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Eric Zee, MD

  • “My goal is to give each family personalized care.”

I became a pediatrician because I wanted to be an advocate for children, and I feel very fortunate to serve our community's families and children.

Kids see doctors differently than adults. As a doctor I tend to be informal. I don't wear a tie or a white coat — that's by design. I want children and families to feel comfortable when they see me. I try to talk to the kids as much as possible and not talk through them to parents. I feel this leads to more personalized care.

Communication is key in medicine and the foundation of personalized care. Pediatrics presents a unique opportunity for that communication, because I'm speaking with both parents and children. I listen to my patients' and their parents' questions fully and then make sure they both understand my thoughts and recommendations. More than anything, that two-way communication is key.

Especialidades médicas y/o especialidades quirúrgicas

Pulmonary

Trabajo y educación

Educación

FUHS/The Chicago Medical School, North Chicago, IL, 6/4/1999

Últimos años de residencia

University of Texas Southwestern Medical Center, Dallas, TX, 6/30/2002

Subespecialidad

University of Colorado, Aurora, CO, 6/30/2005

Certificado(s) de especialidad

Pediatric Pulmonary, American Board of Pediatrics

Pediatrics, American Board of Pediatrics

Todo Publicaciones

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): 62027

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): L10210

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