Daniel G. Remick, M.D.
Professor and Director, Autopsy Service and Electron Microscopy
Campus Address:
M2210 Med Sci I
1301 Catherine Road
Ann Arbor, Michigan USA 48109-0602
Phone: 734/763-6454
FAX: 734/763-6476
remickd@umich.edu
More information on Dr. Remick's research lab is available here.
Biography | Clinical Interests | Research Interests | Selected Publications
Departmental Annual Report
Brief Biography
Dr. Remick received a B.S. in chemistry from the University of Minnesota in 1978 He obtained an M.D. from the Mayo Medical School, Rochester, Minnesota in 1982. Following a Residency and Post-Doctoral Fellowship in Immunopathology, both at the University of Michigan, he joined the Faculty at the University of Michigan in 1986. He became the Director of the Autopsy Service in 1987 and the Director of the Electron Microscopy Service in 1994.
Dr. Remick is actively involved in teaching medical students in both the first and second year pathology laboratories. He serves on a study section for the National Institutes of Health and is on the editorial board of the Journal of Immunology and Shock. In addition to extensive scientific research and publication, Dr. Remick has been active in the Michigan Association of Medical Examiners and is presently Chair of that organization.
Clinical Interests
Autopsies, quality assurance, clinical chemistry, clinical immunology, and forensic pathology.
Research Interests
Sepsis, cytokines, reactive oxygen intermediates, reactive
nitrogen intermediates, chemokines, and asthma.
My research focuses on understanding the mediators of inflammation. We are addressing the events that lead to up regulation of the cytokines which are protein mediators of inflammation. Once the cytokines are elevated, we are interested in determining how they injure cells and organs, and how the cells/organs attempt to protect themselves from damage. Our research focused on three principal areas.
The first system is a murine model of sepsis caused by ligation and puncture the cecum. This is a polymicrobial sepsis which more closely mimics the clinical scenario. Our investigations have shown that standard therapies will improve survival in this model. However newer attempts to use immunomodulation have not yielded any significant improvement. Therefore, this model closely recapitulates the clinical observations in treating human patients. We are in the process of attempting to decipher the immune mediators responsible for the altered pathophysiology in sepsis.
Our second line of investigation involves the study of intracellular reactive oxygen intermediates. We believe that these reactive oxygen intermediates serve as intracellular second messengers to regulate cytokine gene expression. We're attempting to decipher the five prime gene sequences responsible for recognizing the increase in intracellular reactive oxygen. Our investigations are also evaluating reactive nitrogen intermediates.
The third area involves the development of a new murine model of asthma. For this model, we intend to collect host dust from the homes of children who have asthma. This house dust will be tested for the presence of cockroach allergens. The dust will then be used to immunize the mice followed by an aerosol challenge with the same house dust. We will attempt to determine which inflammatory mediators are responsible for the onset of the pulmonary inflammation.
Several methods are presently working within the laboratory. These include immunohistochemistry and in situ hybridization. Western lots are also routinely performed. Newer molecular biology methods are used including RT-PCR and gene transfer.
Recent Publications
Call, D. R., J. A. Nemzek, S. J. Ebong,
G. R. Bolgos, D. E. Newcomb, G. K. Wollenberg, and D. G. Remick. 2001.
Differential local and systemic regulation of the murine chemokines KC
and MIP2. Shock 4:278.
Remick, D. G., D. R. Call, S. J. Ebong, D. E. Newcomb, P. Nybom, J. A.
Nemzek, and G. E. Bolgos. 2001. Combinantion immuntherapy with soluble
tumor necrosis factor receptors plus interleukin 1 receptor antagonist
decreases sepsis mortality. Critical Care Medicine 29:473.
Remick, D. G., D. E. Newcomb, G. L. Bolgos, and D. R. Call. 2000. Comparison
of the mortality and inflammatory response of two models of sepsis: lipopolysaccharide
vs. cecal ligation and puncture. Shock 13:110.
Nemzek, J. A., D. E. Newcomb, D. R. Call, and D. G. Remick. 1999. Plasma
interference in an enzyme-linked immunosorbant assay using a commercial
matched antibody pair. Immunological Investigations 28:209.
Villarete, L. H., and D. G. Remick. 1997. Nitric oxide regulation of interleukin-8
gene expression. Shock 7:29.