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唐朝枢，北京大学医学部生理与病理生理学教授，博士研究生导师。曾任国家九七三项目（心脑血管疾病发病和防治基础研究）首席科学家，长期从事心血管生理及病理机制方面的科研和教学工作。兼任《生理学报》、《北京大学学报（医学版）》，《中国动脉硬化杂志》，《中华老年多器官功能障碍杂志》和《国际病理科学和临床杂志》副主编，《中华医学杂志》、《中华心血管病杂志》和《中国医学科学院学报》等杂志编委。参编、主编《病理生理学》教科书及《休克学》、《老年心脏病学》和《动脉粥样硬化性心血管病.基础与临床》等专著多部。至今已发表SCI收录论文120余篇。曾获国家科技进步二等奖（1998年），部委一等奖（1991、1997、2003和2005年）、二、三等奖等多项奖项。
Tang Chao Shu, A Professor of Department of Physiology and Pathophysiology, Peking University Health Science Center, tutor of doctor as well. Professor Tang has been engaged in teaching and research work of physiology and pathological mechanism of cardiovascular system. He was a chief scientist of the State Major Basic Research Development Program of the People’s Republic of China “973”.He is an associate editor of Journals including “Acta Physiologica Sinica”, “Progress in Physiological Science”, “Journal of Peking University(Health sciences)”, “ Chinese Journal of arteriosclerosis”, “Chinese Journal of Multiple Organ Diseases in the Elderly”, “International Journal of Pathology and Clinical Medicine”,etc. And he is an editor of Journals including “Chinese Medical Journal”, and “Chinese Journal of Cardiology”, “Acta Academiae Medicinae Sinicae”,etc. As a editor, He wrote many books including “ Pathophysiology” , “Shock”, “Atherosclerotic Cardiovascular Diseases: Basic and Clinical Medicine”,etc. So far, he has published more than 150 original research papers collected in Science Cited Index(SCI). The major awards he has been granted include a second-class National Prize for Progress in Science and Technology (1998), four first-class awards at the ministerial/provincial levels (1991,1997,2003,2005, respectively), and many other awards.
齐永芬博士
Yong Fen Qi, Ph.D.
Phone：010-82802851
Fax： 010-82802851
E-mail：yongfenqi@163.com
学习经历
1982.9-1987.7 衡阳医学院 医疗系 本科生 获学士学位
1990.9-1993.7 北京医科大学 寄生虫学教研室 研究生 获硕士学位
1999.9-2002.7 北京大学医学部 生理与病理生理学系 研究生 获博士学位
工作经历
1987.7-1990.8 衡阳医学院 寄生虫学教研室 助教
1993.8-1999.8 北京医科大学 寄生虫学教研室 讲师
2002.8-2003.8 北京大学医学部 生理与病理生理学系 讲师
2003.9-2008.7 北京大学医学部 生理与病理生理学系 副教授
2009.2-2009.8 美国中弗罗里达大学医学院 分子生物学中心 访问学者
2008.8- 北京大学医学部 病原生物学系 教授
至今已发表50余篇SCI论文， H-index 为11.
Education and Training
1999,9 ~ 2002,7 Ph. D Degree was awarded by Peking University. Beijing, China
1990,9 ~ 1993,7 Master Degree of Science( M.S.) Department of Parasitology, Beijing Medical University, Beijing, China
1982,9 ~1987,7 Bechalor Degree of Medicine( equivalent to MD), Department of Medicine, Heng Yang Medical College, Heng Yang, Hunan, China
Work Experience:
2008.8~now Professor of Physiology
2009.2~2009.8 Visiting scholar, Biomolecular Science Center, College of Medicine, University of Central Florida
2003,9~ 2008.8 Associate professor of Department of Physiology and Pathophysiology
Peking University Health Science Center
2002,7 ~2003,8 Lecture of Department of Physiology and Pathophysiology
Peking University Health Science Center
1993,8~1999 Lecture, Department of Parasitology, Beijing Medical University, Beijing, China
1987,8~1990 Assistant , Department of Parasitology, Heng Yang Medical College, Heng Yang, Hunan Province, China
So far, she has published more than 50 original research papers collected in Science Cited Index(SCI). H-index is 11.
研究室成员
吴伟：副教授
鱼艳荣：讲师
贾默稚：讲师
朱永红: 技术员
黄婕：技术员
滕旭：博士生
段晓辉：博士生
常晋瑞：硕士生
赵蕾：硕士生
实验室概述
本研究室以心血管疾病（缺血心肌损伤，心力衰竭，血管钙化，高血压，动脉粥样硬化）发病的生理及病理生理学基础作为主要研究目标，以心血管活性多肽为切入点，重点研究疾病发病过程中活性多肽的分子内调控和分子间的网络调控，以及心血管疾病发病过程中的细胞内信号转导机制。
研究方向与热点：方向：1. 心血管活性多肽的生理调节机制和心血管疾病发病的细胞内信号传导机制；2. 细胞损伤时内源性保护物质的变化及其作用机制；3. 血管钙化的发病机制。 研究热点：同一基因表达的心血管活性大分子内不同肽段间相互作用与活性多肽功能多样性的关系；血管钙化时血管平滑肌细胞向成骨样细胞表型转换的细胞信号传导机制；心血管疾病过程中内源性活性物质的变化及其在细胞损伤中的作用与作用的细胞信号传导机制。
研究内容：
1. 心血管活性多肽的生理调节机制和心血管疾病发病过程中活性多肽的细胞内信号转导机制
（1） 对于已知的心血管活性多肽研究其新机制，尤其是“分子内调控”的机制
（2） 对新发现的活性多肽研究其生物学效应及作用机制，研究其在心血管疾病发病中的病理生理意义，开拓心血管疾病预警和早期诊断的新型生物学标志分子，提出相应预警指标和预期预防措施
2. 细胞损伤时内源性保护物质的变化及其作用机制
（1）心力衰竭时内源性活性多肽的保护作用及其机制研究
（2）心肌缺血再灌注损伤时内源性活性多肽的作用及其机制研究
（3）细胞损伤时内源性保护物质变化及其作用机制，阐明心血管损伤性疾病（心肌缺血再灌注损伤，血管钙化，高血压，动脉粥样硬化）的发病机制理论并提出内源性细胞保护的新的治疗模式
3. 血管钙化发病机制
（1）血管钙化时血管旁/自分泌功能改变及改变的血管旁/自分泌因子间的相互作用
（2）血管钙化时血管平滑肌细胞向成骨样细胞表型转换的细胞信号传导机制
Research Description:
The main research aim is focused on physiological and pathophysiological basis of cardiovascular diseases including ischemic myocardial injury, heart failure, vascular calcification, hypertension and atherosclerosis. As cardiovascular bioactive peptides a target, we mainly investigated both for intra-molecular regulation of peptides and for interactions with its sib peptides, we also explore the intracellular signal transduction of pathogenesis of cardiovascular diseases.
Research Direction
1. The physiological regulatory mechanism of cardiovascular bioactive peptides and intracellular signal transduction mechanism of these peptides in pathogenesis of cardiovascular diseases.
2. The alteration and mechanism of endogenous protective substances in cardiovascular cells injury.
3. The pathogenetic mechanism of vascular calcification.
Research Hotspots
1. The interaction among different bioactive fragments derived from the same cardiovascular macromolecular peptide and the functional diversity relations of these small peptide fragments.
2. The interaction between different bioactive peptides and their
functional diversity relations in the target cell signal transduction pathways.
3. The cell signal transduction mechanism during vascular smooth mucle cells(VSMCs) transforming into osteoblast-like phenotype in vascular calcification.
4. The alteration and potential action mechanism of endogenous protective substances during cardiovascular diseases and cell injury.
1. The physiological regulatory mechanism of cardiovascular bioactive peptides and their intracellular signal transduction mechanism in pathogenesis of cardiovascular diseases.
(1) To investigate the novel effective mechanism of cardiovascular bioactive peptides, especially the “intramolecular pattern”;
(2) Try to study the biological effects and action mechanism of the newly discovered peptides, to elucidate their pathophysiological implications in cardiovascular diseases; to explore early warning and diagnosis novel biological marker of cardiovascular diseases, and to raise corresponding early warning index and expectation preventive measures of the cardiovascular diseases;
2. The alteration and potential action mechanism of endogenous protective substances in cell injury.
(1) The protective effects of the endogenous bioactive peptides and their mechanism in heart failure.
(2) The protective effects of the endogenous bioactive peptides and their mechanism in myocardial ischemic/ reperfusion injury;
(3) Study of changes and regulatory mechanism of endogenous protective substances in cell damage, and demonstrate pathogenetic theory of cardiovascular injured diseases including myocardial ischemia/reperfusion injury, vascular calcification, hypertension and atherosclerosis), and raise a new therapeutic model of endogenous cell protection.
3. The pathogenetic mechanism of vascular calcification
(1) The functional change of autocrine/ paracrine and the interactive alterations of various autocrine/ paracrine factors in vascular calcification.
(2) The intracellular signal transduction mechanism during vascular smooth muscle cells transforming into osteoblast-like phenotype in vascular calcification.
Selected Publications（articles as the first or corresponding author）：
3． Zhang GG, Teng X, Liu Y, Cai Y, Zhou YB, Duan XH, Song JQ, Shi Y, Tang CS, Yin XH, Qi YF*. Inhibition of endoplasm reticulum stress by ghrelin protects against ischemia/reperfusion injury in rat heart. Peptides. 2009;30(6):1109-1116.
6. Pan CS, Jin SJ, Cao CQ, Zhao J, Zhang J, Wang X, Tang CS, Qi YF*.The myocardial response to adrenomedullin involves increased cAMP generation as well as augmented Akt phosphorylation. Peptides. 2007; 28: 900-909.
8. Jia YX, Pan CS, Yang JH, Liu XH, Yuan WJ, Zhao J, Tang CS, Qi YF*. Altered arginine/nitric oxide synthase/nitric oxide pathway in the vascular adventitia of rats with sepsis. Clin Exp Pharmacol Physiol. 2006; 33: 1202–1208.
9. Jia YX, Pan CS, Zhang J, Geng B, Zhao J, Gerns H, Yang J, Chang JK, Tang CS, Qi YF*. Apelin protects myocardial injury induced by isoproterenol in rats. Regul Peptides 2006；133：147–154.
10. Ren YS, Yang JH, Zhang J, Pan CS, Yang J, Zhao J, Pang YZ, Tang CS, Qi YF*. Intermedin 1–53 in central nervous system elevates arterial blood pressure in rats. Peptides. 2006; 27:74 –79.
11. Yang JH, Pan CS, Jia YX, Zhang J, Zhao J, Pang YZ, Yang J, Tang CS, Qi YF*. Intermedin1-53 activates L-arginine/nitric oxide synthase/nitric oxide pathway in rat aortas. Biochem Biophys Res Commun 2006;341:567–572.
12. Pan CS， Jiang W， Wu SY， Zhao J， Pang YZ, Tang CS, Qi YF*. Potentiated response to adrenomedullin in myocardia and aortas in spontaneously hypertensive rat. Basic Res Cardiol 2006;101:193-203.
13. Wu SY, Pan CS, Geng B, Zhao J, Yu F, Pang YZ, Tang CS, Qi YF*. Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats1 Acta Pharmacol Sin 2006; 27 (3): 299–306.
14. Jia YX, Yang JH, Pan CS, Geng B, Zhang J, Xiao Y, Zhao J, Gerns H, Yang J, Chang JK, Wen JK, Tang CS,Qi YF*. Intermedin1-53 protects the heart against isoproterenol-induced ischemic injury in rats. Eur J Pharmacol. 2006;549(1-3):117-123.
19. Yang JH, Jia YX, Pan CS, Zhao J, Ouyang M, Yang J, Chang JK, Tang CS, Qi YF*. Effects of intermedin(1-53) on cardiac function and schemia/reperfusion injury in isolated rat hearts. Biochem Biophys Res Commun. 2005;327(3):713-719.
20. Yang JH, Qi YF*, Jia YX, Pan CS, Zhao J, Yang J, Chang JK, Tang CS. Protective effects of intermedin/adrenomedullin2 on ischemia/reperfusion injury in isolated rat hearts. Peptides. 2005;26 : 501–507.
21. Qi YF, Dong LW, Pan CS, Zhang J, Geng B, Zhao J, Tang CS. Adrenomedullin induces heme oxygenase-1 gene expression and cGMP formation in rat vascular smooth muscle cells. Peptides 2005；26：1257–1263.
22. Pan CS, Yang JH, Cai DY, Zhao J, Gerns H, Yang J, Chang JK, Tang CS, Qi YF*. Cardiovascular effects of newly discovered peptide intermedin/adrenomedullin 2 . Peptides .2005;26: 1640–1646.
23. Pan CS, Jiang W, Zhong GZ, Zhao J, Pang YZ, Tang CS , Qi YF*. Hypertension induced by nitric oxide synthase inhibitor increases responsiveness of ventricular myocardium and aorta of rat tissue to adrenomedullin stimulation in vitro. Life Sci 2005；78：398–405.
24. Chang L, Xu JX, Zhao J, Pang YZ, Tang CS, Qi YF*. Taurine antagonized oxidative stress injury induced by homocysteine in rat vascular smooth muscle cells. Acta Pharmacol Sin. 2004;25(3):341-346.
25. Chang L, Zhao J, Xu J, Jiang W, Tang CS, Qi YF*. Effects of taurine and homocysteine on calcium homeostasis and hydrogen peroxide and superoxide anions in rat myocardial mitochondria.Clin Exp Pharmacol Physiol. 2004 ;31(4):237-243.
26. Pan CS, Qi YF*, Wu SY, Jiang W, Li GZ, Tang CS. The role of adrenomedullin and its receptor system in cardiovascular calcification of rat induced by vitamin D3 plus nicotine. Peptides. 2004; 25:601-608.
27. Pan CS, Qi YF*, Wang SH, Zhao J, Bu DF, Li GZ, Tang CS. Alterations of adrenomedulin and its receptor system components in calcified vascular smooth muscle cells. Regul peptides 2004;120:77-83.
28. Ding WH, Chu SY, Jiang HF, Cai DY, Pang YZ, Tang CS, Qi YF*. Plasma mitochondrial coupling factor 6 in patients with acute myocardial infarction. Hypertens Res. 2004;27(10):717-722.
29. Qi YF, Wang SH, Zhang BH, Bu DF, Tang CS, Du JB. Changes of amount of ADM mRNA and RAMP2 mRNA in calcified vascular smooth muscle cells. Peptides.2003;24(2): 287-294.
30. Qi YF, Bu DF, Niu DD, Shi YR, Wang SH, Pang YZ, Tang CS, Du JB. Effects of different peptide fragments derived from proadrenomedullin on gene expression of adrenomedullin gene. Peptides. 2002; 23:1141-1147. |
