CIT ID: 6780
Program date: Tuesday, June 10, 2008, 12:00:00 PM
Presented by: Christopher Marx, Harvard University

Abstract:

Microbes present an opportunity to study evolution on a small scale, both in time and space – and to address particularly vexing biological questions such as how organisms adapt to complex, changing environments. An emerging leader in the field of experimental evolution, Dr. Marx approaches this question by studying the evolution of physiological systems in microbial populations.

Lecture series presented by National Institute of General Medical Sciences, the Office of Science Education, and the National Human Genome Research Institute. For more information, visit
http://www.nigms.nih.gov/News/Meetings/EvolutionSeries2008

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CIT ID: 6226
Program date: Wednesday, June 04, 2008, 3:00:00 PM
Presented by: Huda Akil, University of Michigan

Abstract:

This lecture will summarize our research aimed at understanding the biology of mood disorders, including efforts at identifying genetic vulnerability factors and at characterizing the consequences of these illnesses on the brain. It will describe a combination of genome-wide association and candidate genetic studies, post-mortem gene expression profiling and downstream analyses in animal models. It will offer examples of how these “discovery approaches” can lead to unexpected insights into the molecular neurobiology of mood and emotions.

This lecture will also discuss the limitations of the strategies used to date given the unique challenges intrinsic to complex brain diseases, particularly mood disorders. It will end by proposing an integrated approach, termed “Circuit Neuromics”—a framework for meeting these challenges, and for discovering both the antecedents of dysregulated moods and the consequences of these disorders on brain function.

The research to be presented reflects collaborative work in the laboratories of H. Akil and S. J. Watson, as well as a broader team effort by members of an NIMH Conte Center and the Prizker Neuropsychiatric Research Consortium. Collaborators include Drs. J.D. Barchas, W.E. Bunney, E.G. Jones, R. M. Myers, A.F. Schatzberg, S.J. Watson and their colleagues.

Huda Akil is the Gardner Quarton Distinguished University Professor of Neuroscience and Psychiatry at the University of Michigan, and the co-Director of the Molecular and Behavioral Neuroscience Institute (MBNI). Dr. Akil has made seminal contributions to the understanding of the neurobiology of emotions, including pain, anxiety, depression and substance abuse. Early on, she focused on the role of the endorphins and their receptors in pain and stress responsiveness. She and her colleagues provided the first physiological evidence for a role of endorphins in the brain; and showed that endorphins are activated by stress and cause pain inhibition, a phenomenon they termed Stress-Induced Analgesia. She defined how the postranslational processing of opioid precursors is modulated by stress, and demonstrated the coordinate actions of the neuropeptide products on behavior. Her research group, in collaboration with Dr. Stanley Watson, characterized the anatomy of the opioid peptides and their receptors, cloned two types of opioid receptors and conducted structure-function analyses defining the molecular basis of high affinity and selectivity towards the endogenous ligands.

Dr. Akil has investigated the molecular and neural mechanisms underlying stress reactivity and their relation to anxiety and depression. She demonstrated that social defeat in rodents activates unique neural pathways that resemble those altered in human depression. She and her colleagues have focused on the role of the steroid stress hormone receptors in emotionality, demonstrating the involvement of the mineralocorticoid receptor in human depression. She and her collaborators have created transgenic mouse models that overexpresses either the mineralocorticoid receptor or the glucocorticoid receptor selectively in forebrain and studied the impact on anxiety and stress responses. They have shown that the glucocorticoid receptor over-expressor exhibits increased emotional lability and enhanced responsiveness to antidepressants, two features of bipolar (manic-depressive) illness.

Dr. Akil is one of the key investigators in a major research consortium using genomic tools to uncover the pattern of gene expression associated with major depression and bipolar illness in human postmortem brains. This team is currently conducting a genome-wide search for the allelic genetic variants involved in bipolar illness.

Dr. Akil’s scientific contributions have been recognized with numerous honors and awards. These include the Pacesetter Award from the National Institute on Drug Abuse (NIDA) in 1993, and with Dr. Stanley Watson, the Pasarow Award for Neuroscience Research in 1994. In 1998, she received the Sachar Award from Columbia University and the Bristol Myers Squibb Unrestricted Research Funds Award. Dr. Akil is the past President of the American College of Neuropsychopharmacology (1998) and the past President of the Society for Neuroscience (2004). She was elected as a Fellow of the American Association for the Advancement of Science in 2000 and to the American Academy of Arts and Sciences in 2004. In 1994, she was elected to the membership of the Institute of Medicine (IOM) of the National Academy of Science and currently serves on its Council.

More information available at
http://www.mbni.med.umich.edu/mbni/faculty/akil/akil.html

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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CIT ID: 6779
Program date: Tuesday, May 27, 2008, 12:00:00 PM
Presented by: Mohamed Noor, Duke University

Abstract:

Evolution and Medicine

Lecture series presented by National Institute of General Medical Sciences, the Office of Science Education, and the National Human Genome Research Institute. For more information, visit
http://www.nigms.nih.gov/News/Meetings/EvolutionSeries2008

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	Enhanced Audio Podcast	47:08			Enhanced Video Podcast	47:08

CIT ID: 6224
Program date: Wednesday, May 21, 2008, 3:00:00 PM
Presented by: Vishva Dixit, Ph.D., Vice President, Early Discovery Research Genentech, Inc., San Francisco, California

Abstract:

The NIH Director's Wednesday Afternoon Lecture Series: http://www1.od.nih.gov/wals/schedule.htm

Proper regulation of inflammation is essential for combating pathogen invasion and maintaining homeostasis. Whereas hypo-responsive hosts succumb to infections, unchecked inflammatory reactions promote a variety of debilitating and fatal conditions including septic shock, autoimmune disease, atherosclerosis, graft rejection, and cancer. Pathogens, host immune cell ligands, and pro-inflammatory cytokines such as Tumor Necrosis Factor-a (TNF-a), Interleukin-1-b (IL1-b), and Lipopolysaccharide (LPS) induce an array of inflammatory responses by activating a variety of cell types. Although much is known about how inflammatory responses are initiated and sustained, less is known about how inflammation is attenuated to maintain a homeostatic balance.


The A20 protein is now recognized as a central, negative feedback inhibitor, of NF-kB mediated inflammatory responses. It was originally discovered as an NF-kB inducible gene that was recruited to the assembled proximal signaling complex of pro-inflammatory receptors by virtue of being able to bind to other proximal signaling adaptors including TRAFs and RIP. Analysis revealed seven repeats of a novel type of Cys2/Cys2 zinc finger motif at the carboxy terminus that possessed E3 ligase activity and a amino terminal Ovarian Tumor (OTU) domain that exhibited deubiquitinating activity. Both enzymatic activities were shown to act in concert to attenuate NF-kB signaling from pro-inflammatory receptors.

Dixit is profiled in the April 1, 2004, issue of Nature: http://www.nature.com/nature/journal/v428/n6982/full/nj6982-586c.html

BIOGRAPHICAL SKETCH: Vishva Dixit, a native of Kenya, East Africa, finished medical school at the top of his class at the University of Nairobi in 1980. Following an year of internship, he pursued further medical training at Washington University School of Medicine in St. Louis, Missouri. As a resident in the Department of Pathology, Vishva was fortunate to be awarded a Josiah Macy fellowship that allowed him to interrupt his residency training and do a postdoctoral fellowship in the Department of Biological Chemistry pursuing the biochemistry of extracellular matrix components. Following completion of residency training in 1986 Vishva joined the Department of Pathology at The University of Michigan as Assistant Professor. He rose through the ranks to be appointed full professor in 1995. During his tenure at Michigan his laboratory worked in many areas including matrix biology and on the characterization of a novel family of receptor protein tyrosine kinases. However, he is best known for his work on apoptosis. His laboratory published a series of groundbreaking papers in the mid nineties in which they defined the molecular components of the death receptor pathway. This importance of this work is reflected in the fact that Vishva was the second most highly cited scientist in all scientific disciplines in 1997. In recognition of these contributions in 1996 he was awarded the Warner-Lambert/Parke-Davis Award in Experimental Pathology. He joined Genentech in 1997 as Director on Molecular Oncology. Under his stewardship the Department has excelled in both basic and translational research and is second to none in the Biotechnology sector. Vishva has published well over a hundred scientific articles and has a significant number of patents to his name.


More information available: http://www.gene.com/gene/research/sci-profiles/phychem/dixit/profile.html

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