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Who is Jeff Sands?
Researcher and Clinician


Jeff was born in Boston, MA. When he was young, he was fascinated by the manned space program and by the US going to the moon in the 1960s. That started his interest in science. In addition, he always enjoyed math. However, he found that he enjoyed applying math more than performing pure math.

Experiments Beat Modeling
When it came time to select a college, Jeff chose Harvard College. He chose Harvard because he felt that it would provide a top-notch liberal arts education while also providing a solid math and science education. While in college, Jeff began looking for a senior honor thesis project.

Originally, he wanted to perform mathematical modeling of proximal tubule function in the kidney. However, his advisor steered him to a renal physiologist at Harvard Medical School (Harvard had a Physiology Department in the 1970s). Jeff was allowed to design and execute his own experiments using electrophysiology. He found this experience to be extremely interesting and wanted to continue studying renal physiology. He knew this would mean either pursuing a Ph.D. or an M.D. degree. He graduated with his Bachelor’s degree in applied math in 1977.

M.D. or Ph.D.?
As he was trying to decide between pursuing an M.D. or a Ph.D. degree, Jeff’s advisors suggested he should think about getting an M.D. degree, since they thought that researchers with M.D. degrees had an easier time getting National Institutes of Health (NIH) grants to support their research. Of course, as it turns out, the opposite is true. However, Jeff followed their advice and applied to medical school at Boston University School of Medicine.

Medical School
Once in medical school Jeff focused on internal medicine and then did a nephrology fellowship so that he could get back to doing renal physiology. He found that studying the urine concentrating mechanism was, for him, an excellent combination of applied math, mathematical modeling, and intriguing physiological questions.

After Dr. Sands graduated from Medical School in 1981, he first did an Internal Medicine residency at the University of Chicago. After 2 years, he moved to Bethesda, MD, to the NIH for a postdoctoral fellowship in renal physiology. In 1988, he did a clinical nephrology fellowship at Emory University in Atlanta, GA, as a condition of his joining the faculty at that school in 1989.

Being an M.D. and a Medical School Faculty Member
Currently, Dr. Sands holds the position of Professor of Medicine and of Physiology and Director of the Renal Division at Emory University. His job involves research, teaching, patient care, and administration.

His major focus is on his NIH-funded renal physiology research. Dr. Sands’ research is directed at understanding the physiology of the renal inner medulla and the urine concentrating mechanism. He is currently studying the molecular physiology of urea transporters and water channels. Dr. Sands uses a combination of isolated perfused tubule studies to measure transport, antibodies to measure changes in the amount or location of the transport proteins, and Northern analysis to measure changes in mRNA. Studies are performed in rats treated to produce physiological and pathophysiological models of human conditions. Research areas being addressed include: 1) long-term regulation of urea transport proteins in rat models of human diseases such as diabetes, 2) mechanisms by which vasopressin rapidly regulates urea transport, and 3) regulation of urea transporter genes.

In addition, he gives lectures to medical students and teaches students, residents, and fellows on rounds in the teaching hospitals. As Director of the Renal Division, Dr. Sands leads a group of 25-30 faculty and 15 fellows.

For Fun
Dr. Sands enjoys playing tennis and bridge, watching sports, and doing things with his kids.

He also is active in his professional societies (American Physiological Society and American Society for Nephrology). For APS, Dr. Sands has dual roles: that of Editor of American Journal of Physiology: Renal Physiology and an elected member of the APS Council, which governs the Society.

Advice for an Undergraduate Student
You can pursue physiology either by obtaining an M.D., as I did, or by obtaining a Ph.D. This is a difficult decision. Medical school involves considerable expense and extra years of clinical training. However, it gives you an excellent idea of what is relevant to human disease. Obtaining a Ph.D. is a more straight-forward degree path and often does not require taking on debt. As a Ph.D. physiologist, you get more time for your research. One can also consider an M.D./Ph.D., which gives you the best of both worlds but also takes longer. A dedicated M.D. who manages to get some research training along the way and does a full length post-doctoral fellowship does not need to get a joint degree to be successful. However, M.D./Ph.D. programs usually allow the graduates to emerge debt-free.

Recent Publications
1. Kato, A., J.D. Klein, C. Zhang, and J.M. Sands. Angiotensin II increases vasopressin-stimulated facilitated urea permeability in rat terminal IMCDs. Am. J. Physiol. Renal Physiol. 279: F835-F840, 2000.m. J. Physiol. Renal Physiol. 279: F835-F840, 2000.

2. Bradford, A.D., J.M. Terris, C.A. Ecelbarger, J.D. Klein, J.M. Sands, C.-L. Chou, and M.A. Knepper. 97 and 117 kDa forms of the collecting duct urea transporter UT-A1 are due to different states of glycosylation. Am. J. Physiol. Renal Physiol. 281: F133-F143, 2001.

3. Bagnasco, S.M., T. Peng, M.G. Janech, A. Karakashian, and J.M. Sands. Cloning and characterization of the human urea transporter UT-A1 and mapping of the human Slc14a2 gene. Am. J. Physiol. Renal Physiol. 281: F400-F406, 2001.

4. Timmer, R.T., J.D. Klein, S.M. Bagnasco, J.J. Doran, J.W. Verlander, R.B. Gunn, and J.M. Sands. Localization of the urea transporter UT-B protein in human and rat erythrocytes and tissues. Am. J. Physiol. Cell Physiol. 281: C1318-C1325, 2001.

5. Zhang, C., J.M. Sands, and J.D. Klein. Vasopressin rapidly increases the phosphorylation of the UT-A1 urea transporter activity in rat IMCDs through PKA. Am. J. Physiol. Renal Physiol. 282: F85-F90, 2002.

6. Kim, Y.-H., D.-U. Kim, K.-H. Han, J.-Y. Jung, J.M. Sands, M.A. Knepper, K.M. Madsen, and J. Kim. Expression of urea transporters in the developing rat kidney. Am. J. Physiol. Renal Physiol. 282: F530-F540, 2002.

7. Peng, T., J.M. Sands, and S.M. Bagnasco. Glucocorticoids inhibit transcription and expression of the UT-A urea transporter gene. Am. J. Physiol. Renal Physiol. 282: F853-F858, 2002.

8. Klein, J.D., D.L. Quach, J.M. Cole, K. Disher, A.K. Mongiu, X. Wang, K.E. Bernstein, and J.M. Sands. Impaired urine concentration and the absence of tissue ACE: the involvement of medullary transport proteins. Am. J. Physiol. Renal Physiol. 283: 517-524, 2002.

9. Wagner, L., J.D. Klein, J.M. Sands, and C. Baylis. Urea transporters are widely distributed in endothelial cells and mediate inhibition of L-arginine transport. Am. J. Physiol. Renal Physiol. 283: 578-582, 2002.

10. Kim, D.U., J.M. Sands, and J.D. Klein. Changes in renal medullary transport proteins during uncontrolled diabetes mellitus in rats. Am. J. Physiol. Renal Physiol. 285: F303-F309, 2003.

11. Jung, J.Y., K.M. Madsen, K.H. Han, C.W. Yang, M.A. Knepper, J.M. Sands, and J. Kim. Expression of urea transporters in potassium depleted mouse kidney. Am. J. Physiol. Renal Physiol. 285: F1210-F1224, 2003.

12. D.U. Kim, J.M. Sands, and J.D. Klein. Role of vasopressin in diabetes mellitus-induced changes in medullary transport proteins involved in urine concentration in Brattleboro rats. Am. J. Physiol. Renal Physiol. 286: F760-F766, 2004.

13. Li, C., J.D. Klein, W. Wang, M.A. Knepper, S. Nielsen, J.M. Sands, and J. Frokiaer. Altered expression of urea transporters in response to ureteral obstruction. Am. J. Physiol. Renal Physiol. 286: F1154-F1162, 2004.

14. Fröhlich, O., J.D. Klein, P.M. Smith, J.M. Sands, and R.B. Gunn. Urea transport in MDCK cells that are stably transfected with UT-A1. Am. J. Physiol. Cell Physiol. 286: C1264-C1270, 2004.

15. Lim, S.W., C. Li, B.K. Sun, W.Y. Kim, K.H. Han, Y.W. Oh, J.U. Lee, P.F. Kador, M.A. Knepper, J.M. Sands, J. Kim, and C.W. Yang. Long-term treatment with cyclosporine decreases aquaporins and urea transporters in rat kidney. Am. J. Physiol. Renal Physiol. 287: F139-F151, 2004.

16. Kim, D.U., J.D. Klein, S. Racine, S.P. Murrell, and J. M. Sands. Urea may regulate urea transporter protein abundance during osmotic diuresis. Am. J. Physiol. Renal Physiol. 287: in press, 2004.