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| 1 | AMPK and cardiac remodelling显示文摘Cardiac remodelling is generally accepted as a critical process in the progression of heart failure. Myocyte hypertrophy,inflammatory responses and cardiac fibrosis are the main pathological changes associated with cardiac remodelling.AMP-activated protein kinase(AMPK) is known as an energy sensor and a regulator of cardiac metabolism under normal and ischaemic conditions. Additionally, AMPK has been shown to play roles in cardiac remodelling extending well beyond metabolic regulation. In this review, we discuss the currently defined roles of AMPK in cardiac remodelling and summarize the effects of AMPK on cardiac hypertrophy, inflammatory responses and fibrosis and the molecular mechanisms underlying these effects. In addition, we discuss some pharmacological activators of AMPK that are promising treatments for cardiac remodelling. | Yenan Feng Youyi Zhang Han Xiao | 2018 | Science China(Life Sciences)2018，61，1： | 17 |
| 2 | Galectin-3-centered paracrine network mediates cardiac inflammation and fibrosis upon β-adrenergic insult显示文摘Rapid over-activation of β-adrenergic receptors (β-AR) following acute stress initiates cardiac inflammation and injury by activating interleukin-18 (IL-18),however,the process of inflammation cascades has not been fully illustrated.The present study aimed to determine the mechanisms of cardiac inflammatory amplification following acute sympathetic activation.With bioinformatics analysis,galectin-3 was identified as a potential key downstream effector of β-AR and IL-18 activation.The serum level of galectin-3 was positively correlated with norepinephrine or IL-18 in patients with chest pain.In the heart of mice treated with β-AR agonist isoproterenol (ISO,5 mg kg^(-1)),galectin-3 expression was upregulated markedly later than IL-18 activation,and Nlrp3^(-/-)and Il18^(-/-)mice did not show ISO-induced galectin-3 upregulation.It was further revealed that cardiomyocyte-derived IL-18 induced galectin-3 expression in macrophages following ISO treatment.Moreover,galectin-3deficiency suppressed ISO-induced cardiac inflammation and fibrosis without blocking ISO-induced IL-18 increase.Treatment with a galectin-3 inhibitor,but not a β-blocker,one day after ISO treatment effectively attenuated cardiac inflammation and injury.In conclusion,galectin-3 is upregulated to exaggerate cardiac inflammation and injury following acute β-AR activation,a galectin-3 inhibitor effectively blocks cardiac injury one day after β-AR insult. | Guomin Hu Jimin Wu Huijun Gu Xiangning Deng Wenli Xu Shan Feng Shuaixing Wang Yao Song Zhengda Pang Xiuling Deng Aleksandr E.Vendrov Nageswara R.Madamanchi Marschall S.Runge Xinyu Wang Youyi Zhang Han Xiao Erdan Dong | 2023 | Science China(Life Sciences)2023，66，5： | 3 |
| 3 | OPTIMAL RESERVE PRICE IN STATIC AND DYNAMIC SPONSORED SEARCH AUCTIONS显示文摘Sponsored search advertising is a significant revenue source for search engines.To ameliorate revenues,search engines often set fixed or variable reserve price to in influence advertisers' bidding. This paper studies the optimal reserve price for a generalized second-price auction(GSP) under both static and dynamic settings.We show that if advertisers' per-click value has an increasing generalized failure rate,the search engine's revenue rate is quasi-concave and hence there exists an optimal reserve price under both settings.Different from a static GSP auction where the optimal reserve price is proved to be constant,in a dynamic setting the optimal reserve price is dependent on not only advertisers' per-click values,but also the number of ad links sold.A search engine should gradually raise reserve price as more qualified advertisers arrive,and maintain the same threshold after all first-page positions are occupied. | Wei YANG Jun QIAO Youyi FENG Baichun XIAO | 2013 | Journal of Systems Science and Systems Engineering2013，22，4： | 2 |
| 4 | A continuous-time seat control model for single-leg flights with no-shows and optimal overbooking upper bound显示文摘 | Youyi Feng Baichun Xiao | 2005 | European Journal of Operational Research2005，，2： | 1 |
| 5 | Maximizing revenues of perishable assets with a risk factor显示文摘 | FENG Youyi XIAO Baichun | 1999 | Operations Research1999，47，2： | 1 |
| 6 | Integration of pricing and capacity allocation for perishable products显示文摘 | Youyi Feng Baichun Xiao | 2006 | European Journal ol Operational Research2006，168，： | 1 |
| 7 | A continuous-time yield management model with multiple prices and reversible price changes 显示文摘 | Feng Youyi Xiao Baichun | 2000 | Management Science2000，，5： | 1 |
| 8 | Optimal Policies of Yield Management with Multiple Predetermined Prices显示文摘 | Feng Youyi Xiao Baichun | 2000 | Operations Research2000，48，2： | 1 |
| 9 | Optimal Policies of Yield Mana- gement with Multiple Predetermined Prices显示文摘 | Feng Youyi Bai Chunxiao | 2000 | Operations Research2000，，48： | 1 |
| 10 | A continuous-time yield management model with multiple prices and reversible price changes显示文摘 | Feng Youyi Xiao Baichun | 2000 | Management Science2000，46，5： | 1 |
| 11 | A Continuous-Time Yield Mana- gement Model with Multiple Prices and Reversible Price Changes 显示文摘 | Youyi Feng Baichun Xiao | 2000 | Management Science2000，46，5： | 1 |
| 12 | Optimal Starting Times for End-of-Season Sales and Optimal Stopping Times for Pro- motional Fares显示文摘 | Youyi Feng Guillermo Gallego | 1995 | Management Science1995，41，8： | 1 |
| 13 | A continuous2time yield management model with multiple prices and reversible price changes 显示文摘 | Feng Youyi Xiao Baichun | 2000 | Management Science2000，46，5： | 1 |
| 14 | Exercise training attenuates angiotensinⅡ-induced cardiac fibrosis by reducing POU2F1 expression显示文摘Background:Exercise training protects against heart failure.However,the mechanism underlying the protective effect of exercise training on angiotensinⅡ(AngⅡ)-induced cardiac fibrosis remains unclear.Methods:An exercise model involving C57BL/6N mice and 6 weeks of treadmill training was used.AngⅡ(1.44 mg/kg/day)was administered to induce cardiac fibrosis.RNA sequencing and bioinformatic analysis were used to identify the key factors mediating the effects of exercise training on cardiac fibrosis.Primary adult mouse cardiac fibroblasts(CFs)were used in vitro.Adeno-associated virus serotype 9 was used to overexpress POU domain,class 2,transcription factor 1(POU2F1)in vivo.Results:Exercise training attenuated AngⅡ-induced cardiac fibrosis and reversed 39 gene expression changes.The transcription factor regulating the largest number of these genes was POU2F1.Compared to controls,POU2F1 was shown to be signififcantly upregulated by AngⅡ,which is itself reduced by exercise training.In vivo,POU2F1 overexpression nullified the benefits of exercise training on cardiac fibrosis.In CFs,POU2F1 promoted cardiac fibrosis.CCAAT enhancer-binding proteinβ(C/EBPβ)was predicted to be the transcription factor of POU2F1and verified using a dual-luciferase reporter assay.In vivo,exercise training activated AMP-activated protein kinase(AMPK)and alleviated the increase in C/EBPβinduced by AngⅡ.In CFs,AMPK agonist inhibited the increase in C/EBPβand POU2F1 induced by Ang II,whereas AMPK inhibitor reversed this effect.Conclusion:Exercise training attenuates AngⅡ-induced cardiac fibrosis by reducing POU2F1.Exercise training inhibits POU2F1 by activating AMPK,which is followed by the downregulation of C/EBPβ,the transcription factor of POU2F1. | Na Feng Haiyi Yu Yueshen Wang Youyi Zhang Han Xiao Wei Gao | 2023 | Journal of Sport and Health Science2023，12，4： | 0 |
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