Search

Your search keyword '"Yan Xiangyu"' showing total 494 results
Start Over Author "Yan Xiangyu" Publication Year Range Last 50 years
494 results on '"Yan Xiangyu"'

2. Multi-Interactive-Modality based Modeling for Myopia Pro-Gression of Adolescent Student

Author

Yan, Xiangyu, Han, Gongen, Fang, Can, and Jing, Xuan

Subjects
Computer Science - Human-Computer Interaction
Abstract

Myopia is a common visual disorder that affects millions of people worldwide and its prevalence has been increasing in recent years. Environmental factors, such as reading time, viewing distance, and ambient lighting, have been identified as potential factors in the development of myopia. In this study, we investigated the relationship between three major factors and myopia in 120 adolescents. By collecting environmental images of the adolescents in the learning state as well as retinal fundus images, we proposed an environmental visual load (EVL) model to extract the potential information in these images. Through experimental data analysis, we found that these three major factors are closely related to the severity of myopia, and that the simultaneous exacerbation of these factors sharply increases the myopia of the eye. Our results suggest that interventions targeting these environmental factors may help prevent and manage myopia., Comment: 9 pages, 5 figures

Published
2023

12. The application of large language models in medicine: A scoping review

Author

Meng, Xiangbin, Yan, Xiangyu, Zhang, Kuo, Liu, Da, Cui, Xiaojuan, Yang, Yaodong, Zhang, Muhan, Cao, Chunxia, Wang, Jingjia, Wang, Xuliang, Gao, Jun, Wang, Yuan-Geng-Shuo, Ji, Jia-ming, Qiu, Zifeng, Li, Muzi, Qian, Cheng, Guo, Tianze, Ma, Shuangquan, Wang, Zeying, Guo, Zexuan, Lei, Youlan, Shao, Chunli, Wang, Wenyao, Fan, Haojun, and Tang, Yi-Da

Published
2024
Full Text
View/download PDF

43. Von Willebrand factor exacerbates heart failure through formation of neutrophil extracellular traps.

Author

Mang, Ge, Chen, Jianfeng, Sun, Ping, Ma, Ruishuang, Du, Jingwen, Wang, Xiaoqi, Cui, Jingxuan, Yang, Mian, Tong, Zhonghua, Yan, Xiangyu, Wang, Dongni, Xie, Huiqi, Chen, Yujia, Yang, Qiannan, Kong, Yingjin, Jin, Jiaqi, Wu, Jian, Zhang, Maomao, and Yu, Bo

Subjects
VON Willebrand factor, KNOCKOUT mice, HOMEOSTASIS, RNA sequencing, HEART failure, LABORATORY mice
Abstract

Background and Aims Heart failure (HF) is a leading cause of mortality worldwide and characterized by significant co-morbidities and dismal prognosis. Neutrophil extracellular traps (NETs) aggravate inflammation in various cardiovascular diseases; however, their function and mechanism of action in HF pathogenesis remain underexplored. This study aimed to investigate the involvement of a novel VWF-SLC44A2-NET axis in HF progression. Methods NET levels were examined in patients with HF and mouse models of transverse aortic constriction (TAC) HF. PAD4 knockout mice and NET inhibitors (GSK-484, DNase I, NEi) were used to evaluate the role of NETs in HF. RNA sequencing was used to investigate the downstream mechanisms. Recombinant human ADAMTS13 (rhADAMTS13), ADAMTS13 , and SLC44A2 knockouts were used to identify novel upstream factors of NETs. Results Elevated NET levels were observed in patients with HF and TAC mouse models of HF. PAD4 knockout and NET inhibitors improved the cardiac function. Mechanistically, NETs induced mitochondrial dysfunction in cardiomyocytes, inhibiting mitochondrial biogenesis via the NE-TLR4-mediated suppression of PGC-1α. Furthermore, VWF/ ADAMTS13 regulated NET formation via SLC44A2. Additionally, sacubitril/valsartan amplifies the cardioprotective effects of the VWF-SLC44A2-NET axis blockade. Conclusions This study established the role of a novel VWF-SLC44A2-NET axis in regulating mitochondrial homeostasis and function, leading to cardiac apoptosis and contributing to HF pathogenesis. Targeting this axis may offer a potential therapeutic approach for HF treatment. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

44. Protosappanin A Protects DOX‐Induced Myocardial Injury and Cardiac Dysfunction by Targeting ACSL4/FTH1 Axis‐Dependent Ferroptosis.

Author

Cui, Jingxuan, Chen, Yujia, Yang, Qiannan, Zhao, Peng, Yang, Mian, Wang, Xiaoqi, Mang, Ge, Yan, Xiangyu, Wang, Di, Tong, Zhonghua, Wang, Penghe, Kong, Yingjin, Wang, Naixin, Wang, Dongni, Dong, Nana, Liu, Mingyang, E, Mingyan, Zhang, Maomao, and Yu, Bo

Subjects
MYOCARDIAL injury, HEART diseases, CARDIOTOXICITY, IRON ions, HEART injuries, DOXORUBICIN
Abstract

Doxorubicin (DOX) is an effective anticancer agent, but its clinical utility is constrained by dose‐dependent cardiotoxicity, partly due to cardiomyocyte ferroptosis. However, the progress of developing cardioprotective medications to counteract ferroptosis has encountered obstacles. Protosappanin A (PrA), an anti‐inflammatory compound derived from hematoxylin, shows potential against DOX‐induced cardiomyopathy (DIC). Here, it is reported that PrA alleviates myocardial damage and dysfunction by reducing DOX‐induced ferroptosis and maintaining mitochondrial homeostasis. Subsequently, the molecular target of PrA through proteome microarray, molecular docking, and dynamics simulation is identified. Mechanistically, PrA physically binds with ferroptosis‐related proteins acyl‐CoA synthetase long‐chain family member 4 (ACSL4) and ferritin heavy chain 1 (FTH1), ultimately inhibiting ACSL4 phosphorylation and subsequent phospholipid peroxidation, while also preventing FTH1 autophagic degradation and subsequent release of ferrous ions (Fe2+) release. Given the critical role of ferroptosis in the pathogenesis of ischemia‐reperfusion (IR) injury, this further investigation posits that PrA can confer a protective effect against IR‐induced cardiac damage by inhibiting ferroptosis. Overall, a novel pharmacological inhibitor is unveiled that targets ferroptosis and uncover a dual‐regulated mechanism for cardiomyocyte ferroptosis in DIC, highlighting additional therapeutic options for chemodrug‐induced cardiotoxicity and ferroptosis‐triggered disorders. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results