Clinical Focus

  • Pediatric Pulmonology

Academic Appointments

Professional Education

  • Board Certification: American Board of Pediatrics, Pediatric Pulmonology (2006)
  • Residency: University of Texas Southwestern Medical Center (2002) TX
  • Fellowship: University of Colorado (2005) CO
  • Board Certification: American Board of Pediatrics, Pediatrics (2002)
  • Medical Education: FUHS/The Chicago Medical School (1999) IL

Contact

  • Academic
    ezee@stanford.edu
    University - Academic staff Department: Pediatrics - Pulmonary Medicine Position: Clinical Associate Professor
    • 6121 Hollis Street
    • Suite 2
    • Emeryville,  California  94608 
  • Clinical (Primary)  Stanford Childrens Health 6121 Hollis St Ste 2 Emeryville, CA 94608 (510) 457-4236 (fax)

Additional Clinical Info

Additional Info

  • Mail Code: 5882

All Publications

  • A pilot study of heated and humidified low flow oxygen therapy: An assessment in infants with mild and moderate bronchiolitis (HHOT AIR study) PEDIATRIC PULMONOLOGY Chen, D. Y., Zee, E. D., Gildengorin, G., Fong, E. W. 2019; 54 (5): 620–27

    View details for DOI 10.1002/ppul.24267

    View details for Web of Science ID 000468315500016

  • Hypoxia upregulates lung microvascular neurokinin-1 receptor expression. American journal of physiology. Lung cellular and molecular physiology Zee, E. D., Schomberg, S., Carpenter, T. C. 2006; 291 (1): L102-10

    Abstract

    Subacute exposure to moderate hypoxia can promote pulmonary edema formation. The tachykinins, a family of proinflammatory neuropeptides, have been implicated in the pathogenesis of pulmonary edema in some settings, including the pulmonary vascular leak associated with exposure to hypoxia. The effects of hypoxia on tachykinin receptor and peptide expression in the lung, however, remain poorly understood. We hypothesized that subacute exposure to moderate hypoxia increases lung neurokinin-1 (NK-1) receptor expression as well as lung substance P levels. We tested this hypothesis by exposing weanling Sprague-Dawley rats to hypobaric hypoxia (barometric pressure 0.5 atm) for 0, 24, 48, or 72 h. Hypoxia led to time-dependent increases in lung NK-1 receptor mRNA expression and lung NK-1 receptor protein levels at 48 and 72 h of exposure (P < 0.05). Immunohistochemistry and in situ NK-1 receptor labeling with substance P-conjugated fluorescent nanocrystals demonstrated that hypoxia increased NK-1 expression primarily in the pulmonary microvasculature and in alveolar macrophages. Hypoxia also led to increases in lung substance P levels by 48 and 72 h (P < 0.05) but led to a decrease in preprotachykinin mRNA levels (P < 0.05). We conclude that subacute exposure to moderate hypoxia upregulates lung NK-1 receptor expression and lung substance P peptide levels primarily in the lung microvasculature. We speculate that this effect may contribute to the formation of pulmonary edema in the setting of regional or environmental hypoxia.

    View details for DOI 10.1152/ajplung.00286.2005

    View details for PubMedID 16461432