BackgroundThe role of postoperative adjuvant treatment for sinonasal malignant melanoma remains unclear. This study evaluates the impact of three different surgical and postoperative adjuvant treatment modalities: surgery alone(open and endoscopic approaches), surgery plus radiotherapy and surgery, radiotherapy plus chemotherapy on survival of patients with primary sinonasal malignant melanoma (SMM).MethodsThe data of 69 patients who underwent primary surgical treatments at Eye & ENT hospital of Fudan University between January 1st, 2000 and December 31st, 2010 were retrospectively reviewed. Survival comparison of different surgical and postoperative adjuvant treatment modalities (surgery alone, surgery plus radiotherapy and surgery, radiotherapy plus chemotherapy), as well as survival comparison between open and endoscopic surgical approaches were performed. Curves depicting survival were performed using Kaplan-Meier method. Statistical analysis was performed using log-rank test software SPSS19 and p < .05 is considered as statistically significant.ResultsThe median overall survival time was found to be 18 months for surgery alone (27 cases), 32 months for surgery plus radiotherapy (24 cases), 42 months for surgery, radiotherapy plus chemotherapy (18 cases). The 3 and 5 year survival rates for groups mentioned above were 14.8% and 5.6%, 45.1% and 31.6%, 55% and 32.1%, respectively. Statistical significances were found not only between surgery alone and surgery plus radiotherapy treatment group (P = 0.012), but also surgery alone and surgery, radiotherapy plus chemotherapy group (P = 0.002). There was no statistically significant survival difference found between the two different surgical approaches (41 cases for open approach and 28 cases for endoscopic approach).ConclusionsSinonasal malignant melanoma is a disease with a poor prognosis. Patients who underwent surgery plus radiotherapy or surgery, radiotherapy plus chemotherapy had better survival outcomes than those underwent surgery alone. Endoscopic approach provided similar survival outcome as an open approach.

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Background: Chronic administration of D-galactose (D-gal) results in oxidative stress and chronic inflammatory aging. Age-related changes in the brain result in neurovascular damage and blood-brain barrier (BBB) dysfunction. However, little is known regarding D-gal-induced neurovascular damage, as well as the protective effects of huperzine A. Objective: The purpose of this study was to utilize a D-gal-induced rat model to investigate the activation of neurovascular inflammatory damage and apoptosis in the rat hippocampus and to understand whether huperzine A alleviates D-gal-induced neuronal and vascular inflammatory injury. Methods: Aging rats were treated with D-gal (300 mg/kg s.c. for 8 weeks), were coadministered D-gal and huperzine A (D-gal 300 mg/kg and huperzine A 0.1 mg/kg s.c. for 8 weeks) or served as the saline-treated control group rats (same volume of saline given subcutaneously for 8 weeks). Changes in hippocampal morphology and biomarkers of inflammatory damage were analyzed. Results: Our study revealed that chronic administration of D-gal resulted in the activation of glia and vascular endothelial cells and upregulation of mRNA and protein levels of cell-associated adhesion molecules and inflammatory cytokines via nuclear factor (NF)-κB inhibitor degradation and NF-κB nuclear translocation. The inflammatory injury caused significant BBB dysfunction, decreased density of tight junctions (TJs) and apoptosis in the rat hippocampus. Coadministration of huperzine A not only markedly inhibited the D-gal-induced increase in acetylcholinesterase (AChE) activity, but also alleviated D-gal-induced neurovascular damage by inhibiting D-gal-induced NF-κB activation, improving cerebrovascular function and suppressing the D-gal-induced decrease in the density and protein levels of TJs and cell apoptosis. Conclusions: Our findings provided evidence that D-gal induced a proinflammatory phenotype mediated by NF-κB in the rat hippocampus. Moreover, huperzine A suppressed D-gal-induced neurovascular damage and BBB dysfunction, partly by preventing NF-κB nuclear translocation. The inhibiting effect of huperzine A on AChE activity might play an important role in attenuating D-gal-induced inflammatory damage.

Our findings provide evidence that HRH4 rs77485247 and rs77041280 polymorphisms may be associated with the risk of AR and the efficacy of H1 antihistamines for the treatment of AR patients.