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Introduction and details of Ye Maoqing.
Male, master tutor, studied in the United States after graduating from Wuhan University in 2005, specializing in the study of congenital heart disease in children, and joined the American Heart Association. 1 1 After returning to China in, he focused his work on China. At present, he is a full-time associate researcher at the Institute of Advanced Translational Medicine of Tongji University, an associate researcher at the Key Laboratory of Arrhythmia of the Ministry of Education, and a tutor for master students of internal medicine at Dongfang Hospital affiliated to Tongji University, and is committed to the molecular genetic etiology of human congenital heart disease and the molecular mechanism of cardiovascular development.

Educational background from September 2000 to June 2005:

Doctoral student, School of Life Sciences, Wuhan University, majoring in biochemistry and molecular biology.

1September 1995 ~ June 2000:

Hubei Medical University (now Wuhan University Medical College) First Clinical Medical College, Bachelor of Medicine.

Work background 09/20 1 1~

associate research fellow

Tongji University Oriental Hospital, Key Laboratory of Arrhythmia, Ministry of Education

Tongji university institute of advanced translational medicine

09/2005~09/20 1 1

Postdoctoral researcher

Department of Pediatrics, University of California, San Diego: Basic Research.

Department of Pediatric Cardiology, Radi Children's Hospital, San Diego: Clinical Study.

03/ 1999~06/2000: undergraduate clinical practice in the third hospital of Wuhan.

111998 ~ 02/1999: undergraduate clinical practice in the First People's Hospital of Hubei Province.

During his stay in the United States, five academic papers have been published, among which the first author published three papers in SCI journals, three in international conferences, the highest impact factor 14.6 circulation, and the second author 1 comments (the first author is a correspondent, with the impact factor1.44 JACC).

Research topic research direction 1. Screening of heart disease-causing genes

In the previous work, we collected DNA samples from children with congenital heart disease, and determined the location of chromosome defects by in situ fluorescence hybridization, gene chip and PCR technology, and successfully found a new gene ETS- 1 related to human heart disease. At present, we are continuing to carry out relevant research, using the advantages of clinical resources of Tongji University School of Medicine/Shanghai Oriental Hospital to find new human congenital heart disease-causing genes. At the same time, it is also hoped that this method and system can be used to screen specific adult heart disease-related genes.

Research direction 2. Through the analysis of transgenic mouse model, the development process of mammalian heart and the pathogenesis of congenital heart disease were studied.

With the rapid development of transgenic animal experimental technology, the research technology of animal specific gene physiological function has been very mature. In the study of cardiovascular diseases, using transgenic mouse model technology, it has been possible to achieve site-specific knockout, mutation and modification of specific genes in specific tissues at specific development time. These new technologies can help us to clarify the function of genes in heart development and the pathogenesis of heart disease. We are using knockout and mutant mouse models to study the role of transcription factors ETS- 1 and NOTCH- 1 in mammalian heart development.

The role of1.k08 # hl070640-01a1iglons gene superfamily in heart development and heart diseases, National Institutes of Health (NIH).

2. South Dakota "1020" subcontract, Sanford Health Research Institute.

3. Effects of Cell-to-Cell Interaction and Cell-to-Extracellular Matrix Interaction on Heart Function and Diseases, National Institutes of Health (NIH)

4. Comparison of atenolol and losartan in the treatment of Marfan syndrome in National Institutes of Health (NIH)

5. Etiological analysis of congenital heart disease in Children's Heart Institute.

6. Genotyping of patients with 6.UCSD pediatric/RCSD Jacobson syndrome.

Representative paper 1. Ye Maoqing, Chris Coldren, Xing Qunliang, Teresa Martina, Elizabeth Goldman, D Woodrow Benson, Dunbar Ivey, MB Perryman, Lee Ann Sinha-Garrett, paul gross Field. The deletion of the key region gene ETS- 1 in Jacobson syndrome leads to ventricular septal defect in mice. Human molecule Geics. (20 10, 19(4), 648-56)

2. Xing Qunliang *, Sun Yunfu *, Ye Maoqing * (co-first author), Maria Cecilia Simia, Jody Martin, Ann Rearden, Kari Wu, Henry Powell, Sylvia Evans and Chen Ju. The targeted combination of Pink 1 and Pink 2 from rat myocardium leads to dilated heart disease and early death after birth. Circulation. 2009, 120 (7), 568-76. (* * Same as the first author)

3. Ye Maoqing, Rabih Hamze, Amy Geddes, Nisi Valchi, Benjamin Perryman, paul gross Field, the deletion of JAM-C, a candidate gene for heart defect in Jacobson syndrome, leads to normal heart phenotype in mice. 2009 American Journal of Medical Geics, Part A, 149A(7), 1438- 1433.

4. paul gross Field, Ye Maoqing and Richard Harvey. Low plasticity left ventricular syndrome: a new Geic view. 2009 Journal of American College of Cardiology, 53 (12), 1072- 1074. (the first author of the tutor).

5. Xia,,,, Zou. Purification and Properties of Acid deoxyribonuclease from Cordyceps Mycelia. 2004. Journal of Biochemical and Molecular Biology, 37(4), 466-473.

6. Tong Yinyi,,, Zou, thermodynamic characteristics of chemical and thermal denaturation of bovine immunoglobulin G. 2005。 Journal of China Chemistry, 63( 22), 2047-2054.

7. Liang Xingqun, Sun Yunfu, You Ergen Schneider,,,, Shoumo Bhattacharya, Ann Rearden, Sylvia Evans, Chen Ju. Pinch 1 is necessary for the normal development of cranial nerves and cardiac neural crest-derived structures. 2007. Circulation Research, 100, 527-535.