Andrea has a demonstrated history of working with various medical practices around the Bay Area and within the biotechnical industry as a Health Care Quality Specialist and Clinical Researcher. She received her Bachelor’s Degree in Molecular Biology with an emphasis on Human Health and the Environment in 2011 from the University of California, Berkeley. She later received her Master’s Degree in Health Care Quality in 2015 from the George Washington University School of Medicine and Health Sciences. Andrea’s research interests include understanding brain bases of emotion, motivation, and reward to identify structure of natural behavior. She is committed to improving quality of life of those with complex mental health disorders.

Current Role at Stanford

Clinical Research Coordinator for the BITS Study which tests the feasibility of adding ten in-home decluttering sessions to the Building in Treasures (BIT) Workshop as an intervention to help improve symptoms of hoarding disorder. Project is funded by the Department of Psychiatry and Behavioral Sciences of Stanford University and the National Institute of Health.

- Serve as the primary contact with research participants, sponsors, and regulatory agencies.
- Perform clerical duties in the preparation of regulatory monitoring, inspections, and audits. Maintain all forms and documents, including consent forms and master subject logs.
- Collect and manage patient and laboratory data for research. Maintain research project databases, develop flow sheets, and complete study documents/case report forms.
- Assist with screening, recruiting, and obtaining consent of study participants. Schedule and/or call subjects for appointments; contact participants with reminders or other requirements. Review medical records and/or perform telephone or in-person interviews to gather data, as needed.
- Process study compensation payments and thank you letters to subjects upon completion of trial activities. Assist with post-study activities, as needed.
- Determine effective strategies for promoting and recruiting research participants and retaining participants in long-term clinical trials.


Education & Certifications

  • MSHS, Health Care Quality, George Washington University School of Medicine and Health Sciences (2015)
  • BS, Molecular Environmental Bio, University of California, Berkeley, Emphasis on Human Health and the Environment (2011)


All Publications

  • High Altitude and Acute Mountain Sickness and Changes in Circulating Endothelin-1, Interleukin-6, and Interleukin-17a HIGH ALTITUDE MEDICINE & BIOLOGY Boos, C. J., Woods, D. R., Varias, A., Biscocho, S., Heseltine, P., Mellor, A. J. 2016; 17 (1): 25-31


    Hypoxia induces an inflammatory response, which is enhanced by exercise. High altitude (HA) leads to endothelial activation and may be proinflammatory. The relationship between endothelial activation, inflammation, and acute mountain sickness (AMS) and its severity has never been examined.Forty-eight trekkers were studied during a progressive trek at 3833, 4450, and 5129 m at rest postascent (exercise), and then again at rest 24 hours later. Twenty of the subjects were also tested at rest pre- and postexercise at sea level (SL) at 6 weeks preascent. We examined plasma levels of the interleukin 6 (IL-6), 17a (IL-17a), and endothelin-1 (ET-1) along with oxygen saturation (SpO2) and Lake Louise scores (LLS).ET-1 (5.7 ± 2.1 vs. 4.3 ± 1.9 pg/mL; p < 0.001), IL-6 (3.3 ± 3.3 vs. 2.4 ± 2.3 pg/mL; p = 0.007), and IL-17a (1.3 ± 3.0 vs. 0.46 ± 0.4 pg/mL; p < 0.001) were all overall significantly higher at HA versus SL. There was a paired increase in ET-1 and IL-6 with exercise versus rest at SL, 3833, 4450, and 5129 m (p < 0.05). There was a negative correlation between LLS and SpO2 (r = -0.32; 95% confidence interval [CI] -0.21 to -0.42; p < 0.001) and a positive correlation between LLS and IL-6 (r = 0.16; 0.0-0.27; p = 0.007) and ET-1 levels (r = 0.29; 0.18-0.39; p < 0.001. Altitude, ET-1, IL-6, and SpO2 were all univariate predictors of AMS. On multivariate analysis, ET-1 (p = 0.002) and reducing SpO2 (p = 0.02) remained as the only independent predictors (overall r(2) = 0.16; p < 0.001) of AMS. ET-1 (p = 03) and SpO2 were (p = 0.01) also independent predictors of severe AMS (overall r(2) = 0.19; p < 0.001).HA leads to endothelial activation and an inflammatory response. The rise in ET-1 and IL-6 is heavily influenced by the degree of exercise and hypoxia. ET-1 is an independent predictor of both AMS and its severity.

    View details for DOI 10.1089/ham.2015.0098

    View details for Web of Science ID 000372177700018

    View details for PubMedID 26680502