Keynote Speakers
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Research interests include developing degradable polymeric biomaterials that can be used for tissue engineering, drug delivery, and fundamental polymer studies. The platform polymer technology involves the development of multifunctional monomers that form degradable crosslinked networks via a radical polymerization. Specific targets of his research include: scaffolding for cell and growth factor delivery in bone and cartilage regeneration; controlling stem cell differentiation and growth factor delivery; and investigating the influence of monomer structure on resulting network macroscopic and microscopic properties.
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George Q. Daley, M.D., Ph.D. is the Samuel E. Lux IV Professor of Hematology/Oncology and the Director of the Stem Cell Transplantation Program at Children's Hospital Boston, Professor of Biological Chemistry and Molecular Pharmacology at Harvard Medical School, and an investigator of the Howard Hughes Medical Institute. He is past-President of the International Society for Stem Cell Research ('07-'08), and formerly Chief Resident in Medicine at MGH ('94-'95). Dr. Daley received his bachelor's degree magna cum laude from Harvard University (1982), a Ph.D. in biology from MIT (1989), and the M.D. from Harvard Medical School summa cum laude (1991). Dr. Daley has received the NIH Director’s Pioneer Award, the Judson Daland Prize from the American Philosophical Society, the E. Mead Johnson Award from the American Pediatric Society, and the E. Donnall Thomas Prize from the American Society for Hematology. He has been elected a member of the Institute of Medicine of the National Academies, fellow of the American Academy of Arts and Sciences and the American Association for the Advancement of Science, and a member of the American Society for Clinical Investigation, American Association of Physicians, and American Pediatric Societies.
Daley's research contributions include the derivation of patient-specific induced pluripotent stem cells for over a dozen human diseases, demonstration of combined gene and cell therapy via customized stem cells, and creation of a murine model of human chronic myeloid leukemia that validated BCR/ABL as a drug target. His current research emphasizes the derivation of hematopoietic stem cells from pluripotent stem cell sources, reprogramming technologies for producing personalized patient-specific stem cells, and study of oncogenic and developmental pathways related to the Lin28/let-7 microRNA regulatory network.
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Dr. Geoffrey C. Gurtner is a Professor of Surgery at Stanford within the division of Plastic Surgery. He is a magna cum laude graduate of Dartmouth College and an AOA graduate of the University of California-San Francisco School of Medicine. He completed a general surgery residency at the Massachusetts General Hospital/Harvard Medical School program, a plastic surgery residency at the NYU School of Medicine and received advanced training in microsurgery at the University of Texas-MD Anderson Cancer Center. He is the author of over 100 peer-reviewed publications and is an Editor of the most widely read textbook in the field, Grabb & Smith’s Plastic Surgery. Dr. Gurtner’s NIH funded laboratory seeks to understand how organisms respond to injury and how to reactivate nascent pathways of tissue regeneration. Dr. Gurtner has an active role in medical technology development and has founded start-up companies in the aesthetic, wound healing and cardiovascular spaces.
Geoffrey Gurtner's Lab is interested in understanding the mechanism of new blood vessel growth following injury and how pathways of tissue regeneration and fibrosis interact in wound healing.
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Charles Murry is Professor of Pathology at the University of Washington in Seattle, and Director of the Center for Cardiovascular Regenerative Biology. He obtained his Ph.D. and M.D. from Duke University, and did a fellowship in vascular biology at the University of Washington under Stephen M. Schwartz, M.D., Ph.D. His laboratory’s research focuses on myocardial infarctions and the heart’s lack of intrinsic regenerative ability. Work centers on the biology of myocardial infarction, both in defining the molecular mechanisms that underlie the heart's normal wound healing processes and in developing molecular and cell-based approaches to improve infarct repair. They are a multidisciplinary group, doing basic work in molecular biology and regulation of gene expression, cell biology, tissue engineering, mouse models of disease, and analyses of human tissues. More specifically, the Murry Laboratory’s research involve the following: 1) Stem cell studies that entail both adult and embryonic stem cells, with an aim to develop cellular approaches to regenerate the heart. In addition to continuing analysis of human tissues, the goals are to develop mouse models that allow them to identify the progenitor cells, factors that trigger mobilization and homing, and identify the pathways that regulate transdifferentiation of the progenitors to other cell types, particularly cardiomyocytes; 2) ''Molecular Pharmacology'' for control of cell proliferation studies involving induction of cell replication in response to a small, synthetic molecule both in vitro and in vivo. This system may allow control of proliferation after cell grafting, such that optimal repair of myocardial infarcts can be effected pharmacologically. This system works well in skeletal muscle cells and endothelial cells, with extension to control proliferation of stem cell-derived cardiomyocytes; 3) Tissue engineering for creation of a ''patch'' of contractile tissue ex vivo, implanted onto an infarcted heart for cardiac repair. Current approaches involve seeding cells onto synthetic, biodegradable scaffolds and utilizing a ''cells in gels'' approach, where cells are seeded into hydrophilic gels containing microencapsulated growth factors and cytokines for timed release; and 4) Regulation of the heart's intrinsic repair response using a mouse model of myocardial infarction developed to take advantage of numerous genetic models. The lab is currently screening knockout strains to define the major mitogens i.e., bFGF, that regulate endothelial cell and fibroblast proliferation post-infarction.
Our lab studies the biology of myocardial infarction (heart attacks), and in particular, how the heart heals after infarction. We are interested in discovering the cells and molecules that normally regulate infarct repair and in developing new strategies to prevent the onset of heart failure after infarction. In recent years, we have become particularly interested in harnessing the potential of adult and embryonic stem cells to regenerate cardiac muscle and the coronary circulation.
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The Poss lab is investigating the biology of spectacular regenerative events in zebrafish to discover new cellular mechanisms, and we are also developing new tools to interrogate regeneration deeply at the molecular level. Over the next several years, we will pursue fundamental aspects of organ regeneration—most importantly, how tissue renewal is stimulated by injury, and how newly created cells recognize position and functionally incorporate into existing tissue.
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Our research focuses on the cross-talk between the immune and the nervous systems, in health and disease. Over the last decade, we have formulated and developed a concept suggesting that adaptive immunity, in concert with resident microglia and recruited blood-borne monocytes, plays a key role in central nervous system plasticity. Thus, we have shown that immune cells regulate a wide range of neural functions including stem cell renewal and fate decisions, some aspects of hippocampal dependent cognitive activity, and recovery and repair following injury.
Research in the Tidball lab is directed toward understanding processes that regulate skeletal muscle wasting and regeneration. Exploring the mechanisms through which the immune system can modulate skeletal muscle wasting, injury, regeneration and growth is a particular focus of the lab. Discoveries in the Tidball lab over the past 15 years have shown that immune cells, especially myeloid cells, play a major role in modulating muscle injury and repair that occur in chronic, muscle wasting diseases and following acute injuries. For example, their findings have shown that macrophages and eosinophils are key effector cells in the pathogenesis of Duchenne muscular dystrophy. Ongoing investigations in the lab are revealing the identity of specific molecules released by myeloid cells that promote muscular dystrophy. However, recent findings in the lab have also shown that regulatory interactions between cytotoxic, M1 macrophages in dystrophic muscle and anti-inflammatory, M2a macrophages are important in regulating the balance between the death of dystrophic muscle and regenerative processes. This work shows that the experimental manipulation of the balance between the functions of M1 and M2a macrophages can affect the severity of muscular dystrophy, suggesting that manipulation of macrophage phenotype in vivo may have potential therapeutic value for the treatment of the disease. Other investigations in the Tidball lab concern the proteolytic mechanisms that contribute to sarcopenia, the process through which muscle wasting occurs during the aging process. The Tidball lab uses proteomic approaches to identify specific, key substrates in proteolytic cascades that lead to muscle wasting. Subsequent experimentation relies on genetic manipulations designed to disrupt the cascades, with the goal of reducing sarcopenia. Identification of the mechanisms through which pro-inflammatory, Th1 cytokines can modulate muscle wasting during aging by influencing the state of activation proteases that drive muscle wasting is also major component of the sarcopenia investigations in the Tidball lab.
