Objective: This systematic review investigates the long-term effect of cochlear implantation (CI) on clinical outcomes in tinnitus patients with sensorineural hearing loss (SNHL). Database Sources: PubMed, Embase, and the Cochrane Library were searched from inception to 30 April 2024. Manual searches of reference lists supplemented these searches when necessary. Review Methods: Original studies included in the meta-analysis had to contain comparative pre- and postoperative data for SNHL patients who underwent CI. Outcomes measured were the Tinnitus Handicap Inventory (THI), Visual Analog Scale (VAS), and Tinnitus Questionnaire (TQ). Results: A total of 28 studies comprising 853 patients showed significant tinnitus improvement after CI: THI mean difference (MD) −14.02 [95%CI −15.29 to −12.76, p < 0.001], TQ MD −15.85 [95%CI −18.97 to −12.74, p < 0.05], and VAS MD −3.12 [95%CI −3.49 to −2.76, p < 0.05]. Subgroup analysis indicated a significant difference between follow-up periods in THI (p < 0.0001) and VAS loudness (p = 0.02). Conclusions: Cochlear implantation substantially improves tinnitus in patients with hearing loss, though the effect may diminish over time. Further research is needed to confirm these findings.

The objective of this research was to create a prognostic model focused on genes related to ubiquitination (UbRGs) for evaluating their clinical significance in head and neck squamous cell carcinoma (HNSCC) patients. The transcriptome expression data of UbRGs were obtained from The Cancer Genome Atlas (TCGA) database, and weighted gene co-expression network analysis (WGCNA) was used to identify specific UbRGs within survival-related hub modules. A multi-gene signature was formulated using LASSO Cox regression analysis. Furthermore, various analyses, including time-related receiver operating characteristics (ROCs), Kaplan–Meier, Cox regression, nomogram prediction, gene set enrichment, co-expression, immune, tumor mutation burden (TMB), and drug sensitivity, were conducted. Ultimately, a prognostic signature consisting of 11 gene pairs for HNSCC was established. The Kaplan–Meier curves indicated significantly improved overall survival (OS) in the low-risk group compared to the high-risk group (p < 0.001), suggesting its potential as an independent and dependable prognostic factor. Additionally, a nomogram with AUC values of 0.744, 0.852, and 0.861 at 1-, 3-, and 5-year intervals was developed. Infiltration of M2 macrophages was higher in the high-risk group, and the TMB was notably elevated compared to the low-risk group. Several chemotherapy drugs targeting UbRGs were recommended for low-risk and high-risk patients, respectively. The prognostic signature derived from UbRGs can effectively predict prognosis and provide new personalized therapeutic targets for HNSCC.

Tinnitus is a prevalent and distressing medical symptom, and no effective pharmacological treatment currently exists. Despite significant advances, tinnitus remains a scientific enigma. To explore the molecular underpinnings of tinnitus, we developed a noise-induced tinnitus model in mice and utilized metabolomics to identify key differences in metabolic pathways. Our results revealed that oxidative stress-related pathways, including glutathione (GSH) metabolism, were significantly enriched in the auditory cortex of mice exhibiting tinnitus-like behavior. To further explore the role of oxidative stress, we examined the involvement of nuclear factor erythroid 2-related factor 2 (Nrf2) in tinnitus by conducting experiments in Nrf2 knockout (Nrf2-KO) mice. While Nrf2-deficient mice did not develop spontaneous tinnitus or hearing loss, they displayed increased susceptibility to prolonged tinnitus-like behavior after noise exposure. This was accompanied by heightened microglial activation, neuroinflammation, and significant alterations in gut microbiota composition, including greater diversity and dysbiosis. Our findings highlight a novel mechanism underlying tinnitus, emphasizing the role of oxidative stress in the auditory cortex and its connection to noise-induced tinnitus. The deficiency of Nrf2 in mice increases their susceptibility to tinnitus, suggesting that Nrf2 may serve as a promising therapeutic target for preventing noise-induced tinnitus.