Even with protective head bandages, 1.5-T MRI in patients with CIs led to a variety of adverse events, including discomfort or pain and displacement of the internal magnet. Therefore, sedation and careful head positioning may be appropriate for some patients with CIs who undergo MRI, and these patients should be carefully monitored to decrease the likelihood of such adverse effects.

Meniere's disease is an inner ear disorder that can manifest as fluctuating vertigo, sensorineural hearing loss, tinnitus, and aural fullness. However, the pathologic mechanism of Meniere's disease is still unclear. In this study, we evaluated autoimmunity as a potential cause of Meniere's disease. In addition we tried to find useful biomarker candidates for diagnosis. We investigated the protein composition of human inner ear fluid using liquid column mass spectrometry, the autoimmune reaction between circulating autoantibodies in patient serum and multiple antigens using the Protoarray system, the immune reaction between patient serum and mouse inner ear tissues using western blot analysis. Nine proteins, including immunoglobulin and its variants and interferon regulatory factor 7, were found only in the inner ear fluid of patients with Meniere's disease. Enhanced immune reactions with 18 candidate antigens were detected in patients with Meniere's disease in Protoarray analysis; levels of 8 of these antigens were more than 10-fold higher in patients than in controls. Antigen-antibody reactions between mouse inner ear proteins with molecular weights of 23–48 kDa and 63–75 kDa and patient sera were detected in 8 patients. These findings suggest that autoimmunity could be one of the pathologic mechanisms behind Meniere's disease. Multiple autoantibodies and antigens may be involved in the autoimmune reaction. Specific antigens that caused immune reactions with patient's serum in Protoarray analysis can be candidates for the diagnostic biomarkers of Meniere's disease.

Kim SH, Kim KX, Raveendran NN, Wu T, Pondugula SR, Marcus DC. Regulation of ENaC-mediated sodium transport by glucocorticoids in Reissner's membrane epithelium. 's membrane epithelium forms much of the barrier that produces and sustains the large ionic differences between cochlear endolymph and perilymph. We have reported that Reissner's membrane contributes to normal cochlear function by absorbing Na ϩ from endolymph via amiloridesensitive channels in gerbil inner ear. We used mouse Reissner's membrane to 1) identify candidate genes involved in the Na ϩ transport pathway, 2) determine whether their level of expression was regulated by the synthetic glucocorticoid dexamethasone, and 3) obtain functional evidence for the physiological importance of these genes. Transcripts were present for ␣-, ␤-, and ␥-subunits of epithelial Na ϩ channel (ENaC); corticosteroid receptors GR (glucocorticoid receptor) and MR (mineralocorticoid receptor); GR agonist regulator 11␤-hydroxysteroid dehydrogenase (HSD) type 1 (11␤-HSD1); Na ϩ transport control components SGK1, Nedd4-2, and WNKs; and K ϩ channels and Na ϩ -K ϩ -ATPase. Expression of the MR agonist regulator 11␤-HSD2 was not detected. Dexamethasone upregulated transcripts for ␣-and ␤-subunits of ENaC (ϳ6-and ϳ3-fold), KCNK1 (ϳ3-fold), 11␤-HSD1 (ϳ2-fold), SGK1 (ϳ2-fold), and WNK4 (ϳ3-fold). Transepithelial currents from the apical to the basolateral side of Reissner's membrane were sensitive to amiloride (IC50 ϳ0.7 M) and benzamil (IC50 ϳ0.1 M), but not EIPA (IC50 ϳ34 M); amilorideblocked transepithelial current was not immediately changed by forskolin/IBMX. Currents were reduced by ouabain, lowered bath Na ϩ concentration (from 150 to 120 mM), and K ϩ channel blockers (XE-991, Ba 2ϩ , and acidification from pH 7.4 to 6.5). Dexamethasone-stimulated current and gene expression were reduced by mifepristone, but not spironolactone. These molecular, pharmacological, and functional observations are consistent with Na ϩ absorption by mouse Reissner's membrane, which is mediated by apical ENaC and/or other amiloride-sensitive channels, basolateral Na ϩ -K ϩ -ATPase, and K ϩ -permeable channels and is under the control of glucocorticoids. These results provide an understanding and a molecular definition of an important transport function of Reissner's membrane epithelium in the homeostasis of cochlear endolymph.

We found that VEMP latencies are increased in BPPV patients, which may signify neuronal degenerative changes in the macula of the saccule. When an extensive neuronal damage was suspected by VEMP results such as "no response" in VEMP, the disease progress showed a chronic and resistive course. Therefore, we propose that VEMP could be a useful method to determine a clinical prognosis of patients with BPPV.

Highlights d Cleaved inner ear cochlin LCCL secretes to perilymph space post-bacterial infection d LCCL induces bacterial aggregation in the scala tympani d Spatiotemporal innate immune response by LCCL protects the sensory organ of Corti d LCCL rescues Coch À/À mouse post-Pseudomonas inner ear infection hearing loss

4. Laryngoscope, 127:921-926, 2017.

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