About Us > LLU Health Care Otolaryngology Department - Research Information

Research projects

Alfred Simental, MD

Utilization of videoassisted thyroid and parathyroidectomy.

This is a prospective clinical study to evaluate the utilization, complication and techniques of minimally invasive thyroid and parathyroid surgery.

Timothy T.K. Jung, MD, PhD

1) Inflammatory Mediators of Otitis Media and Inner Ear Function

This is a study of the role of eicosanoids and other inflammatory mediators (IMs) in the pathogenesis of otitis media. Prostaglandins, leukotrienes and platelet-activating factor (PAF) are measured in the middle ear fluids from humans and experimentally induced animal otitis media by HPLC and radioimmunoassay. Eicosanoids are also measured in human cholesteatoma and granulation tissue. Effects of inhibitors of arachidonic acid metabolism and PAF-blocker on the outcome of experimental otitis media are tested. Also effect of IMs on the inner ear function is tested after round window membrane application of these IMs by measurements of auditory brainstem response, cochlear blood flow, and otoacoustic emissions. Effect of IMs on morphology of isolated outer hair cells from chinchilla cochlea are tested by superfusing IMs into the media containing these cells.

2) Ciliary Abnormality and Dysfunction in the Pathogenesis of Radiation Induced Otitis Media with Effusion

The purpose of this study is to determine the role of cilia in the pathogenesis of radiation induced otitis media. Morphology and function of cilia of eustachian tubes in normal and radiation-treated chinchillas are studied using scanning and transmission electron microscopy, light microscopy of temporal bone histopathology, and the rate of dye transport. The result of this study will be helpful to find the morphologic and functional effects of radiation treatment on the cilia of the eustachian tube as a cause of otitis media. Effect of radioprotector, WR 2721 on radiation induced injury to ciliated cells of eustachian tubes is studied.

3) Role of Arachidonic Acid Metabolites in Salicylate Ototoxicity

Since high doses of salicylates such as aspirin cause tinnitus and hearing loss and also inhibit PG-synthesis by blocking cyclooxygenase in the arachidonic acid (AA) cascade, we suspected that the inhibition of prostaglandin (PG) synthesis in the inner ear may be the underlying pathogenesis of ototoxicity of salicylates. Indeed, we found that treatment with high doses of salicylates decreased PG levels and increased leukotriene (LT) levels in the perilymph. Our investigation on the role of AA metabolites in salicylate ototoxicity is continuing by correlating hearing loss with levels of AA metabolites in the perilymph after treatment of AA metabolites on the round window membrane and treatment with PGI2-analog and/or leukotriene inhibitor. Changes in the cochlear blood flow after treatment of salicylates are determined also. Effect of leukotriene inhibitor on salicylate induced morphologic changes of cochlear isolated outer hair cells is investigated. Morphology of isolated outer hair cells from chinchilla cochlea is investigated after exposure of these cells to salicylate with or without LT inhibitors. Results of this study can be clinically applicable to prevent salicylate-induced ototoxicity and even other types of hearing loss by manipulating cochlear blood flow.

4) Arachidonic Acid Metabolites in Nasal Polyps and Nasal Mucosa

Aspirin-sensitivity associated with nasal polyposis and asthma is a well known syndrome and is probably mediated by leukotrienes in the lipoxygenase pathway of the arachidonic acid metabolism. Arachidonic acid metabolites are determined in the nasal polyps and nasal mucosa. Concentrations of prostaglandins and leukotrienes are determined by radioimmunoassay and high performance liquid chromatography (HPLC). Effects of steroids and lipoxygenase inhibitors on the growth of the polyps are assessed in vitro using tissue culture system. This study will provide useful information in developing medical treatment for nasal polyps.

[ENT homepage]