ABSTRACT
BACKGROUND: Innate/adaptive immunity is the key to anti-tumor therapy. However, its causal relationship to Gastrointestinal (GI) cancer remains unclear. METHODS: Immunity genes were extracted from the MSigDB database. The Genome-wide association studies (GWAS) summary data of GI cancer were integrated with expression quantitative trait loci (eQTL) and DNA methylation quantitative trait loci (mQTL) associated with genes. Summary-data-based Mendelian randomization (SMR) and co-localization analysis were used to reveal causal relationships between genes and GI cancer. Two-sample MR analysis was used for sensitivity analysis. Single cell analysis clarified the enrichment of genes. RESULTS: Three-step SMR analysis showed that a putative mechanism, cg17294865 CpG site regulating HLA-DRA expression was negatively associated with gastric cancer risk. HLA-DRA was significantly differentially expressed in monocyte/macrophage and myeloid cells in gastric cancer. CONCLUSION: This study provides evidence that upregulating the expression level of HLA-DRA can reduce the risk of gastric cancer.
Subject(s)
Adaptive Immunity , DNA Methylation , Gastrointestinal Neoplasms , Genome-Wide Association Study , Immunity, Innate , Mendelian Randomization Analysis , Quantitative Trait Loci , Humans , Immunity, Innate/genetics , Adaptive Immunity/genetics , Gastrointestinal Neoplasms/genetics , Gastrointestinal Neoplasms/immunology , Stomach Neoplasms/genetics , Stomach Neoplasms/immunology , HLA-DR alpha-Chains/genetics , CpG Islands/genetics , MultiomicsABSTRACT
Objective: To investigate the effects of 36 h total sleep deprivation (TSD) on object working memory by event related potential(ERP). Methods: We used a pre-post-design, sixteen healthy college students (age range: 21-28 years, mean age: 23 years) received object working memory tasks while awake and after 36 hours of TSD and simultaneously recording electroencephalograph (EEG) data while completing 2-back object working memory tasks. ERP data were statistically analyzed using repeated measurements analysis of variance to observe the changes in the working memory-related P2, N2 and P3 components. Results: After 36 h TSD, the latency of N2 waves related to object working memory significantly was prolonged (Pï¼0.05), and the amplitude was decreased, but difference did not reach statistical significance (Pï¼0.05). The latency of P2 was significantly prolonged after TSD (Pï¼0.05). There was no significant difference in the change of latency and amplitude of P3 waves (Pï¼0.05). Conclusion: 36 h of total sleep deprivation affected working memory-related components and impaired object working memory capacity.
