Current student at Stanford University School of Medicine. Born in Huntington Beach, CA.
Honors & Awards
Future Leader in Science, Sanofi Institut Pasteur Award (2017)
U.S. Presidential Champion of Change, The White House, Obama Administration (2016)
Chancellor's Award of Distinction, University of California (2016)
Highest Achievement in Academic Excellence, University of California (2016)
Excellence in Research Distinction, University of California (2016)
Academic Scholarship, Anthem Blue Cross (2014)
One of 10 "Students Who Will Change the World", University of California (2014)
Endowed Research Award, Bill & Melinda Gates Foundation (2013)
Education & Certifications
B.A., University of California at Irvine, Anthropology (2017)
"United States Patent (Provisional) Caloric restriction for improving survival and neurological outcome", University of California, Sep 28, 2019
"United States Patent 20170348479 Adhesive system for drug delivery device", Insulet Corporation, Dec 7, 2017
Current Clinical Interests
- Medical Translational Research
Adolescent Vulnerability to Heightened Emotional Reactivity and Anxiety After Brief Exposure to an Obesogenic Diet.
Frontiers in neuroscience
2020; 14: 562
Background: Emerging evidence demonstrates that diet-induced obesity disrupts corticolimbic circuits underlying emotional regulation. Studies directed at understanding how obesity alters brain and behavior are easily confounded by a myriad of complications related to obesity. This study investigated the early neurobiological stress response triggered by an obesogenic diet. Furthermore, this study directly determined the combined impact of a short-term obesogenic diet and adolescence on critical behavioral and molecular substrates implicated in emotion regulation and stress.Methods: Adolescent (postnatal day 31) or adult (postnatal day 81) Lewis rats were fed for 1 week with an experimental Western-like high-saturated fat diet (WD, 41% kcal from fat) or a matched control diet (CD, 13% kcal from fat). We used the acoustic fear-potentiated startle (FPS) paradigm to determine the effects of the WD on cued fear conditioning and fear extinction. We used c-Fos mapping to determine the functional influence of the diet and stress on corticolimbic circuits.Results: We report that 1-week WD consumption was sufficient to induce fear extinction deficits in adolescent rats, but not in adult rats. We identify fear-induced alterations in corticolimbic neuronal activation and demonstrate increased prefrontal cortex CRHR1 messenger RNA (mRNA) levels in the rats that consumed the WD.Conclusion: Our findings demonstrate that short-term consumption of an obesogenic diet during adolescence heightens behavioral and molecular vulnerabilities associated with risk for anxiety and stress-related disorders. Given that fear extinction promotes resilience and that fear extinction principles are the foundation of psychological treatments for posttraumatic stress disorder (PTSD), understanding how obesogenic environments interact with the adolescent period to affect the acquisition and expression of fear extinction memories is of tremendous clinical relevance.
View details for DOI 10.3389/fnins.2020.00562
View details for PubMedID 32694970
Recovery from Coma Post-Cardiac Arrest Is Dependent on the Orexin Pathway
JOURNAL OF NEUROTRAUMA
2017; 34 (19): 2823–32
Cardiac arrest (CA) affects >550,000 people annually in the United States whereas 80-90% of survivors suffer from a comatose state. Arousal from coma is critical for recovery, but mechanisms of arousal are undefined. Orexin-A, a hypothalamic excitatory neuropeptide, has been linked to arousal deficits in various brain injuries. We investigated the orexinergic system's role in recovery from CA-related neurological impairments, including arousal deficits. Using an asphyxial CA and resuscitation model in rats, we examine neurological recovery post-resuscitation in conjunction with changes in orexin-A levels in cerebrospinal fluid (CSF) and orexin-expressing neurons. We also conduct pharmacological inhibition of orexin post-resuscitation. We show that recovery from neurological deficits begins between 4 and 24 h post-resuscitation, with additional recovery by 72 h post-resuscitation. Orexin-A levels in the CSF are lowest during periods of poorest arousal post-resuscitation (4 h) and recover to control levels by 24 h. Immunostaining revealed that the number of orexin-A immunoreactive neurons declined at 4 h post-resuscitation, but increased to near normal levels by 24 h. There were no significant changes in the number of neurons expressing melanin-concentrating hormone, another neuropeptide localized in similar hypothalamus regions. Last, administration of the dual orexin receptor antagonist, suvorexant, during the initial 24 h post-resuscitation, led to sustained neurological deficits. The orexin pathway is critical during early phases of neurological recovery post-CA. Blocking this early action leads to persistent neurological deficits. This is of considerable clinical interest given that suvorexant recently received U.S. Food and Drug Administration approval for insomnia treatment.
View details for DOI 10.1089/neu.2016.4852
View details for Web of Science ID 000411672700016
View details for PubMedID 28447885
View details for PubMedCentralID PMC5647501