Eugene Chang

Interests

Research

IRB #201107701: The airway in obstructive sleep apneaIRB #201301714: Understanding sinonasal disordersIRB # : NasalCell junction proteins in health and disease; electrophysiological transport in airway epithelial cells; craniofacial and sinus development; chronic models of sinusitis; nasal polyposis; porcine cystic fibrosis model; large animal models of infection; gene therapy; human molecular genetics; cell biology; immunology and allergy

Courses

Scholarly Contributions

Journals/Publications

• Chang, E. (2024). Does the use of extended reality (XR) simulation improve surgical/procedural learning and patient outcomes compared to standard training methods?: a systemic review.. Simulation in Healthcare, 19(1S), S98-S111. doi:10.1097/SIH.0000000000000767
• Grimm, D. R., Beswick, D. M., Maoz, S. L., Wang, E. W., Choby, G. W., Kuan, E. C., Chan, E. P., Adappa, N. D., Geltzeiler, M., Getz, A. E., Humphreys, I. M., Le, C. H., Abuzeid, W. M., Chang, E., Jafari, A., Kingdom, T. T., Kohanski, M. A., Lee, J. K., Nayak, J. V., , Palmer, J. N., et al. (2024). SNOT-22 subdomain outcomes following treatment for sinonasal malignancy: A Prospective, multicenter study.. Int Forum Allergy Rhinol, 14(8), 1314-1326. doi:10.1002/alr.23338
• Maoz, S. L., Golzar, A., Choby, G., Hwang, P. H., Wang, E. W., Kuan, E. C., Adappa, N. D., Geltzeiler, M., Getz, A. E., Humphreys, I. M., Le, C. H., Pinheiro-Neto, C. D., Fischer, J. L., Chan, E. P., Abuzeid, W. M., Chang, E., Jafari, A., Kingdom, T. T., Kohanski, M. A., , Lee, J. K., et al. (2024). University of Washington Quality of Life subdomain outcomes after treatment of sinonasal malignancy: A prospective multicenter study. Int Forum Allergy Rhinol. doi:10.1002/alr.23386
• Narendran, N., Volpe, S., Ramadan, I., Herbert, J. R., LaFleur, B., Samargandy, S., Le, C. H., & Chang, E. (2024). A prospective longitudinal study assessing the impact of rhinovirus and bacterial infections in acute exacerbations of chronic rhinosinusitis. Int Forum Allergy Rhinol. doi:10.1002/alr.23431
• Palumbo, S., Irish, J., Narendran, N., Stern, D. A., Volpe, S., Le, C. H., Starks, R., Bosco, A., Martinez, F. D., & Chang, E. (2024). The rs6967330 minor allele in CDHR3 is a significant risk factor for severe acut exacerbations in CRS. J Allergy Clin Immunol. doi:10.1016/j.jaci.2024.09.025
• Fleseriu, C. M., Beswick, D. M., Maoz, S. L., Hwang, P. H., Choby, G., Kuan, E. C., Chan, E. P., Adappa, N. D., Geltzeiler, M., Getz, A. E., Humphries, I. M., Le, C. H., Abuzeid, W. M., Chang, E., Jafari, A., Kingdom, T. T., Kohanski, M. A., Lee, J. K., Nabavizadeh, S. A., , Nayak, J. V., et al. (2023). Predictive factors for decreased baseline quality of life in patients with sinonasal malignancies.. Int Forum Allergy Rhinol. doi:10.1002/alr.23261
• Maoz, S. L., Wang, E. W., Hwang, P. H., Choby, G., Kuan, E. C., Fleseriu, C. M., Chan, E. P., Adappa, N. D., Geltzelier, M., Getz, A. E., Humphreys, I. M., Le, C. H., Abuzeid, W. M., Chang, E., Jafari, A., Kingdom, T. T., Kohanski, M. A., Lee, J. K., Lazor, J. W., , Nabavizadeh, A., et al. (2023). Long-term quality of life after treatment in sinonasal malignancy: A prospective, multicenter study.. Int Forum Allergy Rhinol, 13(11), 2030-2042. doi:10.1002/alr.23171
• Volpe, S., Irish, J., Palumbo, S., Lee, E., Herbert, J., Ramadan, I., & Chang, E. (2023). Viral infections and chronic rhinosinusitis. J Allergy Clin Immunol, 152(4), 819-826. doi:10.1016/j.jaci.2023.07.018
• Chang, E. H., Pouladi, N., Guerra, S., Jandova, J., Kim, A., Li, H., Li, J., Morgan, W., Stern, D. A., Willis, A. L., Lussier, Y. A., & Martinez, F. D. (2022). Epithelial cell responses to rhinovirus identify an early-life-onset asthma phenotype in adults. The Journal of allergy and clinical immunology, 150(3), 604-611.
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  The study of pathogenic mechanisms in adult asthma is often marred by a lack of precise information about the natural history of the disease. Children who have persistent wheezing (PW) during the first 6 years of life and whose symptoms start before age 3 years (PW) are much more likely to have wheezing illnesses due to rhinovirus (RV) in infancy and to have asthma into adult life than are those who do not have PW (PW).
• Lee, H. S., Volpe, S. J., & Chang, E. (2022). The role of viruses in the inception of chronic rinosinusitis.. Clin Exp Otorhinolaryngol, 15(4), 310-318. doi:10.21053/ceo.2022.01004
• Bailey, C. E., Grauer, J. S., Chen, P. G., Rangarajan, S. V., Chan, Y., Tewfik, M. A., Marino, M. J., Torabi, M., Le, C. H., & Chang, E. (2021). Development of a self-directed sinonasal surgical anatomy video curriculum: Phase 1 validation. Int Forum Allergy Rhinol.
• Orlandi, R. R., Kingdom, T. T., Smith, T. L., Bleier, B., DeConde, A., Luong, A. U., Poetker, D. M., Soler, Z., Welch, K. C., Wise, S. K., Adappa, N., Alt, J. A., Anselmo-Lima, W. T., Bachert, C., Baroody, F. M., Batra, P. S., Bernal-Sprekelsen, M., Beswick, D., Bhattacharyya, N., , Chandra, R. K., et al. (2021). International consensus statement on allergy and rhinology: rhinosinusitis. Int Forum Allergy Rhinol, 11, 213-739.
• Chang, E. (2020). How our specialty can contribute and benefit from COVID-19 research. Int Forum Allergy Rhinol, 10(12), 1274-1275. doi:10.1002/alr.22719
• Chang, E., & Mitts, K. B. (2020). Genetics of chronic rhinosinusitis. J Allergy Clin Immunol, 145(3), 777-779.
• Chang, E., Willis, A. L., Romanoski, C. E., Cusanovich, D. A., Pouladi, N., Li, J., Lussier, Y. A., & Martinez, F. D. (2020). RV Infections in asthmatics increase ACE2 expression and cytokine pathways implicated in COVID-19. Am J Respir Crit Care Med.
• Kato, K., Chang, E., Chen, Y., Lu, W., Kim, M. M., Niihori, M., Hecker, L., & Kim, K. C. (2020). MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke invivo. Am J Physiol Lung Cell Mol Physiol, 319(1), L82-L90.
• Richards, J. P., Done, A. J., Barber, S. R., Jain, S., Son, Y. J., & Chang, E. (2020). Virtual coach: the next tool in functional endoscopic sinus surgery education. Int Forum Allergy Rhinol, 10(1), 97-102.
• Vaidyanathan, S., Salahudeen, A. A., Sellers, Z. M., Bravo, D. T., Choi, S. S., Batish, A., Le, W., Baik, R., de la, O. S., Kaushik, M. P., Galper, N., Lee, C. M., Teran, C. A., Yoo, J. H., Bao, G., Chang, E., Patel, Z. M., Hwang, P. H., Wine, J. J., , Milla, C. E., et al. (2020). High-efficiency, selection-free gene repair in airway stem cells from cystic fibrosis patients rescues CFTR function in differentiated epithelia. Cell Stem Cell, 4, 161-171.
• Willis, A. L., Calton, J. B., Calton, J., Kim, A. S., Lee, R., Torabzadeh, E., Billheimer, D. D., Le, C. H., Martinez, F. D., & Chang, E. (2020). RV-C infections result in greater clinical symptoms and epithelial responses compared to RV-A infections in patients with CRS. Allergy.
• Kato, K., Song, B. H., Howe, C. L., & Chang, E. (2019). A Comprehensive Systematic Review of the association between Airway Mucins and Chronic Rhinosinusitis. American Journal of Rhinology & Allergy, 33(4), 433-48.
• Kim, A., Willis, A. L., Laubitz, D., Sharma, S., Song, B., Chiu, A., Le, C., & Chang, E. (2019). The effect of maxillary sinus antrostomy size on the sinus microbiome. International Forum of Allergy and Rhinology, 9(1), 30-38.
• Vaidyanathan, S., Salahudeen, A. A., Sellers, Z. M., Bravo, D. T., Choi, S. S., Batish, A., Le, W., De La O, S., Kaushik, M. P., Galper, N., Lee, C. M., Bao, G., Chang, E., Wine, J. J., Milla, C. E., Desai, T. J., Nayak, J. V., Kuo, C. J., & Porteus, M. H. (2019). Highly Efficient Repair of the F508 Mutation in Airway Stem Cells of Cystic Fibrosis Patients with Functional Rescue of the Differentiate Epithelia. bioRxiv. doi:10.1101/561183
• Vaidyanathan, S., Salahudeen, A., Sellers, Z. M., Bravo, D. T., Choi, S., Batish, A., Le, W., Delao, S., Lee, C., Teran, C. A., Boa, G., Chang, E., Patel, Z. M., Hwang, P. H., Wine, J. J., Milla, C., Desai, T., Nayak, J., Kuo, C. J., & Porteus, M. (2019). High Efficicney, Selection-Free Gene Repair in Airway Stem Cells from Cystic Fibrosis Patients Rescues CFTR Function in Differentiated Epithelia. Cell Stem Cell, 26(2), 161-74.
• Chang, E., Stern, D. A., Willis, A. L., Guerra, S., Wright, A. L., & Martinez, F. D. (2018). Early life risk factors for chronic sinusitis: a longitudinal birth cohort study. J Allergy and Clin Immunology, 141(4), 1291-1297.
• Christensen, D. N., Franks, Z. G., McCrary, H. C., Saleh, A. A., & Chang, E. (2018). A systematic review of the association between cigarette smoke exposure and chronic rhinosinusitis.. Otolaryngology-Head and Neck Surgery.
• Christensen, D. N., Franks, Z. G., McCrary, H. C., Saleh, A. A., & Chang, E. (2018). A systematic review of the association between cigarette smoke exposure and chronic rhinosinusitis. Otolaryngology-Head and Neck Surgery.
• Noutsios, G. T., Willis, A. L., Ledford, J. G., & Chang, E. (2017). Novel role of surfactant protein A in bacterial sinusitis. Int Forum Allergy Rhinol.
• Palejwala, S. K., Sharma, S., Le, C. H., Chang, E., & Lemole, G. M. (2017). Complications of advanced kadish stage esthesioneuroblastoma: single institution experience and literature review. Cureus, 9(5):1245.
• Palejwala, S. K., Sharma, S., Le, C. H., Chang, E., Erman, A. B., & Lemole, G. M. (2017). Complex skull base reconstruction in Kadish D esthesioneuroblastoma: case report. J Neurol Surg Rep, 78(2): e86-92.
• Barry, J. Y., Le, C. H., Baumann, J., Skinker, L., Chiu, A. G., & Chang, E. (2016). Endoscopic resection of maxillary sinus keratocystic odontogenic tumors. Laryngoscope. doi:10.1002/lary.25920
• Barry, J. Y., McCrary, H. C., Kent, S., Saleh, A. A., Chang, E. H., & Chiu, A. G. (2016). The Triple Aim and its implications on the management of chronic rhinosinusitis. American journal of rhinology & allergy, 30(5), 344-50.
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  Accountable care organizations (ACO) and alternative payment models are a sign of the change in reimbursement from fee-for-service to value-based reimbursement. The focus of health care under ACOs is represented by the Triple Aim: to improve the experience of health care, improve the health of populations, and reduce the per capita costs. Individuals with chronic rhinosinusitis (CRS) are heavy consumers of health care services. Results of recent studies have indicated that there is the potential for improved outcomes and cost savings from early surgical intervention. Adhering to the principles of the Triple Aim may signal a paradigm shift in regard to timing of intervention for CRS in certain patients.
• Calton, J. B., Koripella, P. C., Willis, A. L., Le, C. H., Chiu, A. G., & Chang, E. H. (2016). Paranasal sinus size is decreased in CFTR heterozygotes with chronic rhinosinusitis. International forum of allergy & rhinology.
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  Cystic fibrosis (CF) heterozygotes with a single mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene are at significantly higher risk to develop chronic rhinosinusitis (CRS). However the reasons why remain unknown. We tested the hypothesis that CFTR heterozygotes would have smaller sinus volumes than healthy controls. To exclude sinus disease as a confounding factor we also assessed paranasal sinus volume in those with CRS, but without known CFTR mutations.
• Chang, E. H., Willis, A. L., McCrary, H. C., Noutsios, G. T., Le, C. H., Chiu, A. G., Mansfield, C. J., Reed, D. R., Brooks, S. G., Adappa, N. D., Palmer, J. N., Cohen, N. G., Stern, D. A., Guerra, S., & Martinez, F. D. (2016). Association between the CDHR3 rs6967330 risk allele and chronic rhinosinusitis. The Journal of allergy and clinical immunology.
• Faucett, E. A., Larsen, B. T., Khan, R., Chiu, A. G., & Chang, E. H. (2016). A Diagnostic Dilemma: Multiple Primary Intracranial Tumors Without Vestibular Schwannomas. The Annals of otology, rhinology, and laryngology, 125(11), 938-942.
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  Sinonasal schwannomas with intracranial extension are exceedingly rare, with only 7 cases reported in the literature. Schwannomas can be isolated or multiple and are commonly associated with familial disorders such as neurofibromatosis 2 (NF 2) or familial schwannomatosis or in sporadic cases seen in sporadic schwannomatosis. Nearly all people with NF2 older than 30 years of age will have the hallmark of bilateral vestibular schwannomas (VS). This case highlights a reported case of an adult with separate primary intracranial tumors. We review the diagnostic criteria of NF2 and schwannomatosis, a recently described third variant of neurofibromatosis. In this case, we incorporate family history, histopathology, and the pathophysiology of both disorders to help determine a diagnosis for this patient.
• Le, C., McCrary, H. C., & Chang, E. (2016). Cystic Fibrosis Sinusitis. Advances in oto-rhino-laryngology, 79, 29-37.
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  Cystic fibrosis (CF) is an autosomal recessive genetic disorder caused by mutations in the CF transmembrane conductance regulator gene(CFTR) resulting in impaired ion transport. Nearly all people with CF will develop chronic rhino-sinusitis (CRS) and present with the characteristic viscous mucus, impaired mucociliary clearance and chronic inflammation/infection of the sinonasal cavity. While some individuals with CF can appear relatively asymptomatic in terms of their sinus disease, commonly reported symptoms include anosmia, headache, facial pain, nasal obstruction, chronic congestion and nasal discharge. Nasal endoscopy typically reveals mucosal edema, purulent discharge and nasal polyposis. Computed tomography (CT) imaging classically demonstrates the distinguishing findings of sinus hypoplasia or aplasia with generalized opacification, medial bulging of the lateral sinonasal sidewall and a demineralized uncinate process. Current treatment for CF sinusitis includes the use of hypertonic saline, topical and systemic steroids, antibiotics and endoscopic surgery. Research investigating novel therapies designed at targeting the primary defect of CF is showing promise for reversal of CF sinus disease, in addition to potential for disease prevention.
• Willis, A. L., Calton, J. B., Carr, T. F., Chiu, A. G., & Chang, E. H. (2016). Differentiating live from dead: a novel profile of the sinus microbiome.. American Journal of Rhinology and Allergy.
• Carr, T. F., Hill, J. L., Chiu, A., & Chang, E. H. (2015). Alteration in Bacterial Culture After Treatment With Topical Mupirocin for Recalcitrant Chronic Rhinosinusitis. JAMA otolaryngology-- head & neck surgery, 1-5.
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  Topical mupirocin therapy is used to treat symptomatic chronic sinusitis (CRS). However, the potential adverse impact of this therapy on the sinus microbiota has not been well quantified.
• Chang, E. (2018). The role of surfactant protein-A in sinusitis. Current Opinion in Allergy and Clinical Immunology Journal. doi:Ref MS No ACI190112
• Chang, E. H., & Zabner, J. (2015). Precision Genomic Medicine in Cystic Fibrosis. Clinical and translational science, 8(5), 606-10.
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  The successful application of precision genomic medicine requires an understanding of how a person's genome can influence his or her disease phenotype and how medical therapies can provide personalized therapy to one's genotype. In this review, we highlight advances in precision genomic medicine in cystic fibrosis (CF), a classic autosomal recessive genetic disorder. We discuss genotype-phenotype correlations in CF, genetic and environmental modifiers of disease, and pharmacogenetic therapies that target specific genetic mutations thereby addressing the primary defect of cystic fibrosis.
• Chang, E. H., Lee, J. H., & Zabner, J. (2010). Tryptase does not alter transepithelial conductance or paracellular permeability in human airway epithelial cells. American journal of rhinology & allergy, 24(2), 126-8.
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  Cell tight junction proteins create a barrier between airway epithelial cells to limit paracellular transport from the apical to basolateral surface. This barrier can impede the entry of respiratory pathogens and toxins from the airway lumen into the systemic circulation. Mast cell-mediated inflammation in the human airway can cause a disruption of this barrier. Tryptase is one of the major mediators released by mast cells and has been studied extensively in diseases such as asthma, reflux, and sinusitis. We hypothesize that tryptase may play a role in airway paracellular permeability by disrupting the cell tight junction proteins.
• Chang, E. H., Tang, X. X., Shah, V. S., Launspach, J. L., Ernst, S. E., Hilkin, B., Karp, P. H., Abou Alaiwa, M. H., Graham, S. M., Hornick, D. B., Welsh, M. J., Stoltz, D. A., & Zabner, J. (2015). Medical reversal of chronic sinusitis in a cystic fibrosis patient with ivacaftor. International forum of allergy & rhinology, 5(2), 178-81.
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  Chronic sinusitis is universal in cystic fibrosis (CF) and our current treatments are ineffective in reversing sinus disease. The objective of this work was to determine if increasing CF transmembrane conductance regulator (CFTR) activity by ivacaftor could treat CF sinus disease and assess its effect on primary sinus epithelial cultures.
• Kim, A., Laubitz, D., Sharma, S., Song, B., Chiu, A., Le, C., & Chang, E. (2018). Virtual FESS simulation using 3D-printed models for mixed reality nasal endoscopy. Otolaryngology-Head and Neck Surgery.
• Potter, N. J., Graham, S. M., Chang, E., & Greenlee, J. D. (2015). Bioabsorbable plate cranial base reconstruction. Laryngoscope. doi:10.1002/lary.24991
• Sharma, S., McCrary, H., Romero, E., Kim, A., Chang, E., & Le, C. (2018). A prospective, randomized single-blinded trial for improving health outcomes in rhinology by the use of personalized video recordings.. Int Forum Allergy Rhinol.
• Williams, A. L., Calton, J. B., Chiu, A. G., & Chang, E. H. (2015). Dead or alive: Deoxyribonuclease I sensitive bacteria and implications for the sinus microbiome. American journal of rhinology & allergy.
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  Recently, there has been tremendous interest in the sinus microbiome and how it relates to disease. However, a lack of a standardized sample collection and DNA extraction methods makes comparison of results across studies nearly impossible. Furthermore, current techniques fail to identify which components of the microbiome are actually alive within the host at the time of sampling.
• Chang, E. H. (2014). New insights into the pathogenesis of cystic fibrosis sinusitis. International forum of allergy & rhinology, 4(2), 132-7.
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  People with cystic fibrosis (CF) sinus disease have developmental sinus abnormalities with airway bacterial infection, inflammation, impaired mucociliary clearance and thick obstructive mucus. The pathophysiology of airway disease in CF is not completely understood, and current treatments in CF sinus disease ameliorate symptoms but do not provide a cure.
• Kopelovich, J. C., Baker, M. S., Potash, A., Desai, L., Allen, R. C., & Chang, E. H. (2014). The hybrid lid crease approach to address lateral frontal sinus disease with orbital extension. The Annals of otology, rhinology, and laryngology, 123(12), 826-30.
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  This study aimed to describe the hybrid lid crease approach in conjunction with functional endoscopic sinus surgery (FESS) for lateral frontal sinus disease with orbital extension.
• Fletcher, A., Choi, J., Awadalla, M., Potash, A. E., Wallen, T. J., Fletcher, S., & Chang, E. H. (2013). The effect of geniglossal advancement on airway flow using a computational flow dynamics model. The Laryngoscope, 123(12), 3227-32.
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  Obstructive sleep apnea (OSA) is a sleep disorder caused by partial or complete collapse of the pharyngeal airway. Genioglossal advancement (GGA) is a well-tolerated surgical procedure intended to address hypopharyngeal collapse, yet there are few studies that monitor changes in airflow dynamics at this site. Computation fluid dynamics (CFD) utilizes airflow simulation to predict changes in airflow after anatomic manipulation.
• Potash, A. E., Wallen, T. J., Karp, P. H., Ernst, S., Moninger, T. O., Gansemer, N. D., Stoltz, D. A., Zabner, J., & Chang, E. H. (2013). Adenoviral gene transfer corrects the ion transport defect in the sinus epithelia of a porcine CF model. Molecular therapy : the journal of the American Society of Gene Therapy, 21(5), 947-53.
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  Cystic fibrosis (CF) pigs spontaneously develop sinus and lung disease resembling human CF. The CF pig presents a unique opportunity to use gene transfer to test hypotheses to further understand the pathogenesis of CF sinus disease. In this study, we investigated the ion transport defect in the CF sinus and found that CF porcine sinus epithelia lack cyclic AMP (cAMP)-stimulated anion transport. We asked whether we could restore CF transmembrane conductance regulator gene (CFTR) current in the porcine CF sinus epithelia by gene transfer. We quantified CFTR transduction using an adenovirus expressing CFTR and green fluorescent protein (GFP). We found that as little as 7% of transduced cells restored 6% of CFTR current with 17-28% of transduced cells increasing CFTR current to 50% of non-CF levels. We also found that we could overcorrect cAMP-mediated current in non-CF epithelia. Our findings indicate that CF porcine sinus epithelia lack anion transport, and a relatively small number of cells expressing CFTR are required to rescue the ion transport phenotype. These studies support the use of the CF pig as a preclinical model for future gene therapy trials in CF sinusitis.
• Stoltz, D. A., Rokhlina, T., Ernst, S. E., Pezzulo, A. A., Ostedgaard, L. S., Karp, P. H., Samuel, M. S., Reznikov, L. R., Rector, M. V., Gansemer, N. D., Bouzek, D. C., Alaiwa, M. H., Hoegger, M. J., Ludwig, P. S., Taft, P. J., Wallen, T. J., Wohlford-Lenane, C., McMenimen, J. D., Chen, J., , Bogan, K. L., et al. (2013). Intestinal CFTR expression alleviates meconium ileus in cystic fibrosis pigs. The Journal of clinical investigation, 123(6), 2685-93.
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  Cystic fibrosis (CF) pigs develop disease with features remarkably similar to those in people with CF, including exocrine pancreatic destruction, focal biliary cirrhosis, micro-gallbladder, vas deferens loss, airway disease, and meconium ileus. Whereas meconium ileus occurs in 15% of babies with CF, the penetrance is 100% in newborn CF pigs. We hypothesized that transgenic expression of porcine CF transmembrane conductance regulator (pCFTR) cDNA under control of the intestinal fatty acid-binding protein (iFABP) promoter would alleviate the meconium ileus. We produced 5 CFTR-/-;TgFABP>pCFTR lines. In 3 lines, intestinal expression of CFTR at least partially restored CFTR-mediated anion transport and improved the intestinal phenotype. In contrast, these pigs still had pancreatic destruction, liver disease, and reduced weight gain, and within weeks of birth, they developed sinus and lung disease, the severity of which varied over time. These data indicate that expressing CFTR in intestine without pancreatic or hepatic correction is sufficient to rescue meconium ileus. Comparing CFTR expression in different lines revealed that approximately 20% of wild-type CFTR mRNA largely prevented meconium ileus. This model may be of value for understanding CF pathophysiology and testing new preventions and therapies.
• Chang, E. H., Pezzulo, A. A., Meyerholz, D. K., Potash, A. E., Wallen, T. J., Reznikov, L. R., Sieren, J. C., Karp, P. H., Ernst, S., Moninger, T. O., Gansemer, N. D., McCray, P. B., Stoltz, D. A., Welsh, M. J., & Zabner, J. (2012). Sinus hypoplasia precedes sinus infection in a porcine model of cystic fibrosis. The Laryngoscope, 122(9), 1898-905.
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  Chronic sinusitis is nearly universal in humans with cystic fibrosis (CF) and is accompanied by sinus hypoplasia (small sinuses). However, whether impaired sinus development is a primary feature of loss of the cystic fibrosis transmembrane conductance regulator (CFTR) or a secondary consequence of chronic infection remains unknown. Our objective was to study the early pathogenesis of sinus disease in CF.
• Dlouhy, B. J., Madhavan, K., Clinger, J. D., Reddy, A., Dawson, J. D., O'Brien, E. K., Chang, E., Graham, S. M., & Greenlee, J. D. (2012). Elevated body mass index and risk of postoperative CSF leak following transsphenoidal surgery. Journal of neurosurgery, 116(6), 1311-7.
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  Postoperative CSF leakage can be a serious complication after a transsphenoidal surgical approach. An elevated body mass index (BMI) is a significant risk factor for spontaneous CSF leaks. However, there is no evidence correlating BMI with postoperative CSF leak after transsphenoidal surgery. The authors hypothesized that patients with elevated BMI would have a higher incidence of CSF leakage complications following transsphenoidal surgery.
• Lacruz, R. S., Smith, C. E., Moffatt, P., Chang, E. H., Bromage, T. G., Bringas, P., Nanci, A., Baniwal, S. K., Zabner, J., Welsh, M. J., Kurtz, I., & Paine, M. L. (2012). Requirements for ion and solute transport, and pH regulation during enamel maturation. Journal of cellular physiology, 227(4), 1776-85.
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  Transcellular bicarbonate transport is suspected to be an important pathway used by ameloblasts to regulate extracellular pH and support crystal growth during enamel maturation. Proteins that play a role in amelogenesis include members of the ABC transporters (SLC gene family and CFTR). A number of carbonic anhydrases (CAs) have also been identified. The defined functions of these genes are likely interlinked during enamel mineralization. The purpose of this study is to quantify relative mRNA levels of individual SLC, Cftr, and CAs in enamel cells obtained from secretory and maturation stages on rat incisors. We also present novel data on the enamel phenotypes for two animal models, a mutant porcine (CFTR-ΔF508) and the NBCe1-null mouse. Our data show that two SLCs (AE2 and NBCe1), Cftr, and Car2, Car3, Car6, and Car12 are all significantly up-regulated at the onset of the maturation stage of amelogenesis when compared to the secretory stage. The remaining SLCs and CA gene transcripts showed negligible expression or no significant change in expression from secretory to maturation stages. The enamel of CFTR-ΔF508 adult pigs was hypomineralized and showed abnormal crystal growth. NBCe1-null mice enamel was structurally defective and had a marked decrease in mineral content relative to wild-type. These data demonstrate the importance of many non-matrix proteins to amelogenesis and that the expression levels of multiple genes regulating extracellular pH are modulated during enamel maturation in response to an increased need for pH buffering during hydroxyapatite crystal growth.
• Sinn, P. L., Cooney, A. L., Oakland, M., Dylla, D. E., Wallen, T. J., Pezzulo, A. A., Chang, E. H., & McCray, P. B. (2012). Lentiviral vector gene transfer to porcine airways. Molecular therapy. Nucleic acids, 1, e56.
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  In this study, we investigated lentiviral vector development and transduction efficiencies in well-differentiated primary cultures of pig airway epithelia (PAE) and wild-type pigs in vivo. We noted gene transfer efficiencies similar to that observed for human airway epithelia (HAE). Interestingly, feline immunodeficiency virus (FIV)-based vectors transduced immortalized pig cells as well as pig primary cells more efficiently than HIV-1-based vectors. PAE express TRIM5α, a well-characterized species-specific lentiviral restriction factor. We contrasted the restrictive properties of porcine TRIM5α against FIV- and HIV-based vectors using gain and loss of function approaches. We observed no effect on HIV-1 or FIV conferred transgene expression in response to porcine TRIM5α overexpression or knockdown. To evaluate the ability of GP64-FIV to transduce porcine airways in vivo, we delivered vector expressing mCherry to the tracheal lobe of the lung and the ethmoid sinus of 4-week-old pigs. One week later, epithelial cells expressing mCherry were readily detected. Our findings indicate that pseudotyped FIV vectors confer similar tropisms in porcine epithelia as observed in human HAE and provide further support for the selection of GP64 as an appropriate envelope pseudotype for future preclinical gene therapy studies in the porcine model of cystic fibrosis (CF).Molecular Therapy - Nucleic Acids (2012) 1, e56; doi:10.1038/mtna.2012.47; published online 27 November 2012.
• Chang, E. H., Lacruz, R. S., Bromage, T. G., Bringas, P., Welsh, M. J., Zabner, J., & Paine, M. L. (2011). Enamel pathology resulting from loss of function in the cystic fibrosis transmembrane conductance regulator in a porcine animal model. Cells, tissues, organs, 194(2-4), 249-54.
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  Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR), a phosphorylation- and ATP-regulated anion channel. CFTR expression and activity is frequently associated with an anion exchanger (AE) such as AE2 coded by the Slc4a2 gene. Mice null for Cftr and mice null for Slc4a2 have enamel defects, and there are some case reports of enamel anomalies in patients with CF. In this study we demonstrate that both Cftr and AE2 expression increased significantly during the rat enamel maturation stage versus the earlier secretory stage (5.6- and 2.9-fold, respectively). These qPCR data im- ply that there is a greater demand for Cl(-) and bicarbonate (HCO₃⁻) transport during the maturation stage of enamel formation, and that this is, at least in part, provided by changes in Cftr and AE2 expression. In addition, the enamel phenotypes of 2 porcine models of CF, CFTR-null, and CFTR-ΔF508 have been examined using backscattered electron microscopy in a scanning electron microscope. The enamel of newborn CFTR-null and CFTR-ΔF508 animals is hypomineralized. Together, these data provide a molecular basis for interpreting enamel disease associated with disruptions to CFTR and AE2 expression.
• Chang, E. H., Pezzulo, A. A., & Zabner, J. (2011). Do cell junction protein mutations cause an airway phenotype in mice or humans?. American journal of respiratory cell and molecular biology, 45(2), 202-20.
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  Cell junction proteins connect epithelial cells to each other and to the basement membrane. Genetic mutations of these proteins can cause alterations in some epithelia leading to varied phenotypes such as deafness, renal disease, skin disorders, and cancer. This review examines if genetic mutations in these proteins affect the function of lung airway epithelia. We review cell junction proteins with examples of disease mutation phenotypes in humans and in mouse knockout models. We also review which of these genes are expressed in airway epithelium by microarray expression profiling and immunocytochemistry. Last, we present a comprehensive literature review to find the lung phenotype when cell junction and adhesion genes are mutated or subject to targeted deletion. We found that in murine models, targeted deletion of cell junction and adhesion genes rarely result in a lung phenotype. Moreover, mutations in these genes in humans have no obvious lung phenotype. Our research suggests that simply because a cell junction or adhesion protein is expressed in an organ does not imply that it will exhibit a drastic phenotype when mutated. One explanation is that because a functioning lung is critical to survival, redundancy in the system is expected. Therefore mutations in a single gene might be compensated by a related function of a similar gene product. Further studies in human and animal models will help us understand the overlap in the function of cell junction gene products. Finally, it is possible that the human lung phenotype is subtle and has not yet been described.
• Stoltz, D. A., Meyerholz, D. K., Pezzulo, A. A., Ramachandran, S., Rogan, M. P., Davis, G. J., Hanfland, R. A., Wohlford-Lenane, C., Dohrn, C. L., Bartlett, J. A., Nelson, G. A., Chang, E. H., Taft, P. J., Ludwig, P. S., Estin, M., Hornick, E. E., Launspach, J. L., Samuel, M., Rokhlina, T., , Karp, P. H., et al. (2010). Cystic fibrosis pigs develop lung disease and exhibit defective bacterial eradication at birth. Science translational medicine, 2(29), 29ra31.
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  Lung disease causes most of the morbidity and mortality in cystic fibrosis (CF). Understanding the pathogenesis of this disease has been hindered, however, by the lack of an animal model with characteristic features of CF. To overcome this problem, we recently generated pigs with mutated CFTR genes. We now report that, within months of birth, CF pigs spontaneously developed hallmark features of CF lung disease, including airway inflammation, remodeling, mucus accumulation, and infection. Their lungs contained multiple bacterial species, suggesting that the lungs of CF pigs have a host defense defect against a wide spectrum of bacteria. In humans, the temporal and causal relations between inflammation and infection have remained uncertain. To investigate these processes, we studied newborn pigs. Their lungs showed no inflammation but were less often sterile than controls. Moreover, after introduction of bacteria into their lungs, pigs with CF failed to eradicate bacteria as effectively as wild-type pigs. These results suggest that impaired bacterial elimination is the pathogenic event that initiates a cascade of inflammation and pathology in CF lungs. Our finding that pigs with CF have a host defense defect against bacteria within hours of birth provides an opportunity to further investigate CF pathogenesis and to test therapeutic and preventive strategies that could be deployed before secondary consequences develop.
• Chang, E. H., Lobe, T. E., & Wright, S. K. (2009). Our initial experience of the transaxillary totally endoscopic approach for hemithyroidectomy. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery, 141(3), 335-9.
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  To report our initial experience with the transaxillary totally endoscopic (TATE) approach to the thyroid gland.
• Chang, E. H., & Hamilton, G. S. (2008). Novel technique for peritonsillar abscess drainage. The Annals of otology, rhinology, and laryngology, 117(9), 637-40.
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  We propose a novel technique for peritonsillar abscess (PTA) drainage in which the patient is lying in the Trendelenburg position. We provide evidence that this novel technique is relatively safe and effective in PTA drainage.
• Vore, A. P., Chang, E. H., Hoppe, J. E., Butler, M. G., Forrester, S., Schneider, M. C., Smith, L. L., Burke, D. W., Campbell, C. A., & Smith, R. J. (2005). Deletion of and novel missense mutation in POU3F4 in 2 families segregating X-linked nonsyndromic deafness. Archives of otolaryngology--head & neck surgery, 131(12), 1057-63.
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  To analyze the physical manifestations and genetic features of 2 families segregating X-linked deafness, which is most commonly reported to be caused by mutations of the POU domain gene POU3F4 at the DFN3 locus.
• Chang, E. H., Menezes, M., Meyer, N. C., Cucci, R. A., Vervoort, V. S., Schwartz, C. E., & Smith, R. J. (2004). Branchio-oto-renal syndrome: the mutation spectrum in EYA1 and its phenotypic consequences. Human mutation, 23(6), 582-9.
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  EYA1 mutations cause branchio-oto-renal (BOR) syndrome. These mutations include single nucleotide transitions and transversions, small duplications and deletions, and complex genomic rearrangements. The last cannot be detected by coding sequence analysis of EYA1. We sought to refine the clinical diagnosis of BOR syndrome by analyzing phenotypic data from families segregating EYA1 disease-causing mutations. Based on genotype-phenotype analyses, we propose new criteria for the clinical diagnosis of BOR syndrome. We found that in approximately 40% of persons meeting our criteria, EYA1 mutations were identified. Of these mutations, 80% were coding sequence variants identified by SSCP, and 20% were complex genomic rearrangements identified by a semiquantitative PCR-based screen. We conclude that genetic testing of EYA1 should include analysis of the coding sequence and a screen for complex rearrangements.
• Husein, M., Chang, E., Cable, B., Karnell, M., Karnell, L. H., & Canady, J. W. (2004). Outcomes for children with submucous cleft palate and velopharyngeal insufficiency. The Journal of otolaryngology, 33(4), 222-6.
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  To review the outcomes of children with submucous cleft palate who also have velopharyngeal insufficiency (VPI).
• Ruf, R. G., Xu, P., Silvius, D., Otto, E. A., Beekmann, F., Muerb, U. T., Kumar, S., Neuhaus, T. J., Kemper, M. J., Raymond, R. M., Brophy, P. D., Berkman, J., Gattas, M., Hyland, V., Ruf, E., Schwartz, C., Chang, E. H., Smith, R. J., Stratakis, C. A., , Weil, D., et al. (2004). SIX1 mutations cause branchio-oto-renal syndrome by disruption of EYA1-SIX1-DNA complexes. Proceedings of the National Academy of Sciences of the United States of America, 101(21), 8090-5.
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  Urinary tract malformations constitute the most frequent cause of chronic renal failure in the first two decades of life. Branchio-otic (BO) syndrome is an autosomal dominant developmental disorder characterized by hearing loss. In branchio-oto-renal (BOR) syndrome, malformations of the kidney or urinary tract are associated. Haploinsufficiency for the human gene EYA1, a homologue of the Drosophila gene eyes absent (eya), causes BOR and BO syndromes. We recently mapped a locus for BOR/BO syndrome (BOS3) to human chromosome 14q23.1. Within the 33-megabase critical genetic interval, we located the SIX1, SIX4, and SIX6 genes, which act within a genetic network of EYA and PAX genes to regulate organogenesis. These genes, therefore, represented excellent candidate genes for BOS3. By direct sequencing of exons, we identified three different SIX1 mutations in four BOR/BO kindreds, thus identifying SIX1 as a gene causing BOR and BO syndromes. To elucidate how these mutations cause disease, we analyzed the functional role of these SIX1 mutations with respect to protein-protein and protein-DNA interactions. We demonstrate that all three mutations are crucial for Eya1-Six1 interaction, and the two mutations within the homeodomain region are essential for specific Six1-DNA binding. Identification of SIX1 mutations as causing BOR/BO offers insights into the molecular basis of otic and renal developmental diseases in humans.
• Chang, E. H., Van Camp, G., & Smith, R. J. (2003). The role of connexins in human disease. Ear and hearing, 24(4), 314-23.
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  Connexins are the building blocks of gap junctions. In forming a gap junction, six connexins oligomerize to form a hexameric torus called a connexon. The number of gap junctions in a cell ranges from a few to over 105 and imparts to interconnected cells a uniform phenotype. The crucial role that gap junctions play in normal physiology is reflected by the diverse spectrum of human diseases in which allele variants of different gap junction genes are implicated. In particular, mutations in GJB2 are a major cause of autosomal recessive non-syndromic deafness. This discovery has impacted medical practice and makes it incumbent on clinicians to familiarize themselves with the genetic advances that are rapidly occurring in our field.
• Lee, M. H., Qu, Z., Fishbein, G. A., Lamp, S. T., Chang, E. H., Ohara, T., Voroshilovsky, O., Kil, J. R., Hamzei, A. R., Wang, N. C., Lin, S. F., Weiss, J. N., Garfinkel, A., Karagueuzian, H. S., & Chen, P. S. (2001). Patterns of wave break during ventricular fibrillation in isolated swine right ventricle. American journal of physiology. Heart and circulatory physiology, 281(1), H253-65.
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  Several different patterns of wave break have been described by mapping of the tissue surface during fibrillation. However, it is not clear whether these surface patterns are caused by multiple distinct mechanisms or by a single mechanism. To determine the mechanism by which wave breaks are generated during ventricular fibrillation, we conducted optical mapping studies and single cell transmembrane potential recording in six isolated swine right ventricles (RV). Among 763 episodes of wave break (0.75 times x s(-1) x cm(-2)), optical maps showed three patterns: 80% due to a wave front encountering the refractory wave back of another wave, 11.5% due to wave fronts passing perpendicular to each other, and 8.5% due to a new (target) wave arising just beyond the refractory tail of a previous wave. Computer simulations of scroll waves in three-dimensional tissue showed that these surface patterns could be attributed to two fundamental mechanisms: head-tail interactions and filament break. We conclude that during sustained ventricular fibrillation in swine RV, surface patterns of wave break are produced by two fundamental mechanisms: head-tail interaction between waves and filament break.

Presentations

• Chang, E. (2023). Viruses in sinusitis. A2DRC Conference. University of Arizona.
• Chang, E. (2023, February). Sinus surgery complications - how to prepare, avoid and correct. ENT in the Desert.
• Chang, E. (2023, Spring). A virtual portfolio for skull base surgical training. 8th Annual ABRD-Flinn Research Conference.
• Chang, E. (2022, February). Anosmia, long-haul COVID, timing of COVID trachs, upper airway stenosis, omicron variant and more panel. ENT in the Desert.
• Chang, E. (2022, February). Avoiding complications in sinus surgery. ENT in the Desert.
• Chang, E. (2022, February). Case presentations - surgery or biologic and why?. ENT in the Desert.
• Chang, E. (2022, February). Evaluation of the patient with nasal obstructions. ENT in the Desert.
• Chang, E. (2022, February). How to grade success in CRSwNP. ENT in the Desert.
• Chang, E. (2022, February). Novel techniques in surgical planning, practice and education. ENT in the Desert.
• Chang, E. (2022, February). Updates on a longitudinal study of outcomes between biologic and surgical patients for CRSwNP. ENT in the Desert.
• Chang, E., Le, C., & Bailey, C. E. (2022). Teaching Sinus Anatomy: Efficacy of Self-Directed Online Sinonasal Anatomy Learning Modules. 68th ARS at AAO-Head and Neck Surgery Foundation Academy Meeting.
• Chang, E. (2021, April). Prevalence and features of CRS worldwide. International Congress of ORL-HNS, Seoul South Korea. Seoul South Korea.
• Le, C., Bailey, C. E., & Chang, E. (2021). Phase 2 Validation of a Self-directed Sinonasal Video Curriculum. AAO-Head and Neck Surgery Foundation Academy Meeting.
• Chang, E. (2019, Fall). Genome-virome interactions in CRS. A2DRC.
• Chang, E. (2019, February). Emerging Techniques/Innovations: Intraoperative Navigation and Beyond. ENT in the Desert. Scottsdale Marriott at McDowell Mountains: UofA.
• Chang, E. (2019, March). Genome-virome Interactions in the Pathogenesis of Unified Airway Disease. Asthma UK Centre Research Seminar. London, England: Imperial College London.
• Chang, E. (2019, March). Incorporating mixed-reality and virtual reality coaching in neurohinologic surgery. Virtual Reality and Healthcare Symposium. UofA: UofA.
• Chang, E. (2018, August). Rhinovirus and chronic rhinosinusitis. A2DRC.
• Chang, E. (2018, February). Management of challenging surgical cases. ENT in the Desert.
• Chang, E. (2018, February). The Sinonasal Microbiome. ENT in the Desert.
• Chang, E. (2018, February). Treating patients from 9 to 90. ENT in the Desert.
• Chang, E. (2018, July). Rhinology and Skull Base Surgery. Otolaryngology Resident Didactics.
• Chang, E. (2018, June). The Role of Rhinovirus in Airway Disease. A2DRC Research Update Seminar.
• Chang, E. (2017, April 2017). Advances and challenges in managing cystic fibrosis. Targeted therapy for CFTR mutations in CF sinusitis. ARS at COSM. San Diego: American College of Surgeons Combined Otolaryngology Spring Meeting (COSM).
• Chang, E. (2017, Feb 2017). Contemporary surgical management of Samter's triad. ENT in the Desert. Loews Ventana Canyon: University of Arizona.
• Chang, E. (2017, Feb 2017). Genotype-phenotype-endotype in ENT: how will this affect my practice?. ENT in the Desert. Loews Ventana Canyon: University of Arizona.
• Chang, E. (2017, Feb 2017). Unified airway panel. ENT in the Desert. Loews Ventana Canyon: University of Arizona.
• Chang, E. (2017, June). Nasal polyps-an otolaryngologists' perspective, living with sinus disease. Novartis Training Program: Asthma, Sinus Disease and Uriticaria. Tucson: Novartis.
• Chang, E. (2017, March 2017). Unified airway: beyond atopy. AAAAI. Atlanta: American Academy of Allergy, Asthma and Immunology.
• Chang, E. (2017, March). Tackling problematic sinusitis: benchtop to better outcomes. Pediatric Sinusitis and CFTR-Mediated CRS. Scottsdale, Arizona: Mayo Clinic.
• Chang, E. (2017, Sep 2017). Genome-virome interactions in chronic sinusitis. AAO Conference. Chicago: American Academy of Otolaryngology.
• Willis, A. L., Noutsios, G. T., & Chang, E. (2017, March). Histamine enhances rhinovirus C binding in differentiated sinus epithelial culture. AAAAI Meeting. Atlanta, GA: American Academy of Allergy, Asthma and Immunology.
• Chang, E. (2016, March 2016). The Field of Medicine. Future Health Leaders Alliance (FHLA) Student GroupUniversity of Arizona.

Poster Presentations

• Chang, E., Le, C., & Bailey, C. E. (2021). Development of a Multi-Media Educational Model of Sinonasal Anatomy: Face and Content Validity. Combined Otolaryngology Spring Meeting Virtual Conference.

Others

• Chang, E. (2024, February). Biologics Versus Surgery for Nasal Polyps: What's the Consensus?. ENT in the Desert.
• Chang, E. (2024, February). Panel Moderator: Multi-disciplinary therapy for patients with CRS. ENT in the Desert.
• Chang, E. (2024, February). Panel: Medicine's Future-What do we need to know?. ENT in the Desert.
• Chang, E. (2024, February). Using Technology to Train Better Surgeons. ENT in the Desert.
• Chang, E. (2023, February). Panel: Case-based discussion of approaches to patients with CRSwNP. ENT in the Desert.
• Chang, E. (2023, February). Panel: Frontal sinus surgery: balloon, hybrid or complete surgery, a case-based approach. ENT in the Desert.
• Chang, E. (2023, May). Panel: Tissue histopathology and clinical endotyping: Implications for patient care. COSM Meeting.
• Chang, E. (2022, February). Panel: Multi-disciplinary Type 2 airway. ENT in the Desert.
• Chang, E. (2021, April). Panel: Current and future changes to rhinology education. COSM.
• Chang, E. (2020, January). Panel moderator: Type-2 mediated airway and asthma symposium. ENT in the Desert.
• Jain, S., Lee, S., Barber, S., Chang, E., & Son, Y. (2020, Dec). Virtual reality based hybrid simulation for functional endoscopic sinus surgery manuscript. IISE Transactions on Healthcare Systems Engineering.
  More info

  Published Manuscript
• Chang, E. (2019, February). Panel Moderator: From upper to lower airway: diagnosis, treatment, outcomes for allergic rhinitis, sinusitis and severe asthma. ENT in the Desert.
• Chang, E. (2019, February). Panel: Challenging Cases. ENT in the Desert.
• Chang, E. (2019, February). Panel: Rhinology Cases. ENT in the Desert.
• Chang, E. (2019, June). Panel Moderator: 1) Current Phenotypes of CRS: Do age, gender and atopic status matter?  2) Channels, pumps and ionic distrubances in CRS. Rhinoworld, Chicago.
• Chang, E. (2018, Summe). Top Tucson Doctors 2018. Tucson Lifestyle Magazine. http://www.tucsonlifestyle.com/bestof/top-doctors/
• Chang, E. (2017, March). The unified airway: beyond atopy. The role of RV in CRS and asthma. AAAAI Meeting, Atlanta.
• Noutsios, G. T., Romero, E., Willis, A. L., Calton, J. T., Ledford, J. G., & Chang, E. (2017, March). Expression of Surfactant Protein A in human nasal epithelial cells after infection with rhinovirus C in the presence of histamine. AAAAI Meeting, Atlanta.
• Chang, E., & Martinez, F. D. (2016, May). An association between the CDHR3 SNP and chronic rhinosinusitis. American Thoracic Society, San Francisco.
• Chang, E., & Wallen, T. (2013, January). “An in vitro organoid model of sinus development.”. American Rhinologic Society, Vancouver, Canada.
• Chang, E., Fletcher, A., Choi, J., Awadalla, M., Potash, A., & Fletcher, S. (2013, January). “The effect of genioglossal advancement on airway volume and flow characteristics using a computational flow dynamics (CFD) model.”. Triological society, Scottsdale, AZ.
• Chang, E., Wallen, T., Zabner, J., & Welsh, M. J. (2012, January). “Olfactory measurements of newborn CF pigs.”. Academy of Otolaryngology, Washington, DC.
• Chang, E., Potash, A., Desai, L., & Allen, R. (2011, January). “The open approach to the frontal sinus in an endoscopic era.”. Academy of Otolaryngology, San Francisco, CA.
• Chang, E., Pezzulo, A., Stoltz, D., & Zabner, J. (2010, January). “Role of CFTR on Sinus Development and Disease.”. Academy of Otolaryngology, Boston, MA.
• Chang, E., Brookes, J. T., Kilborn, S. A., Kirby, P. A., & Smith, R. J. (2009, January). “Endoscopic removal of giant cell reparative granuloma of the sinus: case report and review of the literature”. Rhinology World: Pennsylvania, PA 2009..
• Chang, E., Lee, J. H., & Zabner, J. (2009, January). “Tryptase does not alter paracellular permeability in Human Airway Epithelia.”. Rhinology World: Pennsylvania, PA.
• Chang, E., Lobe, T. E., & Wright, S. K. (2008, January). “Our initial experience of the Trans-Axillary Total Endoscopic Approach (TATE) for hemithyroidectomy”. Academy of Otolaryngology National Meeting: Chicago, IL.
• Chang, E., Cho, P., & Choi, K. (2007, February). “Are airbags protective in maxillofacial injury?”. Triological Combined Sections Meeting: Marco Island, FL.
• Chang, E., Cho, P., & Choi, K. (2005, January). “Are airbags protective in maxillofacial injury?”. Iowa Advances in Trauma Meeting: Iowa City, IA,.
• Chang, E. H., Cucci, N. C., & Vervoort, R. A. (2003, January). Defining Branchio-Oto-Renal syndrome and determining the role EYA1 mutations make to this phenotype.. American Society for Human Genetics meeting: Los Angeles, CA, 2003.
• Chang, E. H., Meyer, N. C., Cucci, R. A., & Smith, R. J. (2003, January). Genetic testing for EYA1 mutations in persons with Branchio-Oto-Renal (BOR) syndrome.. ASPO National Meeting: Nashville, Tennessee.
• Chang, E. H., Meyer, N. C., Cucci, R. A., & Smith, R. J. (2003, January). Genotype-phenotype correlations between EYA1 and Branchio-oto-renal (BOR) syndrome.. International Congress of Genetics: Melbourne, Australia.
• Chang, E., Husein, M., Cable, B., Karnell, M., & Canady, J. (2003, January). “Long-term Outcomes for Children with Submucous Cleft Palate that have Velopharyngeal Insufficiency.”. Canadian Society of Otolaryngology meeting: Toronto, Canada.