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南京市鼓楼区中老年居民幽门螺杆菌感染 现状及相关因素研究
引用本文:赵莹,张志红,刘杰静,白剑英,徐建军,邱勇,郭卫伟.南京市鼓楼区中老年居民幽门螺杆菌感染 现状及相关因素研究[J].中国预防医学杂志,2014,15(1):1-4.
作者姓名:赵莹  张志红  刘杰静  白剑英  徐建军  邱勇  郭卫伟
作者单位:山西医科大学公共卫生学院环境卫生学教研室,山西太原030001
基金项目:国家自然科学基金(30700655;81072261);2009年度山西省高等学校优秀青年学术带头人支持项目(晋教科20096号)
摘    要:摘要:目的 了解南京市鼓楼区中老年居民幽门螺杆菌(HP)感染现状及其危险因素,为制定正确有效的 预防措施提供依据。方法 2017年5~8月对南京市鼓楼区935例居民进行尿素14C 呼气试验测定,分析其 感染率;同时应用调查问卷开展危险因素调查,采用单因素和多因素logistic回归分析幽门螺杆菌相关危险 因素。结果 935例居民中366例(39.14%)HP阳性;单因素logistic回归分析显示有消化道疾病史、消 化道不适、是否吃辛辣和方便食品与HP感染有关(犘<0.05);多因素logistic回归模型拟合发现消化道疾 病史与HP感染负相关,而吃辛辣和方便食品与HP感染正相关(犘<0.05)。结论 南京市鼓楼区居民幽 门螺杆菌感染率较全国水平低,但感染仍普遍存在,应加强对消化道疾病的筛查与治疗,大力宣传健康安 全的饮食习惯,积极预防幽门螺杆菌感染与传播。 关键词:中老年;幽门螺杆菌;危险因素;问卷调查;流行病学研究 中图分类号:R183.4  文献标识码:A  文章编号:1009 6639 (2019)01 0001 05

关 键 词:交通相关PM2  5  凋亡  P  ERK蛋白  p-JNK蛋白  p38蛋白  JNK拮抗剂SP600125  p38拮抗  剂SB203580

Effect of MAPK signaling pathway on CEM-6T cell apoptosis induced by traffic-related PM2.5
ZHAO Ying,ZHANG Zhi hong,LIU Jie-jing,BAI Jian-ying,XU Jian-jun,QIU Yong,GUO Wei-wei.Effect of MAPK signaling pathway on CEM-6T cell apoptosis induced by traffic-related PM2.5[J].China Preventive Medicine,2014,15(1):1-4.
Authors:ZHAO Ying  ZHANG Zhi hong  LIU Jie-jing  BAI Jian-ying  XU Jian-jun  QIU Yong  GUO Wei-wei
Institution:Department of Environmental Health, School of Public Health, Shanxi Medical University, Taiyuan, Shan:xi030001, China
Abstract:ObjectiveTo explore the effect of MAPK signaling pathway on CEM-6T cell apoptosis induced by traffic related PM2.5, and to provide experimental evidence for understanding the mechanism of immunotoxic ity. Methods CEM 6T cells were exposed to PM2.5 at the doses of 0, 20, 80 and 320 mg/L for 24h or 48h. Western Blot was used to assess the effect of PM2.5 on p ERK, p-JNK and p38 inside cells. Meanwhile, the antagonists SP600125 for p JNK and SB203580 for p38 were also applied for further verification of the effect. One-way ANOVA was used for data statistical analysis. Results The p-ERK protein expression in CEM 6T cells decreased along with an increased exposure doses and time frames to traffic-related PM2.5. The lowest p-ERK protein level was noticed in cells exposed to the highest dose of 320 mg/L PM2.5 which had a significant difference compared to saline control (P〈0.05) . While, the p JNK1, p-JNK2 and p38 protein levels elevated in cells along with the increased doses of PM2.5 exposure. When cells were exposed to320 mg/L PM2.5, the differences of the above three protein levels were statistically significant compared to saline control (P-~0.0,5) . However, the addition of antagonists of p-JNK and p38 prior to the exposure could block the increases of p JNK2 and p38 protein levels, especially at the dose of 320mg/L. Conclusion Traffic related PM2.5 may induce CEM-6T cells apoptosis through the MAPK signaling pathway.
Keywords:Traffic-related PM2  5 Apoptosis p ERK p-JNK p38 Antagonist
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