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Richard A. Hawkins, PhD
Dr. Hawkins began his academic career at San Diego State University where he earned a degree in Life Sciences, magna cum laude in 1963. After brief assignments on the faculty at San Diego State, Dr. Hawkins entered Harvard University in 1964 (full scholarship) and received a PhD Degree in Physiology from that prestigious institution in 1969.
From Harvard, Dr. Hawkins became a Research Fellow at Oxford University, from 1969 to 1971 with Sir Hans Krebs (Nobel Prize recipient) where he became seriously interested and involved in research on the brain. After Oxford, Dr. Hawkins held research positions in the National Institute for Mental Health and from 1974 until 1976 he served as Chief of the Physical Sciences Branch of the Food and Drug Administration of the US Department of Health Education and Welfare.
This was followed by faculty appointments at New York University as Associate Professor of Experimental Neurosurgery and Physiology (1976-1977), and at Penn State (1977-1988) where Dr. Hawkins was Professor of Anesthesiology and Physiology and Chief of the Division of Anesthesiology and Metabolic Research.
In 1988, Dr. Hawkins came to Finch University (now Rosalind Franklin University), serving as Professor and Chairman of the Department of Physiology and Biophysics until assuming the position of Executive Vice President for Academic Affairs in June 1993. In December 1998, Dr. Hawkins was named Provost and subsequently President of the University in April 1999. Dr. Hawkins resigned as President at the end of 2002 to resume his teaching and research career as Professor of Physiology.
Throughout his academic career, Dr. Hawkins has maintained his significant original research on the brain -- supported by grants from the National Institutes of Health and other agencies. Dr. Hawkins has published many original scientific articles, and has achieved international recognition for his discoveries and the development of important new knowledge that he has shared freely with the scientific communities here and abroad.
Dr. Hawkins, who is fluent in Spanish, married Enriqueta Elias (from Valencia, Spain) and resides in Chicago, Illinois. Dr. and Mrs. Hawkins have two sons: Richard (MD ’00) and Paul (PhD ’95, MD ’97) both of whom are Anesthesiologists.
- Rasgado-Flores, H., Mokashi, A., and Hawkins, R.A., Na+-dependent transport of taurine is found only on the abluminal membrane of the blood-brain barrier. Journal of Experimental Neurology 233:457-462, 2011.
- Hawkins R.A., Viña. J. R., Darryl R. Peterson, D. R. O’Kane, R. , A. Mokashi, A. and Ian A. Simpson, I. A., Amino acid transport across each side of the blood-brain barrier. in Amino Acids in Nutrition and Health (J.P.F. D’Mello ed), CABI, Oxford, 2011, pp 191-214.
- Devraj K., Klinger M., Meyers R., Mokashi A., Hawkins R.A., and Simpson I.A. GLUT-1 glucose transporters in the blood-brain barrier: differential phosporylation. Journal of Neuroscience Research. 12:1913-1925, 2011
- Hawkins R.A., Mokashi A., Dejoseph M.R, Viña J.R., Fernstrom J.D. Glutamate permeability at the blood-brain barrier in insulinopenic and insulin-resistant rats. Metabolism. 59:258-66, 2010.
- Hawkins R.A.: The blood-brain barrier and glutamate. American Journal of Clinical Nutrition 90: 867S-874S, 2009.
- Devraj K., Geguchadze R, Klinger M.E., Freeman W.M., Mokashi A., Hawkins R.A., and Simpson I.A. Improved membrane protein solubilization and clean-up for optimum two-dimensional electrophoresis utilizing GLUT-1 as a classic integral membrane protein. Journal of Neuroscience Methods. 184:119-23, 2009.
- Hawkins R.A., Simpson I.A. Mokashi, A. and Viña, J.R.,: Pyroglutamate stimulates Na+-dependent amino-acid transport across the blood-brain barrier. FEBS letters 580: 4382-4386, 2006.
- O’Kane R.L., Viña, J.R., Simpson, I.A., Zaragoza, R., Mokashi, A. and Hawkins, R.A.: Cationic amino acid transport across the blood-brain barrier is mediated exclusively by system y+. American Journal of Physiology, 291 :E412-419, 2006.
- Hawkins, R.A., O’Kane, R.L., Simpson, I.A., and Viña, J.R.: Structure of the blood brain barrier and its role in transport of amino acids. Journal of Nutrition 136: 218S-226S, 2006.
- Hawkins, R.A., Mokashi, A., Simpson I.A. An active transport system in the blood-brain barrier may reduce levodopa availability. Journal of Experimental Neurology, 195: 267-271, 2005.
- O’Kane, R.L. Viña J.R., Simpson I.A. and Hawkins, R.A.: Na+-dependent neutral amino acid transporters (A, ASC and N) of the blood-brain barrier: mechanisms for neutral amino acid removal. American Journal of Physiology Endocrinology and Metabolism. . American Journal of Physiology, 287: E622-629, 2004.
- O’Kane, R.L. and Hawkins, R.A.: A Na+-dependent carrier of large neutral amino acids exists at the abluminal membrane of the blood-brain barrier. American Journal of Physiology, 285:E1167-E1173. 2003.
- Hawkins, R.A., Peterson D.R. and Viña J.R. The complementary membranes forming the blood-brain barrier. IUBMB Life, 54:101-107, 2002.
- Simpson I.A., Vannucci S.J., DeJoseph M.R., and Hawkins R.A. Glucose transporter asymmetries in the bovine blood-brain barrier Journal of Biological Chemistry, 20; 276(16):12725-9. 2001.
- O’Kane, R.L., Martinez-Lopez, I., DeJoseph, M.R., Viña, J.R., Hawkins, R.A. Na+-dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) of the blood-brain barrier. A Mechanism for glutamate removal. Journal of Biological Chemistry, 274:31891-31895, 1999.
- Lee, W-J., Hawkins, R.A., Viña, J.R., and Peterson, D.R. Glutamine transport by the blood-brain barrier: a possible mechanism for nitrogen removal. American Journal of Physiology, 274: C1101-C1107, 1998.
- Hawkins, P.A., DeJoseph, M.R. and Hawkins, R.A.: Diurnal rhythm returns to normal after elimination of portacaval shunting. American Journal of Physiology, 274:E426-E431, 1998.
- Lee, W-J, Peterson, D.R., Sukowski, E.J. and Hawkins, R.A.: Glucose transport by isolated plasma membranes of the bovine blood-brain barrier. American Journal of Physiology, 272:C1552-C1557, 1997.
- Hawkins, P.A., DeJoseph, M.R., Viña, J.R., and Hawkins, R.A.: Comparison of the metabolic disturbances caused by end-to-side and by side-to-side portacaval shunts. Journal of Applied Physiology, 80: 885-891, 1996.
- Hawkins, P.A., DeJoseph, M.R. and Hawkins, R.A.: Eliminating metabolic abnormalities of portacaval shunting by restoring normal liver blood flow. American Journal of Physiology, 270: E1037-E1042, 1996.
- Hawkins, P.A., DeJoseph, M.R. and Hawkins, R.A.: Reversal of portacaval shunting normalizes brain energy consumption in most brain structures. American Journal of Physiology, 271:E1015-E1020, 1996.
- Hawkins, R.A., Jessy, J., Mans, A.M. and DeJoseph, M.R.: Effect of reducing brain glutamine synthesis on metabolic symptoms of hepatic encephalopathy. The Journal of Neurochemistry, 60:1000-1006, 1993.
- DeJoseph, M.R. and Hawkins, R.A.: Glucose consumption decreases throughout the brain only hours after portacaval shunting. American Journal of Physiology, 260:E613-E619, 1991.
- Jessy, J., DeJoseph, M.R., and Hawkins, R.A.: hyperammonemia depresses glucose consumption throughout the brain. The Biochemical Journal, 277:693-696, 1991.
- Hawkins, R.A. and Jessy, J.: hyperammonemia does not impair brain function in the absence of net glutamine synthesis. The Biochemical Journal, 277:697-703, 1991.
- Mans, A.M., DeJoseph, M.R., Davis, D.W., Viña, J.R. and Hawkins, R.A.: Early establishment of cerebral dysfunction after portacaval shunting. American Journal of Physiology, 259:E104-E110, 1990.
- Jessy, J., Mans, A.M., DeJoseph, M.R., and Hawkins, R.A.: hyperammonemia causes many of the changes found after portacaval shunting. The Biochemical Journal, 272:311-317, 1990.
We are involved in two projects. The first is the transport of essential nutrients across the blood-brain barrier using isolated cell constituents in vitro and autoradiography in vivo. Our focus has been on glucose and amino acid carriers in the constituent membranes of the blood-brain barrier, as well as those in intracellular pools. Both the luminal and abluminal membranes of endothelial cells, which constitute the blood-brain barrier, are isolated as vesicles, and various measurements made. We are testing the hypothesis that the distribution, ion dependency, and kinetics of transport proteins favor the delivery of glucose and essential amino acids to the brain, but prevent accumulation of nonessential amino acids that may serve as neurotransmitters.
The second subject is hepatic encephalopathy, a significant cause of morbidity and mortality worldwide that is caused by elevated ammonia in circulation when blood bypasses the liver. We showed that reducing the incorporation of ammonia into brain glutamine could mitigate the disease and possibly reverse it. The remaining work to be done is to provide definitive evidence that inhibiting brain glutamine synthetase activity can prevent hepatic encephalopathy long-term, and that inhibiting brain glutamine synthetase activity can reverse established hepatic encephalopathy.