Background: Mutations in GJB2 are the most common molecular defects responsible for autosomal recessive nonsyndromic hearing impairment (NSHI). The mutation spectra of this gene vary among different ethnic groups.

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Objective The aim of this study was to compare the outcomes of lateral temporal bone resection and pedicled temporalis muscle flap stuffing with external auditory canal closure with those of canal wall down mastoidectomy for the treatment of mastoid osteoradionecrosis. Study Design Prospective nonrandomized case-control clinical study. Setting Department of Otolaryngology of the First People's Hospital of Foshan. Subjects and Methods Seventy-seven postirradiation nasopharyngeal carcinoma patients with mastoid osteoradionecrosis were included. Forty patients (40 ears) underwent lateral temporal bone resection in the temporalis muscle flap group. Their pedicled temporalis muscle flaps were laid on the surgical cavity, and the external canal opening was simultaneously closed. Thirty-seven patients (37 ears) underwent a canal wall down mastoidectomy in the mastoidectomy group. The surgical wounds and complications following surgery were retrospectively analyzed. Results The patients were followed for 2 years. The percentage of patients with purulent otorrhea and persistent osteoradionecrosis in the temporalis muscle flap group was lower than that in the mastoidectomy group. Conclusion Our preliminary results suggest that lateral temporal bone resection with the pedicled temporalis muscle flap filled into the surgical cavity, followed by closure of the external auditory canal, represents a valuable approach for treating mastoid osteoradionecrosis.

The Hippo/Yes-associated protein (YAP) signaling pathway has been shown to be able to maintain organ size and homeostasis by regulating cell proliferation, differentiation, and apoptosis. The abuse of aminoglycosides is one of the main causes of sensorineural hearing loss (SSNHL). However, the role of the Hippo/YAP signaling pathway in cochlear hair cell (HC) damage protection in the auditory field is still unclear. In this study, we used the YAP agonist XMU-MP-1 (XMU) and the inhibitor Verteporfin (VP) to regulate the Hippo/YAP signaling pathway in vitro. We showed that YAP overexpression reduced neomycin-induced HC loss, while downregulated YAP expression increased HC vulnerability after neomycin exposure in vitro. We next found that activation of YAP expression inhibited C-Abl-mediated cell apoptosis, which led to reduced HC loss. Many previous studies have reported that the level of reactive oxygen species (ROS) is significantly increased in cochlear HCs after neomycin exposure. In our study, we also found that YAP overexpression significantly decreased ROS accumulation, while downregulation of YAP expression increased ROS accumulation. In summary, our results demonstrate that the Hippo/YAP signaling pathway plays an important role in reducing HC injury and maintaining auditory function after aminoglycoside exposure. YAP overexpression could protect against neomycin-induced HC loss by inhibiting C-Abl-mediated cell apoptosis and decreasing ROS accumulation, suggesting that YAP could be a novel therapeutic target for aminoglycosides-induced sensorineural hearing loss in the clinic.