Background: Studies have shown that the lipid metabolism mediator leukotriene and prostaglandins are associated with the pathogenesis of allergic rhinitis (AR). The aim of this study was to identify key lipid metabolism-related genes (LMRGs) related to the diagnosis and treatment of AR. Materials and methods: AR-related expression datasets (GSE75011, GSE46171) were downloaded through the Gene Expression Omnibus (GEO) database. First, weighted gene co-expression network analysis (WGCNA) was used to get AR-related genes (ARRGs). Next, between control and AR groups in GSE75011, differentially expressed genes (DEGs) were screened, and DEGs were intersected with LMRGs to obtain lipid metabolism-related differentially expressed genes (LMR DEGs). Protein-protein interaction (PPI) networks were constructed for these LMR DEGs. Hub genes were then identified through stress, radiality, closeness and edge percolated component (EPC) analysis and intersected with the ARRGs to obtain candidate genes. Biomarkers with diagnostic value were screened via receiver operating characteristic (ROC) curves. Differential immune cells screened between control and AR groups were then assessed for correlation with the diagnostic genes, and clinical correlation analysis and enrichment analysis were performed. Finally, real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was made on blood samples from control and AR patients to validate these identified diagnostic genes. Results: 73 LMR DEGs were obtained, which were involved in biological processes such as metabolism of lipids and lipid biosynthetic processes. 66 ARRGs and 22 hub genes were intersected to obtain four candidate genes. Three diagnostic genes (LPCAT1, SGPP1, SMARCD3) with diagnostic value were screened according to the AUC > 0.7, with markedly variant between control and AR groups. In addition, two immune cells, regulatory T cells (Treg) and T follicular helper cells (TFH), were marked variations between control and AR groups, and SMARCD3 was significantly associated with TFH. Moreover, SMARCD3 was relevant to immune-related pathways, and correlated significantly with clinical characteristics (age and sex). Finally, RT-qPCR results indicated that changes in the expression of LPCAT1 and SMARCD3 between control and AR groups were consistent with the GSE75011 and GSE46171. Conclusion: LPCAT1, SGPP1 and SMARCD3 might be used as biomarkers for AR.

Objective: To investigate the characteristics of sleep disorders and anxiety in patients with tinnitus, their influencing factors, and the role of sleep disorders as mediators.Methods: The general conditions and disease characteristics of 393 patients with tinnitus presented to the Changzheng Hospital of the Naval Medical University from 2018 to 2021 were collected. All patients accepted questionnaires such as Tinnitus Handicap Inventory (THI), Pittsburgh Sleep Quality Index (PSQI) and Self-rating Anxiety Scale (SAS), and then the characteristics and the influencing factors of sleep disorders and anxiety were analyzed.Results: Among the 393 tinnitus patients, 213 cases (54.19%) were diagnosed with sleep disorders, and 78 cases (19.85%) were diagnosed with anxiety, including 25 men (32.1%) and 53 women (67.9%). Binary regression showed that gender, hearing loss, tinnitus severity, and sleep disorders severity were positively associated with anxiety. Multiple logistic regression analysis showed that female gender (OR = 2.526, P = 0.008), hearing loss (OR = 2.901, P = 0.003, tinnitus severity (OR = 1.863, P = 0.003) and sleep disorders (OR = 2.510, P = 0.001) were the independent risk factors of anxiety. The mediating effect of sleep disorders between tinnitus severity and anxiety accounted for 27.88% of the total effect size.Conclusion: Females patients with hearing loss, moderate to severe tinnitus, and sleep disorders were at greater risk for anxiety, with sleep disorders partially mediating the anxiety associated with tinnitus.

Rationale: Gustation is important to several biological functions in mammals. However, chemotherapy drugs often harm taste perception in cancer patients, while the underlying mechanism is still unclear for most drugs and there is no effective way to restore taste function. This study investigated the effects of cisplatin on the taste cell homeostasis and gustatory function.