Effects of otolaryngological diseases on sleep quality, anxiety, and depression: a multicenter observational study.

Background: The impact of otolaryngological diseases on sleep quality, anxiety, and depression has garnered significant attention. However, research has primarily focused on unveiling the effects of only one or two specific diseases, without analyzing the impact of multiple concurrent diseases. Furthermore, investigation into the interaction mechanisms among these factors has been lacking.

The IRF2/CENP-N/AKT signaling axis promotes proliferation, cell cycling and apoptosis resistance in nasopharyngeal carcinoma cells by increasing aerobic glycolysis.

Background: Centromere protein N (CENP-N) has been reported to be highly expressed in malignancies, but its role and mechanism in nasopharyngeal carcinoma (NPC) are unknown.

Methods: Abnormal CENP-N expression from NPC microarrays of GEO database was analyzed. CENP-N expression level was confirmed in NPC tissues and cell lines.

PLAC8 gene knockout increases the radio-sensitivity of xenograft tumors in nude mice with nasopharyngeal carcinoma by promoting apoptosis.

In vitro cell experiments showed that knocking out the placenta-specific protein 8 (PLAC8) gene significantly increased the sensitivity of tumor cells to radiation. This study used two nude mouse models of nasopharyngeal carcinoma (NPC) to investigate the radio-sensitization and molecular mechanism of PLAC8 knockout . The expression of PLAC8 in 120 NPC tissues and 30 nasopharyngitis (NPG) tissues was detected by immunohistochemistry (IHC) to analyze the relationship between PLAC8 and neck lymph node metastasis and prognosis in NPC patients.

Overexpression of Notch2 enhances radiosensitivity via inhibition of the AKT/mTOR signaling pathway in nasopharyngeal carcinoma.

Our previous study found that in nasopharyngeal carcinoma (NPC) cells, overexpression of Notch2 can inhibit epithelial-mesenchymal transition (EMT), which plays a vital role in mediating radiosensitivity. The purpose of this study was to explore the radiosensitizing efficacy of the Notch2 gene in NPC cells and its potential mechanism. We used the recombinant plasmid transfection technique to establish Notch2-overexpressing 5-8 F and CNE-2 NPC cells.

Integrated analysis of deregulation microRNA expression in head and neck squamous cell carcinoma.

MicroRNAs (miRNAs) play critical roles in carcinogenesis and development of cancers. In this study, we analyzed the eccentrically expressed miRNAs in head and neck squamous cell carcinoma (HNSCC) tissues based on the miRNA-Seq data of HNSCC patients available in the Cancer Genome Atlas database. Aberrant expression of 2589 miRNAs was detected in HNSCC tissues (1128 downregulated and 1461 upregulated).

Plac8-mediated autophagy regulates nasopharyngeal carcinoma cell function via AKT/mTOR pathway.

To explore the relationship between autophagy and cell function, we investigated how PLAC8-mediated autophagy influences proliferation, apoptosis and epithelial-mesenchymal transition (EMT) in NPC. Colony formation analyses and CCK8 assays were used to assess the proliferative capacity of NPC cells. Transmission electron microscopy (TEM) was used to identify autophagosomes.

The diagnostic value of measurement of cochlear length and height in temporal bone CT multiplanar reconstruction of inner ear malformation.

Conclusion: The cochlear length (CL) and cochlear height (CH) measured through MPR will provide for more accurate quantitative diagnosis of inner ear malformation, and are subsequently convenient for calculating cochlear duct length (CDL) before cochear implant.

Objectives: Qualitative and quantitative diagnosis of inner ear malformation in deaf patients through multiplanar reconstruction (MPR) was performed to provide a reference for cochlear implants.

Methods: One hundred and two cases without sensorineural deafness and 560 patients with sensorineural deafness had MPR of temporal bone computed tomography performed to obtain the standardized cochlear-view and oblique coronal-view images.