Bio


I am a Bioengineering PhD student in the Radiological Sciences Laboratory. My research interest is in advancing magnetic resonance imaging (MRI) techniques to understand brain physiology, enhance disease diagnosis, and improve patient care. Before joining Stanford Bioengineering in 2024, I investigated the impact of congenital heart defects on neurodevelopment as part of the Pediatric Heart and Brain Research Group at UCSF. I graduated from the University of San Francisco in 2021 with a BS in Chemistry and Mathematics.

Education & Certifications


  • Bachelor of Chemistry, University of San Francisco, Chemistry, Mathematics (2021)
  • B.S., University of San Francisco, Chemistry, Mathematics (2021)

Current Research and Scholarly Interests


Characterization of brain waste clearance with motion-encoding MRI

All Publications


  • Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease. Pediatric cardiology DeRose, L., Martin, M., George, E., Silva, K. L., Gallegos, F. N., Steurer, M., Xu, D., McQuillen, P., Peyvandi, S. 2026

    Abstract

    Neurodevelopmental impairments are common in congenital heart disease (CHD) and fetal brain volume is an important predictor of outcomes. Social determinants of health (SDOH) and environmental factors influence brain growth in other populations and likely play a neurodevelopmental role in CHD. This study evaluated the influence of SDOH and environmental factors on fetal and neonatal brain volume, growth, and risk of brain injury in CHD. This prospective single-center longitudinal cohort study enrolled fetuses with severe CHD to undergo third-trimester fetal and preoperative brain MRIs. Controls underwent third-trimester brain MRIs. Participants completed SDOH and environmental exposure surveys. Fetal and neonatal brain volumes, brain growth, and presence of white matter injury (WMI) were assessed. 57 CHD patients and 24 controls were enrolled, resulting in 33 fetal and 44 neonatal MRIs in the CHD group and 21 fetal control MRIs. Several SDOH and environmental factors, including maternal smoking, were associated with smaller brain volume and slower brain growth in CHD but not in controls. With CHD, repeated-measures analysis showed smaller fetal brain volume (coeff: - 13.3, 95% CI - 25.5, - 1.1, p = 0.03) and slower growth (coeff: - 2.5, 95% CI - 5.0, - 0.07, p = 0.04) with exposure to any risk factor. Patients with moderate to severe WMI had significantly lower mean COI scores compared to those with no or minimal WMI (58.28 vs. 37.28, p = 0.04), but lost significance when adjusted for GA. SDOH and environmental exposures influence fetal brain growth and preoperative brain injury risk in CHD. These results highlight additive environmental prenatal risks which may be amenable to early intervention.

    View details for DOI 10.1007/s00246-026-04308-x

    View details for PubMedID 42184039

    View details for PubMedCentralID 4533222

  • Patterns of MRI Brain Injury in Children after Out-of-Hospital Cardiac Arrest. AJNR. American journal of neuroradiology Shih, J. J., Baker, A., Vassar, R., Mehta, N., Wietstock, S. O., Amorim, E., George, E., Lindan, C., Glenn, O., Hetts, S., Martin, M., McCulloch, C. E., Xu, D., Li, Y. 2026; 47 (4): 1081-1088

    Abstract

    Pediatric out-of-hospital cardiac arrest (OHCA) is associated with a high rate of morbidity and mortality from hypoxic-ischemic brain injury. The patterns and evolution of brain injury on MRI after pediatric OHCA have not been well described. The purpose of this study was to evaluate regional brain injury patterns on MRI after pediatric OHCA and its association with clinical factors.We analyzed a retrospective cohort of pediatric patients aged between 48 hours and 18 years who experienced OHCA between 2016-2023 and underwent brain MRI containing DWI and T2-weighted sequences within 8 days postarrest. Two neuroradiologists independently scored the presence or absence of signal abnormality in the cortex, WM, globus pallidus, putamen/caudate, thalamus, posterior limb of the internal capsule (PLIC), hippocampus, brainstem, and cerebellum.Of the 68 patients included, 46 (68%) exhibited brain injury on initial MRI, with the most common locations being the cortex (50%), putamen/caudate (43%), and WM (40%). First MRI was obtained at a median of 3 (interquartile range 1-4) days postarrest. Patients with WM injury were younger (median age 1.4 years) than those without WM injury (3.6 years; P = .01), and those with PLIC injury were younger (median age 0.4 years) than those without PLIC injury (3.5 years; P = .003). Longer time to return of spontaneous resuscitation was associated with injury across a greater number of brain regions (P < .001). Among 11 patients who underwent 2 MRIs within 8 days, WM injury occurred more frequently on later imaging (36% on first MRI versus 73% on second MRI; P < .05).Patterns of injury after pediatric OHCA are influenced by patient age, timing of imaging, and cardiac arrest characteristics. The evolving distribution of injury, such as delayed appearance of WM injury, and greater vulnerability of WM and PLIC in younger patients, highlights the importance of considering clinical context when interpreting postarrest brain MRI. Recognizing these patterns may aid in identifying hypoxic-ischemic injury, especially when clinical history is limited.

    View details for DOI 10.3174/ajnr.A9057

    View details for PubMedID 41136331

    View details for PubMedCentralID PMC13045892

  • Effect of Fetal Brain Oxygenation and Volume on Brain Maturation and Neurodevelopmental Outcomes in Congenital Heart Disease. Radiology George, E., Liu, J., Martin, M., Kuang, A., Scheffler, A., Christopher, L., Xu, D., McQuillen, P., Peyvandi, S. 2025; 317 (1): e250651

    Abstract

    Background Neurodevelopmental delay is a cause of long-term morbidity in congenital heart disease (CHD). There are limited data on the effects of the fetal period on later neurodevelopment. Purpose To assess the effect of impaired fetal brain oxygenation and fetal brain volume on perinatal brain maturation and early neurodevelopmental outcomes. Materials and Methods In this secondary analysis of a single-center prospective study (April 2017 to November 2024), fetuses with CHD and normal fetuses underwent third-trimester fetal brain MRI with T2* mapping to assess oxygenation. Those with CHD underwent neonatal MRI, and neurodevelopmental testing at 30 months of age with the Bayley Scales of Infant and Toddler Development. T2* and brain volume were indexed by sex and gestational age to controls, to generate residuals. The associations of residual fetal T2* and residual fetal brain volume with brain volume growth rate from fetal to neonatal MRI, neonatal white matter (WM) apparent diffusion coefficient and fractional anisotropy, and neurodevelopment at 30 months were assessed using univariable and multivariable linear regression models. Results The study included 80 individuals (mean gestational age at fetal brain MRI, 34.0 weeks ± 0.9 [SD]; 52 male fetuses; 60 fetuses with CHD, 20 controls). There was no evidence of an association of residual fetal T2* with perinatal brain growth rate (β = 0.06 [95% CI: -0.00, 0.12]; P = .06), WM apparent diffusion coefficient (P = .11), WM fractional anisotropy (P = .21), or 30-month neurodevelopment (motor, P = .99; language, P = .89; cognition, P > .99). In multivariable analysis, single ventricle physiology was associated with worse motor scores than transposition of the great arteries (β = -19.87 [95% CI: -39.61, -0.13]; P = .049), while residual fetal brain volume was positively associated with language score (β = 0.79 [95% CI: 0.05, 1.54]; P = .04). Conclusion Fetal brain oxygenation was not associated with perinatal brain maturation or early neurodevelopmental outcomes, but fetal brain volume and lesion complexity (as represented by lesion type) were associated with improved language and worse motor outcomes, respectively. © RSNA, 2025 Supplemental material is available for this article.

    View details for DOI 10.1148/radiol.250651

    View details for PubMedID 41055496