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Facial nerve schwannoma (FNS) is a benign, slow-growing schwannoma that originates from Schwann cells. Facial nerve schwannoma is the most common tumor of the facial nerve but rare and only accounts for 0.15% to 0.8% of intracranial neurinomas. It may be manifested as asymmetric hearing loss, facial palsy, and hemifacial spasm. A 56-year-old woman was transferred to our department, because of pain behind the right ear and spasm of the right lateral muscle for more than 2 years and pulsatile tinnitus for half a year. Based on the preoperative medical history, physical signs, and auxiliary examination, it was diagnosed with jugular foramen (JF) space-occupying lesion. We removed the tumor through the infratemporal fossa type A approach and found that the tumor originated from the facial nerve. After the tumor resection, sural nerve transplantation was performed. The patient demonstrated postoperative facial palsy (House-Brackman grade VI) and was smoothly discharged after good recovery. Facial nerve schwannoma rarely invades the JF, and the most common tumor in the JF is the glomus jugular tumor, followed by the posterior cranial schwannoma. They have common symptoms, making it difficult to obtain a correct diagnosis. Clinical data, medical history, and auxiliary examinations should be carefully analyzed to avoid misdiagnosis or mistreatment. Infratemporal fossa type A approach is an effective method for treating FNS of JF. [ABSTRACT FROM AUTHOR]

Background: Mitochondrial proteins assume a pivotal role in the onset and progression of diverse diseases. Nonetheless, the causal interconnections with sensorineural hearing loss (SNHL) demand meticulous exploration. Mendelian randomization analysis is a method used in observational epidemiological studies to predict the relationship between exposure factors and outcomes using genetic variants as instrumental variables. In this study, we applied this analytical approach to two distinct samples to predict the causal impact of mitochondrial proteins on SNHL., Methods: Two-sample Mendelian randomization analyses were executed to scrutinize the predicted associations between 63 mitochondrial proteins (nuclear-encoded) and SNHL, utilizing summary statistics derived from genome-wide association studies. Assessments of pleiotropy and heterogeneity were carried out to gauge the robustness of the obtained findings., Results: Four mitochondrial proteins exhibited a suggestive causal relationship with the susceptibility to SNHL. Dihydrolipoamide dehydrogenase (DLD; OR = 0.9706, 95% CI = 0.9382-0.9953, p = 0.0230) was linked to a diminished risk of SNHL. Conversely, elevated levels of mitochondrial ribosomal protein L34 (MRPL34; OR = 1.0458, 95% CI = 1.0029-1.0906, p = 0.0362), single-pass membrane protein with aspartate-rich tail 1 (SMDT1; OR = 1.0619, 95% CI = 1.0142-1.1119, p = 0.0104), and superoxide dismutase 2 (SOD2; OR = 1.0323, 95% CI = 1.0020-1.0634, p = 0.0364) were associated with an elevated risk of SNHL., Conclusion: This research utilized Mendelian randomization analysis to predict the relationship between mitochondrial proteins and SNHL. It provides a potential viewpoint on the etiology and diagnosis., Competing Interests: Competing interests: The authors disclose no conflicts of interest., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of Otology & Neurotology, Inc.)

Background: Uncontrolled cellular proliferation may result in the progression of diseases such as cancer that promote organism death. Programmed cell death (PCD) is an important mechanism that ensures the quality and quantity of cells, which could be developed as a potential biomarker for disease diagnosis and treatment., Methods: RNA-seq data and clinical information of nasopharyngeal carcinoma (NPC) patients were downloaded from the Gene Expression Omnibus (GEO), and 1548 PCD-related genes were collected. We used the "limma" package to analyze differentially expressed genes (DEGs). The STRING database was used for protein interaction analysis, and the least absolute shrinkage and selection operator (Lasso) and support vector machines (SVMs) regression analyses were used to identify biomarkers. Then, the timeROC package was used for classifier efficiency assessment, and the "CIBERSORT" package was used for immune infiltration analysis. Wound healing and transwell migration assay were performed to evaluate migration and invasion., Results: We identified 800 DEGs between our control and NPC patient groups, in which 59 genes appeared to be PCD-related DEGs, with their function closely associated with NPC progression, including activation of the PI3K-Akt, TGF-β, and IL-17 signaling pathways. Furthermore, based on the STRING database, Cytoscape and six algorithms were employed to screen 16 important genes ( GAPDH , FN1 , IFNG , PTGS2 , CXCL1 , MYC , MUC1 , LTF , S100A8 , CAV1 , CDK4 , EZH2 , AURKA , IL33 , S100A9 , and MIF ). Subsequently, two reliably characterized biomarkers, FN1 and MUC1 , were obtained from the Lasso and SVM analyses. The Receiver operating characteristic (ROC) curves showed that both biomarkers had area under the curve (AUC) values higher than 0.9. Meanwhile, the enrichment analysis showed that in NPC patients, the FN1 and MUC1 expression levels correlated with programmed cell death-related pathways. The enrichment analysis and cellular experimental results indicated that FN1 and MUC1 were overexpressed in NPC cells and associated with programmed cell death-related pathways. Importantly, FN1 and MUC1 severely affected the ability of NPC cells to migrate, invade, and undergo apoptosis. Finally, medroxyprogesterone acetate and 8-Bromo-cAMP acted as drug molecules for the docking of FN1 and MUC1 molecules, respectively, and had binding capacities of -9.17 and -7.27 kcal/mol, respectively., Conclusion: We examined the PCD-related phenotypes and screened FN1 and MUC1 as reliable biomarkers of NPC; our findings may promote the development of NPC treatment strategy., Competing Interests: The authors declare no conflict of interest., (© 2024 The Author(s). Published by IMR Press.)

Background: Nasopharyngeal carcinoma (NPC) is an aggressive and highly metastatic malignant tumor. Despite recent therapeutic advances, resistance to Taxol (the generic name of paclitaxel) therapy remains a major challenge in clinical management. Therefore, it is imperative to explore the potential mechanisms of paclitaxel resistance in NPC. This study aimed to investigate the expression of aldehyde dehydrogenase 2 (ALDH2) in NPC cells and its critical role in paclitaxel resistance., Methods: Paclitaxel-resistant cell line CNE1/Taxol (CNE1-TR), a drug-resistant cell line, was established by exposing the CNE1 nasopharyngeal carcinoma cell line to progressively increasing concentrations of paclitaxel. Furthermore, we investigated the role of ALDH2 in paclitaxel resistance and the function of exosomes using cell culture, Western blotting, reverse transcription-polymerase chain reaction (RT-PCR), Cell Counting Kit-8 (CCK-8), and nanoparticle tracking analysis., Results: The results showed that in the presence of paclitaxel, the CNE1-TR cells manifested higher survival rate and half-maximal inhibitory concentration (IC50) value compared to the parental cell line, indicating strong resistance to paclitaxel. CNE1-TR cells had significantly upregulated mRNA and protein levels of ALDH2. In addition, exosome analysis showed that CNE1-TR cells were able to deliver ALDH2 via exosomes, increasing paclitaxel resistance in the recipient cells. We observed that the ALDH2 expression levels and paclitaxel resistance in CNE1-TR cells were effectively reduced by blocking the release of exosomes., Conclusion: ALDH2 is not only a key molecular marker indicative of therapeutic efficacy, but also a potential therapeutic target for developing novel anticancer strategies. By blocking the exosomal transport of ALDH2 or directly inhibiting its activity, it may be possible to overcome paclitaxel resistance, thus improving the success rate of clinical treatment.