UW
Cardiovascular Pathology Training Program
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Steve's Phone Numbers: office 206 543 0258 cell 206 579 7635 home 206 325 3955 Steve's email: steves@u.washington.edu Assistant's email (more reliable): jparedes@u.washington.edu Steve's personal website: www.vasculata.com
CURRICULUM VITAE Stephen M. Schwartz, M.D., Ph.D. Dr. Schwartz is currently Professor of Pathology and Director of the Cardiovascular Pathology Training Program Over the long term, Dr. Schwartz has devoted his career to vascular biology. Along with a small group of colleagues, he pioneered this new field in the 1970s. Later he went on to organize the First Gordon Conference on Vascular Biology, the first molecular vascular biology meeting, and the IXth International Vascular Biology Meeting. In 1993 he founded the North American Vascular Biology Organization along with Michael Gimbrone. Dr. Schwartz’s research efforts over this time have covered a wide scope of vascular biology. His original work, as a Ph.D. student with Earl Benditt, described the ultrastructural basis of arterial permeability and response to injury. The latter work, continued in collaboration with Alec Clowes and Michael Reidy, pioneered the “3-wave model” of vascular response to angioplasty. This model is the basis for most current work on restenosis in cardiology and vascular surgery. Recent efforts of Dr. Schwartz's laboratory have been focused on smooth muscle lineages. The laboratory has shown that smooth muscle cells belong to distinct lineages or subsets. Unique properties of these subsets may account for monoclonality of atherosclerotic lesions and for the special properties of the arterial intima that contribute to progression of atherosclerosis. The lab’s efforts have included identification of subset unique gene products by comparative hybridization and array display. These have included c-FLIP – a gene implicated in regulation of plaque death, osteopontin – a gene implicated in plaque calcification, elastin – a gene implicated in neural crest origin and RGS-5, an arterial gene likely to be critical to control of mass in hypertension. Current projects include: 1) Clonal variation in lineage-specific genes by smooth muscle cells from blood vessels; 2) Role of cell adhesion molecules in plaque contraction; 3) Identification of lineage-specific genes by rapid sequencing; 4) Role of apoptosis in vascular remodeling; 5) Development of a model for advanced atherosclerosis.
PERSONAL DATADate of Birth: January 1, 1942, Boston, Massachusetts
Family: Wife: Barbara Rae Schwartz Daughter: Havivah Devora (born 1973) Graduate Student, French Literature University of Pennsylvania Son: Hillel Tsvi (born 1974) Graduate Student, Molecular Genetics Massachusetts Institute of Technology
Home Address: 934 - 21st Avenue East Seattle, Washington 98112
Office Address: Department of Pathology University of Washington Vascular Biology/Box 357335 Seattle, WA 98195-7335
Office Phone: (206) 543-0258
FAX: (206) 543-5657
E-mail: STEVES@U.WASHINGTON.EDU
Websites: http://www.pathology.washington.edu/labs/schwartz/ http://members.tripod.com/SMSchwartz/
EDUCATIONHarvard College, B.A. in Biology, 1963 (under K.R. Porter‑-Chromatolysis)
Boston University School of Medicine, M.D., 1967 (under A. Cohen -- Harvard Medical School, 1967, senior fellowship (under G. Majno -- Vascular Injury) University of Washington, Ph.D. in Experimental Pathology, 1973 (under Earl Benditt --Endothelial Function) University of Goteborg, M.D. (Honorary), 1989 CLINICAL POSTGRADUATE TRAININGResidency and Postdoctoral Training: Department of Pathology, University of Washington School of Medicine, 1973.
OUTSIDE INTERESTS
Photography: Dr. Schwartz has taught masters classes at Orange Coast College, Boating: Dr. Schwartz has worked on and owned cruising boats for 30 years. History of Judaism and Christianity
RESEARCH (Major findings and period of study in italics. Fellows marked by * now hold major positions in academia or industry) Endothelial Structure Function (Identification of permeability pathways across aortic endothelium [1973]; Cell kinetics of the vessel wall [1975]) Dr. Schwartz's interest in blood vessels began at Harvard College, where he was introduced to electron microscopy and cell biology by Dr. Keith Porter. Using these methods, Dr. Schwartz began studying vascular responses to injury under Dr. Guido Majno. After medical school, Dr. Schwartz undertook a Ph.D. thesis with Dr. Earl Benditt. This work at Harvard Medical School included ultrastructural studies of aortic endothelial permeability pathways. Because the permeability studies implied focal areas of cell death in the endothelium, Dr. Schwartz developed cell kinetic methods later widely used by his lab and others to study responses of vessels to injury.
Endothelial Growth Control
(Identification of v-cadherin, a cell-cell adhesion molecule in endothelial
cells [1990]; First demonstration of apoptosis in the vessel wall [1984, 1985])
The work on endothelial cells with Dr. Hansson* was probably the first study of apoptosis in the vessel wall. These in vivo studies progressed to studies of how endothelium is organized in vitro. Dr. Heimark* was the first to demonstrate contact inhibition in cultured endothelium. Dr. Bavisotto discovered that FGF stimulated loss of the contact inhibition and disappearance of the cell-cell adhesion activity. This led to an attempt to relate contact inhibition of growth to stimulation of growth by FGF. The obvious focus of interest was on the cell junction. Drs. Heimark* and Schwartz developed methods for selective mapping of endothelial membrane proteins. They found that membrane preparations from these cells have the ability to mimic contact inhibition of movement and replication. One of these proteins had the properties of a vascular cadherin. Continuing this work after leaving the lab, Dr. Heimark* continued with Dr. Suzuki et al. to identify cadherin V, a protein controlling endothelial cell-cell adhesion.
Pharmacology of Smooth
Muscle Replication (Development of cell kinetic “three-wave model” fo
rvascular injury [1978, 1981, 1984]; Identification of polyploidy in
hypertensive smooth muscle [1981]) Other fellows in the lab have used pharmacologic tools to define the mechanisms controlling gene expression by intimal cells. Dr. Majesky*, using Dr. Schwartz's cell kinetic methods, was the first person to map the patterns of gene expression following balloon injury in vivo. Dr. Daemen, with Dr. Schwartz, showed that angiotensin and the -adrenergic system control smooth muscle responses in vivo, but that these effects were very different for normal medial smooth muscle vs. the smooth muscle cells that comprise the neointima formed after injury. A graduate student in the laboratory, Dr. Joseph Su extended this work. We can now define in vivo a pathway from angiotensin II to smooth muscle replication via -adrenergic receptors or via FGF, depending on the vessel bed.
Smooth Muscle
Developmental Biology (Identification of first endothelial cellsforming aorta
in mouse embryo [1991])
Smooth Muscle Diversity
(Identification of smooth muscle subsets [1989, 1990, 1993]; First use of
cloning in vascular biology; Identification of subset-specific genes) In fact, the pup cells, but not the adult cells, express PDGF-B. The lab set out, therefore, to characterize other molecular differences as possible lineage markers for two different kinds of smooth muscle. Dr. Giachelli*, working with Drs. Majesky* and Schwartz, identified a series of genes, called "Pup-Intimal" genes (or "" genes). Expression of genes is typical of smooth muscle from neointimal vascular tissue as well as from pup. These genes are found at low levels or not found in smooth muscle from adult animals. Mr. Han van Neck, a graduate student, looked at the role of determination genes in controlling differences between pup and adult cells and showed that the difference between pup and adult smooth muscle cells was reflected in their distinct responses to the muscle lineage gene MyoD1. Another postdoctoral fellow, Dr. Lemire, showed that clones could be isolated from the vessel wall with or properties, the latter distinctive cells derived from "Medial-Unmanipulated" vessel wall. At this point it is clear that in vitro smooth muscle cells contain at least two subpopulations. Subpopulations, however, are only of interest if they have distinct functions in vivo. Genes cloned on the basis of belonging to the phenotype in vitro also appear to mark the intimal phenotype seen in atherosclerosis and in the neointima that appears after injury. Continuing in this line, Dr. Giachelli* has cloned other pup-intimal genes and has shown that these may play a critical role in the vascular response to injury. One of these genes, osteopontin, plays intriguing roles in migration and proliferation of smooth muscle cells and is a major focus of this lab. As already noted, we now have an extensive effort focused on the biology of osteopontin including embryology and function. As part of this effort we identified the receptors for osteopontin. One of these, integrin v3, may play a key role in smooth muscle and endothelial migration after injury. The integrin work progressed under a graduate student, Karen Yee, and postdoctoral fellow Yuji Ikari*. They identified the integrins responsible for fibrin-mediated gel contraction. Dr. Ikari identified the serum proteins responsible for cell spreading. To our surprise these did not include vitronectin but consisted of three antiproteases. Current efforts are directed at identification of the protease. Studies of Atherosclerotic Plaque (First identification of tissue factor in plaque [1989]; First studies of apoptosis in plaque [1995]; Cloning of c-FLIP [1997]) In the 1990’s the lab became more focused on human disease. This began with a sabbatical at Genentech which produced the first in situ hybridization studies of human plaque. The most important data showed tissue factor in plaque. This work was done in the laboratory of Rik Derynck with a fellow of Dr. Derynck’s, Cy Wilcox*. Later efforts to work on death in plaque included the first studies of plaque apoptosis with Martin Bennett* and cloning the c-FLIP with David Han.
Kinetics and Clonality in
Humans (Identification of clonal populations in the atherosclerotic plaque
[1985, 1986]; First use of arrays to study blood vessels [1999]; Identification
of signatures for specific arteries [2000]) Dr. Schwartz revisited an old issue in an effort to look at the atherosclerotic lesion from a different point of view. Dr. Murry*, working with other fellows in the group, has developed a set of methods that allow the application of several molecular biologic methods to tissues on slides. One of these methods has allowed Dr. Murry to microdissect slides, demonstrate that plaques are indeed monoclonal, and identify the monoclonal cell -- the smooth muscle cell of the plaque cap. Dr. Murry's demonstration of monoclonality confirms earlier work by Dr. Schwartz's mentor, Dr. Benditt, and opens up a new area of research -- the attempt to identify the genetic basis for monoclonality. Efforts in the latter direction are beginning to bear fruit. Another fellow, Dr. Bennett*, has shown an apoptotic mechanism that is unique to the plaque-derived smooth muscle cell. Current cloning efforts in the lab are directed at identifying new genes that are specific for human smooth muscle subsets. Ongoing efforts in collaboration with Drs. Joseph Miano and Eric Olson have identified homeobox genes, Hox B7 and C9, as distinctive to certain smooth muscle subsets. Along with a postdoctoral fellow, Dr. Larry Adams, Dr. Schwartz developed ways to use expression arrays in the vessel wall. This led to identification of expression sets specific for different arteries as well as sets specific for different layers of the arterial wall and the atherosclerotic plaque. One gene that marks arteries as a clone is a member of the RGS family, implicating RGS transcription and G-protein signaling in pressure responses of arteries. Advanced Mouse Lesions (First demonstration of atherosclerotic lesions with progression and scarring [2000]) Most recently the laboratory has published data on atherosclerotic mice, providing the first model for the terminal lesion of atherosclerosis by identifying a site that shows advanced features similar to those in man. REVIEW PANELSBasic Science Review Board, Veterans Administration, 1979-1982 NIH Hypertension SCOR Review Panel, 1979 American Heart Association Project Review Committee, 1980-1981 NHLBI Project Review Committee B, 1982-1985 Committee on Prize for Young Investigators, American Heart Association, 1984 American Type Culture Collection Committee, 1982 NHLBI Centers of Excellence Committee, 1988 NHLBI Manpower Committee (1989- ) Chair, NHLBI Minority Recruitment Committee, 1993.
PROFESSIONAL SOCIETIESAmerican Society for Investigative Pathology, 1977- American Society for Cell Biology, 1978- American Heart Association (Atherosclerosis) Scientific Council, 1977- North American Vascular Biology Organization, 1993-
HONORS, AWARDS, MEETING CHAIRMANSHIPSAlpha Omega Alpha, 1966 American Heart Association Established Investigatorship, 1977-1982 Candlelight Lecturer, European Artery Club, Hindasgaden, 1982; Venice, 1992 President, Blood Vessel Club, 1982- Chairman, Molecular Biology of the Vessel Wall meeting, 1983 Pluto Club (Association of Academic Pathologists), 1984- Chair, Atherosclerosis Gordon Conference, 1987 Founding Chair (with Paul DiCorleto) of Vascular Biology Gordon Conference, 1988 M.D. (honorary, Sahlgrenska, Sweden, 1989) Fellow, Japan Society for Promotion of Science, 1990 Co-founder (with Dr. Michael Gimbrone), North American Vascular Biology Organization, 1993 Dutch Federation Prize (Federatie van Medisch Wetenschappelijke Verenigingen in Nederland -FEDERA) Annual Dutch Prize for outstanding biomedical research. September 23, 1993, Nijmegen, The Netherlands First Kerckhoff lecturer, Max Planck Institute, Bad Nauheim, Germany, 1993 Schlomo Eisenberg Memorial Lecturer, European Atherosclerosis Society, European Atherosclerosis Society, Utrecht, The Netherlands, 1995 President, North American Vascular Biology Organization, 1995 Chair, International Vascular Biology Meeting, 1996 Fellow, AHA Council for High Blood Pressure Research, 1997 MILITARY SERVICE
United States Naval Reserve, active reserve, 1968-1973
EDITORIAL BOARDSAmerican Journal of Pathology Arteriosclerosis, Thrombosis and Vascular Biology Atherosclerosis Biochemical Journal (2001-present) Circulation Research Circulation Hypertension Journal of Clinical Investigation Journal of Microvascular Research Journal of Molecular and Cellular Cardiology (2000-present) Science (1986-1988) Thrombosis and Haemostasis, Associate Editor (1999-present) Vascular Medicine Editor, Cellforum (electronic forum for cell and molecular biology; sponsored by the American Assoc. of Pathologists and the American Society of Cell Biologists, 1984-1989) Sysop, Medsig Scientific Medicine Forum, Compuserve, 1991 - 1996 PROFESSIONAL APPOINTMENTSPostdoctoral Trainee, 1968-1973, Department of Pathology, University of Washington Assistant Director of Laboratories, Long Beach Naval Medical Center, United States Navy Medical Corps Assistant Professor, Department of Pathology, University of Washington, 1973-1979 Associate Professor, Department of Pathology, University of Washington, 1979-1984 Professor, Department of Pathology, University of Washington, 1984-present Adjunct Professor of Bioengineering, University of Washington, 1985-present Adjunct Professor of Cardiology, Department of Medicine, University of WA, 1993-present CONSULTING ACTIVITIESDr. Schwartz has been employed by Asahi Pharmaceuticals, Biogen, Cardiovascular Therapeutics, Daiichi Pharmaceuticals, Otsuka Pharmaceuticals, Centocor, COR Therapeutics, Parke Davis, Bristol-Meyers, Hoffman-LaRoche, Eli Lilly, Marion Merril Dow, Sandoz, Astra, Biogen, Centocor and Genentech as a vascular biology consultant. He currently serves as permanent consultant to the Berlex Corporation.
TEACHING RESPONSIBILITIESPathology Coordinator Washington, Alaska, Montana, Idaho Regional Medical Education Program, 1974-1979 Course Chairperson, Pathology Independent Study Program, 1975-1978 Course Chairperson, Pathology, 1979-1981 DEPARTMENTAL ADMINISTRATIONGraduate Program Director in Pathology, 1979-1983; 1991-1993 Curriculum Director in Pathology, 1983-1995 Research Advisor, Residency Program, 1985-1995 Seminar Director, 1999-present MINORITY AFFAIRSIn 1993, Dr. Schwartz chaired a task force on minority recruitment for the NHLBI whose recommendations were adopted as policy by the NHLBI in 1995. These include additions to training grants to recruit minority candidates, assignment of responsibilities to institutions hosting training grants to coordinate minority recruitment, development of partnerships between minority schools and research institutions, and efforts by the NHLBI to provide investigators with more information about minority candidates. RESEARCH ADMINISTRATION/RESEARCH GRANTSNIH Reaction to Injury Program Project, 1980-present (Stephen Schwartz, Principal Investigator and Program Director): This is a program of six projects directed to basic mechanisms of vascular developmental biology. Component investigators include Drs. Michael Reidy, Stephen Hauschka, Mark Bothwell, Helene Sage, Daniel Bowen-Pope, and Cecilia Giachelli. Dr. Schwartz's project has focused on the unique properties of intimal vs. medial smooth muscle cells in the rat artery following angioplasty. Drs. Giachelli and Schwartz have cloned two sets of genes, genes and genes, which appear unique to each set of cells. Current focus is on studying the function and control of expression of these genes. NIH Cardiovascular Pathology Training Grant, 1978-present (Stephen Schwartz, Principal Investigator and Program Director): This is a multi-department training program with six predoctoral and 10 postdoctoral fellows. Thirty faculty members are affiliated with this grant, representing the Departments of Pathology, Medicine, Biochemistry, Biological Structure, Laboratory Medicine, Pharmacology, Physiology and Biophysics, Surgery, and the Fred Hutchinson Cancer Research Center. NIH University of Washington Specialized Center of Research in Atherosclerosis (UW SCOR-A), 1991-1996 (Stephen Schwartz, Principal Investigator and Program Director): This is a new program devoted to use of human tissues to study ontogeny of atherosclerosis. All SCORs are required to have a clinical component. Component investigators include Drs. James McDougall (virology), Cecilia Giachelli (osteopontin), Russell Ross (macrophage), Jon Tait (annexin), Kazuo Fujikawa (annexin), Samir Deeb (lipoprotein lipase), John Harlan (leukocytes), and Kenneth Kaushansky (adherence receptor promoters). This SCOR is the first in the nation to have pathology as its clinical component. Dr. Schwartz's project is directed toward extending the study of smooth muscle cell subtypes to human smooth muscle cells. Using a variety of methods, his group has now cloned a series of homeobox genes and an integrin that appear to be specific for certain smooth muscle subsets in humans. NIH Endothelial Injury in Small Vessels, 1978-present (Merit Award) (Stephen Schwartz, Principal Investigator): This RO1 grant addresses the pharmacology of smooth muscle replication in response to injury. This was the founding grant for most of the cell kinetic studies that today underlie modern restenosis research. Current efforts have extended this effort to the microvascular level. We now have a discrete model for injury in resistance arteries and believe that this may prove useful in understanding hypertensive hyperplasia. NIH Collaborative RO1: Cell Survival Pathways in Vascular Smooth Muscle Cells (Stephen Schwartz, Principal Investigator). The central hypothesis is that rupture of atherosclerotic plaques is caused in part by loss of normal mechanisms that protect smooth muscle cells from programmed cell death. In this grant, we will attempt to identify and characterize components of cell survival and cell death pathways in vascular smooth muscle cells with a specific effort at identifying pathways that are likely to prevent plaque rupture. The Specific Aims are: (1) To test the hypothesis that cell-death resistant cultured smooth muscle cells possess amplified survival signals, which are essential for maintaining normal integrity of the vessel wall; (2) To test the hypothesis that smooth muscle cell death in atherosclerotic plaques is caused by aberrant expression of cell survival and cell death machinery; (3) To develop and characterize a model of in vivo gene transfer to atherosclerotic plaques in the carotid arteries of mice, and to determine whether the inflammation associated with adenoviral arterial gene delivery causes plaque rupture; and, (4) To test the hypothesis that local overexpression of the Fas/Fas ligand complex is sufficient to cause plaque rupture NIH RO1 Properties of the Intimal Smooth Muscle Cell (Stephen Schwartz, Principal Investigator). This is a study of human atherosclerotic tissue. The overall objective of this proposal is to explore the properties that distinguish plaque smooth muscle cells from normal medial smooth muscle. This objective grows out of three simple facts: (1) the intima is defined by the properties of the intimal smooth muscle cell; (2) atherosclerosis is a focal disease of the arterial intima, and (3) the cells of the atherosclerotic lesion comprise a clone.The Specific Aims are: (1) to determine the time course of monoclonality; (2) to determine whether clonal expansion occurs in vitro; (3) to define intimal-unique genes that mark the plaque smooth muscle cell; (4) to examine the relative role of cell death in expansion of the intima and loss of the media at sites of atherosclerotic progression; and (5) to look for mutations or genetic instability that could confer a proliferative or anti-apoptotic advantage on plaque smooth muscle cells. Berlex Grant. (Stephen Schwartz, Principal Investigator) This is an effort at developing systems to identify the role of cell death in progression of the atherosclerotic plaque. NIH 1 PO1 Genomic and Genetic Approaches to Plaque Rupture (Stephen Schwartz, Principal Investigator). Project 3: Critical Role of Macrophage Death in Plaque progression (Schwartz) and Core C: Administrative Core (Schwartz) An ongoing program devoted to final events in atherosclerosis, that is rupture of the atherosclerotic plaque. The hypothesis explored is that macrophage death plays a critical role in progression of the lesion. To test this hypothesis, we propose a combination of an in vitro assay designed to identify genes controlling macrophage death and an animal model already demonstrated to show spontaneous plaque rupture. Work done under this program has the potential to identify novel therapeutic approaches to dealing with the progression from existing atherosclerotic lesions to atherosclerotic lesions that become clinically significant.
SUMMARY OF CURRENT GRANT SUPPORT
TRAINING RESPONSIBILITIES1974 - present: Director, Pathology Summer Lecture Series. This is a summer series devoted to experimental pathology at a cellular and molecular level. Past lecturers have included Morris Karnovsky, Christian de Duve, Keith Porter, Renato Baserga, John Buchanan, Gunter Blobel, Daniel Mazia, Barry Glickman, Anthony Means, Isaiah Fidler, Ralph Bradshaw, Vincent Marchesi, and Joost Oppenheim. 1978 - 1981: Course Chairman, Human Biology 520. This is an introductory course for first year Medical School students. 1979 - 1983: Graduate Program Director, Department of Pathology 1979 - 1983: Co-Principal Investigator: Cardiovascular Pathology Training Grant (HL07312). 1983 - present: Principal Investigator: Cardiovascular Pathology Training Grant (HL07312). 1983 - present: Co-Principal Investigator: Pathobiology Training Grant (GM07187). Principal Investigator: Lawrence Loeb. Drs. Loeb and Schwartz have designed this as an innovative program intended to train M.D.s for research. The emphasis is on post-M.D. doctoral level training. Students are encouraged to pursue a second doctorate. 1983 - present: Departmental Curriculum Chairman. 1987 - 1995: Chair, Residency Research Committee. 1991 - 1995: Graduate Program Director, Department of Pathology TRAINING EXPERIENCEDr. Schwartz has been director of a laboratory involved in predoctoral and postdoctoral training since 1977. His past trainees include: POSTDOCTORAL (Fellows’ work described in RESEARCH section)Fellows Term at UW Current Status
*Corinne
M. Gajdusek, Ph.D.
1979-1981 Research Assistant Professor,
*Michael
A. Reidy, Ph.D.
1978-1979 Professor of Pathology,
Ulrich Delvos, M.D.
1979-1980 Director of Clinical
*Gary
K. Owens, Ph.D.
1979-1981 Professor, Physiology,
Sandra Harris-Hooker,
Ph.D.,
1978-1981 Asst. Prof., Pathology
*Goran
Hansson, M.D., Ph.D.
1981-1983 Professor, Molecular
*Ronald
L. Heimark, Ph.D.
1981-1987 Assistant Professor
David W. Vintner, Ph.D.
1984-1986 Asst. Prof., Pathology,
*Mark
W. Majesky, Ph.D.
1984-1988 Associate Prof., Pathology
*David
Gordon, M.D.
1985-1986 Associate Prof., Pathology
Charles S. Chen, M.D.
1985-1988 Asst.
Prof., Medicine
Rodney Dilley, Ph.D.
1986-1987 Research Staff, Baker Medical
Mat J.A.E. Daemen, M.D.
1987-1988 Professor and Chair, Pathology,
*J.
Douglas Coffin, Ph.D.
1989-1990 Assoc. Prof. of Molecular Genetics
*Cecilia
M. Giachelli, Ph.D.
1988-1991 Associate Professor, Bioengineering
Hiroshi Okazaki, M.S.
1989-1991 Res. Director, Kirin Pharmaceutical
John J. Medina, Ph.D.
1988-1993 Founding Director and CEO
Denis deBlois, Ph.D.
1990-1994 Assistant Professor,
*Charles
Murry, M.D., Ph.D.
1990-1994 Assistant Professor, Dept. of
*Edward
R. O'Brien, M.D.
1991-1994 Assistant Professor, Division of
*Joan
Lemire, Ph.D.
1991-1994 Acting Instructor
Martin Bennett, M.D., Ph.D.
1993-1995 Professor, British Heart Foundation
Stephan Regenass, Ph.D.
1994-1995 University of Basel,
Junichi Taguchi, M.D.
1993-1996 Professor of Cardiology,
Masaaki Hoshiga, M.D.,
Ph.D.
1994-1996 Chair, Cardiology
Uriel Malyankar, Ph.D.
1994-1996 Scientist, Curagen Corp.
David Courtman,
Ph.D.
1994-1997 Asst. Prof. & Director of Research,
*Larry
Adams, Ph.D.
1994-present Postdoctoral Fellow,
Ick-Mo Chung, M.D., Ph.D.
1995-1997 Assistant Professor of Cardiology,
Hong-Seog Seo
1995-
1997 Associate Professor of Medicine,
*David
K. M. Han, Ph.D.
1995-1998 Assistant Professor
Leo Hofstra,
M.D.
1996-
1997 Cardiologist
*Yuji
Ikari, M.D.
1996-
1999 Associate Director
Takahito Itoh, M.D.,
Ph.D.
1996-
1999 Associate Director
Toshio Imanishi, M.D.,
Ph.D.
1997-1999 Associate Professor, Cardiology
Sumi Paranjape,
Ph.D.
1998-
present Postdoctoral Fellow,
Danielle Methot, Ph.D.
1998-present Postdoctoral Fellow,
Xi Wang, Ph.D.
2000-present Postdoctoral Fellow,
Noboru, Wtanabe, M.D.,
Ph.D.
2000-present Postdoctoral Fellow,
Lil Pabon, Ph.D.
2001-present Postdoctoral Fellow, PREDOCTORAL
Sydney C. Selden, III,
Ph.D.
1977-1980 Grants Management Office, |
SCHWARTZ LAB