Dr. Fabry is Professor of Medicine at the Albert Einstein College of Medicine. She received a BS in Chemistry from Stanford University and a PhD in Molecular Biophysics from Yale University. She has been a member of the NIH Sickle Cell Advisory Committee and has served on NIH review panels for Biophysics, Biophysical Chemistry, and Hematology. She is currently a member of the Editorial Boards of Blood and the Journal of Biological Chemistry.
Dr. Fabry has used biophysical techniques (infrared spectroscopy, magnetic resonance relaxation, and magnetic resonance imaging) to study enzyme mechanisms, water movement across red cell membranes, and oxygenation and perfusion in transgenic mouse models of hemoglobinopathies. She was one of the first to recognize the effects of deoxyhemoglobin on chemical shift and relaxation in red cell suspensions and to connect these effects with the change in magnetic susceptibility of deoxyhemoglobin that is the basis for the BOLD (blood oxygen level dependent) effect in MRI. She developed a density gradient centrifugation technique that displays the distribution of red cell density (directly proportional to MCHC) present in whole blood and has used this approach to demonstrate volume regulation and the effect of cation transport on MCHC in red blood cells of humans and transgenic mice. During the last fifteen years she has been instrumental in developing and characterizing transgenic mouse models for three major hemoglobinopathies: HbS, HbC, and HbE. Dr. Fabry has extensive experience in managing complex transgenic colonies; the colony at AECOM has more than thirty different transgenes and knockouts. Her work on sickle transgenic mice has focused on exploring the in vivo interactions between HbS and naturally occurring anti-sickling hemoglobins such as HbF and their effect on cation transport, red cell density, polymerization, blood flow in the microcirculation (perfusion), blood oxygenation (BOLD effect), and nitric oxide and arginine. With Jose Romero and Richard Kennan, she has demonstrated that arginine supplementation of sickle transgenic mice reduces MCHC (intracellular hemoglobin concentration) by partially inhibiting Gardos channel activity and improves perfusion and reduces deoxyhemoglobin levels in the brain. Many of these approaches are being applied to sickle cell patients.
Book Chapters and Reviews:
22. Fabry, ME. Laboratory Diagnosis of Hemoglobin Disorders, and Animal Models for Their Study. In Disorders of Hemoglobin: Genetics, Pathophysiology, Clinical Management. Editors: MH Steinberg, BG Forget, DR Higgs, and RL Nagel. Cambridge University Press, US, 2000.
23. Nagel RL and Fabry ME. The panoply of animal models for sickle cell anaemia. British J Hematology, 112:19-25, 2001.
24. Fabry ME, Acharya SA, Suzuka SM, Nagel RL. Solubility measurement of the sickle polymer. Methods Mol Med. 2003;82:271-287.
25. Fabry ME, Bouhassira EE, Suzuka SM, Nagel RL. Transgenic mice and hemoglobinopathies. Methods Mol Med. 2003;82:213-241.
26. Nagel RL, Fabry ME, Steinberg MH. The paradox of hemoglobin SC disease. Blood Rev. 2003;17:167-178.
27. Atweh GF, DeSimone J, Saunthararajah Y et al. Hemoglobinopathies. Hematology (Am Soc Hematol Educ Program ). 2003;14-39.
28. Kaul, DK, and Fabry, ME. In vivo studies of sickle red blood cells. Microcirculation, 2004, 11: 153-165.
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