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Biomedical Seminars |
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Wednesday May 7, 2008 NOON |
Ge Wang, Ph.D.
Title:Biomedical Imaging with X-ray and Bioluminescence
Date: Wednesday, May 7, 2008
Location: VCOM, 3rd floor CME Room
Sponsor: Dr. Yunbo Li
Name: Ge Wang, Ph.D.
Academic Address: Pritchard Professor & Director of Biomedical Imaging Division
VT-WFU School of Biomedical Engineering & Sciences
Virginia Polytechnic Institute & State University
1880 Pratt Drive, Suite 2000, MC-0493
Blacksburg, VA 24061, USA e-mail: ge-wang@ieee.org
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Ge Wang received his BE Degree in electrical engineering from Xidian University, Xian, China, in 1982, MS in remote sensing from Graduate School of Academia Sinica, Beijing, China, in 1985, and MS and PhD in electrical and computer engineering from State University of New York, Buffalo, in 1991 and 1992. He was Instructor and Assistant Professor with Department of Electrical Engineering, Graduate School of Academia Sinica in 1984–1988, Instructor and Assistant Professor with Mallinckrodt Institute of Radiology, Washington University, St. Louis, MO, in 1992-1996. He was Associate Professor with University of Iowa from 1997-2002, and then Professor with Departments of Radiology, Biomedical Engineering, Mathematics, Civil Engineering, Electrical and Computer Engineering, and Director of the Center for X-Ray and Optical Tomography, University of Iowa. Currently, he is Director of the Biomedical Imaging Division and Samuel Reynolds Pritchard professor, WFU-VT School of Biomedical Engineering and Sciences at Virginia Polytechnic Institute and State University, Blacksburg, VA.
His academic and research interests include: computed tomography; bioluminescence tomography; and systems medicine. He and his coauthors have published over 400 journal articles and conference papers, including the first paper on spiral/helical cone-beam CT, the first paper on bioluminescence tomography and the first paper on interior tomography. He is the founding Editor-in-Chief for International Journal of Biomedical Imaging, and Associate Editors for IEEE Trans. Medical Imaging and Medical Physics. He is an IEEE Fellow, SPIE Fellow and an AIMBE Fellow. He is also recognized by a number of awards for academic achievements.
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Tuesday September 18, 2007 NOON |
Koh Fujinaga, Ph.D.
Title: Transcriptional elongation control in AIDS, cancer and cardiac hypertrophy
Date: Tuesday September 18, 2007
Location: VCOM, 3rd floor CME Room
Sponsor: Dr. Hara Misra
Name: Koh Fujinaga, Ph.D., Assistant Professor
Department of Medicine, Division of Infectious Diseases,and Department of Molecular Biology and Microbiology
Case Western Reserve University School of Medicine.
Address: 2109 Adelbert Road, BRB1024, LC 4984, Cleveland OH 44106-4984
Tel: 216-368-5259
FAX: 216-368-2034
e-mail: kxf32@cwru.edu
Web site: http://www.cwru.edu/med/microbio/fujinaga.html
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Education:
Ph.D. (Molecular Virology): Department of Medicine, Hokkaido University, Sapporo, Japan, 1997.
M.S. (Biochemistry): Department of Chemistry, Faculty of Science, Hokkaido University, Sapporo, Japan, 1993.
B.S. (Chemistry): Department of Chemistry, Faculty of Science
Hokkaido University, Sapporo, Japan, 1991.
Research Experience:
2002-present: Assistant Professor: Division of Infectious Diseases, Case Western Reserve University School of Medicine.
Postdoctoral Research Associate: Department of Medicine, Microbiology and Immunology,
1997-2002: University of California, San Francisco (B. Matija Peterlin
Lab.).
Professional Summary:
My main research interest is to investigate the transcriptional regulation mechanism in various diseases by focusing on the function of two cellular transcription factors, the positive transcription elongation factor b (P-TEFb) and the negative transcription elongation factor (NELF). Though I initially published several papers concerning the role of P-TEFb in HIV transcription, I subsequently discovered that P-TEFb also performs crucial functions in non-HIV systems such as breast cancer and cardiac hypertrophy. These unexpected results led me to expand my research into cancer and developmental and cardiovascular biology. I would like to continue two main projects that are currently ongoing in my laboratory: (1) The role of NELF in HIV transcription and latency, and (2) the role of P-TEFb in cardiac development and hypertrophy. Within a year or two, I will attempt to obtain a seed grant (R21) for the heart research and an R01 grant for the NELF/HIV project. I will also continue collaborations established while at Case with specialists in fields including cancer biology, immunology, and structural, developmental and cardiac biology. In the long run, I would like to study the mechanism by which P-TEFb/NELF-mediated eukaryotic transcription systems are regulated in the normal and diseased state. I will mainly employ HIV infection and cardiac development as model systems in the beginning, and will expand my research field into other biological systems. I would also like to apply my knowledge of P-TEFb/NELF to translational research such as drug development and gene therapy.
ABSTRACT:
The elongation of transcription has been recognized as a tightly regulated transcriptional step where both negative and positive factors are involved.
Over the last few years, it has been demonstrated that P-TEFb (the positive transcription elongation factor b) plays a central role in many human diseases that include AIDS, various forms of cancer, autoimmune diseases and cardiac hypertrophy. In particular, we have recently demonstrated that P-TEFb is required for transcription mediated by cellular DNA-bound transactivators such as estrogen receptor (ER) and myocyte enhancer factor 2 (MEF2). Also, our previous studies have indicated that NELF (negative transcription elongation factor) plays an important role in the establishment of latent HIV infection by counteracting P-TEFb. Therefore, we hypothesize that the cross-talk between P-TEFb and NELF is a key step in the regulation of transcriptional elongation in the normal state, and its deregulation causes aberrant transcription control that results in disease conditions. I will present our recent studies on the role of P-TEFb in ER- and MEF2-dependent transcription and the involvement of NELF in HIV transcription, as well as our attempt to construct dominant negative P-TEFb mutants that can block HIV transcription.
Recent Publications:
- Anand K., Schulte A., Fujinaga K., Scheffzek K., and Geyer M. Cyclin box structure of the
P-TEFb subunit Cyclin T1 derived from a fusion complex with EIAV Tat. J.Mol. Biol.
(2007) in press.
- Wittman B.M., Fujinaga K., Deng H., Ogba N., and Montano M.M. The breast cell growth
inhibitor, estrogen down-regulated gene 1 (EDG1), modulates a novel functional interaction
between estrogen receptor alpha and transcription elongation factor cyclin T1. Oncogene
(2005) 1-13.
- Fujinaga K., Irwin D., Huang, Y., Taube R., Kurosu T., and Peterlin B. M. Dynamics of HIV
transcription; P-TEFb phosphorylates RD and dissociates negative factors from TAR. Mol.
Cell. Biol. (2004) 24:787-795.
- Fujinaga K., Irwin D., Taube R., Zhang, F., Geyer M., and Peterlin B. M. A minimal Chimera
between human cyclin T1 and Tat binds TAR and activates HIV transcription in murine cells.
J. Virol.(2002) 76:12934-12939.
- Fujinaga K., Irwin, D., Geter, M., and Peterlin, B. M. Optimized chimeras between kinase
innactive, mutant Cdk9 and truncated Cyclin T1 proteins inhibit efficiently Tat transacrtivayion
and HIV replication. J. Virol. (2002) 76:10873-10881.
- Taube R., Lin X., Irwin D., Fujinaga K., and Peterlin B. M. Interaction between P-TEFb and
the C-terminal domain of RNA Polymerase II activates transcriptional elongation from sites
upstream or downstream of target genes. Mol. Cell. Biol. (2002) 22: 321-331.
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Wednesday, September 12 , 2007 NOON |
Henry H. Bauer, Ph.D.
Title: Truth Stranger Than Fiction: HIV is Not The Cause of AIDS
Date: Wednesday September 12, 2007
Location: VCOM, 3rd floor CME Room
Phone: 540-951-2107
Email:hhbauer@vt.edu
www.henryhbauer.homestead.com
School Affiliation: Virginia Tech
Professor Emeritus of Chemistry & Science Studies
Dean Emeritus of Arts & Sciences
Virginia Polytechnic Institute & State University
Address: 1306 Highland Circle, Blacksburg VA 24060-5623
Sponsor: Dr. Hara Misra |
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Professional Summary:
For twenty-five years, Henry Bauer taught chemistry and carried on research in electrochemistry, at the Universities of Sydney (Australia), Michigan, Southampton (England), and Kentucky. During that time he published 3 books and about 100 articles, chapters, and reviews. In the 1970s he turned to history, philosophy, and sociology of science, and became a founding member of the Center for the Study of Science in Society at Virginia Polytechnic Institute & State University. His special interests are, how to differentiate science from pseudo-science, and what the role of anomalies and unorthodoxies is in the progress of science. He taught in the undergraduate program in Humanities, Science & Technology and the graduate program in Science & Technology Studies. His publications on these topics include 6 books and several dozen chapters, articles, and reviews. From 1978 until 1986, Bauer served as Dean of the College of Arts & Sciences, described with some poetic license in the memoir, "To Rise Above Principle". When political correctness came to Virginia Tech, Bauer joined the National Association of Scholars, and he founded and edited (1993--99) Virginia Scholar, newsletter of the Virginia Association of Scholars http://filebox.vt.edu/faculty/aaup/index4.html). Upon retirement from teaching, he became Editor-in-Chief of the Journal of Scientific Exploration.
Abstract:
Accumulated results of HIV tests in the United States show that the tests are not tracking an infection, still less a sexually transmitted infection. Comparisons with AIDS data show that HIV and AIDS are not correlated over time, or geographically, or in how they affect men and women, or in how they affect members of different racial groups. HIV is not the cause of AIDS.
How could medical science have got it so wrong? To historians of science and medicine, there is nothing remarkable about that. Science has progressed for several centuries via smaller and bigger “scientific revolutions”: overturning and proving wrong what the professional consensus had believed right up to the time of the revolution.
Recent Books:
- The Origin, Persistence and Failings of HIV/AIDS Theory
McFarland, 2007; ISBN 0-7864-3048-6
- Knowledge Monopolies: Science and Medicine Gone Wrong
manuscript under review by publisher
- Science or Pseudoscience: Magnetic Healing, Psychic Phenomena, and Other Heterodoxies, University of Illinois Press 2001; paperback ed. 2004
- Fatal Attractions: The Troubles with Science
New York: Paraview Press 2001
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Tuesday August 7, 2007 NOON |
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Ann Marie Nelson, M.D., F.C.A.P., F.A.S.C.P.
Seminar Title: The Altered Host Response in HIV Infection and AIDS
Date: Tuesday August 7, 2007
Location: VCOM, 3rd floor CME Room
Title: Chief, Division of AIDS Pathology and Emerging Infections
Chief, Distance Learning Activity
Expertise: Infectious Disease Pathology (AIDS, HIV, Emerging Infections, Tropical Diseases, Host Response and Pathogenesis)
Continuing Medical Education (Pathology, Clinical-Pathology Correlation – Courses, written and electronic formats)
Address:
Department of Environmental and Infectious Disease Sciences
Armed Forces Institute of Pathology, Bldg 54
6825 16th Street, NW
Washington, DC 20306-6000
Tel: 202 782-2260
FAX: 202 782-9160
E-mail: nelsona@afip.osd.mil
Sponsor: Dr. JiM Palmieri |
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Dr. Nelson is board certified in anatomic and clinical pathology and has more than 20 years experience in global infections including five years in Africa working on HIV, AIDS, malaria and tuberculosis. She has been Chief, Division of AIDS Pathology and Emerging Infectious Diseases at the Armed Forces Institute of Pathology (AFIP) since 1994 and oversees one of the world’s largest registries of HIV and AIDS pathology. She is committed to improving health care by promoting more rapid and more accurate diagnoses, especially in parts of the world where resources are limited. In order to address these issues she has founded the International Pathology and Laboratory Medicine Initiative.
In 1986 she joined the staff of the Department of Infectious and Parasitic Diseases Pathology at the AFIP and was assigned as chief of the pathology component of Projet SIDA, one of the first international AIDS programs in Africa. The project, located in Kinshasa, DRC (ex-Zaire) was co-sponsored by the CDC, the NIH, the Tropical Medicine Institute of Antwerp, and the AFIP. During her 5 year tour (1986-1991), the project was able to renovate and equip a histopathology unit at the University of Kinshasa and autopsy suites at the university and at the city morgue of Kinshasa. The pathology unit provided diagnostic support for Projet SIDA studies, and conducted one of the first large autopsy studies to define causes of HIV and AIDS-associated mortality in sub-Saharan Africa. The AFIP portion of the project also trained pathology residents, histopathology technicians and autopsy assistants.
Dr. Nelson is chief of the new distance learning program for pathology services in the DoD and VA. Under her guidance, the Distance Learning Program has provided more than 60 live conferences and 20 hours of DVD’s on current issues in pathology and laboratory medicine. She has authored or co-authored more than 40 manuscripts in peer-reviewed journals, 18 chapters in medical textbooks, and is co-editor of two books on the pathology of emerging infections and co-editor of a monograph on global aspects of infectious disease pathology. She has given more than 150 lectures and poster presentations throughout the US, as well as Africa, Australia, China, Europe, Mexico, and South America (in Spanish and French as well as English) and directed 15 courses on various aspects of infectious disease pathology. She serves as the Editor of Histopathology for the journal Clinical Infectious Diseases and section editor for the Annals of Diagnostic Pathology.
Abstract:
A complex combination of alterations in host response occurs over the stages of HIV infection. The defects are seen in both acute and chronic phases of inflammation. If we understand the usual histologic reaction to infective agents in the immune competent host we can predict the most likely cause of a given reaction. Predictions can also be made in an immunocompromised host if we understand how the underlying deficiency can alter the histologically observable immune response.
The normal host has several mechanisms to prevent and control infection. Non-specific barriers (skin and mucosal surfaces) block entry of microorganisms into the host. If these fail, the body has an incremental defense system that evolves from a nonspecific “innate” reaction to a highly specific “adaptive” response. Acute inflammation is primarily controlled by the "innate" defense system and can function with humoral, cellular or combined immune deficiencies if the neutrophil count is adequate and there is active myelopoiesis. The cellular immune system modulates all aspects of immunity including control of intracellular pathogens, tumor surveillance, healing and repair. Cell-mediated immunity and delayed-type hypersensitivity are mediated by T-cells, natural killer cells, macrophages, and various cytokines. In advanced stages of HIV infection the marked disruption of lymphoid tissue and loss of follicular dendritic cells limits the host’s ability to process antigen and mount specific responses to pathogens. There are qualitative and quantitative defects in CD4 cells due to HIV infection. The resulting indirect effects include loss of cytokines production, dysregulation of B-cell function, loss of CMI, and “holes” in the immunologic repertoire that may not be restored with the use of antiretroviral therapy.
Resent Peer-reviewed Journal Articles
- Hofman, P, Nelson AM. The pathology induced by highly active antiretroviral therapy against human immunodeficiency virus: an update. Current Medicinal Chemistry, 2006, 13:3121-32.
- Thompson LD, Fisher SI, Chu WS, Nelson A, Abbondanzo SL. HIV-associated Hodgkin lymphoma: A clinicopathologic and immunophenotypic study of 45 cases. Am J Clin Pathol. 2004;121:727-38.
- Nelson AM. The cost of disease eradication: Smallpox and bovine tuberculosis. In: Food and Agricultural Security. New York Academy of Sciences, 2000;894:83-91.
- Lewin-Smith MR, Klassen MK, Frankel SS, Nelson AM. Pathology of human immunodeficiency virus infection: infections conditions. Ann Diagn Pathol 1998;2:181-194.
- Klassen MK, Lewin-Smith MR, Frankel SS, Nelson AM. Pathology of human immunodeficiency virus infection: Noninfections conditions. Ann Diagn Pathol 1997;1:57-64.
- Frankel SS, Wenig BM, Burke AP, Mannan P, Thompson LDR, Abbondanzo SL, Nelson AM, Pope M, Steinman RM. Replication of HIV-1 in dendritic cell-derived syncytia at the mucosal surface of the adenoid. Science, 1996;272:115-7X. (Dr. Frankel won USCAP Castleman Award,1997 and AFIP John Hill Britton Award for this article)
Recent Book Chapters
- Lemons-Estes F, Nelson AM. Protozoal and algal infections In: Barnhill RL, Crowson, AN. Textbook of Dermatopathology, 2nd Ed. The McGraw-Hill Co Inc 2004; 23:535-546.
- Horsburgh CR Jr, Nelson AM. Mycobacterial diseases of the gastrointestinal tract. In: Blaser MJ, et al. editors Infections of the gastrointestinal tract. 2nd Edition Raven Press, Ltd. 2002, 831-845.
- Kayembe K, Nelson AM, Colebunders RL. Opportunistic infections and diseases. In: Essex M, et al. editors. AIDS in Africa, 2nd Ed. Plenum Publishers Corportation, 2002.
- Horsburgh CR, Nelson AM. Mycobacterium avium. In: Nelson AM, Horsburgh CR Jr (editors) Pathology of Emerging Infections 2. ASM Press, Washington, DC, 1998(9):193-214.
- Blumberg HM, Nelson AM. Tuberculosis. In: Nelson AM, Horsburgh CR Jr (editors). Pathology of Emerging Infections 2. ASM Press, Washington, DC, 1998:167-192.
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Tuesday, June 19, 2007 NOON |
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John P. Williams, Ph.D.
Title: Mim-1 Signaling Inside and Outside of the Bone Microenvironment
Date: Tuesday June 19, 2007
Location: VCOM, 3rd floor CME Room
Phone: (859) 323-5049 x231
Email:johnwilliams@uky.edu
School Affiliation: University of Kentucky
Department of Internal Medicine
Division of Nephrology, Bone and Mineral Metabolism
Address: 800 Rose Street, MN521, Lexington, KY 40536
Sponsor: Dr. Hara Misra |
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Professional Summary:
I obtained my Ph.D. in 1987, doing my dissertation studies on the role of reversible protein phosphorylation in regulating fluid secretion from tick salivary glands. The nature of these biochemical studies led me to postdoctoral training at Washington University, St. Louis; investigating the roles of calcium and calmodulin in protein phosphorylation cascades in the insulin signal transduction pathway. Calcium signaling, glucose homeostasis and protein phosphorylation have been the focus of my research interests since that time and I moved these into the field of bone metabolism in 1993, while working in the Department of Pathology at the University of Alabama at Birmingham. Since 1995 I have been primary or senior author on thirteen manuscripts and coauthor on six others published in the bone field. I have continued my investigations into these aspects of bone metabolism since joining the Division of Nephrology, Bone and Mineral Metabolism at the University of Kentucky in 2000.
Abstract:
The overall research focus of my laboratory is regulation of bone turnover. Currently, the primary focus of my laboratory is to determine the biological function of an osteoclast-secreted chemokine (mim-1) that I identified. Mim-1 was first reported to be expressed specifically by hematopoietic cells. Bone mass is a function of the net balance between osteoblast and osteoclast activity, the cells that synthesize and degrade bone, respectively. Cellular communication between these opposing cells has long been postulated but remains poorly understood. Mim-1 stimulates migration and differentiation of osteoblast precursor cells and matrix mineralization by mature osteoblasts. We are investigating the mechanisms by which these effects are regulated. Our hypothesis is that mim-1 is an osteoclast-secreted anabolic chemokine responsible for recruiting osteoblastic precursor cells to areas of recent bone resorption, stimulating osteoblast differentiation and subsequent mineralization thereby efficiently replacing lost bone. This represents a novel anabolic signaling pathway involved in maintaining and regulating bone mass. In addition, we have recently demonstrated that mim-1 is expressed outside of bone. Because bone, skin and kidney are dependent on mesenchymal cell differentiation we performed immunostaining in mouse and human skin sections as well as human kidney sections. Mim-1 is clearly evident in hair follicles, basal keratinocytes and sebaceous glands and is also up-regulated in specific tumors including malignant melanoma and renal papillary tumors. In kidney, mim-1 is localized in glomeruli and collecting tubules.
Recent Publications:
This manuscript is the most complete characterization of the regulation of mim-1 expression. Very little is known about the biological function of the protein.
Ness, S.A., Marknell, A., and Graf, T. (1989). The myb oncogene product binds to and activates the promyelocyte-specific mim-1 gene. Cell 59: 1115-1125.
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Wednesday, June 13, 2007 NOON |
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Li Zhang, Ph.D.
Title: From yeast to human astrocytes: global molecular mechanisms governing cellular responses to environmental stressors
Date: Wednesday June 13, 2007
Location: VCOM, 3rd floor CME Room
Phone: 212-781-1038
School Affiliation: Columbia Center for Environmental Health in Northern Manhattan
Mailing Address: 60 Haven Avenue, B-106, New York, NY 10016
Phone: 212-781-1038
Fax: 212-781-1038
Email: lz2115@columbia.edu
Sponsor: Dr. Hara Misra |
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| Research Focus: Dr. Li Zhang’s research focuses on oxygen sensing, heme signaling and molecular actions of environmental neurotoxicants. Defects in oxygen sensing and heme signaling in humans cause serious diseases, including cancers, neurological and hematological diseases. Altered heme metabolism is also associated with schizophrenia. Dr. Zhang’s research goal is to decipher the molecular events underlying numerous diseases associated with oxygen sensing, heme signaling, and environmental neurotoxicants. |
Professional Summary:
Dr. Li Zhang earned her BS degree in chemistry and PhD degree in biochemistry. She received rigorous training at UCLA and MIT in biochemistry, molecular and cellular biology, and genetics. As a faculty member at NYU School of Medicine and Mailman School of Public Health, Columbia University, she taught and directed research in diverse areas of biomedical sciences. During the past 12 years, Dr. Zhang taught medical, MPH and graduate students in biochemistry, molecular and cellular biology, genetics and toxicology. Her laboratory has performed research in various areas of physiology, molecular and cellular biology, and genomics and published research articles regarding oxygen sensing, heme signaling, cell signaling, transcriptional regulation, and neural signaling. Her research goal is to understand the molecular and genomic mechanisms governing cellular responses to changes in the environment, such as hypoxia, by applying multidisciplinary approaches.
Degrees received:
- 1984, BS., Chemistry, Zhongshan University, China
- 1990, Ph.D., Biochemistry, Molecular and Cellular Biology
Teaching and Research Positions:
1995-2000 Assistant Prof., NYU School of Medicine
2001-2003 Associate Prof., NYU School of Medicine
2004 Associate Prof., Mailman School of Public Health, Columbia University
2004- Professor, Mailman School of Public Health, Columbia University
Abstract:
My laboratory investigates the molecular mechanisms by which living organisms or cells respond to environmental stressors, including hypoxia, manganese and common pesticides. Hypoxia is implicated in the pathogenesis of many diseases ranging from stroke to cancer. Human exposure to manganese or pesticides is associated with neurological disturbances. In yeast, heme mediates oxygen regulation of many genes. By applying genomic and computational approaches, we elucidated the global regulatory network mediating oxygen and heme regulation in yeast. Furthermore, we used biochemical, cellular and genomic approaches to elucidate the molecular mechanisms by which astrocytes respond to hypoxia, manganese and common pesticides. Potential global mechanisms underlying cellular responses to these stressors will be presented.
Recent Publications:
- Sengupta A, Hon T, Zhang L*. 2005. Heme Deficiency Suppresses the Expression of Key Neuronal Genes and Causes Neuronal Cell Death. Mol. Brain Res. 137: 23-30
- Mense SM, Sengupta A, Zhou M, Lan C, Bentsman G, Volsky DJ, Zhang L*. 2006. Gene expression profiling reveals the profound upregulation of hypoxia-responsive genes in primary human astrocytes. Physiol Genomics 25: 435-49
- Mense SM, Zhang L*. 2006. Heme: a versatile signaling molecule controlling the activities of diverse regulators ranging from transcription factors to MAP kinases. Cell Res 16: 681-92
- Mense SM, Sengupta A, Lan C, Zhou M, Bentsman G, Volsky DJ, Whyatt RM, Perera FP, Zhang L*. 2006. The Common Insecticides Cyfluthrin and Chlorpyrifos Alter the Expression of a Subset of Genes with Diverse Functions in Primary Human Astrocytes. Toxicological Sciences 93: 125-35
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Tuesday, June 12, 2007 2 p.m. |
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Jolynne Ruth Tschetter, Ph.D.
Title: Autoimmunity: Harnessing Cytotoxic T Lymphocytes to Control B Cells
Institute: Virginia Polytechnic Institute and State University
College of Veterinary Medicine,
Large Animal Clinical Sciences, 0442
Phase II, Duckpond Drive,
Blacksburg, VA 24061
Date: Tuesday, June 12, 2007 2 p.m.
Location: VCOM, 3rd floor CME Room
Phone: 540-231-1775(office), 540-231-9049 (lab)
Email: tschette@vt.edu
Sponsor: Dr. Hara Misra |
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Abstract:
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by chronic inflammation affecting diverse organs including skin, joints, kidneys, blood and brain. SLE affects multiple organs through the production of autoantibodies to numerous nuclear antigens including single-stranded (ss) DNA, double-stranded (ds) DNA and several nuclear antigens. Early diagnosis and appropriate medical intervention significantly help control the disease; however, diagnosis often takes >1 year. The parent-into-CB6 F1 model of graft-versus-host disease (GVHD) provides an example of induced immune dysregulation resulting in a disease similar to SLE. While it is currently impossible to pinpoint the time and specific events that define the onset of autoimmunity in humans, parent-into-F1 GVHD has a defined moment of induction (the intravenous (iv) injection of parental splenocytes) and can be used to study early events in the induction of autoimmune disease.
Professional Experience:
Research Assist. Professor, Virginia Polytechnic Institute and State University, Virginia-Maryland Regional College of Veterinary Medicine, Large Animal Clinical Sciences, Blacksburg, VA. 2006 to present.
Research Scientist, Virginia Polytechnic Institute and State University, Virginia-Maryland Regional College of Veterinary Medicine, Large Animal Clinical Sciences, Blacksburg, VA. 2004-2005.
Professional Summary:
Dr. Jolynne Tschetter received her doctoral degree in 1997 with specialization in immune responses to persistent viral infections from Washington State University, Pullman, WA. Following an Intramural Research Training Award fellowship from the National Institutes of Health (NIH), she was hired as a Research Scientist at a small biotechnology company. In 2004, she joined the Large Animal Clinical Sciences department at Virginia Tech as a Research Scientist and became a Research Assistant Professor in 2006.
Recent Publications:
- J Dascanio, J Tschetter, A Gray, and K Bridges. 2006. Use of quantitative real-time polymerase chain reaction to examine endometrial tissue. Animal Reproduction Science. 94:254-258
- JR Tschetter, AT Blikslager, D Little, RD Howard, SL Woody, LM Beex and MV Crisman. 2005. Detection of Differentially Regulated Genes in Ischemic Equine Intestinal Mucosa. Equine Veterinary Journal. 37(4):319-24.
- Ward, JM, N Nikolov, JR Tschetter, JB Kopp, FJ Gonzalez, S Kimura and RM Siegel. 2004. Progressive glomerulonephritis and histiocytic sarcoma associated with macrophage functional defects in CYP1B1-deficient mice. Toxicologic Pathology. 32:1-9.
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Tuesday May 15, 2007 NOON |
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Ali Iranmanesh, M.D.
Title: Functional Genomics Data Analyst
Institute: Virginia Bioinformatics Institute
Mailing Address: VA Medical Center (151)
1970 Roanoke Blvd.
Salem, VA 24153
United States
540-983-1015
Title: Hypogonadism in the aging male
Date: Tuesday May 15, 2007
Location: VCOM, 3rd floor CME Room
Phone: 540-983-1015
Email: ali.iranmanesh@med.va.gov
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Professional Summary:
Chief of the Endocrine Section, Director of the Endocrine Laboratory, and Coordinator for Research, VA Medical Center, Salem, VA
Degrees received:
- University of Tehran, School of Medicine, MD, 1969
- Sinai Hospital of Detroit, Internal Medicine 1976
- Wayne State University, Endocrinology/Metabolism, 1978
Medical School Appointments:
- Professor of Medicine, Edward Via Virginia College of Osteopathic Medicine
- Associate Professor of Medicine (Endocrinology), University of Virginia School of Medicine, Charlottesville, VA
Abstract:
Aging in men is associated with a gradual and subtle decline in the reproductive hormone outflow, with a decrement approximated at 30-50% by the sixth through eighth decades of life. On the other hand, low testosterone concentrations forecast relative sarcopenia, osteopenia, visceral fat accumulation, detectable cognitive impairment, and altered mood. Such clinical implications of androgen deficiency in aging male and the potential clinical demand for therapeutic intervention underscore the need for better understanding of the underlying mechanisms. In this context, advancing age could project disruption of normal physiology at any or all of the three dominant sites in the gonadal network, namely, hypothalamus, pituitary gland, and testis, via compromised humoral signals known as gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), and testosterone, individually or jointly. To this end, the notion of joint anomaly appears to be more attractive due to the fact that in an interlink network with feedback and feed forward adaptation, no single gland could act in isolation to maintain homeostasis. Within this concept, testosterone availability is assumed to be adjusted on a minute-by-minute basis by repeated decremental and incremental signaling interactions among GnRH, LH, and testosterone. Clinical studies predict that hypoandrogenemia and altered LH secretion in aging male could arise singly or jointly from: (1) attenuated hypothalamic GnRH feed forward drive, (2) impaired-Leydig cell steroidogenesis, and/or (3) reduced negative feedback by testosterone.
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Thursday May 3rd, 2007 NOON |
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Saroj Kant Mohapatra, MBBS, MD
Title: Functional Genomics Data Analyst
Institute: Virginia Bioinformatics Institute
Address: Bioinformatics Facility
Washington Street
Blacksburg, VA 24061
United States
(540) 231-0938
Title: A Novel Method for Discovery of Tumor Markers
Date: Thursday May 3rd, 2007
Time: 12:00 (Noon)
Location: VCOM, 3rd floor CME Room
VCOM Host: Dr. Hara Misra
Email: saroj@vt.edu
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Professional Summary:
After training in medicine (MBBS, Utkal University) and biochemistry (MD, Banaras Hindu University), Dr. Mohapatra completed several teaching assignments in India and Nepal. Since 1998, he has been steadily following the role of computers in medical research. He studied neural networks with Prof. N. Pradhan at Bangalore, India and participated in a serious bioinformatics project at Karmanos Cancer Institute, Detroit, USA under supervision of Prof. Michael A Tainsky. More recently he has been working at VBI, Blacksburg on microarray data analysis and integration of high-throughput datasets. He has a strong interest in discovery of clinically relevant patterns in high-dimensional data.
Areas of Interest:
Biochemistry (including metabolism, molecular and cell biology) was my main focus of study during this post-graduate program. Studied some subjects with anxiety neurosis and observed correlation between the levels of psychological stress (through interview) and serum lipids (various lipoprotein fractions of cholesterol).
Abstract:
Early detection of malignancy was attempted through combination of high-throughput selection and array-based detection of antigens associated with presence of cancer. In the first stage, a set of cancer-related antigens were selected using serum immunoglobulins from a positive subject as bait and validated using macroarrays and sequence analysis. These clones were further pursued with two-color microarrays (with fluorescent detection of IgG reactivity). Machine learning methods were employed to build a classifier which was then validated on an independent dataset. The results provide proof of principle and draw attention to both biological and informatics issues involved.
Recent Publications:
Chatterjee M, Mohapatra S, et al. (2006) Diagnostic markers of ovarian cancer by high-throughput antigen cloning and detection on arrays. Cancer Res. 66(2):1181-90.
Nowak JE, Chatterjee M, Mohapatra S, Dryden SC, Tainsky MA. (2006) Direct production and purification of T7 phage display cloned proteins selected and analyzed on microarrays. Biotechniques. 40(2):220-7.
Khan ZH, Mohapatra S, Khodiar PK, Ragu Kumar SN (1998) Artificial neural network and medicine. Indian J Physiol Pharmacol. 42(3):321-42
Khan ZH, Mohapatra S, Ragu Kumar SN (1997) Multimedia in health. Natl Med J India. 10(5):237-41
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Thursday April 12, 2007 NOON |
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Ms. Ann K. Peton
Title: Mapping Data for/with Research
Date: Thursday April 12, 2007
Time: 12:00 (Noon)
Sharp Location: CME Seminar Room, 3rd Floor, VCOM
VCOM Host: Dr. Hara Misra
Web Site: http://www.mappinghealth.com/index.html |
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| Ann K. Peton has over 20 years experience managing, coordinating, and/or facilitating GIS projects and training in support of public, non-profit and private healthcare, governmental and environmental organizations and associations. Her dedication and passion to the application and education of others as to the value that mapping and other technologies may provide within rural America, has made her a much sought after consultant, speaker and trainer.
Ann lives in Jefferson City, Missouri with her husband and 7 children.
Past Clientele include:
- American Osteopathic Association
- HHS’ Health Resources Services Administrations’ Office of Rural Health Policy
- National Rural Health Association
- National Organization of State Offices of Rural Health (NOSORH)
- Health Professions Network (HPN) of Allied Health Professionals
- Rural Health Resource Center
- National Center for Rural Health Works
- DeBusk College of Osteopathic Medicine
- City of New York’s Human Resources Administration
- American Ambulance Association
- Critical Injury Foundation
- State of Alabama’s Department of Children’s Affairs
- Oklahoma State University Rural Health Policy and Research Center
- Pennsylvania’ Community Action Partnership
- Health Education Industry Partnership (HEIP)
- State of Idaho’s Governor’s Office of State and Community Affairs
- National Association of Development Organizations (NADO)
Presentation Content:
Ms. Peton will share her experiences gained over the last 20 years on the application of Geographic Information Systems (GIS), electronic data management and other information technologies in support of healthcare delivery, management, policy and planning activities. Demonstrations of how other colleges, clinicians, researchers and healthcare organizations have been and are considering the application of geographic information system will be provided throughout her presentation, closing with a video on how GIS is being used to support the threat of the Pandemic Flu. She also wishes to hear how the staff and faculty view these experiences and GIS, in general, could be utilized to support Virginia College of Osteopathic Medicine’s research, clinical program development, marketing and advocacy.
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Monday, March 12, 2007 NOON |
Periannan Kuppusamy, Ph.D.
Professor, Department of Internal Medicine
College of Medicine & Public Health
6971 Cunningham Drive, New Albany, OH 43054
The Ohio State University, Columbus, OH
614-933-8877 (H); 614-292-8998 (W); 614-446-8877 (mobile)
Email: kuppusamy.1@osu.edu
URL: http://heartlung.osu.edu/2418.cfm?id=A4B6AE72-6351-4885-AB09-6CD9FBEF10B9
Title: Oxygen-sensing in Myocardial Stem Cell Therapy Date: Monday, March 12, 2007
Time: 12:00 (Noon)
Location: CME Seminar Room, 3rd Floor, VCOM
VCOM Host: Dr. Yunbo Li
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Education:
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B. Sc. 1975 and M,Sc. 1977 |
University of Madras, Chennai (Chemistry)
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Ph.D. 1985 |
Indian Institute of Technology (Chemistry/Spectroscopy)
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Faculty Positions:
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Professor of Internal Medicine & Biomedical Engineering, William D. and Jacquelyn L. Wells Chair in Imaging Research; Director, Center for Biomedical EPR Spectroscopy & Imaging; Associate Director, Davis Heart and Lung Research Institute;The Ohio State University Medical Center, Columbus, OH 43210
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Professional Summary:
Dr. Periannan Kuppusamy received his doctoral degree in 1986 with specialization in EPR (electron paramagnetic resonance) spectroscopy from Indian Institute of Technology, Madras, India. Following a Fogarty Fellowship from the National Institutes of Health (NIH), he joined the Johns Hopkins University School of Medicine in 1987 as a Research Fellow in the Division of Cardiology. He became a faculty in 1991 and was promoted to Associate Professor in 2001. In July 2002 he joined the Ohio State University, where he is currently a Professor in the Department of Internal Medicine. He also serves as the Director of the Biomedical EPR (electron paramagnetic resonance) Spectroscopy & Imaging Facility in the DHLRI and Small Animal Imaging Resources in the Comprehensive Cancer Center.
Title: Oxygen-sensing in Myocardial Stem Cell Therapy
Abstract:
Oxygen is a critical determinant in the prediction of treatment outcome of several disease including surgical interventions, cancer therapy, tissue graft, and cell therapy. There is a great need for methods capable of reliable noninvasive measurement and monitoring of oxygen concentration in tissues. EPR oximetry, which uses oxygen-sensitive probes to enable reliable and accurate measurements of concentrations of oxygen (pO2) in tissues, has many potential advantages. We have developed innovative approaches using oxygen-sensing nano/microcrystalline probes to perform noninvasive cellular/tissue oximetry/imaging in a variety of applications including myocardial ischemia/reperfusion injury, cellular cardiomyoplasty (cell therapy), organ transplantation, angiogenesis, cancer therapy, and wound healing. Of particular interest to our group is the application of EPR oximetry to monitor stem cell therapy in the heart. We used the oxygen-sensing nanoparticulate spins (OxySpin) to label stem cells to monitor their migration and in situ pO2 in the infarct myocardium following cell therapy. The bifunctional nature of the probe, namely cell-tracking and oxygen-sensing at the same time, combined with the magnetic resonance-based noninvasive detection offers a unique opportunity for long-term monitoring of cell therapy under in vivo conditions. We have demonstrated that the probe can be internalized in a variety of cells in culture. We used the noninvasive EPR technology to track/image skeletal myoblasts (stem cells) labeled with OxySpins and to simultaneously monitor in situ pO2 for several weeks after cell transplantation in a mouse model of myocardial infarction. The results clearly established the feasibility of in vivo tracking of the stem cells for several weeks and showed the retention and differentiation of the cells into myotubes with a significant increase in pO2 at the site of engraftment.
Background Readings:
- Wisel, S., Chacko, S. M., Kuppusamy, M. L., Pandian, R. P., Khan, M., Kutala, V. K., Bury, R. W., Sun, B., Kwiatkowski, P., and Kuppusamy, P. Labeling of skeletal myoblasts with a novel oxygen-sensing spin probe for noninvasive monitoring of in situ oxygenation and cell therapy in heart. Am. J. Physiol. (Heart and Circ. Physiol.) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17142337
- Pandian, R. P., Young-Il, K., Woodward, P., Zweier, J. L., and Kuppusamy, P. Open molecular framework in lithium octabutoxy-naphthalocyanine paramagnetic crystal: Implications for the detection of oxygen and nitric oxide by EPR spectroscopy. J. Mater. Chem. 16, 3609-3620 (2006).
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Monday February 19, 2007 NOON |
Martha J Wunsch MD FAAP FASAM
Associate Professor, VCOM
Virginia College of Osteopathic Medicine
Department of Addiction Medicine
Address: 2265 Kraft Drive, Blacksburg, Va 24060
Telephone: 540-231-4477
Email: mwunsch@vcom.vt.edu
Title: Prescription Drug Mortality in Western Virginia: Identification of Older Women as a Risk Group for Death
Date: Monday, February 19, 2007
Time: 12:00 (Noon)
Location: VCOM, 3rd floor Rocovich Board Room
VCOM Host: Dr. Hara Misra
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Biographical Summary: Dr. Wunsch is a graduate of Albion College, majoring in Cultural Anthropology and Sociology. She earned her doctorate in medicine at the Uniformed Services University of the Health Sciences in 1983 where she began her career as a Commissioned Officer in the United States Public Health Service. She completed residency training at Los Angeles Children's Hospital and was Board Certified in Pediatrics in 1987. She served as a general pediatrician, and then Maternal Child Health Officer and Chief of Substance Abuse for the Tucson Area Indian Health Service. After leaving the Indian Health Service, she was the Project Officer for Healthy Start, an initiative in the Maternal Child Health Bureau, HHS, to reduce infant mortality in the Aberdeen Area, Indian Health Service. She practiced general pediatrics in a community setting for 7 years (1993-2000) and in 2000 returned to training as the Hoff Addiction Medicine Fellow at Medical College of Virginia, Virginia Commonwealth University. She was an Assistant Professor of Pediatrics, Internal Medicine and Psychiatry at VCU and BIRCWH Scholar with a focus on the treatment of neonatal opioid withdrawal from 2001-2002. In 2002, she became the Chair of Addiction Medicine at the Virginia College of Osteopathic Medicine where she has developed and teaches a four year course in Addiction Medicine.
Dr. Wunsch's clinical and research interests include prescription drug abuse, pregnancy and addiction, and the treatment of neonatal opioid withdrawal. She is Medical Director of ARS Pantops Opioid Treatment Program, a National Mentor for the Buprenorphine Physician Clinical Support System, a member of the American Academy of Pediatrics Committee on Substance Abuse, serves on the Board of Directors for the American Society of Addiction Medicine and was Co-Chair of the 2005 ASAM research conference "State of the Art in Addiction Medicine", and is Co-Editor of the Journal of Addiction Medicine. She is the Principle Investigator for NIDA R03 DA 019047-01A1: "Opioid Mortality in Southwestern Virginia" and has received pharmaceutical funding support to study rural prescription drug abuse in Southwestern Virginia.
Board Certifications:
1987 Pediatrics;
1990, 2002 Addiction Medicine, American Society of Addiction Medicine
ABSTRACT:
In 308 medical examiner deaths involving drugs from predominantly rural Western Virginia, deaths from prescription drugs occur at a substantially higher rate relative to the rest of the state and the country as a whole. This is consistent with epidemiological data indicating that death from prescription drugs is a particular problem in rural areas. However, one group?women aged 35-54?exhibits an unexpectedly high death rate from prescription drugs. By comparison, younger people aged 15-24 have a lower death rate than do older women. The older women also appear to engage in a different pattern of use and misuse of these medications than the younger people. Fewer have a history of substance misuse or abuse and most hold prescriptions for the medications involved in their deaths, including opioids, benzodiazepines, and antidepressants prescribed for chronic pain, depression, and anxiety. However legitimate their access to the drugs, these women suffer a death rate nearly triple the national average for women from drugs. The data suggest that particular care and vigilance is needed in prescribing prescription medications when treating women for chronic pain, depression, and anxiety.
Current Research
Opioid Mortality in Southwestern Virginia. (PI) RO3 DA019047-01A1. Funded by NIDA/NIH August 2005. This project will conduct intensive retrospective chart reviews of the 575 opioid related deaths in southwestern Virginia utilizing a multidisciplinary team.
The Development and Implementation Assessment of a Tobacco Use Prevention Model for Youth with Psychiatric Disorders. (Consultant) Virginia Tobacco Settlement Foundation. PI: P Mazarros PhD) This a study that will address prevention of tobacco use in young children by developing an intervention based on clinical experience and the research literature.
Addiction Severity Indexes in Probationers and Parolees, District 28, Radford Virginia. (PI) A study of addiction among prisoners and probationers in the New River Valley. Funded by Purdue Pharma LP. January 2005-March 2006
Maternal Attachment and Neonatal Opioid Withdrawal. (PI) Case studies of pregnant women in medication assisted treatment with methadone and the affect of the severity of neonatal opioid withdrawal on attachment. ARS Pantops Clinic. September 2004-2005.
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Tuesday February 20, 2007 NOON |
Webster L. Santos
Virginia Tech
Department of Chemistry
Address: 401B Davidson Hall, Blacksburg, VA 24061
Telephone: 540-231-5742
Email: wsantos@vt.edu
Web site:www.chem.vt.edu/chem-dept/wsantos
Title: RNA Interacting Polynucleotides (RIPtides): Targeting Hepatitis C Virus RNA with small molecules and proteins
Date: Tuesday, February 20, 2007
Time: 12:00 (Noon)
Location: VCOM, 3rd floor CME Conference Room
VCOM Host: Dr. Hara Misra
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Dr. Santos received his B.S. and Ph.D. degrees in synthetic chemistry at the Department of Chemistry at the University of Virginia under Professor Timothy L. Macdonald. He performed his postdoctoral training in the Department of Chemistry and Chemical Biology at Harvard University as a NIH postdoctoral fellow under Professor Gregory L. Verdine. In 2006, he moved to the Department of Chemistry at Virginia Tech as an assistant professor.
Dr. Santos' research interest lies at the interface between chemistry and biology. His primary focus is the synthesis of novel molecular entities that can be used as probes in studying the biological functions of proteins involved in the Malarial parasite plasmodium falciparum. These molecules are transition state analogs based on borinic acid scaffold. In addition, he is developing new strategies and embarking on the unconventional approach of targeting the mRNA of proteins implicated in neurological disease states such as Parkinson's and Alzheimer's diseases with small molecules. In organic chemistry, he is employing a chemical biology approach in evolving nucleic acid polymers, such as RNA, to discover molecular scaffolds that can catalyze chemical reactions. One of his goals is to use modular RNA to perform the total synthesis of natural products, where one product can arise from a complex pool of starting materials.
SUMMARY: A general strategy of discovering novel ligands that bind to specific folded, globular RNA structures was developed. By performing hybridization using microarrays consisting of all possible combination of 4- to 8-mer 2'-OMe RNA sequences (87,296) with the IIId stem loop region of hepatitis C virus internal ribosome entry site (HCV-IRES), lead RNA-interacting polynucleotide sequences (RIPtides) were discovered. Biophysical characterization of RIPtides was performed using fluorescence polarization and gel-shift assays. Functional assays revealed that RIPtides inhibited HCV-IRES mediated cap-independent translation effectively.
AWARDS:
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2002-2006 |
Ruth L. Kirschtein Postdoctoral Fellow (NRSA), Harvard University
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2000-2002 |
NIH NRSA Pre-doctoral Fellowship, University of Virginia |
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2002 |
Third Prize Winner, Robert J. Huskey Graduate Research Symposium, University of Virginia |
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1998-1999 |
Outstanding Graduate Teaching Assistant Award (University-wide), University of Virginia |
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1996-1997 |
Semi-finalist for Seven Society Teaching Fellowship, Secret Seven Society, University of Virginia |
RECENT PUBLICATIONS: -
Banerjee, A.; Santos, W.L. and Verdine, G.L. Disulfide trapping and structural characterization of an early intermediate in the pathway of damage search by MutM. Science, 2006, 311, 1153.
- Johnson, A.A.; Santos, W.L.; Marchand, C.; Amin, R.; Verdine, G.L. and Pommier, Y. Interaction between HIV-1 integrase Q148 and a viral DNA cytosine is required for strand transfer. J. Biol. Chem., 2006, 281, 461.
- Santos, W.L.; Heasley, B.H.; Jarosz, R.; Carter, K.M.; Lynch, K.R. and Macdonald, T.L. Synthesis and biological evaluation of phosphonic and thiophosphoric acid derivatives of lysophosphatidic acid. Bioorg. Med. Chem. Lett. 2004,14, 3473.
- Kapetanovic, I.M.; Torchin, C.D.; Strong, J.M.; Yonekawa, W.D.; Lu, C.; Li, A.P.; Dieckhaus, C.M.; Santos, W.L.; Macdonald, T.L.; Sofia, R.D. and Kupferberg, H.J. Reactivity of atropaldehyde, a felbamate metabolite in human liver tissue in vitro. Chem. Biol. Interact. 2002, 142, 119-34.
- Roller, S. G.; Dieckhaus, C. M.; Santos, W.L.; Duane Sofia, R. and Macdonald, T. L. Oxidation of 3-carbomoyl-2-phenylpropionaldehyde, a felbamate metabolite, by aldehyde dehydrogenase 1: significance in detoxification of felbamate. Chem. Res. Toxicol. 2002, 15, 815-24.
PATENTS:
- Santos, W.L. and Verdine, G.L. Oligonucleotide microarrays comprising nucleic acid analogs for hybridization with target RNA, including RNA in nucleoprotein complexes. PCT Int. Appl. 2005, 60 pp.
- Lynch, K.R.; Macdonald, T. L.; Heise, C.H.; Santos, W.L. and Okusa, M.D. Novel Lysophosphatidic Acid Receptor Agonists and Antagonists. PCT Int. Appl. 2002, 81 pp.
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Monday, October 23, 2006 NOON |
Edward L. Orr, Ph.D.
Biomedical Sciences Program
School of Natural and Health Sciences
Barry University
Miami Shores, Florida 33161-6695
Office Phone: 305-899-3680
E-Mail: eorr@mail.barry.edu
Title: Effects of Head Injury on Dural Mast Cells, Cerebral Cortical Histamine, and Cerebrovascular Permeability Date: Monday, October 23, 2006
Time: 12:00 (Noon)
Location: CME Seminar Room, 3rd Floor, VCOM
VCOM Host: Dr. Hara Misra
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Education:
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1970 |
B.S. (Biology), Cleveland State University, Cleveland, Ohio
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1975 |
Ph.D. (Zoology), University of California, Berkeley.
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Faculty Positions:
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1987-2001 |
Associate Professor of Anatomy and Cell Biology, University of North Texas Health Science Center at Fort Worth (formerly Texas College of Osteopathic Medicine), Fort Worth, Texas |
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2001-2002 |
Acting Assistant Professor of Physiology, University of New England College of Osteopathic Medicine, Biddeford, Maine
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2002-2003 |
Visiting Assistant Professor, Department of Biology, Texas Woman's University, Denton, Texas |
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2004-present |
Associate Professor, Biomedical Sciences Program, School of Natural and Health Sciences, Barry University, Miami Shores, Florida |
Honors and Awards:
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1987-1990 |
National Multiple Sclerosis Society, $112,363, CNS-Associated Mast Cells and Experimental Autoimmune Encephalomyelitis, PI
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1988-1990 |
National Multiple Sclerosis Society, $11,017, Interaction of Ovarian Steroids and Mast cells in the Sensitization and Expression of Experimental
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Professional Summary:
Edward L. Orr, Ph.D. received his Bachelor of Science degree from Cleveland State University in Cleveland, Ohio in 1970 and his Ph.D. from the University of California in Berkeley, California in 1975. After post-doctoral stints at the Dight Institute for Human Genetics at the University of Minnesota and at the Waisman Center for Mental Retardation and the Wisconsin Regional Primate Research Center, both at the University of Wisconsin in Madison, Wisconsin, he joined the faculty in the Department of Anatomy, Texas College of Osteopathic Medicine (now the University of North Texas Health Science Center at Fort Worth; UNTHSC) in 1979. While there, he taught Human Embryology and Medical Neuroscience to first year medical students for over 23 years while carrying out an active research program on the significance and role of histamine and, subsequently, CNS-associated mast cells, in the brain, especially as related to the development and progression of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. After "retiring" from UNTHSC as an Associate Professor in 2001, he then moved with his then wife and their two young children to Portland, Maine where he joined the physiology faculty at the University of New England College of Osteopathic Medicine in Biddeford, Maine for a year before returning to Texas where he then served on the faculty at Texas Womens University in Denton, Texas before joining the faculty in the School of Natural and Health Sciences at Barry University in Miami Shores, Florida in 2004 as an Associate Professor in the Graduate Biomedical Sciences Program. At Barry University, he teaches Neuroanatomy, Histology, Human Embryology, and Endocrinology to Masters students preparing for entry into medical or dental school, as well as Neuroanatomy to first year students in the Podiatric Medicine Program. He has also re-initiated his research activities where he is evaluating the significance and roles of meningeal and other CNS-associated mast cells in response to various forms of head or brain injury. This research is being carried out in collaboration with colleagues at the University of Miami and the Miami Project to Cure Paralysis in nearby Miami, Florida.
Title: Effects of Head Injury on Dural Mast Cells, Cerebral Cortical Histamine, and Cerebrovascular Permeability
Abstract:
In previous research, I had demonstrated that meningeal (dural) mast cells are activated by unilateral cryogenic injury of the mouse head and brain, and that such injuries are accompanied by breakdown of the blood-brain barrier, cerebral edema, and an accumulation of mast cell-derived histamine in the injured cerebral cortex; however, the edema and permeability effects of such cryogenic injuries were not attenuated in mast cell-deficient mice, even though the increase in cerebral cortical histamine did not occur (Orr & Pace, Cryogenic lesions induce a mast cell-dependent increase in cerebral cortical histamine levels in the mouse. Neurochem. Pathol. 8: 43-51. 1984). Disappointed with the apparent lack of significant involvement of dural mast cells and mast cell-derived histamine in this type of brain injury, I discontinued this research direction until recently. I now report that a much more moderate type of head injury (initially, a unilateral craniotomy and, subsequently, simply cutting grooves in the skull) also activates mast cells in the underlying dura mater and that this activation of dural mast cells is accompanied by increases in histamine levels and pial vascular permeability in the subjacent cerebral cortex. Moreover, prior administration of a specific histamine H2-receptor antagonist (zolantidine) significantly and dose-dependently decreases the increase in pial vascular permeability. This research demonstrates that a relatively mild skull injury that does not directly injure the brain results in significant effects on the underlying brain that are mediated in whole or in part by dural mast cells and their released mediators.
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Monday October 9, 2006 NOON |
Dr Rakesh Sharma
Address:A160 COE NHMFL FSU, 1800 E. Paul Dirac Dr., Tallahassee, FL 32310-3706
Telephone: 850-410-6149
Fax: 850-410-6150
Email:
Title: What we can Measure by Magnetic Resonance Imaging and Magnetic Resonance Spectroscopy for Quantitative Anatomy
Date: Monday, October 9, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra
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Current Research Interests:
Technique development for in vivo MRI cell and molecular imaging: - Development of better imaging techniques to improve carbon nanotubes and iron oxide nanoparticle MRI signals
- Development of cell/tissue culture methods for stem cells for MR applications
- Development of in vivo MR spectroscopic imaging and metabolite quantification
Imaging contrast agents development:
- Newer contrast agents (Gene-expression, Gadolinium, Fluoronitromidazole) and apoptosis gene marker imaging agents
Past Research Interests
University of Texas and Methodist Hospital, Houston, TX (October, 1997 - June, 2000) - Localized MRSI of multiple sclerosis lesion in relapsing remitting MS observed serially
- Development of method to assess MS lesion volume by quadruple contrast technique;
- Development of time-dependent lipid rich lesion enhancement by Gadolinium contrast agent
- Development of method for histopathology-MRI characterization of atherosclerosis plaque
- Molecular biology methods(DNA microarray, proteomics, MMP) for carotid artery lesions
- MRI registration, segmentation, image processing, pulse sequence design
ABSTRACT: Quantitative Anatomy is emerging as rapid tool of Radioimaging in both clinical and biomedical research to monitor the effect of drug. Multimodal techniques like Magnetic Resonance Imaging with spectroscopy, Positron Emission Tomography and Molecular imaging provide non-invasive quick insight of tissue characterization and its tissue type with its cellular metabolic details in neurodegenerative disorders of Alzheimer's Disease, Epilepsy, Multiple Sclerosis after Promiscol? therapy. Localized diseases like Atherosclerosis plaque and cardiovascular wall thickening can be measured to evaluate the effect of Lovastatin®. With advanced magnetic resonance imaging operating at high field of 21 Tesla, it has become possible to visualize details of tissues at cellular level after drug therapy.
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Tuesday, September 19, 2006 NOON |
David J. Mokler, Ph.D.
Department of Pharmacology
University of New England
College of Osteopathic Medicine
Address: 11 Hills Beach Road, Biddeford, Maine 04005
Telephone: (Office) (207) 602-2210
(Fax): (207) 602-5931
Email: dmokler@une.edu
Title: Investigations of the Effects of MDMA (Ecstasy) on Neuronal Serotonin and Dopamine Using In Vivo Microdialysis
Date: Tuesday, September 19, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor Rocovich Board Room
VCOM Host: Dr. Hara Misra
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ABSTRACT: MDMA (Ecstasy) is a commonly used drug of abuse. Of great concern has been the neurotoxic effects of MDMA on serotonergic neurons in animals exposed to single high doses or multiple low doses of MDMA. Data from animal studies has shown that this neurotoxicity can be avoided if the animals are pretreated with a selective serotonin reuptake inhibitor such as fluoxetine (Prozac). It has been reported that human MDMA users have pretreated with fluoxetine in an attempt to avoid this possible neurotoxic effect. Furthermore, the SSRIs are commonly prescribed drugs. We have investigated the interactions between MDMA and fluoxetine in terms of extracellular serotonin and dopamine using in vivo microdialysis. In vivo microdialysis allows us to monitor the extracellular concentrations of serotonin and dopamine in the awake, behaving animal. We have examined the extracellular concentrations of serotonin and dopamine in rats ten days after receiving a toxic dose of MDMA alone or pretreated with fluoxetine. MDMA alone decreased extracellular serotonin in the striatum and to a lesser extent in the prefrontal cortex, but did not alter extracellular dopamine in either area. Fluoxetine prevented this effect of MDMA on extracellular serotonin. The combination of fluoxetine and MDMA however produced a decrease in extracellular dopamine in both the striatum and prefrontal cortex. Early studies suggest that this may in fact be a switch in neurotoxicity from serotonin to dopamine neurons.
Education:
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1984-1986 |
Postdoctoral Fellow, Medical College of Virginia, Virginia Commonwealth University, Department of Pharmacology and Toxicology, Richmond, Virginia |
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1979-1984 |
Ph.D., Michigan State University, Department of Pharmacology and Toxicology, and Neurosciences Program (Dual Doctorate), East Lansing, Michigan |
Academic Appointments:
| 2000- present |
Professor of Pharmacology (tenure 1993)
University of New England
College of Osteopathic Medicine |
| 1999-present |
Adjunct Professor
Center for Behavioral Development and Mental Retardation
Department of Psychiatry
Boston University School of Medicine |
| July, 1999- |
Visiting Professor (Sabbatical from UNE) |
| Jan., 2000 |
Center for Behavioral Development and Mental Retardation
Department of Psychiatry
Boston University School of Medicine |
| 1990 - 2000 |
Associate Professor of Pharmacology (tenure 1993)
University of New England
College of Osteopathic Medicine |
| 1986 - 1990 |
Assistant Professor of Pharmacology
University of New England
College of Osteopathic Medicine |
Grants:
| 2004-present |
Consultant, SIDs Program Project, Children s Hospital, Harvard Medical School, Hannah Kinney, M.D., P.I.. |
| 2000-present |
Co-Investigator, National Institute on Child Health and Human Development HD 22539, Prenatal Malnutrition and Mental Retardation, Boston University School of Medicine, Janina Galler, M.D., P.I. |
| 1996 - 1999 |
Consultant, National Institute on Child Health and Human Development HD 22539, Prenatal Malnutrition and Mental Retardation, Boston University School of Medicine, Janina Galler, M.D., P.I.
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| 1991 - 1994 |
PI, National Institute on Drug Abuse DA07316, 5-Hydroxytryptamine Mechanisms of Hallucinogenic Drugs, Total Direct $ 96,575
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Publications:
The following represent the recent work of Dr. Mokler which consists of 55 peer reviewed papers and over 100 abstracts.
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Johnson, D.W., Eodice, P., Winterbottom, H. and Mokler, D.J. Increases in extracellular dopamine release in the nucleus accumbens after acute cocaine are not required for expression of behavioral sensitization in female Sprague-Dawley rats. Pharmacology, Biochemistry and Behavior 65 (4): 659-664, 2000. -
Mokler, D.J., Galler, J.R. and Luebke, J.I. Development and modulation of GABAA receptor-mediated neurotransmission in the CA1 region of prenatally protein malnourished rats. Nutritional Neuroscience 4: 109-119, 2001. -
Morgane, P.J., Mokler, D.J. and Galler, J.R. Effects of prenatal protein malnutrition on the hippocampal formation. Neurosci. Biobehav. Rev. 26(4): 471-483, 2002. -
Morgane, P.J., Mokler, D.J. and Galler, J.R. Malnutrition, central nervous system effects. Encyclopedia of Neuroscience, Elsevier Press, 2003. -
Mokler, D.J., Galler, J.R. and Morgane, P.J. Modulation of 5-HT release from the hippocampus of 30-day old rats exposed in utero to protein malnutrition. Dev. Brain Res. 142(2): 203-208, 2003. -
Turner,T.J., Mokler, D.J., Luebke, J.I. Calcium influx through presynaptic 5-HT3 receptors facilitates GABA release in the hippocampus: In vitro slice and synaptosome studies. Neuroscience 129 (3): 709-718, 2004. -
Morgane, P.J., Galler, J.R., Mokler, D.J. A review of systems and networks of the limbic forebrain/limbic midbrain. Prog. Neurobiol. 75(2): 143-160, 2005. -
Morgane, P.J. and Mokler, D.J. (eds.) Limbic Brain: Structure and Function. Special Issue, Neuroscience and Biobehavioral Reviews, 30(2), 2006. -
Morgane, P.J. and Mokler, D.J. The Limbic Brain: Continuing Resolution. Neuroscience and Biobehavioral Reviews, 30(2), 119-125, 2006. -
Mokler,D.J., Galler, J.R. and Morgane, P.J. Functional inter-relations between the midbrain raph' nuclei as examined by dual-probe microdialysis. Submitted, 2006. -
Mokler, D.J., Torres, O., Galler, J.R. and Morgane, P.J. Stress-induced changes in dopamine and serotonin in the medial prefrontal cortex and dorsal hippocampus of prenatally malnourished rats, Submitted, 2006. - Azie, B.M., Buglio, A.E., Hoffman, J. and Mokler, D.J. Dopamine and serotonin release from the frontal cortex and striatum following MDMA as determined by in vivo microdialysis: Effect of fluoxetine. In preparation.
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| Monday, September 11, 2006 NOON |
Robert R. Luedtke, Ph.D.
Professor, Department of Pharmacology and Neuroscience
Department of Pharmacology and Neuroscience
University of North Texas Health Science Center
Address: 3500 Camp Bowie, Fort Worth, TX 76107
Telephone: (Office) 817-735-2611
(Fax) 817-735-2091
Email: rluedtke@hsc.unt.edu
Title: Development of D3 Dopamine Receptor Subtype Selective Compounds Date:Monday, September 11, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra
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Previous Research Experience:
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1997-2003 | Associate Professor, Department of Pharmacology, UNTHSC |
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1991-1997 | Assistant Professor, Department of Pharmacology, UNTHSC |
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1983-1991 | Research Associate, Department of Pharmacology, University of Pennsylvania. |
Research Awards
| Fulbright Scholar's Award in Molecular Neurobiology | 2004 |
| NIH/ NIDA: R 21 DA16181-01 | 2002 to 2007 (Co.-P.I.) |
| NIH/ NIDA: R-01 DA13584-01 | 2001 to 2005 |
| NIH/ NIDA: R O1 DA12647-01 | 2000 to 2003 (Co.-P.I.) |
| NIH/ NIDA: R-01 DA12205-01 | 1999 to 2001 |
Abstract: The three dopaminergic pathways in the mammalian brain are the nigrostriatal, the mesocorticolimbic and the tuberoinfundibular pathways. Alterations in the dopaminergic pathways are thought to be involved in the pathogenesis of neurological and neuropsychiatric disorders, including Parkinson's Disease and schizophrenia. Modulation of the dopaminergic pathways is also thought to occur following acute or chronic abuse of cocaine and amphetamines.
Molecular genetic studies have defined two types of dopamine receptors, the D1-like (D1 and D5 receptor subtypes) and D2-like (D2, D3 and D4 receptor subtypes) receptors based upon structural and pharmacological similarities. Because of the high degree of homology between D2 and D3 receptor binding sites, it has been difficult to obtain compounds that can bind selectively to either the D2 or the D3 dopamine receptor subtypes. However, we have recently developed D2 and D3 dopamine receptor selective compounds that we hope will be useful pharmacologic tools to precisely define the role of these two D2-like receptor subtypes in a variety of experimental physiological and behavioral situations. The seminar will discuss our research on the development and pharmacological characterization of D2 and D3 receptor subtype selective compounds of varying intrinsic activity. |
| Tuesday August 22, 2006 NOON |
Yunbo Li, MD, PhD
Associate Professor of Medicine and Pharmacology
Associate Director, Center for Environmental & Smoking Induced Disease
The Ohio State University College of Medicine and Public Health
Columbus, Ohio 43210
Title: Pharmacological Upregulation of Cardiovascular Antioxidants & Phase 2 Enzymes: Mechanisms and Chemoprotection
Address: 012C DHLRI, 473 W. 12th Avenue, Columbus, Ohio 43210
Telephone: (Office) 614-292-4811
Email: yunbo.li@osumc.edu
Web site:http://www.heartlung.osu.edu
Date: Tuesday August 22, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra
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Professional summary:
Dr. Li received an MD degree from Shandong Medical University, and a PhD degree in Toxicology/Pharmacology from The Johns Hopkins University. Dr. Li was a visiting scientist in the University of Sydney, Australia, and University of California at Berkeley from 1990 to 1991. Then, he completed a postdoctoral fellowship at The Johns Hopkins University. Dr Li toke his first tenure-track faculty position as an assistant professor of pharmaceutical sciences (pharmacology/toxicology) at St. John's University College of Pharmacy in 2000. He was promoted to an associate professor at the same institute in 2003. In January of 2005, Dr. Li joined The Ohio State University College of Medicine and Public Health. He is currently an associate professor of medicine and pharmacology. He is also the associate director of the Center of Biomedical Technology for the Study of Environmental and Smoking Induced Diseases at The Ohio State University. Dr. Li has published 73 peer-reviewed articles, and written a number of book chapters. He has received numerous institutional and national awards. Dr. Li's research is supported by NIH grants. The current research in his laboratory focuses on the free radical mechanisms of tissue injury and development of pharmacological/chemoprotective strategies for intervention of free radical-mediated disease process.
Abstract: Cardiovascular disease (CVD) remains the number one cause of death in the United States. Considerable evidence supports a causal role for oxidative and electrophilic species in the pathophysiology of various forms of CVD, including myocardial ischemia-reperfusion injury, atherosclerosis, and drug-induced cardiotoxicity. As such, extensive studies have focused on use of exogenous antioxidative compounds, including antioxidant vitamins to prevent or retard the oxidative process underlying CVD. However, clinical trials on use of individual antioxidative compounds, including vitamin E, in the intervention of cardiovascular events have yielded conflicting results, pointing to the limitations associated with using exogenous antioxidants in the management of CVD. We propose a novel strategy for protecting against cardiovascular pathophysiology through drug/chemoprotectant-mediated coordinated upregulation of endogenous antioxidants/phase 2 enzymes in cardiovascular tissue. The coordinated actions of a series of cellular antioxidants/phase 2 enzymes are essential for efficient detoxification of oxidative and electrophilic species. The long-term objective of our research is to develop rational protective/therapeutic strategies to prevent, retard, or even reverse the oxidative degenerative process underlying cardiovascular disorders. Such strategies rely on a profound understanding of the pharmacological inducibility of cardiovascular antioxidants and phase 2 enzymes, and the underlying molecular mechanisms.
Suggested reading: -
Cao Z, Li Y. Potent induction of cellular antioxidants and phase 2 enzymes by resveratrol in cardiomyocytes: protection against oxidative and electrophilic injury. Eur. J. Pharmacol. 489:39-48, 2004.
- Li Y, Cao Z, Zhu H, Trush MA. Differential roles of 3H-1,2-dithiole-3-thione-induced glutathione, glutathione S-transferase and aldose reductase in protecting against 4-hydroxynonenal toxicity in cultured cardiomyocytes. Arch. Biochem. Biophys. 439:80-90, 2005
- Cao Z, Zhu H, Zhang L, Zhao X, Zweier JL, Li Y. Antioxidants and phase 2 enzymes in cardiomyocytes: chemical inducibility and chemoprotection against oxidant and simulated ischemia-reperfusion injury. Exp. Biol. Med. 231:1351-1364, 2006.
- Zhu H, Zhang L, Itoh K, Yamamoto M, Ross D, Trush MA, Zweier, JL, Li Y. Nrf2 controls bone marrow stromal cell susceptibility to oxidative and electrophilic stress. Free Radiac. Biol. Med. 41:132:143, 2006.
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| Thursday July 6, 2006 NOON |
Harihara M. Mehendale, Ph.D.
Professor and Kitty DeGree Chair in Toxicology
Director, Training Program in Toxicology
Department of Toxicology, College of Pharmacy
The University of Louisiana at Monroe (ULM),
Monroe, LA 71209
Title: Liver tissue repair, survival factors and adaptation to injury
Address: 207 Winterpark Drive, West Monroe, LA 71292, USA
Telephone: (off.) 318-342-1691; Alternate (off.): 318 342 1745
Email: mehendale@ulm.edu
Web site:http://rxweb.ulm.edu/pharmacy/mehendale/
Date: Thursday July 6, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra
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Background: Dr. Mehendale received his M.S. and Ph.D. degrees from the Toxicology Program at North Carolina State University. He received his postdoctoral training at the University of Kentucky and at the National Institute of Environmental Health Sciences (NIEHS), before joining NIEHS as a Staff Fellow. In 1975, he joined the University of Mississippi Medical Center as Assistant Professor, rose through the academic ranks to full Professor in 1980. He joined the University of Louisiana at Monroe (ULM) in 1992. His research interests span across pulmonary, hepatic, renal and general toxicology of medicinal, industrial and environmental chemicals. His current area of research emphasis involves understanding the role of tissue repair in the ultimate outcome of tissue injury, the mechanisms in control of cell division and tissue repair as well as the molecular events keying these mechanisms. Current research is focused on the impact of age, diabetes, and diet restriction on toxic effects, mechanisms of progression and regression of injuries, and potential adverse health effects of exposure to combinations of chemicals. He has authored over 275 original research and review articles, as well as book chapters. Dr. Mehendale has received several Honors and Awards for his research and scholarly contributions. In 1988, he received the "Burroughs Wellcome Scholar in Toxicology" award given by the Society of Toxicology, U.S.A. In 1993, he received the Zeneca International Travel Award. In 1995, he was named outstanding researcher at ULM and received the "Researcher of the Year" Award. In 1996, the American Association for the Advancement of Science (AAAS) elected him "Science Fellow". In 1999, he received the Best Paper Award for best paper published in Toxicology and Applied Pharmacology. In 2001, received the Society of Toxicology??s Education Award for his eminent contributions to education in toxicology.
Summary: Liver injury initiated by either the parent drug or its reactive metabolite(s), is known to progress in disease or other physiological states. While we know a great deal about how injury is initiated by drugs, a solid understanding of how injury may progress or regress is lacking.
Recent studies reveal that many events driven by liver biology determine the latter. Progression can result due to destructive action of hydrolytic enzymes, "death proteins" leaking out of necrosed cells on the neighboring partly affected or unaffected cells, thereby setting off a self-perpetuating expansion of injury. Once necrosis is initiated by mechanism-based events, this process occurs even in the absence of the necrogenic drug. Calpain and c-phospholipase A2 (cPLA2) are examples of such hydrolytic 'death proteins'. Compensatory mechanisms such as cell division and over-expression of survival factors by the newly divided cells can prevent this onslaught by the death proteins and expansion of injury. Failed or delayed cell division, as in the case of high doses, or in disease, leads to expansion of injury. Autoprotection and heteroprotection models indicate that stimulation of cell division and tissue repair are critical in overcoming life-threatening liver injury suggesting that adaptive mechanisms can be activated in the liver by priming.
Diabetes is known to sensitize liver to hepatotoxicity. Diabetic rats (type I & type II) are highly sensitive to hepatotoxicity due to impaired compensatory cell division in the diabetic state. However, even in the diabetic state, animal experiments show that it is possible to stimulate efficient cell division by priming and protect the diabetic animals from life-threatening liver toxicity, by overcoming the acute liver failure (ALF)-bound injury. In stark contrast to the diabetic rats, diabetic mice (type I & type II) are resilient to drug-induced hepatotoxicity. Unfortunately, this model has not been investigated enough to find out what we can learn from the mouse about survival strategies. Although much remains to be learned about the murine strategy for survival, what we know from drug toxicity models is that mice are able to compensate rapidly by early and robust stimulation of cell division. Moreover, subchronic priming exposure to chloroform for 30 days protect mice from a subsequent dose of chloroform that normally cause ALF and death, due to prompt stimulation of cell division as an adaptive mechanism. What we learn from these experimental models provide us clues that may be exploited to modify our approaches in dealing with drug-associated liver toxicities.
Suggested reading: Mehenale, H.M. Tissue repair: an important determinant of final outcome of toxicant-induced injury. Toxicolo. Pathol. 33, 41-51, 2005.
Dnyanmote, A. V., Sawant, S. P., Lock, E. A., Latendresse, J. R., and Mehendale, H. M. Diabetic mice are protected from normally lethal nephropathy of 1, 2-dichlorovinyl ??L-cysteine (DCVC): role of nephrogenic tissue repair. Toxicol. Appl. Pharmacol. 211: 133-147, 2006.
Sawant, S. P., Dnyanmote, A. V., Warbrittn, A., Latendresse, J. R., and Mehendale, H. M. Type 2 diabetic rats are sensitive to thioacetamide hepatotoxicity. Toxicol. Appl. Pharmacol. 211: 221-232, 2006.
Limaye, P. B., Apte, U. M., Yu, S., Bhave, V. S., Palkar, P. S., Sawant, S. P., Latendresse, J. L., Reddy, J. K., and Mehendale, H. M. Calpastatin overexpression.
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| Wednesday June 14, 2006 NOON |
Ishwar K. Puri, Ph.D.
Mathematical Model for the Cancer Stem Cell Hypothesis
Address: Virginia Tech, Department of Engineering Science and Mechanics
223 Norris Hall - MC 0219
Blacksburg, VA 24061
Telephone: (540) 231-3243 • Fax: (540) 231-4574
Email: ikpuri@vt.edu
Web site: www.esm.vt.edu Date: Wednesday June 14, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor Board Conference Room
VCOM Host: Dr. Hara Misra
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Background: Professor Ishwar K. Puri has served as Professor and Department Head of Engineering Science and Mechanics at Virginia Tech since 2004. He obtained his Ph.D. (1987), and M.S. (1984) degrees in Engineering Science (Applied Mechanics) from the University of California, San Diego after obtaining a B.Sc. (1982) in Mechanical Engineering from the University of Delhi. He served as an Assistant Research Engineer at the University of California, San Diego from 1987-90. He was appointed as an Assistant Professor in the Mechanical Engineering Department at the University of Illinois at Chicago in 1990, was promoted to the rank of Associate Professor with tenure in 1994, and to the rank of Professor in 1999. He served as Director of Graduate of the Mechanical and Industrial Engineering programs from 1994-97, and 1999-2000. He served as Associate Dean for Research and Graduate Studies (2000-01), and as Executive Associate Dean of Engineering (2001-04). He served on the steering committee of the UIC Institute for Environmental Studies and headed UIC's micro- and nanotechnology initiatives. Professor Puri is a Fellow of the American Society of Mechanical Engineers (ASME) and of the American Association for the Advancement of Science (AAAS). He was a Distinguished Guest of the Swiss Leonard Euler Center of the European Research Community of Fluid Turbulence and Combustion in 1998 and 1999. He was a 1993 American Association for the Advancement of Science-Environmental Protection Agency (AAAS-EPA) Environmental Fellow, a 1992 NASA/Stanford University Center for Turbulence Research Fellow, and a 1991 Visiting Fellow at the University of Cambridge. He has served as a program and peer review panelist for the Department of Energy, US EPA, and NSF. He is an editor of the journal Experimental Heat Transfer. Professor Puri has conducted research through major grants from NASA, NSF, DOE, US EPA, State of Illinois, and industry. He established a European-US consortium to conduct engineering student exchanges at the undergraduate and graduate levels that was funded through the US Department of Education FIPSE program. His students are placed in major corporations and at universities worldwide. He is the author of over 200 archival and conference publications in the fields of combustion, transport phenomena, and computational science and engineering (e.g., related to emissions, self assembly, magnetic fluids, drug targeting, cell mechanics, nanoscale fluid dynamics, and hydrogen storage). He has edited a book on the environmental implications of combustion processes, a textbook on advanced thermodynamics engineering and another on combustion science and engineering.
Summary: stem cells for malignant tumor growth. Various genes that regulate self-renewal in normal stem cells are also found in cancer stem cells. This implies that cancers can occur due to mutations in normal stem cells and early progenitor cells. A predictive mathematical model that is based on the cell compartment method will be presented to pose and validate nonintuitive scenarios proposed through the neural cancer stem cell hypothesis. The growths of abnormal (stem and early progenitor) cells from their normal counterparts will be ascribed with separate mutation probabilities. Stem cell mutations are found to be more significant for the development of cancer than a similar mutation in the early progenitor cells. The model also predicts that, as previously hypothesized, repeated insult to mature cells increases the formation of abnormal progeny, and hence the risk of cancer. Suggested reading: Ganguly, R., and Puri, I.K., Mathematical model for the cancer stem cell hypothesis, Cell Proliferation, 39, 3-14, 2006.
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| Monday, May 8, 2006 NOON |
Stephen Gregory Guill, MS
Title: Sleeping with the Enemy: the Role of Obstructive Sleep Apnea in Chronic Disease Pathology
Address: Lab Coordinator, VIA-TECH Health & Wellness Center, 231A War Memorial Hall
Telephone: 540-231-6374
Email: sguill@vt.edu Date: Monday, May 8, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor Board Conference Room
VCOM Host: Dr. Hara Misra
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Background: Stephen Guill is a Ph.D. candidate at Virginia Tech in the department of Human Nutrition, Foods, and Exercise, with a specialization in Clinical Exercise Physiology. Stephen has also completed doctoral certificates in Gerontology and Molecular Cell Biology and Biotechnology. For the past 6 years, Stephen has supervised laboratory testing and program activities for chronic disease rehabilitation programs at Wake Forest University, where he received his M.S degree in Health and Exercise Science in 2003, and Virginia Tech. Stephen??s current research examines the relationship between obstructive sleep apnea and chronic disease, with an emphasis in metabolic syndrome and diabetes.
Summary: Obstructive sleep apnea (OSA) is an obesity-related condition characterized by repetitive upper airway collapse during sleep. At least 1 in 5 adults may be affected. In addition to excessive daytime sleepiness and impaired cognitive function, individuals with OSA are at greater risk for hypertension and diabetes. This seminar will describe key features of OSA pathology, clinical presentation, and treatment options. Hypothesized mechanistic links between OSA and chronic disease will be explored, including the role of the sympathetic nervous system, intermittent hypoxia and hypercapnia, and fragmented sleep. Finally, recent OSA research conducted at Virginia Tech will be presented, with an emphasis on initiatives for future research. |
| Monday, May 1, 2006 NOON |
Darwin Jorgensen, Ph.D.
Title: "We all work the same way: studies on cardiovascular and respiratory function in certain marine crustaceans"
Mailing Address: Thornhill Professor and Chair
Biology Department
Roanoke College
221 College Lane
Salem, VA 24153
Telephone: (540) 375-2465
FAX (shared): (540) 375-2447 Date: Monday, May 1, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Richard Wyeth
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Research: Dr. Darwin D. Jorgensen has been the Brian H. Th | |