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Objective: To explore the effects of exosomes loaded with circular RNA PARD3 on EBV-miR-BART4-induced stemness and resistance of cisplatin in nasopharyngeal carcinoma side population (NPC-SP) cells through the miR-579-3p/SIRT1/SSRP1 axis. Methods: Sixty-five cancer tissues and 65 noncancerous tissues were collected from NPC patients or patients with rhinitis. The expressions of circPARD3, miR-579-3p, SIRT1, and SSRP1 were detected by qRT-PCR, western blot, or immunohistochemistry. In vivo tumor formation assay was performed in nude mice. Immunofluorescence and qRT-PCR were conducted for the determination of CD44 and CD133 expressions, and flow cytometry combined with Hoechst 33,342 dye efflux for identifying SP cells, CCK-8 and EdU assays for cell proliferation, and Transwell assay for migration and invasion. Results: CircPARD3, SIRT1, and SSRP1 were upregulated while miR-579-3p was downregulated in NPC tissues and cells. CircPARD3 was positively correlated with the expressions of SIRT1 and SSRP1, and miR-579-3p was negatively correlated with circPARD3, SIRT1, and SSRP1. Exosomes loaded with circPARD3 promoted EBV-miR-BART4-induced stemness and cisplatin resistance in NPC-SP cells, while miR-579-3p reversed the effect of exosomal circPARD3 on EBV-miR-BART4-induced stemness and cisplatin resistance in NPC-SP cells. Additionally, miR-579-3p suppressed EBV-miR-BART4-induced stemness and cisplatin resistance in NPC-SP cells by regulating SIRT1. SIRT1 upregulated SSRP1 expression by catalyzing H3K4 methylation and down-regulation of SSRP1 reversed the effect of SIRT1 on EBV-miR-BART4-induced stemness and cisplatin resistance in NPC-SP cells. Conclusion: Exosomes loaded with circPARD3 promoted EBV-miR-BART4-induced stemness and cisplatin resistance in NPC-SP cells through the miR-579-3p/SIRT1/SSRP1 axis. [ABSTRACT FROM AUTHOR]

Background: Neuroimmune communication plays an important role in allergic inflammation, but the neuroimmune regulation of allergic rhinitis remains unclear. Objective: The goal of this study was to investigate the role of CD4-positive T lymphocyte (CD4+ T cells) adhesion to D-U87 neuron-like cells in mediating allergic rhinitis CD4+ T cell differentiation. Methods: D-U87 neuron-like cells were derived from the human glioblastoma U87 cell line. CD4+ T cells were isolated from human peripheral blood using a magnetic separation technique. In vitro coculture of D-U87 neuron-like cells and CD4+ T cells was established. The number of adherent CD4+ T cells was counted using a fluorescence microscope. The percentages of CD4+IFNγ+ and CD4+IL4+ T cells and the levels of IFNγ and IL4 cytokines in the supernatant were measured by flow cytometry. Results: The results showed that the number of adherent CD4+ T cells in patients with allergic rhinitis was significantly higher than that in healthy controls. In allergic rhinitis, the percentage of CD4+IL4+ T cells was significantly increased in the adherent group compared with that in the nonadherent group. Moreover, blocking ICAM1 and E-selectin decreased the number of adherent CD4+ T cells and the percentage of CD4+IL4+ T cells in allergic rhinitis. Conclusion: Adhesion contributes to CD4+IL4+ T cell differentiation in the in vitro coculture system of D-U87 neuron-like cells and allergic rhinitis CD4+ T cells, which may provide new insights into therapeutic strategies for allergic rhinitis. [ABSTRACT FROM AUTHOR]

Background: Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignant tumor worldwide with high morbidity and mortality. However, the diagnosis and molecular mechanisms of HNSCC remains poor. Methods: Robust rank aggregation method was performed to excavate the differentially expressed genes (DEGs) in five datasets (GSE6631, GSE13601, GSE23036, GSE30784, GSE107591) from the Gene Expression Omnibus. Search Tool for the Retrieval of Interacting Genes (STRING) database extracted hub genes from the protein‐protein interaction network. The expression of the hub genes was validated using expression profile from The Cancer Genome Atlas and Oncomine database. The module analysis and disease‐free survival analysis of the hub genes were analyzed by Cytoscape and the Kaplan‐Meier curve, respectively. The expression of hub genes was verified in clinical specimens. The functions of MMP1 which is most important in hub genes were explored in vitro and in vivo. Results: Totally, 235 DEGs were identified in the present study which consists of 103 up‐regulated and 132 down‐regulated genes which were significantly enriched in the molecular function of calcium ion binding followed in the biological process of skin development. The mainly enriched pathways were ECM (extracellular matrix)‐receptor interaction (hsa04512) and protein digestion and absorption (hsa04974). Six hub genes were screened out which showed dramatically increased expression in HNSCC samples compared with normal samples, including COL4A1, MMP1, PLAU, RBP1, SEMA3C, and COL4A2. These hub genes all showed worse disease‐free survival with higher expression and were up‐regulated in HNSCC clinical samples. MMP1 was proved to promote cell growth, migration, and phosphorylation of AKT in vitro and to promote liver metastasis in vivo. Conclusion: Bioinformatics analysis identified six key genes in HNSCC. Of these, MMP1 is the most likely biomarker. It activates the AKT pathway and promotes tumor progression. [ABSTRACT FROM AUTHOR]

With the continuous updating of head and neck surgery concepts and techniques, more and more head and neck surgeries are developing in the direction of refinement.however, the more complete the surgery, the greater the possibility of subsequent nerve exposure and injury. Even a slight perturbation of the nerve may cause serious complications, such as pressure receptor failure.It is necessary to review the mechanisms and the characteristics of baroreceptor failure syndrome after head and neck tumor surgery., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Objective: To investigate the potential risk factors and management of excessive epistaxis after endoscopic endonasal surgery (EES)., Method: Six hundred and forty-one patients who underwent EES in our hospital from December 2011 to December 2012 were reviewed retrospectively. Factors which potentially affect the incidence of excessive epistaxis after EES were analyzed with univariate and multivariate logistic regression model., Result: The incidence rate of excessive epistaxis after EES was 8.4% in our study. Multivariate logistic regression analysis revealed that history of previous EES, along with other four factors, correlated significantly with the occurrence of excessive epistaxis after EES., Conclusions: Previous EES, along with other three factors, may increase the chance of excessive epistaxis after EES, while pre-operative corticosteroid therapy may reduce the risk to some extent.