Objective: Sufferers of tinnitus, especially of the prolonged type, frequently suffer from comorbid depression and anxiety. From the perspective of the network model, this comorbidity is thought to be an interacting system of these two symptoms. In our study, we conducted a network analysis of depression and anxiety comorbidity in tinnitus sufferers, aiming to identify the central and bridge symptoms and make informed suggestions for clinical interventions and psychotherapy. Method: A total of 566 tinnitus sufferers were enrolled in our study. The Patient Health Questionnaire-9 (PHQ-9) and the Generalized Anxiety Disorder 7-Item Questionnaire (GAD-7) were selected to evaluate depression and anxiety symptoms, respectively, followed by network analysis to construct the interacting networks. Results: The findings identified six edges of strongest regularized partial correlations in this network. Of these, three were depression symptoms and three were anxiety symptoms. The anxiety symptoms “Unable to control worry” and “Relaxation difficulty” and the depression symptom “Feeling depressed or hopeless” had the highest expected influence centrality. The analysis results also revealed three bridge symptoms: “Afraid something awful might happen”, “Feeling of worthlessness”, and “Trouble concentrating”. As for “Suicidal ideation”, the direct relations between this symptom and “Afraid something awful might happen” and “Feeling depressed or hopeless” were the strongest. Conclusions: The central and bridge symptoms of the interacting network of depression and anxiety symptoms in tinnitus sufferers can be considered a significant transdiagnostic intervention target for the management of this comorbidity. In particular, clinical prevention and psychotherapy should be implemented, targeting the symptoms that have the strongest associations with suicidal ideation.

Free fatty acids (FFAs) could induce inflammatory responses via various pathways. Ferroptosis is characterized by the accumulation of lipid peroxidation products and fatal reactive oxygen species d... 背景：游离脂肪酸 (FFA) 可通过多种途径诱导炎症反应。铁死亡的特征是由铁积累导致的脂质过氧化产物积累和致命的反应性氧物质, 这可能是炎性损伤的上游事件。目的：研究 FFA诱导的病理毛细胞炎症损伤过程中铁死亡的参与及其机制。材料和方法：我们利用 House Ear Institute-Organ of Corti 1 (HEI-OC1) 细胞系作为体外模型。 棕榈酸 (PA) 被用作 FF...

Hearing loss (HL) is an otolaryngology disease susceptible to environmental pollutants. Volatile organic compounds (VOCs), as a class of chemical pollutants with evaporation propensity, pose a great threat to human health. However, the association between VOCs and HL remains unclear. This study aimed to explore the association between urinary-specific VOC metabolites and HL. It included 1048 participants from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2012. Multivariate linear regression models, smooth curve analysis, and stratified analysis were employed to investigate the relationship between urinary-specific VOC metabolite concentrations and pure tone audiometry (PTA) across three different frequencies. A two-piecewise linear regression model was employed to analyze the threshold effects of urinary-specific VOC metabolites on hearing threshold changes. Furthermore, a comparative toxicogenomics database (CTD) and functional gene enrichment were constructed. An interaction network of transcription factors, genes, and non-coding RNA was constructed to further confirm the upstream and downstream regulatory relationships. Molecular docking analyses were conducted to explore the potential binding modes and critical docking sites. Additionally, a moderation analysis was conducted to investigate the role of oxidative stress in moderating the influence of VOC metabolites on hearing. Multivariate linear regression model discerned a significant correlation between cyanide 2-aminothiazoline-4-carboxylic acid (ATCA) with speech-frequency PTA and N-acetyl-S-(3,4-dihydroxybutyl)-L-cysteine (DHBMA) with high-frequency PTA. The smoothed curve and threshold effect analysis corroborated a positive linear relationship between cyanide ATCA and speech-frequency PTA without a threshold effect only in the 20–34 age group. Additionally, the bioinformatics analysis discovered pathogenic genes related to cyanide-induced HL and suggested that oxidative stress responses play a critical role in this biological process. Furthermore, the moderation effect of total bilirubin (TB), an oxidative stress-associated molecule, was ascertained on the effects of ATCA on hearing. Our findings suggest a potential link between VOC metabolites and hearing and indicate the crucial role of oxidative stress responses in this association.

Background Soldiers are often exposed to high-intensity noise produced by military weapons and equipment during activities, and the incidence of noise-induced hearing loss (NIHL) in many arms is high. Oxidative stress has a significant role in the pathogenesis of NIHL, and research has confirmed that ginsenoside Rd (GSRd) suppresses oxidative stress. Therefore, we hypothesized that GSRd may attenuate NIHL and cochlear hair cell loss, induced by military aviation noise stimulation, through the Sirtuin1/proliferator-activated receptor-gamma coactivator 1α (SIRT1/PGC-1α) signaling pathway.Methods Forty-eight male guinea pigs were randomly divided into four groups: control, noise stimulation, GSRd, and glycerol. The experimental groups received military helicopter noise stimulation at 115 dB (A) for 4 h daily for five consecutive days. Hair cell damage was evaluated by using inner ear basilar membrane preparation and scanning electron microscopy. Terminal dUTP nick end labeling and immunofluorescence staining were conducted. Changes in the SIRT1/PGC-1α signaling pathway and other apoptosis-related markers in the cochleae, as well as oxidative stress parameters were used as readouts.Results Loss of outer hair cells, more disordered cilia, prominent apoptosis, and elevated free radical levels were observed in the experimental groups. GSRd treatment markedly improved morphological changes and apoptosis through decreasing Bcl-2 associated X protein (Bax) expression and increasing Bcl-2 expression. In addition, GSRd upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels, decreased malondialdehyde (MDA) levels, and enhanced the activity of SIRT1 and PGC-1α messenger ribonucleic acid and protein expression.Conclusion GSRd can improve structural and functional damage to the cochleae caused by noise. The underlying mechanisms may be associated with the SIRT1/PGC-1α signaling pathway.