CIT ID: 6211
Program date: Wednesday, February 20, 2008, 3:00:00 PM
Presented by: Cynthia Kenyon, Ph.D., University of California San Francisco

Abstract:

Aging has long been assumed to be a passive consequence of molecular wear and tear. But it’s not so simple. Our discoveries have led to the realization that the aging process, like everything else in biology, is under exquisite regulation, in this case, by a complex, multifaceted hormonal and transcriptional system that affects aging in many species, including mammals. In 1993, we showed that changing a single gene in the small roundworm C. elegans can double its lifespan. This gene encodes an insulin/IGF-1 like receptor, which indicates that aging is regulated hormonally. By manipulating genes and cells, we have now been able to extend the lifespan and period of youthfulness of healthy, active C. elegans by six times. We have found that signals from the reproductive system and sensory neurons influence the lifespan of C. elegans, and these processes, too, may be evolutionarily conserved. These signals act, at least in part, to control the expression of a wide variety of subordinate genes, including antioxidant, stress response, antimicrobial, and novel genes, whose activities act in a cumulative fashion to determine the lifespan of the animal. Some of these subordinate genes can also influence the progression of age-related disease. In this way, this hormone system couples the natural aging process to age-related disease susceptibility.

Cynthia Kenyon graduated valedictorian in chemistry and biochemistry from the University of Georgia, USA, in 1976. She received her PhD from MIT in 1981, where, in Graham Walker’s laboratory, she was the first to look for genes on the basis of their activity profiles, discovering that DNA damaging agents activate a battery of DNA repair genes in E. coli. She then did postdoctoral studies with Nobel laureate Sydney Brenner at the MRC Laboratory of Molecular Biology in Cambridge, UK, studying the development of C. elegans. Since 1986 she has been at the University of California, San Francisco, where she was the Herbert Boyer Distinguished Professor of Biochemistry and Biophysics and is now an American Cancer Society Professor. In 1993, Dr. Kenyon’s discovery that a single-gene mutation could double the lifespan of C. elegans sparked an intensive study of the molecular biology of aging. Dr. Kenyon's findings have now led to the discovery that an evolutionarily-conserved hormone signaling system controls aging in other organisms as well, including mammals. Kenyon has received many honors, including the King Faisal Prize for Medicine, the American Association of Medical Colleges Award for Distinguished Research, the Ilse & Helmut Wachter Award for Exceptional Scientific Achievement, La Fondation IPSEN Prize, and the Inspire Award from the AARP. She is a member of the US National Academy of Sciences, the American Academy of Arts and Sciences, and the US Institute of Medicine, and she has received an honorary doctorate from the University of Paris. She is now the director of the Hillblom Center for the Biology of Aging at UCSF.

The NIH Director's Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide.

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	Enhanced Video Podcast	1:04:08			Enhanced Video Podcast	1:04:08

CIT ID: 6210
Program date: Wednesday, February 13, 2008, 3:00:00 PM
Presented by: Alan Sher, Laboratory of Parasitic Diseases, NIAID

Abstract:

Inflammatory tissue damage is the price the body pays for having an immune system to combat microbial invaders. Indeed, in many situations the immunopathology triggered by infection is more detrimental to the host than the direct toxicity caused by the pathogen itself. This paradoxical yet fundamental feature of the anti-infective immune response is often overlooked in analyses of “host resistance” and in the design of immunologic interventions against infectious disease. Interleukin 10 (IL-10) is a cytokine which the body appears to elaborate primarily as a mechanism for keeping immune responses to infection in check thereby preventing collateral tissue damage. It is thus a key element in host protection against microbial agents. Using models of parasitic infection in which CD4+T cells mount highly polarized Th1 or Th2 cytokine responses, we and our colleagues have shown that IL-10 plays a major role in limiting the pathology induced and in preventing mortality. Our studies have also helped delineate a key function for IL-10 in preventing intestinal inflammation against gut dwelling bacteria and in the maintenance of immunologic homeostasis at that site. Finally, in studying the cellular sources of host protective IL-10, our recent work has revealed that IL-10 can be triggered in the same CD4+ T cells that mediate killing of pathogens thus providing a means of self-control of anti-microbial effector responses. Together these observations underscore the critical importance of immunoregulation in host defense and highlight the insights gained from studies on experimental infection models on the mechanisms used by the body to control inflammation.

Alan Sher received his BA from Oberlin College and his Ph.D from the University of California, San Diego under the supervision of Dr. Melvin Cohn at the Salk Institute. After his post-doctoral training at the National Institute for Medical Research, Mill Hill, UK, he served as a Research Associate and later Assistant Professor in the Department of Pathology, Harvard Medical School. He joined the NIAID’s Laboratory of Parasitic Disease as a Section Head in 1980 and became its Chief in 2003. Dr. Sher is the recipient of the Superior Service Award of the USPHS, the Bailey Ashford Award of the American Society of Tropical Medicine and Hygiene, the Bonazinga Award of the Society for Leukocyte Biology and is a member of the American Academy of Microbiology. He is currently an Editor of the Journal of Experimental Medicine and serves on scientific review panels of the Burroughs Wellcome Fund, the Max Planck Institute and the Board of Directors of The Keystone Symposia. Dr. Sher’s work has focused on the immunology of parasitic and bacterial infection and in particular in the regulation and function of polarized CD4+ T cell responses to these pathogens. Much of this work is carried out in vivo in murine experimental models that have been extensively characterized by his group. Dr. Sher’s laboratory has also made important contributions to the field of innate immunity to infection and in pathogen pattern recognition.

The NIH Director's Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide.

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	Enhanced Audio Podcast	57:25			Enhanced Video Podcast	57:25

CIT ID: 6561
Program date: Tuesday, February 12, 2008, 1:00:00 PM
Presented by: Joan Schwartz and Steven Korn

Abstract:

The primary, long-term goal of the Pathway to Independence (PI or K99/R00) Award program is to increase and maintain a strong cohort of new and talented NIH-supported independent investigators. The PI award program is designed to facilitate a timely transition from a mentored postdoctoral research position to a stable independent research position with independent NIH or other independent research support at an earlier stage than is currently the norm. Support is provided for a total of five years. One or two years of funding is provided to advanced postdoctoral trainees. The trainee then takes the remaining support with him/her when beginning a faculty position in an academic institution. This workshop will provide guidance to NIH postdocs, both U.S. citizens and international scholars, who would like to submit applications to this grant program.

Presenters:

Joan Schwartz, PhD, is Assistant Director, Office of Intramural Research;

Steven Korn, PhD, is Director of Training and Career Development, NINDS.

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	Enhanced Audio Podcast	1:32:45			Enhanced Video Podcast	1:32:45

CIT ID: 6178
Program date: Monday, February 11, 2008, 12:00:00 PM
Presented by: Jeffrey S. Mogil, Ph.D., McGill University

Abstract:

Dr. Mogil is an internationally acclaimed pioneer in the discovery of genes underlying pain sensitivity. His investigations of mice with targeted mutations and inbred strains of mice have revealed interactions between specific genes, genetic background, sex hormones, laboratory environment, and social environment on pain and analgesic responses. Recently his laboratory reported that mice display a form of empathy to the pain responses emitted by their cagemates (Science 312:1967-70, 2006). Dr. Mogil’s NIH Neuroscience lecture will focus on the interface of genes and environment in regulating the sensory and affective components of pain perception.

NIH Neuroscience Seminar Series

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	Description	Runtime			Description	Runtime
	Enhanced Audio Podcast	1:00:20			Enhanced Video Podcast	1:00:20

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