Objective To evaluate the impact of three to four cycles of neoadjuvant chemotherapy (NACT) on the survival of patients with N2-N3 nasopharyngeal carcinoma (NPC).Methods The clinical data of 915 patients with T1-4N2-3M0 NPC from 2007 to 2010 were retrospectively analyzed.A total of 179 patients treated with 3-4 cycles of NACT (NACT≥3 group) were matched with 358 patients treated with 2 cycles of NACT (NACT=2 group) and 179 patients treated without NACT (NACT =0 group,concurrent chemoradiotherapy group) for age,N stage,pathological subtype,and NACT regimen.The Kaplan-Meier method was used to calculate overall survival (OS),disease-free survival (DFS),recurrence-free survival (RFS),and distant metastasis-free survival (DMFS) rates,the log-rank test was used for survival difference analysis and univariate prognostic analysis,and the Cox proportional hazards model was used for multivariate prognostic analysis.Results For the NACT≥ 3,NACT =2,and NACT =0 groups,the 5-year OS rates were 89.4％,81.6％,and 73.7％,respectively (P=O.000),the 5-year DFS rates were 83.2％,69.8％,and 64.2％,respectively (P=O.000),the 5-year RFS rates were 86.0％,76.0％,and 69.3％,respectively (P=0.001),and the 5-year DMFS rates were 86.6％,76.0％,and 68.3％,respectively (P=0.000).Three to four cycles of NACT was an independent protective factor for OS,DFS,RFS,and DMFS in patients with N2-N3 NPC.Conclusion Three to four cycles of NACT can significantly improve the survival of patients with N2-N3 NPC.

As the main weapon of cellular immunity,CD4+ T cells play a vital role in controlling and eliminating infections,and are an important barrier for the body to resist infections.Respiratory tract infectious diseases caused by influenza virus infection have extremely high infectivity,morbidity and mortality.The infection mechanism is relatively complicated and has not been fully ex-plained.The exuberant immune response induced by the body after influenza virus infection is described as a"cytokine storm"which is related to pro-inflammatory cytokines and tissue damage,which may eventually lead to acute lung injury.Therefore,this article sum-marizes the current research progress,focusing on the mechanism of CD4+T cells in the cytokine storm induced by influenza virus in-fection and the impact of acute lung injury,providing relevant ideas and theoretical guidance for follow-up research,with a view to the disease caused by influenza virus bring new and effective methods of diagnosis and treatment.

Influenza is an acute viral respiratory infection that has caused high morbidity and mortality worldwide. Influenza A virus (IAV) has been found to activate multiple programmed cell death pathways, including ferroptosis. Ferroptosis is a novel form of programmed cell death in which the accumulation of intracellular iron promotes lipid peroxidation, leading to cell death. However, little is known about how influenza viruses induce ferroptosis in the host cells. In this study, based on network pharmacology, we predicted the mechanism of action of Maxing Shigan decoction (MXSGD) in IAV-induced ferroptosis, and found that this process was related to biological processes, cellular components, molecular function and multiple signaling pathways, where the hypoxia inducible factor-1(HIF-1) signaling pathway plays a significant role. Subsequently, we constructed the mouse lung epithelial (MLE-12) cell model by IAV-infected in vitro cell experiments, and revealed that IAV infection induced cellular ferroptosis that was characterized by mitochondrial damage, increased reactive oxygen species (ROS) release, increased total iron and iron ion contents, decreased expression of ferroptosis marker gene recombinant glutathione peroxidase 4 (GPX4), increased expression of acyl-CoA synthetase long chain family member 4 (ACSL4), and enhanced activation of hypoxia inducible factor-1α (HIF-1α), induced nitric oxide synthase (iNOS) and vascular endothelial growth factor (VEGF) in the HIF-1 signaling pathway. Treatment with MXSGD effectively reduced intracellular viral load, while reducing ROS, total iron and ferrous ion contents, repairing mitochondrial results and inhibiting the expression of cellular ferroptosis and the HIF-1 signaling pathway. Finally, based on animal experiments, it was found that MXSGD effectively alleviated pulmonary congestion, edema and inflammation in IAV-infected mice, and inhibited the expression of ferroptosis-related protein and the HIF-1 signaling pathway in lung tissues.
Animals ; Mice ; Ferroptosis ; Network Pharmacology ; Reactive Oxygen Species ; Vascular Endothelial Growth Factor A ; Influenza A virus ; Iron ; Hypoxia