A leading clinical researcher, with nearly a decade of working experience in research and management, within both the biotechnical industry and academia, most notably at Stanford University. With a broad skill set covering important facets of healthcare and clinical research, including 3 years as a medical scribe, Varias currently is a serving member of the Rodriguez Translational Therapeutics Laboratory’s Leadership Executive Team as lead coordinator assisting with management of 20+ studies involving individuals with obsessive-compulsive disorder (OCD), suicidal risk factors, and anxiety-related disorders. She holds a Master of Science degree from George Washington University in Health Care Quality and certifications from Stanford’s Clinical Research Operations Program and Vituity’s Medical Scribe Program. Andrea’s research interests include understanding brain bases of natural behavior. She is committed to improving quality of life of those with complex mental health disorders.
Current Role at Stanford
Serving member on the Lab’s Leadership Executive Team as lead clinical research coordinator for studies involving individuals with obsessive-compulsive disorder (OCD) and anxiety-related disorders (including Hoarding Disorder and Post-Traumatic Stress Disorder)
• Conversant in goals, mission and priorities of the Lab and University as primary contact for sponsors, regulatory agencies, Clinical Trials Research Unit, and study participants.
• Demonstrates a high degree of professionalism, initiative and flexibility while managing and auditing all aspects of clinical trials, including development, study start-up, implementation, compliance, and closure of IRB- and FDA-regulated studies.
• Leads a 10-person team of research coordinators and undergraduate assistants focused on research projections/goals, protocol management, and adverse event reporting.
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)
High Altitude and Acute Mountain Sickness and Changes in Circulating Endothelin-1, Interleukin-6, and Interleukin-17a
HIGH ALTITUDE MEDICINE & BIOLOGY
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