Fate of Sudden Deafness Occurring in the Only Hearing Ear: Outcomes and Timing to Consider Cochlear Implantation

The present study was undertaken to learn the outcome of patients with idiopathic sudden sensorineural hearing loss (ISSNHL) in their only hearing ear. Timing to conduct a cochlear implantation was also determined in those who did not recover the hearing. The study group comprised 25 patients who confronted ISSNHL in their only hearing ear. A total of 192 patients, who had ISSNHL in one ear and had normal contralateral ear, served as the control. Demographically there were no significant differences between the groups. The recovery rate was similar between the groups: 64.0% in the experimental and 62.5% in the control group. The duration until the recovery of ISSNHL in the only hearing ear was 5-90 days (average 17.6 days). In the experimental group, 8 patients did not recover from ISSNHL, and underwent cochlear implantation in 6 with satisfactory results. These results suggest that the same treatment is applicable for patients with ISSNHL regardless of whether their contralateral ear is deaf or normal. For those who do not recover from ISSNHL in their only hearing ear, culminating in bilateral deafness, we may consider further definitive treatment including cochlear implantation as early as 3 months after initiating the treatment of ISSNHL.

Cell Surface Tissue Transglutaminase-induced Activation of Phosphoinositol 3-Kinase/Akt Pathway / 체질인류학회지

Multifunctional tissue transglutaminase (tTGase) is found in the cytoplasm and cell surface, as well as in the extracellular matrix. However, it is difficult to determine the exact function of tTGase in each cell compartment. This study focused on the potential role of cell surface tTGase in the process of "outside-in" signal transduction. Immunofluorescence study and western blotting was performed to localize the overexpression of tTGase. tTGaseoverexpressed H9c2/tTGase cells were treated with anti-tTGase antibody to evaluate the potential functions of tTGase on the outside-in signal process. The tTGase level markedly increased in each cell compartment and the culture media of H9c2/tTGase cells that show overexpression of tTGases. Anti-tTGase monoclonal antibody reduced tTGase levels in the whole lysate of H9c2/tTGase cells, and concomitantly increased the activity of the Akt. The results suggest that the cell surface expression of tTGase may be associated with an intracellular signaling pathway via the phosphoinositol-3 kinase/Akt. Phosphorylation of mitogen activated protein kinase family, ERK1/2, and Jun N-terminal Kinase (JNK), was also inhibited in the anti-tTGase antibody-treated H9c2/tTGase cells. These results suggest that cell surface tTGase may regulate intracellular signaling pathways in an autocrine or paracrine manner.