Professional Education


  • Master of Science, University of Southern California (2014)
  • Doctor of Philosophy, University of Southern California (2017)
  • Bachelor of Science, Loyola Marymount University (2009)

Lab Affiliations


All Publications


  • oximetry. Magnetic resonance in medicine Bush, A., Borzage, M., Detterich, J., Kato, R. M., Meiselman, H. J., Coates, T., Wood, J. C. 2017; 77 (6): 2364-2371

    Abstract

    We sought a human blood T2 -oximetery calibration curve over the wide range of hematocrits commonly found in anemic patients applicable with T2 relaxation under spin tagging (TRUST).Blood was drawn from five healthy control subjects. Ninety-three in vitro blood transverse relaxation (T2b ) measurements were performed at 37°C over a broad range of hematocrits (10-55%) and oxygen saturations (14-100%) at 3 Tesla (T). In vivo TRUST was performed on 35 healthy African American control subjects and 11 patients with chronic anemia syndromes.1/T2 rose linearly with hematocrit (r(2)  = 0.96), for fully saturated blood. Upon desaturation, 1/T2 rose linearly with the square of the oxygen extraction, (1-Y)(2) , and the slope was linearly proportional to hematocrit (r(2)  = 0.88). The resulting bilinear model between 1/T2 , (1-Y)(2) , and hematocrit had a combined r(2) of 0.96 and a coefficient of variation of 6.1%. Using the in vivo data, the bilinear model had significantly lower bias and variability than existing calibrations, particularly for low hematocrits. In vivo Bland Altman analysis demonstrated clinically relevant bias that was -6% (absolute saturation) for hematocrits near 30% and rose to + 6% for hematocrits near 45%.This work introduces a robust bilinear calibration model that should be used for MRI oximetry. Magn Reson Med 77:2364-2371, 2017. © 2016 International Society for Magnetic Resonance in Medicine.

    View details for DOI 10.1002/mrm.26311

    View details for PubMedID 27385283

    View details for PubMedCentralID PMC5218988

  • Determinants of resting cerebral blood flow in sickle cell disease AMERICAN JOURNAL OF HEMATOLOGY Bush, A. M., Borzage, M. T., Choi, S., Vaclavu, L., Tamrazi, B., Nederveen, A. J., Coates, T. D., Wood, J. C. 2016; 91 (9): 912-917

    Abstract

    Stroke is common in children with sickle cell disease and results from an imbalance in oxygen supply and demand. Cerebral blood flow (CBF) is increased in patients with sickle cell disease to compensate for their anemia, but adequacy of their oxygen delivery has not been systematically demonstrated. This study examined the physiological determinants of CBF in 37 patients with sickle cell disease, 38 ethnicity matched control subjects and 16 patients with anemia of non-sickle origin. Cerebral blood flow was measured using phase contrast MRI of the carotid and vertebral arteries. CBF increased inversely to oxygen content (r(2)  = 0.69, P < 0.0001). Brain oxygen delivery, the product of CBF and oxygen content, was normal in all groups. Brain composition, specifically the relative amounts of grey and white matter, was the next strongest CBF predictor, presumably by influencing cerebral metabolic rate. Grey matter/white matter ratio and CBF declined monotonically until the age of 25 in all subjects, consistent with known maturational changes in brain composition. Further CBF reductions were observed with age in subjects older than 35 years of age, likely reflecting microvascular aging. On multivariate regression, CBF was independent of disease state, hemoglobin S, hemoglobin F, reticulocyte count and cell free hemoglobin, suggesting that it is regulated similarly in patients and control subjects. In conclusion, sickle cell disease patients had sufficient oxygen delivery at rest, but accomplish this only by marked increases in their resting CBF, potentially limiting their ability to further augment flow in response to stress. Am. J. Hematol. 91:912-917, 2016. © 2016 Wiley Periodicals, Inc.

    View details for DOI 10.1002/ajh.24441

    View details for Web of Science ID 000385237100159

    View details for PubMedID 27263497

    View details for PubMedCentralID PMC4987198