OBJECTIVES: Nasopharyngeal carcinoma is often diagnosed at a late stage due to its concealed location and exhibits marked regional clustering, posing a significant public health challenge in China. This study aims to analyze the disease burden of nasopharyngeal carcinoma in China using the latest 2021 Global Burden of Diseases (GBD) database, providing epidemiological evidence for precise prevention and control of nasopharyngeal carcinoma. METHODS: Age-standardized incidence rate (ASIR), mortality rate, and disability-adjusted life year (DALY) rate were used as indicators of disease burden. Stratified analyses were conducted by age, sex, socio-demographic index (SDI), and relevant risk factors. The autoregressive integrated moving average (ARIMA) model and Bayesian age-period-cohort (BAPC) model were employed to project ASIR trends through 2050. RESULTS: In 2021, China's age-standardized incidence, mortality, and DALY rates of nasopharyngeal carcinoma were 3.4/100 000, 1.5/100 000, and 48.7/100 000, respectively, all higher than the global average. Across all age groups, Chinese males exhibited higher ASIR, mortality, and DALY rates than females. From 1990 to 2021, the disease burden of nasopharyngeal carcinoma in China decreased gradually with rising SDI. The proportion of nasopharyngeal carcinoma burden attributed to alcohol consumption, smoking, and occupational formaldehyde exposure in China exceeded global levels, especially among males. Projections from both models indicate a rising trend in ASIR for males, females, and the general population in China and globally from 2022 to 2050. CONCLUSIONS Over the past 30 years, the disease burden of nasopharyngeal carcinoma in China has decreased with the increasing SDI values but remains higher than the global average. Furthermore, ASIR is projected to increase over the next 30 years. It is imperative for China to enhance healthcare resource allocation for nasopharyngeal carcinoma prevention, diagnosis, and treatment, particularly among high-risk male populations.
Humans ; China/epidemiology* ; Male ; Nasopharyngeal Carcinoma/mortality* ; Female ; Middle Aged ; Nasopharyngeal Neoplasms/mortality* ; Adult ; Incidence ; Global Burden of Disease ; Disability-Adjusted Life Years ; Aged ; Risk Factors ; Adolescent ; Databases, Factual ; Young Adult ; Cost of Illness ; Child ; Bayes Theorem

Objective:To investigate the effects of the novel oral edaravone(EDA)on rats with diabetic encepha-lopathy(DE).Methods:The network pharmacology research methodology was employed to elucidate the mechanism of action of oral EDA in the treatment of diabetes mellitus,identify intersecting targets,and conduct initial validation of these findings in vivo.Thirty male SD rats were randomly assigned to three groups:A normal control(control)group,a diabetic encephalopathy DE(DE)group,and an oral edaravone treatment(DE+EDA)group.Diabetic encephalop-athy was induced in both the DE and DE+EDA groups using the streptozotocin(STZ)method.After successful model-ing,the DE+EDA group received oral administration of EDA,while the other two groups were administered equal doses of saline as controls.Serum samples were examined for lipid release rate,and the protein expression levels of oxidative stress factor 3-nitrotyrosine(3-NT)and apoptotic factor cysteinyl aspartate specific proteinase-3(caspase-3)in brain tissues were detected by Western blot.Brain samples were stained with HE staining to observe the pathological changes.Histopathological changes were observed through hematoxylin-eosin(HE)staining.Results:Network pharmacological analysis yielded 27 core targets,and functional annotation of gene bioprocesses showed that the intersecting targets were mainly enriched in response to oxidative stress and neuronal apoptosis.Serum-related lipid assay showed that the DE+EDA group had significantly improved lipid metabolism disorders compared with the DE group.Additionally,expression levels of 3-NT and caspase-3 were significantly higher in the DE group when compared with controls(P＜0.05);How-ever,both markers exhibited a significant decrease within the DE+EDA treatment cohort as opposed to their counter-parts in the DE group(P＜0.05).HE staining showed that in DE group the cellular arrangement was disordered,the cells were shrunk with intact plasma membrane,and the nuclei were condensed showing karyopyknosis,fragmented and dissolved.Compared with the DE group,the brain tissue in the DE+EDA group was relatively dense and neatly ar-ranged,and the cell karyopyknosis,fragmentation and lysis were significantly improved.Conclusion:Both network pharmacology and in vivo experiments provide preliminary evidence that oral EDA reduces damage in diabetic encepha-lopathy rats.

Objective:To investigate the effects of the novel oral edaravone(EDA)on rats with diabetic encepha-lopathy(DE).Methods:The network pharmacology research methodology was employed to elucidate the mechanism of action of oral EDA in the treatment of diabetes mellitus,identify intersecting targets,and conduct initial validation of these findings in vivo.Thirty male SD rats were randomly assigned to three groups:A normal control(control)group,a diabetic encephalopathy DE(DE)group,and an oral edaravone treatment(DE+EDA)group.Diabetic encephalop-athy was induced in both the DE and DE+EDA groups using the streptozotocin(STZ)method.After successful model-ing,the DE+EDA group received oral administration of EDA,while the other two groups were administered equal doses of saline as controls.Serum samples were examined for lipid release rate,and the protein expression levels of oxidative stress factor 3-nitrotyrosine(3-NT)and apoptotic factor cysteinyl aspartate specific proteinase-3(caspase-3)in brain tissues were detected by Western blot.Brain samples were stained with HE staining to observe the pathological changes.Histopathological changes were observed through hematoxylin-eosin(HE)staining.Results:Network pharmacological analysis yielded 27 core targets,and functional annotation of gene bioprocesses showed that the intersecting targets were mainly enriched in response to oxidative stress and neuronal apoptosis.Serum-related lipid assay showed that the DE+EDA group had significantly improved lipid metabolism disorders compared with the DE group.Additionally,expression levels of 3-NT and caspase-3 were significantly higher in the DE group when compared with controls(P＜0.05);How-ever,both markers exhibited a significant decrease within the DE+EDA treatment cohort as opposed to their counter-parts in the DE group(P＜0.05).HE staining showed that in DE group the cellular arrangement was disordered,the cells were shrunk with intact plasma membrane,and the nuclei were condensed showing karyopyknosis,fragmented and dissolved.Compared with the DE group,the brain tissue in the DE+EDA group was relatively dense and neatly ar-ranged,and the cell karyopyknosis,fragmentation and lysis were significantly improved.Conclusion:Both network pharmacology and in vivo experiments provide preliminary evidence that oral EDA reduces damage in diabetic encepha-lopathy rats.

Objective:To analyze the differentially expressed genes in esophageal squamous cell carcinoma (ESCC) by bioinformatics method, to screen the key genes related to the carcinogenesis and development of ESCC and to find out biomarkers for early diagnosis and prognosis of ESCC.Methods:The ESCC microarray datasets GSE26886, GSE77861, GSE100942, GSE20347, GSE23400, GSE38129 and GSE17351 from gene expression omnibus datasets were downloaded. The differentially expressed genes in ESCC and normal esophageal mucosa tissues of each dataset were screened out, and then the common differentially expressed key genes of seven dataset were selected out. After that, the key differentially expressed genes were analyzed by gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway. Cytoscape software and molecular complex detection were used for protein-protein interaction network (PPI), and the critical hub genes were screened out. The expression of hub genes was divided into high-expression group and low-expression group. The relationship between hub genes and the prognosis of patients with ESCC was analyzed by Kaplan-Meier database.Results:A total of 626 differentially expressed key genes of ESCC were screened out from the seven datasets, including 302 up-regulated genes and 324 down-regulated genes. The results of GO analysis showed that the key differentially expressed genes were mainly involved in collagen binding, regulation of cell cycle and epithelial cell differentiation.The results of KEGG analysis indicated that the differentially expressed genes were focused on extracellular matrix-receptor interaction, p53 signaling pathway and arachidonic acid metabolism signaling pathway. Five hub genes were screened out from PPI, which were collagen type Ⅲ α1 chain ( COL3 A1), collagen type Ⅹ α1 chain ( COL10 A1), collagen type Ⅵ α3 chain ( COL6 A3), collagen type Ⅴ α2 chain ( COL5 A2) and collagen type Ⅰ α1 chain ( COL1 A1). The expression levels of COL3 A1, COL10 A1, COL6 A3, COL5 A2 and COL1 A1 in ESCC tissues were higher than those of normal esophageal mucosa tissues. The prognosis of high-expression group was worse than that of low-expression group. Conclusions:There are differentially expressed genes profiles between ESCC tissues and normal mucosa tissues. COL3 A1, COL10 A1, COL6 A3, COL5 A2 and COL1 A1 are key genes in the genesis and development of ESCC and also related to the prognosis of the patients, which may be new molecular markers for the diagnosis and treatment of ESCC.