Analysis of the Relation Between Periodontitis and Chronic Gastritis/Peptic Ulcer: A Cross-Sectional Study Using KoGES HEXA Data
牙周炎与慢性胃炎/消化性溃疡的关系分析: 一项使用 KoGES HEXA 数据的横断面研究
- 作者列表："Soo Hwan Byun","Chanyang Min","Seok Jin Hong","Hyo Geun Choi","Dong Hee Koh
The aim of the present study was to investigate the association between periodontitis and chronic gastritis/peptic ulcer using a cross-sectional study design. The present prospective cohort study used epidemiological data from the Korean Genome and Epidemiology Study (KoGES) recorded from 2004 to 2016. Among 173,209 participants, 9983 with periodontitis and 125,336 with no periodontitis were selected. Histories of chronic gastritis and peptic ulcer between periodontitis and no periodontitis participants were analyzed. The participants were questioned around any history of hypertension, diabetes mellitus, hyperlipidemia, cerebral stroke, ischemic heart disease, periodontitis, body mass index, smoking, alcohol consumption, nutritional intake, and financial income. Chi-square tests, independent t-tests, two-tailed analyses were used in statistical analysis of the data. The adjusted odds ratio of chronic gastritis was 2.22 (95% confidence interval [CI] = 2.10–2.34, p < 0.001) and that of peptic ulcer was 1.86 (95% CI = 1.74–1.98, p < 0.001) in model 2. This study demonstrated that periodontitis was associated with an increased risk of chronic gastritis/peptic ulcer. These findings provide additional evidence for an association between periodontitis and chronic gastritis/peptic ulcer.
本研究的目的是采用横断面研究设计，调查牙周炎与慢性胃炎/消化性溃疡之间的关系。本前瞻性队列研究使用了 2004 年至 2016 年记录的韩国基因组流行病学学研究 (KoGES) 的流行病学数据。在 173,209 名参与者中，选择 9983 名牙周炎患者和 125,336 名无牙周炎患者。分析牙周炎与无牙周炎患者的慢性胃炎和消化性溃疡病史。询问参与者是否有高血压、糖尿病、高脂血症、脑中风、缺血性心脏病、牙周炎、体重指数、吸烟、饮酒、营养摄入和经济收入。数据统计分析采用卡方检验、独立t检验、双尾分析。慢性胃炎的校正优势比为 2.22 (95% 置信区间 [CI] = 2.10-2.34，p <0.001)，消化性溃疡的校正优势比为 1.86 (95% CI = 1.74-1.98，p <0.001) 在模型 2。本研究表明，牙周炎与慢性胃炎/消化性溃疡的风险增加有关。这些发现为牙周炎和慢性胃炎/消化性溃疡之间的相关性提供了额外的证据。
METHODS::Diffuse gastric cancer (DGC) is a lethal malignancy lacking effective systemic therapy. Among the most provocative recent results in DGC has been that the alter of the cellular cytoskeleton and intercellular adhesion. CD2-associated protein (CD2AP) is one of the critical proteins regulating cytoskeleton assembly and intercellular adhesion. However, no study has investigated the expression and biological significance of CD2AP in gastric cancer (GC) to date. Therefore, the aim of our study was to explore if the expression of CD2AP is associated with any clinical features of GC and to elucidate the underlying mechanism. Immunohistochemistry of 620 patient tissue samples indicated that the expression of CD2AP is downregulated in DGC. Moreover, a low CD2AP level was indicative of poor patient prognosis. In vitro, forced expression of CD2AP caused a significant decrease in the migration and invasion of GC cells, whereas depletion of CD2AP had the opposite effect. Immunofluorescence analysis indicated that CD2AP promoted cellular adhesion and influenced cell cytoskeleton assembly via interaction with the F-actin capping protein CAPZA1. Overall, the upregulation of CD2AP could attenuate GC metastasis, suggesting CD2AP as a novel biomarker for the prognosis and treatment of patients with GC.
METHODS::Aim: To identify the methylated-differentially expressed genes (MDEGs) that may serve as diagnostic markers and therapeutic targets in Epstein-Barr virus-associated gastric cancer (EBVaGC) and to explore the methylation-based pathways for elucidating biological mechanisms of EBVaGC. Materials & methods: Gene expression and methylation profiles were downloaded from GEO database. MDEGs were identified by GEO2R. Pathway enrichment analyses were conducted based on DAVID database. Hub genes were identified by Cytoscape, which were further verified by The Cancer Genome Atlas database. Results: A total of 367 hypermethylated, lowly expressed genes were enriched in specific patterns of cell differentiation. 31 hypomethylated, highly expressed genes demonstrated enrichment in regulation of immune system process. After validation using The Cancer Genome Atlas database, seven genes were confirmed to be significantly different hub genes in EBVaGC. Conclusion: EBVaGC-specific MDEGs and pathways can be served as potential biomarkers for precise diagnosis and treatment of EBVaGC and provide novel insights into the mechanisms involved.
METHODS:Gastric adenocarcinoma, like other cancers, is a multifactorial genetic disease, andmetastasis of cancer cells is one of the main features of this illness. The expressionlevels of the CFL1 gene have been modulated in this pathway. Using small interferingRNA (siRNA) in the treatment of gastric cancer is considered a hopeful genetherapeutic approach. The present study reported the level of CFL1 genes betweentumor and margin and healthy tissue of gastric cancer. Also, the features of a cationicnanoparticle with a polymer coating containing polyacrylic acid and polyethylenei-mine that were used in the delivery of CFL1 siRNA, were shown. Then thecytotoxicity, cellular uptake, and gene silencing efficiency of this nanoparticle wereevaluated with CFL1siRNA. Method:In this study, the CFL1 gene expression was measured in 40 gastricadenocarcinoma, marginal and 15 healthy biopsy samples by a real‐time polymerasechain reaction. Physicochemical characteristics, apoptosis, and inhibition of migrationof the delivery of CFL1 siRNA by nanoparticle and lipofectamine were investigated ingastric cancer cells. Result:The CFL1 expression was remarkably increased in gastric cancer tissues incomparison with the marginal samples and normal tissues (p< .05) and the biomarkerindex for CFL1 was obtained as 0.94, then this gene can be probably used as abiomarker for gastric cancer. After treatment of the AGS cell line by CFL1 siRNA, theCFL1 expression level of mRNA and migration in AGS cells were remarkablysuppressed after transfection. Furthermore, the amount of apoptosis increased(p< .05). Conclusion:Our results demonstrated that CFL1 downregulation in AGS cells caninterdict cell migration. Finally, our outcomes propose that CFL1 can function as anoncogenic gene in gastric cancer and would be considered as a potential purpose ofgene therapy for gastric cancer treatment