Purpose: This study explored the clinical characteristics of patients with tinnitus who responded to sound therapy and established a predictive model to evaluate the effectiveness of this therapy according to the clinical characteristics.
Methods: A retrospective analysis was performed on 991 subjective tinnitus patients who received compound sound therapy in the Department of Otolaryngology of the local hospital from November 2019 to January 2022.
Results: We found that tinnitus patients with different therapeutic effects had significant differences in the tinnitus side ( = 0.
Biochim Biophys Acta Mol Basis Dis
March 2024
Oxidative stress is the common mechanism of sensorineural hearing loss (SNHL) caused by many factors, such as noise, drugs and ageing. Here, we used tert-butyl hydroperoxide (t-BHP) to cause oxidative stress damage in HEI-OC1 cells and in an in vitro cochlear explant model. We observed lipid peroxidation, iron accumulation, mitochondrial shrinkage and vanishing of mitochondrial cristae, which caused hair cell ferroptosis, after t-BHP exposure.
View Article and Find Full Text PDFGenetic factors play an important role in susceptibility to noise-induced hearing loss (NIHL). Alternative splicing (AS) is an essential mechanism affecting gene expression associated with disease pathogenesis at the post-transcriptional level, but has rarely been studied in NIHL. To explore the role of AS in the development of NIHL, we performed a comprehensive analysis of RNA splicing alterations by comparing the RNA-seq data from blood samples from NIHL patients and subjects with normal hearing who were exposed to the same noise environment.
View Article and Find Full Text PDFHair cell death induced by excessive reactive oxygen species (ROS) has been identified as the major pathogenesis of noise-induced hearing loss (NIHL). Recent studies have demonstrated that cisplatin- and neomycin-induced ototoxicity can be alleviated by ferroptosis inhibitors. However, whether ferroptosis inhibitors have a protective effect against NIHL remains unknown.
View Article and Find Full Text PDFEur Arch Otorhinolaryngol
June 2023
Purpose: To explore the diagnostic auditory indicators of high noise exposure and combine them into a diagnostic model of high noise exposure and possible development of hidden hearing loss (HHL).
Methods: We recruited 101 young adult subjects and divided them according to noise exposure history into high-risk and low-risk groups. All subjects completed demographic characteristic collection (including age, noise exposure, self-reported hearing status, and headset use) and related hearing examination.
Idiopathic sudden sensorineural hearing loss (ISSNHL) is an emergency ear disease that is referred to as a sensorineural hearing loss of at least 30 dB in three sequential frequencies and occurs over a period of < 72 h. Because of its etiology, pathogenesis, and prognostic factors, the current treatment methods are not ideal. Previous studies have developed prognostic models to predict hearing recovery from ISSNHL, but few studies have incorporated serum biochemical indicators into previous models.
View Article and Find Full Text PDFPurpose: This study aimed to explore whether sex is influences tinnitus severity and whether the risk factors for tinnitus severity are the same in tinnitus patients of different sexes.
Methods: This was a retrospective study of data from 1427 patients complaining of tinnitus in a local hospital otolaryngology clinic from November 2019 to January 2022. All patients were interviewed and assessed by otoscopy, pure-tone audiometry, tinnitus handicap inventory (THI), visual analogue scale (VAS), and tinnitus refinement test.
The excessive generation of reactive oxygen species (ROS) and mitochondrial damage have been widely reported in noise-induced hearing loss (NIHL). However, the specific mechanism of noise-induced mitochondrial damage remains largely unclear. In this study, we showed that acoustic trauma caused oxidative damage to mitochondrial DNA (mtDNA), leading to the reduction of mtDNA content, mitochondrial gene expression and ATP level in rat cochleae.
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