Honors & Awards

  • Inductee, Gold Humanism Honor Society (2013)
  • MedScholars Research Grant, Stanford University School of Medicine (Awarded January 2012)
  • Excellence in Human Biology Honors Research Award, Stanford University (June 2009)
  • Undergraduate Research Major Grant, Stanford University (Awarded June 2008)

Education & Certifications

  • Bachelor of Arts, Stanford University, HUMBI-BAH (2009)

Stanford Advisors


Work Experience

  • Teaching Assistant for INDE 211, "Creative Writing", Stanford University (2012)


    Stanford, CA

  • Teaching Assistant for SURG 221, "Wilderness Medicine", Stanford University (2012)


    Stanford, CA

  • Tutor for SURG 203, "Human Anatomy", Stanford School of Medicine (2013)


    Stanford, CA

  • Research Technician, Department of Developmental Genetics, Skirball Institute, New York University (2009 - 2010)


    New York, NY


Journal Articles

  • Partial Proteasome Inhibitors Induce Hair Follicle Growth by Stabilizing ß-Catenin. Stem cells Yucel, G., Van Arnam, J., Means, P. C., Huntzicker, E., Altindag, B., Lara, M. F., Yuan, J., Kuo, C., Oro, A. E. 2014; 32 (1): 85-92


    The activation of tissue stem cells from their quiescent state represents the initial step in the complex process of organ regeneration and tissue repair. While the identity and location of tissue stem cells are becoming known, how key regulators control the balance of activation and quiescence remains mysterious. The vertebrate hair is an ideal model system where hair cycling between growth and resting phases is precisely regulated by morphogen signaling pathways, but how these events are coordinated to promote orderly signaling in a spatial and temporal manner remains unclear. Here, we show that hair cycle timing depends on regulated stability of signaling substrates by the ubiquitin-proteasome system. Topical application of partial proteasomal inhibitors (PaPIs) inhibits epidermal and dermal proteasome activity throughout the hair cycle. PaPIs prevent the destruction of the key anagen signal β-catenin, resulting in more rapid hair growth and dramatically shortened telogen. We show that PaPIs induce excess β-catenin, act similarly to the GSK3β antagonist LiCl, and antagonize Dickopf-related protein-mediated inhibition of anagen. PaPIs thus represent a novel class of hair growth agents that act through transiently modifying the balance of stem cell activation and quiescence pathways. Stem Cells 2014;32:85-92.

    View details for DOI 10.1002/stem.1525

    View details for PubMedID 23963711

  • Review of "100,000 Hearts: A Surgeon's Memoir," by Denton Cooley The Pharos Means, C. 2013; Spring : 43-44
  • My First Patient The Intima: A Journal of Narrative Medicine Means, C. 2013
  • Semaphorin-PlexinD1 Signaling Limits Angiogenic Potential via the VEGF Decoy Receptor sFlt1 DEVELOPMENTAL CELL Zygmunt, T., Gay, C. M., Blondelle, J., Singh, M. K., Flaherty, K. M., Means, P. C., Herwig, L., Krudewig, A., Belting, H., Affolter, M., Epstein, J. A., Torres-Vazquez, J. 2011; 21 (2): 301-314


    Sprouting angiogenesis expands the embryonic vasculature enabling survival and homeostasis. Yet how the angiogenic capacity to form sprouts is allocated among endothelial cells (ECs) to guarantee the reproducible anatomy of stereotypical vascular beds remains unclear. Here we show that Sema-PlxnD1 signaling, previously implicated in sprout guidance, represses angiogenic potential to ensure the proper abundance and stereotypical distribution of the trunk's segmental arteries (SeAs). We find that Sema-PlxnD1 signaling exerts this effect by antagonizing the proangiogenic activity of vascular endothelial growth factor (VEGF). Specifically, Sema-PlxnD1 signaling ensures the proper endothelial abundance of soluble flt1 (sflt1), an alternatively spliced form of the VEGF receptor Flt1 encoding a potent secreted decoy. Hence, Sema-PlxnD1 signaling regulates distinct but related aspects of angiogenesis: the spatial allocation of angiogenic capacity within a primary vessel and sprout guidance.

    View details for DOI 10.1016/j.devcel.2011.06.033

    View details for Web of Science ID 000294387300011

    View details for PubMedID 21802375


  • "Examining the effects of sedentary behavior on cognitive performance in a school setting: How is sitting throughout the day affecting student learning?"

    Time Period


    Presented To

    Medical Education Seminar Series



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