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)

Contact

  • Academic
    megmart@stanford.edu
    University - Student Department: Bioengineering Position: Graduate

Additional Info

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. Research square DeRose, L., Martin, M., George, E., Silva, K. L., Nunez-Gallegos, F., Steurer, M., Xu, D., McQuillen, P., Peyvandi, S. 2025

    Abstract

    Background: 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.Methods: 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.Results: 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. CHD subjects from high Childhood Opportunity Index neighborhoods had lower odds of moderate to severe preoperative WMI (OR = 0.16, 95%CI: 0.03, 0.9, p = 0.04).Conclusions: 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 10.21203/rs.3.rs-8206641/v1

    View details for PubMedID 41377966

  • 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

https://orcid.org/0009-0001-3689-1453