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Terry Morgan, MD, PhD
Program Director, Cytopathology Fellowship
Rank: Associate Professor
Clinical Services: Surgical Pathology and Cytopathology
Clinical Interests: Gynecologic Oncology and Placental Pathology
Research Interests: My lab studies the pathology of pregnancy. Specifically, we are investigating the molecular mechanisms mediating renal blood flow and sodium regulation by the kidney during pregnancy. Recent data suggest that the intrarenal renin-angiotensin system is important in sodium regulation during hypervolemia of pregnancy. Transgenic mice that over-express angiotensinogen do not upregulate renal renin expression and fail to expand their plasma volume. This may be a consequence of differences in renal blood flow early in gestation. How mammals regulate renal blood flow during pregnancy is uncertain. Our mouse cDNA microarray studies suggest that intrarenal histamine production may play an important role.
2005    Fellowship    Cytopathology            Stanford University
2003    Fellowship    Surgical Pathology      Stanford University
2002    Residency     Anatomic Pathology    Stanford University
2000    MD, PhD        Medicine                     University of Utah
1989    BS                 Biology                       University of Utah
Anatomic Pathology
Previous Position:
2004-2005    Placental Pathologist, Departments of Pathology and Genetics, Kaiser Permanente, Oakland, CA
2003-2004    Clinical Instructor, Department of Pathology, Stanford University Medical Center
2000-2003    Resident, Department of Pathology, Stanford University Medical Center
1991-2000    MD/PhD Student, Department of Human Genetics, University of Utah
Selected References:
  1. Morgan T., Montgomery K., Mason V., West R., Wang L., van de Rijn M. and J. Higgins. Upregulation of histidine decarboxylase expression in superficial cortical nephrons during pregnancy in mice and women. Kidney Int. 2006 Jul;70(2):306-14.
  2. Morgan T, Rohrwasser A, Zhao L, Hillas E, Cheng T, Ward KJ, Lalouel JM. Hypervolemia of pregnancy is not maintained in mice chronically overexpressing angiotensinogen. Am J Obstet Gynecol. 2006 Jun 20; [Epub ahead of print]
  3. Rohrwasser A., Ishigami T., Gociman B., Lantelme P., Morgan T., Cheng T., Hillas E., Zhang S., Ward K., Bloch-Faure M., Meneton P. and J.M. Lalouel "Renin and Kallikrein in Connecting Tubule of Mouse." Dec;64(6):2155-2162, 2003
  4. Morgan T., and A. Rohrwasser, L. Dillon, L. Zhao, C. Callaway, E Hillas, S. Zhang, T. Cheng, T. Inagami, K. Ward, D. Terreros, J-M Lalouel. "Elements of a paracrine tubular renin-angiotensin system along the entire nephron." Hypertension 34:1265-1274, 1999.
  5. Morgan T., and K. Ward. "New insights into the genetics of preeclampsia." Sem Perinatol 23 (1):14-23, 1999.
  6. Morgan T., C. Craven, J-M Laluoel and K. Ward. "Angiotensinogen T235 variant is associated with abnormal physiologic change of the uterine spinal arteries in first trimester decidua." Am J Ob Gyn 180:95-102, 1998.
  7. Morgan T., C. Craven, L. Nelson, J-M Lalouel and K. Ward. "Angiotensinogen T235 expression is elevated in decidual spiral arteries." J Clin Invest 100 (6):1406-15, 1997.

Last Updated: 08/09/2010