Biomedical Seminars

  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
Web site:

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.

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:

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.

  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

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

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 Upon retirement from teaching, he became Editor-in-Chief of the Journal of Scientific Exploration.

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:

  1. The Origin, Persistence and Failings of HIV/AIDS Theory
    McFarland, 2007; ISBN 0-7864-3048-6
  2. Knowledge Monopolies: Science and Medicine Gone Wrong
    manuscript under review by publisher
  3. Science or Pseudoscience: Magnetic Healing, Psychic Phenomena, and Other Heterodoxies,  University of Illinois Press 2001; paperback ed. 2004
  4. Fatal Attractions: The Troubles with Science
    New York: Paraview Press 2001


  Tuesday August 7, 2007  NOON

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)


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

Sponsor: Dr. JiM Palmieri

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.

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

  1. 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.
  2. 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.
  3. 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.
  4. Lewin-Smith MR, Klassen MK, Frankel SS, Nelson AM. Pathology of human immunodeficiency virus infection: infections conditions. Ann Diagn Pathol 1998;2:181-194.
  5. Klassen MK, Lewin-Smith MR, Frankel SS, Nelson AM. Pathology of human immunodeficiency virus infection: Noninfections conditions. Ann Diagn Pathol 1997;1:57-64.
  6. 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

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. Blumberg HM, Nelson AM. Tuberculosis. In: Nelson AM, Horsburgh CR Jr (editors). Pathology of Emerging Infections 2. ASM Press, Washington, DC, 1998:167-192.


  Tuesday, June 19, 2007 NOON

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

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

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.

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.

  Wednesday, June 13, 2007 NOON

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

Sponsor: Dr. Hara Misra

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

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:

  1. 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
  2. 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
  3. 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
  4. 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
  Tuesday, June 12, 2007  2 p.m.

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)

Sponsor: Dr. Hara Misra

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:

  1. 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
  2. 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.
  3. 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.

Tuesday May 15, 2007  NOON

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

Title: Hypogonadism in the aging male
Date: Tuesday May 15, 2007
Location: VCOM, 3rd floor CME Room
Phone: 540-983-1015


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

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.

Thursday May 3rd, 2007   NOON

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

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).

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

Thursday April 12, 2007   NOON

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:

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.


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)

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


B. Sc. 1975 and M,Sc. 1977 University of Madras, Chennai (Chemistry)
Ph.D. 1985 Indian Institute of Technology (Chemistry/Spectroscopy)

Faculty Positions:

  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

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

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:
  1. 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.);=PubMed&dopt;=Citation&list;_uids=17142337
  2. 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).
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

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

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


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.

Tuesday February 20, 2007   NOON

Webster L. Santos

Virginia Tech
Department of Chemistry
Address: 401B Davidson Hall, Blacksburg, VA 24061
Telephone: 540-231-5742

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

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.


2002-2006 Ruth L. Kirschtein Postdoctoral Fellow (NRSA), Harvard University
2000-2002 NIH NRSA Pre-doctoral Fellowship, University of Virginia
2002 Third Prize Winner, Robert J. Huskey Graduate Research Symposium, University of Virginia
1998-1999 Outstanding Graduate Teaching Assistant Award (University-wide), University of Virginia
1996-1997 Semi-finalist for Seven Society Teaching Fellowship, Secret Seven Society, University of Virginia


  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  1. 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.
  2. 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.
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

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


1970 B.S. (Biology), Cleveland State University, Cleveland, Ohio
1975 Ph.D. (Zoology), University of California, Berkeley.

Faculty Positions:

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
2001-2002 Acting Assistant Professor of Physiology, University of New England College of Osteopathic Medicine, Biddeford, Maine
2002-2003 Visiting Assistant Professor, Department of Biology, Texas Woman's University, Denton, Texas
2004-present Associate Professor, Biomedical Sciences Program, School of Natural and Health Sciences, Barry University, Miami Shores, Florida

Honors and Awards:

1987-1990 National Multiple Sclerosis Society, $112,363, CNS-Associated Mast Cells and Experimental Autoimmune Encephalomyelitis, PI
1988-1990 National Multiple Sclerosis Society, $11,017, Interaction of Ovarian Steroids and Mast cells in the Sensitization and Expression of Experimental

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

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.

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

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

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.

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

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

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.


1984-1986 Postdoctoral Fellow, Medical College of Virginia, Virginia Commonwealth University, Department of Pharmacology and Toxicology, Richmond, Virginia
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


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.
1991 - 1994 PI, National Institute on Drug Abuse DA07316, 5-Hydroxytryptamine Mechanisms of Hallucinogenic Drugs, Total Direct $ 96,575

The following represent the recent work of Dr. Mokler which consists of 55 peer reviewed papers and over 100 abstracts.

  1. 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.

  2. 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.

  3. 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.

  4. Morgane, P.J., Mokler, D.J. and Galler, J.R. Malnutrition, central nervous system effects. Encyclopedia of Neuroscience, Elsevier Press, 2003.

  5. 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.

  6. 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.

  7. 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.

  8. Morgane, P.J. and Mokler, D.J. (eds.) Limbic Brain: Structure and Function. Special Issue, Neuroscience and Biobehavioral Reviews, 30(2), 2006.

  9. Morgane, P.J. and Mokler, D.J. The Limbic Brain: Continuing Resolution. Neuroscience and Biobehavioral Reviews, 30(2), 119-125, 2006.

  10. 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.

  11. 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.

  12. 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.
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

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

Previous Research Experience:
1997-2003Associate Professor, Department of Pharmacology, UNTHSC
1991-1997Assistant Professor, Department of Pharmacology, UNTHSC
1983-1991 Research Associate, Department of Pharmacology, University of Pennsylvania.

Research Awards

Fulbright Scholar's Award in Molecular Neurobiology2004
NIH/ NIDA: R 21 DA16181-012002 to 2007 (Co.-P.I.)
NIH/ NIDA: R-01 DA13584-012001 to 2005
NIH/ NIDA: R O1 DA12647-012000 to 2003 (Co.-P.I.)
NIH/ NIDA: R-01 DA12205-011999 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
Web site:

Date: Tuesday August 22, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra

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:

  1. 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.
  2. 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
  3. 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.
  4. 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.
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
Web site:

Date: Thursday July 6, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra

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.

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
Web site:

Date: Wednesday June 14, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor Board Conference Room
VCOM Host: Dr. Hara Misra

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.

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

Date: Monday, May 8, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor Board Conference Room
VCOM Host: Dr. Hara Misra

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


Research: Dr. Darwin D. Jorgensen has been the Brian H. Thornhill Professor and Chair, Biology Department, Roanoke College since 2003. His research areas include: comparative animal physiology, cardiovascular and respiratory physiology, invertebrate biology, the history and rhetoric of science.

Recent and Selected Professional Publications:

  1. "Distribution of hydrostatic pressure in the branchial chamber of the American lobster, Homarus americanus. (2006). with: A. Hinlicky*. Southeastern Biology 53(2):125. (abstract)
  2. "Unequal hydrostatic pressure distribution in the branchial chamber of the exercising blue crab, Callinectes sapidus." (2006). with: M. Bryant*. Southeastern Biology 53(2):125. (abstract)
  3. "Ventilatory pump effect on circulatory function in the blue crab, Callinectes sapidus. (2006). with E. Brady*. Southeastern Biology 53(2):125. (abstract)
  4. "The Depression of oxygen uptake in blue crabs in response to bacterial challenge" with J. Holman*, K. Burnett, and L. Burnett. (2004). Integrative and Comparative Biology, 43(5). (abstract)
  5. "The Relationship Between Respiratory Pump Function and the Gill Circulation in the American Lobster, Homarus americanus." with J. Herr* and A. Strunk*. (2004). Southeastern Biology 51(2):195. (abstract)
  6. "Respiratory support of submerged walking in the blue crab, Callinectes sapidus." (2000). with: T. Wilkes* and L. Beaulieu*. Southeastern Biology 48(2):53. (abstract)

Summary: My students and I have been studying cardiovascular and respiratory physiology of blue crabs and lobsters. Extremely important to the fisheries industry along the east coast of the U.S. (including our Chesapeake Bay), they are interesting physiological models of how water-breathing animals work. Both species are migratory, walking (and/or swimming) underwater for considerable distances. I will provide an overview of how they work (drawing comparisons to the mammalian situation) and discuss some of our past, current, and future projects

Thursday, March 23, 2006   NOON

Kumar Mallikarjunan

Title: Sniffing out the Discomfort

Mailing Address: 312 Seitz Hall, Virginia Tech
Telephone contact number: 540-231-7937
Web site:

Date: Thursday March 23, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra

Research: Dr. Mallikarjunan, specialized in food engineering, has extensive experience with the development of non-destructive non-contact sensing technologies such as electronic nose and ultrasound for quality evaluation in food products. He also worked in the area of food safety and in prevention of pathogen contamination and treatment of pathogen contaminated food products through thermal and non-thremal processing technologies. He would like to extend his research into biomedical applications and seek collaborative support from VCOM.

Summary: Electronic nose technology, which mimics a biological nose, can overcome some of the difficulties associated with classical odor measurement, and electronic noses have many applications in biomedical industry. They are recently gaining momentum with respect to a variety of applications for diagnostics, routine analysis, prescreening and microbial enumeration. With all the possibilities, still the technology is being pushed by the system manufacturers than pulled by need from the industry. Biomedical industry is very skeptical about the capabilities of the systems, and this presentation will provide an overview of available technologies, systems, applications, and implementation issues. Focus will be given to the pitfalls with these techniques compared to existing analytical methods for odor measurement. Both desktop and handheld-type systems and systems for on-line monitoring will be discussed. Issues like cost, training, sensor drift, statistical limitations, and sampling limitations will be analyzed and future directions for research and development will be discussed. Dr. Mallikarjunan will also discuss the potential for future research collaborations with VCOM faculty.

Tuesday, January 10, 2006

Dongmin Liu, MS PhD

Title: Genistein and pancreatic beta-cell function
Date: Tuesday January 10, 2006
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host: Dr. Hara Misra

Dr. Dongmin Liu received his MS in animal quantitative genetics in China, in 1992. He later obtained his Ph.D in animal nutritional physiology at Virginia Tech in 2000. His Postdoctoral research was in Endocrinology and vascular biologyat the Department of Internal Medicine in the University of Iowa Medical College between 2000-2003.

Research: Dr. Liu discovered a DHEA (a human steroid) receptor in vascular endothelial cells in 2002; received a postdoctoral research award from the University of Iowa Medical College and a postdoctoral fellowship award from the American Heart Association. Started a molecular nutrition position as an assistant professor in the Human Nutrition, Foods and Exercise at Virginia Tech in 2004. Current research in the lab is focusing on to investigate how soy isoflavones modulate vascular and pancreatic beta-cell function, and how DHEA regulates angiogenesis and vascular endothelial apoptosis.

Summary: Although genistein, a soy isoflavone, has beneficial effects on various tissues. It is unclear whether it plays a role in pancreatic beta-cell function. Here we present evidence that genistein increases rapid glucose-stimulated insulin secretion (GSIS) in both insulin secreting cell lines (INS-1 and MIN6) and pancreatic islets of mice and humans. The effect of genistein on GSIS was not dependent on its known effect such as binding to estrogen receptor (ER) or inhibition of protein tyrosine kinase (PTK). Consistent with its effect on GSIS, genistein increases intracellular cAMP and activates protein kinase A (PKA) in both cell lines and the islets by a mechanism that does not involve ER or PTK. The induced cAMP by genistein, at physiological concentrations, may result primarily from enhanced adenylate cyclase activity. Pharmacological or molecular intervention of PKA activation indicated that the insulinotropic effect of genistein is primarily mediated through PKA. In addition, we found that genistein also activates the CRE-regulated gene expression in beta-cells. Furthermore, genistein activates extracellular signal-regulated kinase 1/2 in clonal beta-cells and stimulates the cellular proliferation of beta-cells and pancreatic islets. These findings demonstrated that genistein acts directly on pancreatic beta-cells, leading to activation of the cAMP/PKA signaling cascade to exert an insulinotropic and proliferative effect, thereby providing a novel role of soy isoflavones in the regulation of beta-cell function.

Tuesday September 20, 2005

George Zotalis, M.D.

Title: NF-kB signaling in prostate cancer: a morphoproteomic approach
Date: Tuesday September 20, 2005
Time: 12:00 (Noon)
Location: VCOM, 3rd Floor Board Conference Room
VCOM Host: Dr. Hara Misra

Dr. George Zotalis: Board certified in Anatomic Pathology, American Board of Pathology; Fellow in Cytopathology, Geisinger Medical Center, Danville, PA.; Research fellow, University of Rochester, NY.; Resident in Pathology & Laboratory Medicine, University of Rochester, NY

Dr. Zotalis has interest in skeletal biology and pathology. Upon completion of his pathology training, he pursued further training in basic research at the Musculoskeletal Research Laboratory at the University of Rochester. His present research is in the in vitro interactions between prostate cancer cell lines of different metastatic potential (PC-3, DU-145, LNCaP) and osteoclasts. More specifically, the role of proinflammatory cytokines IL-1, IL-6 and TNF???? in osteoclastic bone resorption induced by malignant cells. Currently, Dr. Zotalis is collaborating with the Geisinger Medical Center on morphoproteomic analyses of prostate cancerand has constructed a tissue microarray to further characterize the status of NF-????B activation in primary, organ-confined, non-metastasizing carcinomas with special emphasis on low-to-intermediate Gleason grade cancers.

Summary: Nuclear Factor-kappa B (NF-kB) signaling has been identified as an important molecular pathway in the pathogenesis of primary and especially metastatic prostate cancer.1,2 NF-kB is a family of heterodimeric transcription factors consisting predominantly of p65 and p50 subunits. Under baseline conditions, NF-kB is sequestered in the cytoplasm bound to the inhibitory complex, IkB. Cellular activation by cytokines, growth factors and other signals can lead to activation of specific IkB kinases that phosphorylate, degrade IkB and release phosphorylated NF-kB dimers to be translocated to the nucleus and initiate transcription of a variety of target genes.3,4 NF-kB is constitutively upregulated in prostate cancer5, a process that seems to be associated with increased IkB kinase activity.6 NF-kB regulates anti-apoptosis7 and is involved in critical steps of the metastatic process.8 The majority of experimental work that has demonstrated an important role for NF-kB in prostate cancer so far, has focused primarily on the more aggressive, androgen-independent, or prostate-specific antigen (PSA)-negative phenotypes such as the ones represented by the PC-3 and DU-145 cell lines.2,9 However the clinical spectrum of prostate cancer is much wider and more complex, a majority of cases fall in the intermediate spectrum of Gleason grading and with widespread use of routine PSA testing, increasing numbers of slow-growing, less aggressive forms of prostate cancer are identified. We have constructed a tissue microarray from radical prostatectomies performed at the Geisinger Medical Center from 1990 to 2000, and used a commercially available polyclonal antibody specific for a phosphorylated form of p65 (p-p65), to investigate the status of NF-kB activation in a group of cases that more accurately reflect the clinical spectrum of the disease, especially as it was changing in the 1990s with the introduction of routine PSA testing. We then correlated the results with follow up information which, for a substantial proportion of our cases, extended beyond the usual 5-year limit. Our hypothesis is that activated NF-kB, as evidenced by nuclear localization of p-p65, correlates with more aggressive disease. Our results depict a strong correlation between p-p65 translocated to the nucleus and recurrence in adenocarcinoma of the prostate. Moreover, the predictive value is independent of Gleason score.
Monday, May 16, 2005

Alexa C. Rosypal, Ph.D.
Center for Molecular Medicine and Infectious Diseases
Department of Biomedical Sciences and Pathobiology
Virginia-Maryland Regional College of Veterinary Medicine
Virginia Polytechnic Institute and State University
1410 Prices Fork Rd., Blacksburg, VA 24061

Title: Emergence of zoonotic canine leishmaniasis in the United States
Monday May 16, 2005
1:30 PM
Location: VCOM, 3rd Floor CME Conference Room
VCOM Host:
Dr. Jeannine Strobl

Dr. Alexa Rosypal received her B.S. from Virginia Tech and her Ph.D. from the Virginia-Maryland Regional College of Veterinary Medicine at Virginia Tech. From 2001-2005, Dr. Rosypal was a Morris Animal Foundation Fellow. Her research interests include Leishmania spp. and other zoonotic protozoan parasites. Dr. Rosypal has published and presented her research in national journals and at international and national meetings.

Summary: Leishmaniasis is an important insect-vectored zoonotic disease in many parts of the world. Leishmania species can cause visceral, cutaneous, and mucocutaneous disease in humans and animals. Dogs are important reservoirs for human visceral leishmaniasis (HVL) and HVL is now considered an opportunistic disease among immunosuppressed individuals. Leishmania infantum, an etiologic agent of zoonotic visceral leishmaniasis, has recently emerged in the foxhound population in the United States and parts of Canada. Current epidemiological data do not implicate sand flies, the insect vector of leishmaniasis, in the transmission of L. infantum in North America. The development of infection models, pathogenesis, diagnostic tests, and alternate transmission mechanisms of a Virginia isolate of L. infantum are discussed.
Thursday, April 28, 2005

Robert S. Jones, D.O., FACP
Berks Infectious Disease Services
301 S. Seventh Ave. Suite 385
West Reading, PA 19611

Title: Invasive Candida Infections: Current Trends and Challenges
Date: Thursday, April 28, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor, CME Conference Room
VCOM Host:
Dr. Jan Willcox

Dr. Robert Jones is Clinical Assistant Professor, Dept. Medicine, Temple University and President of the Berks Infectious Disease Services. Dr. Jones received his BA degree from Gettysburg College, MS from Seton Hall University and Doctor Osteopathic Medicine from Philadelphia College of Osteopathic Medicine, Philadelphia, PA. Presently, Dr. Jones is Certified in Infectious Diseases (ABIM) and is an Associate Hospital Epidemiologist at the Reading Hospital, Reading, Pa. Dr. Jones has published and presented his research in major national medical journals and at professional meetings.

Summary of Presentation: Candida species are the most common cause of fungal infections. They can cause infections ranging from non-life threatening mucocutaneous infections to invasive infections that may involve virtually any organ system. Candida species are currently the fourth most common cause of blood stream infections in the United States with a high attributable mortality. Of particular interest and importance is the increasing prevalence of non-albicans species that are resistant to the azole antifungals. A limited number of antifungal drugs, along with organisms that create a diversity of infections, and a limited ability to perform in-vitro susceptibilities all can create a clinical dilemma in patient care. Such a broad range of infections requires an equally broad range of diagnostic and therapeutic strategies.
Wednesday, April 20, 2005

Abiodun O. Adibi , Ph.D.
Department of Biological Science
Hampton University

Title: Parasitic Disease and Developing Countries:
Should we care?
Date: Wednesday April 20, 2005
Time: 12:00 NOON
Location: VCOM, 1st Floor Dean’s Conference Room
VCOM Host: Dr. Hara Misra

Dr. Abiodun Adibi is presently Associate Professor within the Department of Biology, at Hampton University, Hampton, Virginia. His main reasarch interests include: the study of microbial community in extreme environments, most especially in caves and volcanic regions located in remote areas of Tanzania and the impact of parasitic infections and diseases in developing countries. From 1999 to 2004, Dr. Adibi was Director of the NIH-Funded MARC Honors Program at Hampton University, Hampton, VA.

Summary of Presentation: The primary goal of this presentation is to show the importance of “education” in preventing and controlling parasitic diseases in the endemic areas of the diseases and in the developed countries of the world. This presentation explores some of the important parasitic diseases that are prevalent in different parts of the world. The impacts of the prevalence of these parasitic diseases on developed countries are also discussed. The diseases discussed include those caused by protozoa, nematodes, cestodes and trematodes. The modes of infection, pathologies and distribution of the diseases are discussed.
Tuesday, April 12, 2005

Diana S. Beattie, Ph.D.
Department Chair; Department of Biochemistry and Molecular Pharmacology
West Virginia University
Robert C. Byrd Health Sciences Center

Title: Investigations of the electron transport chain of the African parasite, Trypanosoma brucei, the causative agent of sleeping sickness in humans.
Date: Tuesday, April 12, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor Conference Room
VCOM Host: Dr. Jeannine Strobl

Dr. Diana Beattie received her doctorate degree from the University of Pittsburgh in 1961. She is Department Chair of the Department of Biochemistry and Molecular Pharmacology at West Virginia University. Her research involves investigating the role of cytochrome b and the iron-sulfur protein (ISP) of the cytochrome bc1 complex in the electron transfer and proton releasing reactions that occur at the quinol-oxidizing site of the complex. The second research project involves the electron transport chain of the African parasite, Trypanosoma brucei. Trypanosomes have a dual life cycle in both the bloodstream of the mammalian host and the insect vector. In the mammalian bloodstream, the trypanosomes exist as dividing long slender forms that lack well-developed mitochondria and cyanide-sensitive electron transport. Dr. Beattie has published widely in major biochemistry and bioengineering journals.

Summary of Presentation: My laboratory is investigating the electron transport chain of the African parasite, Trypanosoma brucei, the causative agent of sleeping sickness in humans. It is estimated that 50 million people are at risk for sleeping sickness, with 50,000 new cases reported each year. Trypanosomes have a dual life cycle in both the bloodstream of the mammalian host and the insect vector.
Thursday, April 7, 2005

Francine Marciano-Cabral, Ph.D.
Department of Microbiology and Immunology
Medical College of Virginia Campus
Virginia Commonwealth University
Richmond, Virginia 23298-0678

Title: Free-living Amebae As Agents of CNS Disease
Date: Thursday, April 7, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor, Board Conference Room
VCOM Host:
Dr. Jim Palmieri

Dr. Francine Marciano-Cabral received her M.S. degree from Villanova University and her Ph D. from the University of Connecticut. She conducted her post-doctoral research at Baylor College of Medicine. Dr. Marciano-Cabral is presently a Professor of Microbiology and Immunology at the Medical College of Virginia where she conducts research on Acanthamoeba and other parasitic protozoa. Dr. Marciano-Cabral is a world authority on Acanthamoeba and amoebic encephalitis and has published numerous research papers and review articles in national and international journals.

Summary of Presentation: Free-living amebae belonging to the genera, Naegleria, Acanthamoeba, and Balamuthia can cause fatal infections in humans. One species of Naegleria, N. fowleri, has been associated with fatal Primary Amebic Meningoencephalitis in children and young adults with a history of swimming in fresh water lakes and ponds. Several species of Acanthamoeba can cause Granulomatous Amebic Encephalitis, a chronic progressive disease that occurs more often in immune suppressed or debilitated patients. However, Acanthamoeba can cause amebic keratitis, a painful sight-threatening disease in immune competent individuals. Balamuthia mandrillaris, considered an opportunistic pathogen, also causes Granulomatous Amebic Encephalitis.
Tuesday, March 29, 2005

Ravi F. Saraf, Ph.D.
Department of Chemical Engineering, 212, Othmer Hall
University of Nebraska-Lincoln
Lincoln, NE 68588

Title: DNA Microarray Technology: An Engineer’s Perspective
Date: Tuesday, March 29, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor Conference Room
VCOM Host:
Dr. Hara Misra

Dr. Saraf's training is in polymer science, optics and silicon processing. He received his PhD from the University of Massachusetts, Amherst in 1987, in Polymer Science and Engineering. Dr. Saraf conducted research at IBM’s T.J. Watson Research Center for 12 years studying phenomena in soft-matter influenced by geometric confinement and interfacial forces. In 1999, Dr. Saraf joined the faculty of Chemical Engineering at Virginia Tech where, he shifted his attention to nanometer scale devices for biomedicine & sensors and, biophysics. His group has developed an optical method to study (elastic and viscous) dynamics of tethered biomolecules at single-molecule resolutions by observing deformation in molecular-monolayer at accuracy of 1/100th of a Carbon-to-Carbon bond.

Summary of Presentation: Rapid, inexpensive gene sequencing and mutation analysis is the corner stone of future medicine with the potential to diagnose disease before clinical signs, evaluate the efficacy of an experimental drugs within months compared to years, and personalize medicine. DNA Microarray technology is emerging as the best approach for gene sequencing and mutation analysis at high throughput and low cost. Also known as DNA Chip, microarray analysis is a spotting technique that allows one to perform sequence analysis on hundreds of expressed mRNA (via cDNA synthesis) or chromosomal DNA fragments simultaneously. In microarray analysis, specific binding between 100-500 spots of immobilized single-stranded DNA (ssDNA) fragments of known sequence (the probes) with fluorescent-labeled ssDNA fragments of unknown sequence (the targets) is measured. The technology with its pervasive usage and high visibility has challenges (such a label-interference; background from non-specific binding, and non-linear device response) that limit the robustness and reliability of the data, and confidence level of the inference. This presentation will discuss two methods currently being developed that address the above limitations.
Thursday, February 10, 2005

Charlotte A. Peterson, Ph.D.
Professor of Geriatrics, College of Medicine
University of Arkansas for Medical Sciences
Reynolds Center on Aging, Rm. 3121
629 Jack Stephens Drive , Little Rock, AR 72205

Title: Changes In Myogenic Progenitor Potential With Age
Date: Thursday March 3, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor Conference Room
VCOM Host:
Dr. Richard Wyeth

Charlotte A. Peterson, Ph.D. is a professor of Geriatrics in the Donald W. Reynolds Department of Geriatrics, College of Medicine, with an adjunct appointment in Physiology and Biophysics. She currently serves as Director of the Genomics Facility within the Arkansas Biomedical Research Infrastructure Network (BRIN), Director of the University Microarray Core facility, and Chair of the NIH Cellular Mechanisms of Aging and Development Study Section. Dr. Peterson received a B.S. from University of Notre Dame and a Ph.D. from the University of Virginia, followed by two postdoctoral fellowships, the first at the National Eye Institute at the NIH and the second at Stanford University School of Medicine.

Dr. Peterson's research focuses on elucidation of molecular mechanisms controlling skeletal muscle structure and function. This research is currently funded by the NIH and the VA to study stem cell activity in muscle regeneration; the genetic basis of differences in the muscle inflammatory response to damaging exercise; and mechanisms contributing to restoration of muscle mass following atrophy due to disuse and spinal cord injury. Dr. Peterson's work emphasizes changes that occur with age with the long term goal of preventing frailty and loss of functional independence.
Thursday, February 10, 2005

David J. Feola, Pharm.D.
University of Kentucky Hospital
800 Rose Street, Room C-111
Lexington, KY 40536
Phone: (859) 323-6289

Title: Zidovudine plus sulfamethoxazole
trimethoprim: a common treatment combination's adverse effects on immunity
Date: Thursda, February 10, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor, Board Conference Room
VCOM Host:
Dr. Hara Misra

Dr. David J. Feola received his Pharm.D. from the University of Kentucky College of Pharmacy (1997) and his B.S. Pharmacy, University of Kentucky College Of Pharmacy (1996). He received his BCPS Certification in 2001. Dr. Feola was the recipient of the UKMC Outstanding Pharmacy Resident Award in 2000, the UKMC Residency Program Impact Award (1995-1997), UKCOP Dean EP Sloan Leadership Award, UKCOP Outstanding Graduating Man Award (1995), UKCOP Kappa Psi Graduate Chapter Award, and ACPE-AFPE Association Fellowship in the Pharmaceuticals Sciences.

This presentation will review toxicity profiles of zidovudine and sulfamethoxazole and trimethoprim and discuss the phenotypic analysis of immune cell populations in mice receiving this drug combination. Dr. Feola will discuss data that investigates the mechanism of this combined toxicity on B lymphocytes in bone marrow. A review of the effects of zidovudine plus sulfamethoxazole on the ability of mice to respond to infection and clinical relevance of this interaction will be discussed.
Wednesday, February 2, 2005

Alex Levitov, M.D.
Associate Professor, University of Virginia
Carilion Roanoke Memorial Hospital
Internal Medicine Medical Education
Critical Care Services
Roanoke, VA 24033-3367

Title: Beyond 100% O2
Date: Wednesday, February 2, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor Conference Room
VCOM Host:
Dr. Jim Palmieri

Dr. Alex Levitov was born and educated in Moscow, USSR, and received his MD degree in 1977 from the First Moscow Medical Institute. From 1977-1980, Dr. Levitov conducted research at the Scientific Research Institute of Critical Care with a Residency/Fellowship in Critical Care and Invasive Cardiology at Hamburg University, West Germany. Dr. Levitov had his internal Medicine Internship at Episcopal Hospital, Temple University and his Internal Medicine Residence at Hahnemann University School of Medicine. Dr. Levitov combines his clinical and biomedical skills and has several U.S. patents including the Safety Syringe. His areas of expertise include: diagnosis and treatment of coronary artery disease; treatment of hyperlipidemia; echocardiography in coronary artery disease; outdoor survival/hypothermia; hyperkalemia; and plague/bioterrorism. Dr. Levitov is published in Kardiologiia, Circulation and Journal of Cardiology.
Wednesday, January 12, 2005

Jon E. Sprague, Ph.D.
Chair and Associate Professor of Pharmacology
Virginia College of Osteopathic Medicine
Department of Biomedical Sciences and Pathobiology
Virginia Polytechnic Institute and State University
Title: Uncoupling the Agony from Ecstasy
Date: Wednesday, January 12, 2005
Time: 12:00 NOON
Location: VCOM, 3rd Floor Conference Room
VCOM Host:
Dr. Jeannine Strobl

Dr. Jon Sprague is presently Chairperson and Associate Professor of Pharmacology, Virginia College of Osteopathic Medicine, having come from the Department of Pharmaceutical & Biomedical Sciences, School of Pharmacy, Ohio Northern University, Ada, Ohio in 2004. Dr. Sprague received his B.S. Degree in pharmacology from Ferris State University, Big Rapids, MI in 1989 and his Ph.D. degree in pharmacology and toxicology from Purdue University in 1994.

Body temperature regulation involves a homeostatic balance between heat production and dissipation. Sympathetic agents such as 3,4 methylene dioxy meth amphet amine (MDMA, Ecstasy) can disrupt this balance and as a result can produce an often times life-threatening hyperthermia. The hyperthermia induced by MDMA appears to result from the activation of the sympathetic nervous system (SNS) and the hypothalamic-pituitary-thyroid/adrenal axis. Norepinephrine release mediated by MDMA creates a double edged sword of heat generation through activation of uncoupling protein (UCP3) along with a1- and ß3- adrenoreceptors and loss of heat dissipation through SNS-mediated vasoconstriction. This seminar will review our laboratory’s findings as they relate to the thermogenesis induced by MDMA.
Wednesday, December 1, 2004

Aaron S. Goldstein, Ph.D.
Assistant Professor, Department of Chemical Engineering, Virginia Tech

Biomaterial and Bioreactor Strategies for Ex Vivo Bone Tissue Engineering

Date: Wednesday, December 1, 2004
Time: 12:00 NOON
Location: VCOM
VCOM Host:
Dr. Beverly Rzgalinski

This presentation will discuss 2D flow approaches to characterize the osteoinductive effect of shearing flow, electrospinning approaches to modulate substratum topography, and the combination of degradable segmented polyurethane elastomer foam scaffolds and a perfusion bioreactor for stimulating ex vivo bone tissue development.
Wednesday, November 3, 2004

Martha E. Stokely, Ph.D.
Department of Neuroscience
University of Florida at Gainesville

Understanding neurodegeneration: Endothelin-1 modulates anterograde fast axonal transport in the CNS
Date: Wednesday, November 3, 2004
Time: 11:00 AM
Location: VCOM - Main Floor - Classroom 2
VCOM Host:
Dr. Hara Misra

Martha E. Stokely, Ph.D., received her doctorate degree in 2002 from the University of North Texas Health Science Center for Biomedical Sciences. Her postdoctoral research was conducted at the Department of Pharmacology and Neuroscience, University of North Texas Health Science Center and at the Veterans Administration, Research Service, Malcom Randall VA Medical Center, Gainesville, Florida. Dr. Stokely is currently a Postdoctoral Fellow studying the neurobiology of Aging at the Department of Neuroscience, University of Florida, Gainesville. Her research interests involve chemical intermediaries of neuroglial interactions and anterograde axonal transport. She is a current nominee for the 2003 Lewis Rudin Glaucoma Prize of the New York Academy of Medicine. Wednesday, August 4, 2004
Thursday, September 30, 2004

Sydney Brenner, Ph.D.
Brenner Laboratory, Salk Institute for Biological Studies

The Future of Science and Medicine in the Coming Decade
Via Research Recognition Day 2004-2005
Thursday, September 30, 2004
Location: VCOM
VCOM Host:
Dr. Hara Misra

Sydney Brenner, Ph.D., a distinguished professor, is one of the past century’s leading pioneers in genetics and molecular biology. Most recently, Brenner has been studying vertebrate gene and genome evolution. His work in this area has resulted in new ways of analyzing gene sequences, which has developed a new understanding of the evolution of vertebrates. Among his many notable discoveries, Brenner established the existence of messenger RNA and demonstrated how the order of amino acids in proteins is determined. He also conducted pioneering work with the roundworm, a model organism now widely used to study genetics. His research with Caenorhabditis elegans garnered insights into aging, nerve cell function and controlled cell death, or apoptosis. Dr. Brenner is a recepient of the 2002 Nobel Prize in Physiology or Medicine.

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