Date: 2065438+03-11-30 0: 09: 54 popularity: 605 seal.
Professor Zhu Li graduated from Medical College of Jilin University. The 65438-0992 joint training program was funded by Zheng Scholarship of the Ministry of Health and went to the University of California, San Francisco () to study for a degree. 1999 After graduation, I did postdoctoral research at Thomas Jefferson University. From 2002 to 2008, he worked as a senior research researcher at the University of Pennsylvania in the United States, and from 2008 to 2009, he worked as a supervisor researcher at Bayer Pharmaceutical Company in the United States. Since September 2009, he has been employed as distinguished professor, doctoral supervisor and project leader of Tang Zhongying Hematology Research Center of Suzhou University. Professor Zhu Li is mainly engaged in the research of platelet biology, thrombosis and hemostasis, cardiovascular diseases and so on. The recent major contributions are (1). Firstly, the expression of SEMA4D, a member of semaphore family, was found in platelets, which proved the regulatory mechanism of metalloproteinases ADAM 17 and their soluble SEMA4D forming SEMA4D. (2) Functionally, using model animals and animal models of vascular injury, it is proved for the first time that SEMA4D is involved in platelet activation and thrombosis; (3) Pre-clinical studies show that SEMA4D is involved in the occurrence and development of atherosclerosis and cardiovascular diseases. Published relevant research papers in international core journals such as PNAS and Blood, and obtained 1 US patent, 1 American Heart Association (AHA) research fund and 1 National Institutes of Health (NIH) project. He has written three reviews for international scientific journals such as Journal of Clinical Research (JCI) and participated in the writing of the first and second editions of Platelet. Invited to participate in the evaluation of scientific research funds of American Heart Association and Irish National Institutes of Health. Currently, he is the deputy director of the Atherosclerosis Professional Committee of China Pathophysiology Society, the editorial board member of China Atherosclerosis Journal, and the academic leader in the research direction of blood transformation medicine thrombosis and cardiovascular and cerebrovascular diseases in Jiangsu universities, and he has been supported by the "Six Talent Peaks in Jiangsu Province" project and the National Natural Science Foundation project.
Main research direction: 1. Regulation of megakaryocyte differentiation and platelet production;
2. Platelet activation mechanism and its interaction with coagulation system:
3. Mechanism, prevention and intervention of atherosclerotic thrombotic diseases.
E-mail:zhul@suda.edu.cn
Representative papers (5 papers)
1.WannemacherKM, Zhu L* (co-first author and co-correspondent), Jiang H, Fong KP, Stalker TJ, Lee DY, Tran AN, NeevesK, Maloney S, Kumanogoh A, Kikutani H, Hammer DA, Diamond SL, Brass LF. The decrease of (20 10)Syk activation and the enhancement of contact dependence are the basis of impaired thrombus growth in mice lacking 4D signaling. Blood116: 5707-5715.
2. Zhu L, stalker TJ, Fang KP, Jiang H, Tran A, Creighton I, Li EK, Nevis KB, maloney SF, Kikutani, Kumamoto A, pure E, diamond SL, brass LF. (2009) The destruction of sema4dam can aggravate the platelet hypersensitivity in patients with dyslipidemia and prevent the development of atherosclerosis. Atherosclerosis thrombus biology 29: 1039- 1045.
3.BrassLF, Zhu L, stalker TJ. (2008) A new therapeutic target of platelet vascular interface. Vascular Biology of Atherosclerosis Thrombosis 28: s43-50.
4. Zhu L, Bergmeier W, Wu J, Jiang H, StocktJ, Sieslack M, Fan R, Bumsel L, Xiong Yeguo A, Kikutani, Ta Magney L, Wagner DD, Milla ME, Brasslf. (2007) Dual roles of regulating surface expression and shedding support 4D in platelet response to vascular injury. proc NatlAcad Sci 104: 162 1- 1626。
5. Zhu L, Zilbering A, Wu XD, Kalyankar M, Josef Ji, Jabbour S, Deeb W, Goldstein. (200 1) An anaerobic environment was used to preserve the endogenous activity of protein tyrosine phosphatase isolated from intact cells. FASEB J 15: 1637- 1639。