杰出校友(第一期) – Outstanding Alumni (Issue One)

Issue One (March 2001)

陈列平 Lie Ping CHEN | 卢坤平 Kun Ping LU | 严世都 Shi Du YAN

outstanding-alumni-homepage

PREFACE

Dear Alumni and Friends,

Our association president, Dr. Ruoqing Huang, and Secretary-General, Dr. Yishun Lin, asked me to write articles on behalf of the association to introduce outstanding alumni to our community. The articles are being published in the ” Alumni Gardens ” in the association Website and campus report of Fujian Medical University . We hope the publications will promote the communication and collaboration among alumni in the USA, and between USA and China.

I volunteer to write the articles because I feel like to do it. As many of you may know, I have never been a good writer. When I was a student at Fujian Medical College, I liked to write articles for the Student Radio Station to compliment teachers/professors who gave excellent lectures or made remarkable achievement in scientific research. I was pretty happy because quite a few of my articles were accepted and broadcasted by the station. However, I was quite surprised one day when one of my classmates told me a secret that his friend at the station told him that my writing was pretty bad. The station accepted my articles just because they wanted the articles on those topics. I was very much discouraged by the secret, but I did not give up the writing, because I felt obliged to compliment those teachers/professors who did a good job.  I am now writing the introductory articles of our outstanding alumni, because their achievements have greatly honored our Alma Mater, Fujian Medical University. I am very proud of them, and deeply admire them. I want them to be known by entire community.

We plan to publish two to three issues a year, and introduce three outstanding alumni in an issue. In the first issue, we are introducing Drs Lie Ping CHEN, Kun Ping LU and Shi Du YAN. I am very thankful to the three alumni for allowing me to write about them. I am also asking you to recommend me candidates for future issues. The candidates can be from either USA or China.  Help on writing is highly appreciated. I can be reached at the attached address.

Best wishes to all alumni and friends.

Sincerely,

Defu Zeng
Associate Secretary-General
AAFMUA

Defu Zeng, MD
Senior Research Scientist
Division of Immunology and Rheumatology
Department of Medicine
Stanford University School of Medicine
Stanford, CA 94305
Tel: 650-723-5545 (o); 650-852-0455 (H); Fax: 650-723-3347
Email: defuzeng@stanford.edu

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Lie Ping Chen
陈列平

AN ALL-AROUND CHAMPION: 陈列平 LIEPING CHEN, M.D., Ph.D.

If you were at Fujian Medical College during 1977-1982, I am sure you still remember a special guy named Lieping Chen.  I remembered him as a faster runner and I myself was one of the participants, although I never won any medal. In fact, he was better known as a “muscle man” since he was the champion in all three powerful events (shot put, javelin and disk), and also a good basketball player.  He was famous at Fujian Medical College for sports as a medical student. Now, he is internationally famous for his scientific research. Don’t you think he is really an all-around champion? I certainly think so!

Dr. Lieping Chen is currently Professor of Dermatology and Oncology, Director of Dermatology Research and Investigator, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland. The rapid progress in his career of medical science is amazing, and also encouraging to us. Dr. Chen earned his medical degree from Fujian Medical University (FJMU) in 1982.  After a short stay in the Central Research Laboratory, FJMU, he joined Cancer Institute and Hospital,Chinese Academy of Medical Sciences in Beijing for further training. In 1986, he entered graduate program in Hahnemann Medical College in Philadelphia, and earned his Ph.D. degree in 1989. After postdoctoral training in University of Washington and Bristol-Myers Squibb Pharmaceutical Research Institute in Seattle, WA, with Dr. Karl Erik Hellstrom and Ingegerd Hellstrom, he became a Research Scientist at the Bristol-Myers Squibb Pharmaceutical Research Institute in 1990.  He was subsequently promoted to Senior Research Investigator, Principal Scientist and directed an active research group in studying the mechanisms of immune responses against tumorigenic viruses including human papillomaviruses and EBV, molecular mechanism of lymphocyte co-stimulation of immune cells and development of tumor antigen-based cancer vaccines. In 1997, he moved to the Mayo Medical School, Mayo Clinic at Rochester, Minnesota as Associate Professor and was promoted to Professor of Immunology in 2000. He was recruited to current positions in Johns Hopkins in 2004.

Dr. Chen’s research interests include biochemical, structural and functional aspects of co-signal molecules in lymphocyte activation, and development of novel approaches for immunotherapy of cancers, autoimmune diseases, transplantation rejection and infection. Dr. Chen and his laboratories have published more than 150 papers and he has been invited to deliver more than 120 speeches and lectures in national and international conferences, universities, research institutes and biotechnology and pharmaceutical companies. Dr. Chen has received numerous awards and honors including the Milton Fromer Memory Lectures at the Case Western Reserve University; Kirin Lecture at the University of Texas at Dallas and the Presidential Research Award of Bristol-Myers Squibb Company.  He has been served in many advisory committees of U.S. government and scientific organizations such as NIH¡¯s study sections and special emphasis panels, FDA, NSF and US Army grant review board. He also serves as scientific consultant for Academia Sinica in Taiwan.

Dr. Chen is also collaborating with many scientists in China (Mainland and Taiwan), and participating in many scientific activities. He is currently an Adjunct Professor in Cancer Institute, Shanghai Second Military Medical University, Shanghai, China, and Adjunct Investigator and Professor in the Institute of Biophysics, Chinese Academy of Sciences in Beijing, China. He is also Guest Professor in several universities in mainland China including Beijing University and Beijing Union Medical College, in addition to Fujian Medical University.

Overview of Research Interest:

Molecular description of leukocyte activation and deactivation; biochemical, structural and functional aspects of lymphocyte co-signal molecules; immunology and immunotherapy of cancer, autoimmune diseases, viral infection and transplantation rejection.

A successful immune response consists of highly orchestrated cellular and molecular events. In cellular level, a pathogen will first alert a set of so-called antigen-presenting cells (APC), including dendritic cells and macrophages, leading to stimulation of adaptive components of immune systems including T lymphocytes. Upon elimination of pathogen, expanded T cells contract to basal level. In molecular level, a pathogen is processed by APC and presented in the groove of the major histocompatibility complex (MHC) to T cells with specific receptor (TCR) to initiate intracellular activation program. Outcome of TCR signal, however, is largely determined by a group of co-signal molecules which are also presented on APC and T cells.

Research focus of our laboratory is to identify and characterize co-signal molecules which play key roles in the control of T cell activation and deactivation. Co-signal molecules are essential for the communication of a T cell with virtually all other host cells. During cell-cell contact, specific recognition occurs between co-signal molecules and triggers biochemical signaling, which leads to cascades of transcription and expression of downstream genes in the nucleus. Therefore, co-signaling molecules are among the earliest responding elements of the immune system to antigens. A hallmark for co-signal molecules is that their functions are entirely dependent on TCR signals and the role of co-signal molecules is to control the TCR signal. In the absence of sufficient TCR signaling, co-signal molecules lose their function or function aberrantly. The majority of co-signal molecules are members of the immunoglobulin (Ig) and tumor necrosis factor (TNF) superfamilies. Based on the functional outcomes, co-signal molecules can be further categorized as costimulators or positive costimulatory molecules that enhance TCR-mediated responses, and coinhibitors or negative costimulatory molecules that inhibit tTCR-mediated responses.

The main interest of our laboratory is biochemical, structural and functional studies of co-signal molecules. We are also interested in defining signaling events that induces activation and deactivation of naïve and mature effector T cells. By precise manipulation of these cell surface molecular pathways, we hope to develop new strategies to treat cancer, autoimmune diseases, viral infection and transplantation rejection.

Editorial boards:
Immunology Faculty, Faculty of 1000, 2003-present
Associate Editor, Journal of Immunology, 2004-present
Ad Hoc Reviewer for Scientific Journals:
Blood
British Journal of Cancer
Cancer Gene Therapy
Cancer Immunology and Immunotherapy
Cancer Research
Cellular Immunology
Clinical Cancer Research
Clinical Immunology
European Journal of Immunology
Hepatology
Human Gene Therapy
International Immunology
International Journal of Cancer
Immunity
Immunology Today/Trends in Immunology
Journal of Autoimmunity
Journal of Biological Chemistry
Journal of Clinical Immunology
Journal of Clinical Investigation
Journal of Experimental Medicine
Journal of Immunological Methods
Journal of Immunology
Journal of Infectious Diseases
Journal of Investigative Dermatology
Journal of Leukocyte Biology
Journal of Molecular Medicine
Journal of National Cancer Institute
Mayo Clinic Proceedings
Nature Immunology
Nature Medicine
Nature Reviews Immunology
Oncogene
Proc. Natl. Acad. Sci. USA

Selected Publications:
Chen L, Ashe S, Brady W, Hellström I, Hellström KE, Ledbetter JA, McGowan P and Linsley PS. Costimulation of antitumor immunity by the B7 counterreceptor for T lymphocyte molecules CD28 and CTLA-4. Cell 71:1093-1102, 1992 (citation classic).

Melero I, Shuford WW, Newby SA, Aruffo A, Ledbetter JA, Hellström KE, Mittler R and Chen L. Monoclonal antibodies against the 4-1BB T cell activation molecule eradicate established tumors. Nature Med. 3:682-685, 1997.

Dong H, Zhu G, Tamada K and Chen L. B7-H1, a third member of the B7 family, costimulates T cell proliferation and interleukin-10 secretion. Nature Med. 5:1365-1369, 1999.

Tamada K, Shimozaki K, Chapoval AI, Zhu G, Sica G, Flies D, Boone T, Hsu H, Fu YX, Nagata S, Ni J and Chen L. Modulation of T cell-mediated immunity in tumor and graft versus host disease models through LIGHT costimulatory pathway. Nature Med. 6:283-289, 2000.

Chapoval AI, Ni J, Lau JS, Wilcox RA, Flies DB, Dong H, Sica GL, Zhu G, Tamada K and Chen L. B7-H3: A costimulatory molecule for T cell activation and IFN-g production. Nature Immunol. 2:269-274, 2001.

Sun Y, Chen HM, Subudhi SK, Chen J, Koka R, Chen L and Fu XY. Costimulatory molecule-targeted antibody therapy of a spontaneous autoimmune disease. Nature Med. 8:1405-1413, 2002.

Dong H, Strome SE, Salomao DR, Tamura H, Hirano F, Flies DB, Roche PC, Lu J, Zhu G, Tamada K, Lennon VA, Celis E and Chen L. Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion. Nature Med. 8:793-800, 2002.

Chen L. Antibody gene therapy: Old wine in a new bottle. Nature Med. 8: 333-334, 2002.

Curiel TJ, Wei S, Dong H, Alvarez X, Krzysiek R, Cheng J, Knuston K, Mottram P, Daniel B, Zimmermann MC, David O, Burow M, Gordon A, Dhurandhar N, Myers L, Berggren R, Emilie D, Alvarez RD, Hemminki A, Curiel DT, Lackner A, Chen L* and Zou W.* Blockade of B7-H1 improves myeloid dendritic cell-mediated anti-tumor immunity. Nature Med. 9:562-567, 2003 (*shared senior authorship)

Sica GL,* Choi IH,* Zhu G, Tamada K, Wang S, Tamura H, Chapoval AI, Flies DB, Bajorath J and Chen L. B7-H4, a molecule of the B7 family, negatively regulates T-cell immunity. Immunity 18:849-861, 2003

Curiel TJ, Coukos G, Zou L, Alvarez X, Cheng P, Mottram P, Evdemon-Hogan M, Conejo-Garcia JR, Zhang L, Burow M, Zhu Y, Wei S, Kryczek I, Gordon A, Myers L, Lackner A, Disis ML, Knuston K, Chen L and Zou W. Specific recruitment of regulatory T cells in ovarian carcinoma fosters immune privilege and predicts reduced survival. Nature Med. 10:942-949, 2004

Dong H, Zhu G, Tamada K, Flies DB, van Deursen JMA and Chen L. B7-H1 determines accumulation and deletion of intrahepatic CD8+ T lymphocytes. Immunity 20:327-336, 2004

Chen L. Co-inhibitory molecules of the B7-CD28 family in the control of T-cell immunity. Nature Rev. Immunol. 4:336-347, 2004

(Bio updated February 2005)


 What other alumni talk about Professor Lie Ping Chen:

CC
陈列平

林基祯:在我们的校友当中,有一位非常杰出的科学家,他就是我们福建医大的学术委员会主任,77-级校友陈列平教授。过去读过他的大作多篇,也有幸听过他演讲的免疫负调节理论,受益颇深,对我理解慢性中耳炎这个常见病的发病机制很有帮助,也对人类乳头状瘤引发的头颈部肿瘤的发病机制加深了了解。最近因为校庆回去,再次相遇,了解到了他的研究新进展,颇为欣喜,我相信许多同道对他的研究进展也有兴趣,在此将我所了解到的一些信息放在此与各位校友共同分享。这是一个我们自己的博客,希望各位校友有故事放在此与大家一起分享。谢谢!

美国耶鲁大学的陈列平教授致力于免疫系统的分子调控机制及其临床应用研究二十余年,为该领域的先驱者并首先开创了用免疫调控分子治疗癌症的先河。1999年,陈教授的实验室首先克隆并鉴定了免疫负调控分子(PD-L1, 又称B7-H1), 并于2002年用实验确定肿瘤细胞大量产生PD-L1分子是其不被机体免疫细胞杀死的一个重要原因。他领导的实验室实施了用单克隆抗体阻断PD-L1及其受体PD-1的战略来拆除癌细胞的保护屏障并在动物实验中取得成功。由于他的这一发现,美国著名制药公司百时美-施贵宝(Bristol-Myers Squibb)于2006年生产出对抗PD-1和PD-L1的单克隆抗体并在知名大学包括约翰霍普金斯大学、耶鲁大学,哈佛大学和纽约凯特琳纪念肿瘤中心等十几家医院在296个患有晚期肺癌,肾癌和皮肤癌病人身上进行临床试验。结果表明这是一个非同寻常的抗肿瘤药,能够解救30-50%频于死亡的晚期癌症病人,让他们起死回生,而且用此药治愈后他们当中的绝大多数在5年内没有肿瘤复发。这项结果于2012发表在著名的新英格兰医学杂志(New England Journal of Medicine,Impact factor 35.3)并引起轰动。包括纽约时报(New York Time),CNN,ABC, CBS在内的美国主流媒体均有报道。当时就职于约翰霍普金斯大学陈教授领导的研究小组参与了此项临床试验并且发明了一种甄别技术,用于筛选可能对治疗有效的病人。陈教授的这个新药发明在人类与癌症的斗争中有着里程碑式的意义,标志着晚期癌症并非无药可治,而是科学家们对它不够了解,还没有找到有效的新药而已,至少其中某些晚期癌症病人是如此。陈教授领导的团队现在正在研究用此药物治疗晚期脑肿瘤,胃癌,胰腺癌和乳腺癌并已取得重大进展。

美国耶鲁大学的陈列平教授致力于免疫系统的分子调控机制及其临床应用研究二十余年,为该领域的先驱者并首先开创了用免疫调控分子治疗癌症的先河。1999年,陈教授的实验室首先克隆并鉴定了免疫负调控分子(PD-L1, 又称B7-H1), 并于2002年用实验确定肿瘤细胞大量产生PD-L1分子是其不被机体免疫细胞杀死的一个重要原因。他领导的实验室实施了用单克隆抗体阻断PD-L1及其受体PD-1的战略来拆除癌细胞的保护屏障并在动物实验中取得成功。由于他的这一发现,美国著名制药公司百时美-施贵宝(Bristol-Myers Squibb)于2006年生产出对抗PD-1和PD-L1的单克隆抗体并在知名大学包括约翰霍普金斯大学、耶鲁大学,哈佛大学和纽约凯特琳纪念肿瘤中心等十几家医院在296个患有晚期肺癌,肾癌和皮肤癌病人身上进行临床试验。结果表明这是一个非同寻常的抗肿瘤药,能够解救30-50%频于死亡的晚期癌症病人,让他们起死回生,而且用此药治愈后他们当中的绝大多数在5年内没有肿瘤复发。这项结果于2012发表在著名的新英格兰医学杂志(New England Journal of Medicine,Impact factor 35.3)并引起轰动。包括纽约时报(New York Time),CNN,ABC, CBS在内的美国主流媒体均有报道。当时就职于约翰霍普金斯大学陈教授领导的研究小组参与了此项临床试验并且发明了一种甄别技术,用于筛选可能对治疗有效的病人。陈教授的这个新药发明在人类与癌症的斗争中有着里程碑式的意义,标志着晚期癌症并非无药可治,而是科学家们对它不够了解,还没有找到有效的新药而已,至少其中某些晚期癌症病人是如此。陈教授领导的团队现在正在研究用此药物治疗晚期脑肿瘤,胃癌,胰腺癌和乳腺癌并已取得重大进展。

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Lu_Kun Ping
卢坤平

A RISING STAR, 卢坤平 KUN PING LU, M.D., Ph.D.

Dr. Kun Ping Lu is currently an Associate Professor of Medicine at Harvard Medical School, and an Associate Physician, Beth Israel Deaconess Medical Center, Harvard University. His achievement in medical science research is marvelous. In the past five years, he has published 24 original articles, including one in Cell, two in Nature and two in Science.

We would like to point out that many professors at famous universities in USA did not achieve so many publications in the top journals such as Cell, Nature and Science in their lifetime. Dr. Lu is a Pew Scholar in Biomedical Leukemia Society Scholar.  He is currently conducting several research projects supported by NIH Sciences and a grants, Pew and Leukemia Society, and supervising ten postdoctoral fellows. Dr. Lu is an ad hoc member of NIH Trust study sections of Patho-biochemistry, and Cell Development and Function. He is also a co-founder and chairman of scientific advisory Board of Pintex Pharmaceutical.

Dr. Lu’s laboratory is interested in elucidating molecular mechanisms of the cell cycle and telomere maintenance, as well as in determining how aberrations in these mechanisms leads to cancer and Alzheimer’s disease. They have demonstrated that Pin1 is a phosphorylation-specific prolyl isomerase essential for mitotic regulation and proposed a novel signaling regulatory mechanism: phosphorylation creates binding sites for Pin1, which can then latch on to and isomerize the phosphorylated Ser/Thr-Pro peptide bond. In turn, this may change the shape of the protein, regulating its dephosphorylation, degradation or location in the cell. This new post-phosphorylation regulatory mechanism may help the cell orchestrate the complex events of mitosis.  Significantly, they have found that Pin1 is depleted in brains of patients with Alzheimer’s disease, but is strongly overexpressed in tumor cells.  Furthermore, Pin1 is the first molecule that can restore the biologic function of Alzheimer-associated phosphorylated tau. These results open a new idea for understanding the pathogenesis of cancer and Alzheimer’s disease and designing their therapies.  In addition, they have found that Pin2 is the major telomeric protein expressed in the cell and interacts with several proteins functioning at cell cycle checkpoints and genomic stability.  Thus, Pin2 connects cell cycle control to the telomere regulatory machinery, whose deregulation leads to cancer and aging.

Dr. Lu’s future directions are to elucidate how protein phosphorylation regulates cell cycle progression, how various cell cycle events are coordinated, how the cell division cycle is coordinated with telomere maintenance, how deregulation of the cell cycle and telomeres contributes to cell transformation and/or neurodegenerative diseases, and how these new information can be used to design more effective therapies.  Answers to these questions will be important for elucidating the control of the cell cycle and telomere homeostasis, understanding the pathogenesis of  cancer and neurodegeneration as well as designing effective therapies for these diseases.

We are proud of Dr. Lu’s achievement in medical research and other areas as a alumnus of Fujian Medical University. Dr. Lu obtained his MD from Fujian Medical University in 1984, MS of Pharmacology from Suzhou Medical College, and PhD of Cell Biology from Duke University, a very prestigious University in North Caroline, USA, and obtained his U.S. ECFMG (Educational Commission on Foreign Medical Graduates)Certificate in 1996. Dr. Lu has strong sense of gratitude toward our Alma Mater, Fujian Medical University. He is enthusiastic in helping the development and progress of medical research and education in Fujian Medical University. If you are interested in more details about Dr. Lu’s research, please read his papers (selected publications). You can also contact him at following addresses.

Office Address:

Harvard Institutes of Medicine, HIM1047
Beth Israel Deaconess Medical Center
Harvard Medical School
330 Brookline Avenue
Boston, MA 02215
Email: klu@caregroup.harvard.edu
Associate Physician, Beth Israel Deaconess Medical Center

Reviewer for Scientific Journals
1997-present    EMBO Journal
1998-present    Molecular Biology of Cell; Oncogene
1999-present    Cell Growth & Differentiation
2000-present    Molecular and Cellular Biology; Journal of Cell Biology; Neurobiology of Aging;
Trends in Pharmacological Sciences; Journal of Histochemistry and Cytochemistry;
Human Molecular Genetics;
2001-present    Journal of Cell Sciences; Nature Review Cellular Molecular Biology
2002-present    Genes and Development; Nature Cell Biology; Cancer Research; Cancer Letter,
Journal of Cellular Physiology
2002-present    Editor, Frontier in Biosciences
2003-present    BMC Cell Biology; American Journal of Physiology; FEBS Letters; Neurobiology of Disease
2004-present    Nature; Molecular Cell

Selected Publications:
1.      Lu, K. P. and Hunter, T.  1995, Evidence for a NIMA-like mitotic pathway in vertebrate cells.  Cell81:413-424.

2.      Lu, K. P., Hanes, S. D. and Hunter, T. 1996, A human peptidyl-prolyl isomerase essential for regulation of mitosis.  Nature 380:544-547.

3.      Shen, M., Vogt, V., Haggblom, C., Hunter, T. and Lu, K. P.  1997, Characterization and cell cycle regulation of related human telomeric proteins Pin2 and TRF1 suggests a role in mitosis. Proc. Natl. Acad. Sci. USA 94: 13618-1362.

4.      Yaffe, M., Schutkowski, M., Shen, M., Zhou, X. Z., Stukenberg, P. T., Rahfeld, J.-U., Xu, J., Kuang, J., Kirschner, M. W., Fischer, G., Cantley, L. and Lu, K. P. 1997, Sequence-specific and phosphorylation-dependent proline isomerization: A potential mitotic regulatory mechanism. Science 278:1957-1960 (Comment in Science 278:1883-1884).

5. Ranganathan, R., Lu, K. P., Hunter, T. and Noel, J.  1997, Structural and functional analysis of the mitotic rotamase Pin1 suggests substrate recognition is phosphorylation dependent. Cell 89: 875-886

6.      Lu, P.-J., Zhou, X. Z., Shen, M. and Lu, K. P. 1999, Function of WW domains as phosphoserine or phosphothreonine-binding modules.  Science 283:1325-1328 (Comment in Science 283:1248-1249).

7.      Lu, P.-J., Wulf, G., Zhou, X. Z., Davies, P. and Lu, K. P. 1999, Prolyl isomerase Pin1 restores the function of Alzheimer-associated phosphorylated tau protein. Nature 399:784-788 (News and Views Comment in Nature, 399:739-740).

8.      Lee, S. M. Fang, L., Reimer, C. L., Arizti, P., Lu, K. P. and Aaronson, S. A. 2000, Sustained activation of the MAP kinase cascade by the tumor suppressor p53. Proc. Natl. Acad. Sci. USA 97:8302-8305.

9.      Verdecia, M.A., Bowman, M. E., Lu, K. P., Hunter, T. and Noel, J. P. 2000, Structural basis for phosphoserine-proline recognition by group IV WW domains. Nat. Struct. Biol. 7:639-643 (News and Views Comment in Nat. Struct. Biol. 7:611-6133).

10.  Ryo. A., Wulf, G. M., Nakamura, M. Liou, Y. Lu, K. P. 2001, Pin1 regulates turnover and subcellular localization of beta-catenin by modulating its interaction with the tumor suppressor APC. Nature Cell Biol. 3: 793-801.

11.  Zhou, X.Z. and Lu, K.P. 2001, The Pin2/TRF1-interacting protein PinX1 is a potent telomerase inhibitor.Cell 107: 347-359.

12.  Liou, Y.-C., Ryo, A., Huang, H.-K., Lu, P. J., Fujimori, F., Uchida, T. Bronson, R. Hunter, T. and Lu, K. P.2002, Loss of Pin1 function in the mouse resembles the cyclin D1-null phenotypes. Proc. Natl. Acad. Sci. USA 99:1335-1340 (Track II direct submission).

13.  Zheng, H., You, H., Zhou, X. Z., Murray, S. A., Uchida, T., Wulf, G., Gu, L., Tang, X., Lu, K. P. and Xiao, Z. X. 2002, The prolyl isomerase Pin1 is a regulator of p53 in genotoxic response. Nature 419:849-853 (News and Views Comment in Nature 419:829-831).

14.  Liou, Y.-C., Sun, A., Ryo, A., Zhou, X. Z., Yu, Z.-X., Huang, H.-K., Bronson, R., Uchida, T., Bing, G., Li, X., Hunter, T. and Lu, K. P. 2003, Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration. Nature 424: 556-561.

(bio updated Feb 2005)

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YSDu
严世都

A SUPER FMU GRADUATE: 严世都 SHI DU YAN, M.D., M.S.

Dr. Shi Du Yan is currently an Associate Professor of Department of Pathology, College of Physicians and Surgeons, Columbia University. Everybody knows Columbia University is a very prestigious institute. It is usual that only the productive young scientists and medical doctors from top US universities have the opportunity to obtain a faculty position at Columbia University. However, Dr. Yan, a native graduate of Fujian Medical University (FMU) has exceptionally become the faculty member of Columbia University. Dr. Yan’s success has greatly glorified our Alma Mater. Her success is also very encouraging to our community. I believe there will be more and more native FMU graduates become the faculty members of the prestigious universities and institutes in U.S.

Dr. Yan obtained her MD in the Faculty of Medicine in 1983, and MS in Pathology and Histology from FMU in 1986.  After graduation, she worked as a physician in the Department of Otolaryngology at the 1st Affiliated Hospital of FMU. She became a Postdoctoral Fellow of Department of Otolaryngology at Columbia University in 1988, subsequently became a Postdoctoral Fellow of Physiology and Cellular Biophysics at College of Physicians and Surgeons of Columbia University in 1990. She was promoted to Associate Research Scientist in 1993, and Assistant Professor in 1995 at the Department of Pathology, College of Physicians and Surgeons, Columbia University. Dr. Yan has earned a great deal of awards and honors during her career development in U.S., for example, Young Investigator Award from National Institute of Health (Aging Division) 1995-2000; Senior Research Award from National Institute of Aging (NIA) 1997-2000; Outstanding service on the Alzheimer Association’s Initial Review Board of the Medical and Scientific Advisory Council (1999 Research Grant Program); Senior Research Award from National Institute of Health (Aging Division) 2000-2005, and Review Board in Alzheimer Association 2001-2005. She has been invited as a special Speaker on “Oxidant stress and Alzheimer disease” at professional and International meetings and as an invited Articles or professional book chapter editors.

Dr. Yan’s laboratory discovered two molecules: cell surface receptor called RAGE (receptor for advanced glycation end product) and intracellular enzyme called ABAD (A binding alcohol dehydrogenase). These two molecules are involved in cellular stress, signal transduction, and tumorgenesis. Currently, Her major research projects are 1)to study molecular Mechanisms underlying neurodegeneration and dementia such as Alzheimer’s disease and to develop an effective treatment that will slow and /or halt the progression of Alzheimer’s disease; 2)to study cellular and molecular aspects of the pathomechanism and therapy of murine experimental allergic encephalomyelitis (EAE) using EAE animal model; 3)to study ABAD in tumorgenesis; 4) to study molecular mechanism of diabetics and arteriosclosis.

Dr. Yan’s laboratory is one of those newly built by Columbia University and fully maintains all equipments including cell culture, tissue process, protein purification , molecular biology, and computer facilities. Her laboratory has published 40 papers in world-wild journals including Nature, Nature Medicine, Proceeding of National Academy Sciences, and Journal of Biochemistry. Her laboratory has been collaborated with research scientists from Japan, Germany, Italy, and Saudi Arabia, in addition to US

Dr. Yan has been closely collaborated with our alumni at FMU in China. She was appointed as a Guest Professor of FMU in 1995, and she was the first Guest Professor among us. If you want to know more about Dr. Yan’s research, her recent publication list is attached. If you would like to contact Dr. Yan, she can be reached at the following address.

Office address
Department of Pathology,
College of Physicians and Surgeons,
Columbia University
630 West 168th Street, P&S 17-410
New York, NY 10032

Home address
58 Hamilton Place, Tenafly, New Jersey, NJ 07670
Telephone numbers
212-305-3958 (Work)
201-503-1319 (Home)
212-305-5337 (Fax)
E-mail address
sdy1@columbia.edu

Peer Reviewer

1. American Journal of Pathology
2. Neurobiology of Aging
3. Kidney
4. Journal of Neurochemistry
5. Proceeding National Academic Science U.S.A.
6. FEBS Letters
7. Initial Review Board of the Medical and Scientific Advisory Council of Alzheimer Association
8. Journal of Neuroscience Research
Recent Publications:
1.      *Yan SD, Chen X, Schmidt AM, Brett J, Godman GC, Zou YS, Scott CW, Caputo C, Frappier T, Smith MA, Perry G,Yen SH and Stern D. Glycated tau in Alzheimer disease:  a mechanism for induction of oxidant stress. Proc. Natl. Acad. Sci. USA. 91: 7787-7791, 1994.

2.      Yan SD, Yan S-F, Chen X, Fu J, Chen M, Kuppusamy P, Smith MA, Perry G, Godman GC, Nawroth P, Zweier JL and Stern D: Non-enzymatically glycated tau in Alzheimer¡¯s disease induces neuronal oxidant stress resulting in cytokine gene expression and release of amyloid beta-peptide. Nature Medicine 1 (7): 693 -699, 1995.

3.      Yan SD, Chen X, Fu J, Chen M, Zhu H, Roher A, Slattery T, Zhao L, Nagashima M, Morser J,  Migheli A, Nawroth P, Stern D and Schmidt AM. RAGE and amyloid-beta peptide neurotoxicity in Alzheimer¡¯s disease. Nature 382: 685-691, 1996.

4.      Yan SD, Zhu H, Fu J, Yan S-F, Roher A, Tourtellotte W, Rajavashisth T, Chen X, Godman CG, Stern D and Schmidt AM: Amyloid-ß peptide-receptor for advanced glycation endproduct interaction elicits neuronal expression of macrophage-colony stimulating factor: a proinflammatory pathway in Alzheimer disease. Proc. Natl. Acad. Sci. U. S. A  94:5296-5301,1997.

5.      Yan SD, Fu J, Soto C, Chen X, Zhu H, Al-Mohanna F, Collison K, Zhu A, Stern E, Saido T, Tohyama M, Ogawa S, Roher A and Stern D. An intracellular protein that binds amyloid-beta peptide and  mediates neurotoxicity in Alzheimer¡¯s disease. Nature 389:689-695 1997.

6.      Yan SD, Zhu H, Zhu A,Golabek A, Du H, Roher A, Yu J, Soto C, Schmidt A, Stern D,and Kindy M. Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis. Nature Medicine6(6):643-651, 2000.

7.      Deane R, Yan SD, Submamaryan RK, LaRue B, Jovanovic S, Hogg E, Welch D, Manness L, Lin C, Yu J, Zhu H, Ghiso J, Frangione B, Stern A, Schmidt AM, Armstrong DL, Arnold B, Liliensiek B, Nawroth P, Hofman F, Kindy M, Stern D, Zlokovic B. RAGE mediates amyloid-beta peptide transport across the blood-brain barrier and accumulation in brain. Nature Medicine. 2003 Jul;9(7):907-13. (co-first author)

8.      Yan SS, Wu ZY, Zhang HP, Furtado G, Chen X, Yan SF, Schmidt AM, Brown C, Stern A, LaFaille J, Chess L, Stern DM, Jiang H. Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system. Nature Medicine. 2003 Mar;9(3):287- 93.

9.      Lustbader JW, Cirilli M, Lin C, Xu HW, Takuma K, Wang, N, Caspersen C, Chen X, Pollak S, Chaney M, Trinchese F, Liu S, Gunn-Moore F, Lue LF, Walker DG, Kuppusamy P, Zewier ZL, Arancio O, Stern D, Yan SD, Wu H. (2004) ABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer’s Disease. Science 2004 304: 448-452 (co-corresponding author).

(bio updated Feb. 2005)

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