Signature for Predicting Prognosis and Immune Microenvironment in Papillary Renal Cell Carcinoma

Author

Da,Qingen, Ren,Mingming, Huang,Lei, Qu,Jianhua, Yang,Qiuhua, Xu,Jiean, Ma,Qian, Mao,Xiaoxiao, Cai,Yongfeng, Zhao,Dingwei, Luo,Junhua, Yan,Zilong, Sun,Lu, Ouyang,Kunfu, Zhang,Xiaowei, Han,Zhen, Liu,Jikui, Wang,Tao, Da,Qingen, Ren,Mingming, Huang,Lei, Qu,Jianhua, Yang,Qiuhua, Xu,Jiean, Ma,Qian, Mao,Xiaoxiao, Cai,Yongfeng, Zhao,Dingwei, Luo,Junhua, Yan,Zilong, Sun,Lu, Ouyang,Kunfu, Zhang,Xiaowei, Han,Zhen, Liu,Jikui, and Wang,Tao

Abstract

Qingen Da,1,2,&ast; Mingming Ren,2,&ast; Lei Huang,2 Jianhua Qu,1 Qiuhua Yang,3 Jiean Xu,4 Qian Ma,4 Xiaoxiao Mao,4 Yongfeng Cai,4 Dingwei Zhao,4 Junhua Luo,5 Zilong Yan,1 Lu Sun,2 Kunfu Ouyang,2 Xiaowei Zhang,6 Zhen Han,2 Jikui Liu,1 Tao Wang2 1Department of Hepatobiliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, People’s Republic of China; 2Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, People’s Republic of China; 3Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA, USA; 4Shenzhen Graduate School, Peking University, Shenzhen, People’s Republic of China; 5Department of Urological Surgery, Peking University Shenzhen Hospital, Shenzhen, People’s Republic of China; 6School of Basic Medical Sciences, Peking University, Beijing, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Jikui Liu, Department of Hepatobiliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, People’s Republic of China, Email liu8929@126.com Tao Wang, Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, People’s Republic of China, Email szwangtao@126.comObjective: We aimed to explore the prognostic patterns of ferroptosis-related genes in papillary renal cell carcinoma (PRCC) and investigate the relationship between ferroptosis-related genes and PRCC tumor immune microenvironment.Methods: We obtained the mRNA expression and corresponding clinical data of PRCC from the public tumor cancer genome a

Published
2022

41. Identification and Validation of a Ferroptosis-Related Signature for Predicting Prognosis and Immune Microenvironment in Papillary Renal Cell Carcinoma

Author

Da, Qingen, primary, Ren, Mingming, additional, Huang, Lei, additional, Qu, Jianhua, additional, Yang, Qiuhua, additional, Xu, Jiean, additional, Ma, Qian, additional, Mao, Xiaoxiao, additional, Cai, Yongfeng, additional, Zhao, Dingwei, additional, Luo, Junhua, additional, Yan, Zilong, additional, Sun, Lu, additional, Ouyang, Kunfu, additional, Zhang, Xiaowei, additional, Han, Zhen, additional, Liu, Jikui, additional, and Wang, Tao, additional

Published
2022
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43. Endothelial AMPKα1/PRKAA1 exacerbates inflammation in HFD‐fed mice

Author

Yang, Qiuhua, primary, Ma, Qian, additional, Xu, Jiean, additional, Liu, Zhiping, additional, Mao, Xiaoxiao, additional, Zhou, Yaqi, additional, Cai, Yongfeng, additional, Da, Qingen, additional, Hong, Mei, additional, Weintraub, Neal L., additional, Fulton, David J., additional, Belin de Chantemèle, Eric J., additional, and Huo, Yuqing, additional

Published
2021
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45. Genome and gene evolution of seahorse species revealed by the chromosome‐level genome of Hippocampus abdominalis

Author

He, Libin, primary, Long, Xin, additional, Qi, Jianfei, additional, Wang, Zongji, additional, Huang, Zhen, additional, Wu, Shuiqing, additional, Zhang, Xingtan, additional, Luo, Huiyu, additional, Chen, Xinxin, additional, Lin, Jinbo, additional, Yang, Qiuhua, additional, Huang, Shiyu, additional, Zhou, Qi, additional, and Zheng, Leyun, additional

Published
2021
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46. Deficiency of Myeloid Pfkfb3 Protects Mice From Lung Edema and Cardiac Dysfunction in LPS-Induced Endotoxemia

Author

Xu, Jiean, primary, Wang, Lina, additional, Yang, Qiuhua, additional, Ma, Qian, additional, Zhou, Yaqi, additional, Cai, Yongfeng, additional, Mao, Xiaoxiao, additional, Da, Qingen, additional, Lu, Tammy, additional, Su, Yunchao, additional, Bagi, Zsolt, additional, Lucas, Rudolf, additional, Liu, Zhiping, additional, Hong, Mei, additional, Ouyang, Kunfu, additional, and Huo, Yuqing, additional

Published
2021
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