2017年浙江省杭州市拱墅区登革热暴发疫情调查分析

目的调查2017年浙江省杭州市拱墅区登革热暴发疫情情况及原因，为今后开展登革热防控工作提供参考和依据。方法通过对社区、医院进行主动搜索，对2017年杭州市拱墅区登革热病例进行流行病学个案调查，掌握病例的临床表现、流行病学资料，并对疫情暴发原因进行分析。结果本次疫情共报告登革热病例327例，发病高峰为8月21日至9月15日，病例主要集中分布在运河沿线的4个街道，以＞50岁人员为主，占全部病例的61.16%，职业以离退人员（123例，占37.61%）及家务及待业（76例，占23.24%）为主。 病例发病到诊断时间间隔平均为5.20 d，其中住院病例为3 d（2 ~ 5 d），非住院病例为5 d（3 ~ 7 d），两者差异有统计学意义（Ζ＝6.383，P＜0.001）。结论本次暴发疫情可能是由登革热输入病例或隐性感染者引起的本地传播，建议加强医疗机构登革热诊断水平，提高登革热监测敏感性，长效运行登革热“网格区域责任制”，确保及早发现和控制疫情。     

p16、DAPK和RARβ基因启动子CpG岛甲基化与非小细胞肺癌临床特征的关系

目的 研究非小细胞肺癌(non-smal celllung cancer,NSCLC)患者p16、DAPK和RARβ启动子区CpG岛甲基化对临床特征的影响,探讨其与吸烟的关系.方法 应用甲基化特异性PCR检测200例原发性NSCLC组织和相应正常组织中p16,DAPK和RARβ基因启动子区CpG岛甲基化状况.结果 p16、DAPK和RARβ基因甲基化在癌组织中的检出率分别为51.0%、60.0%和58.0%,均高于其在正常组织中的检出率(分别为12.5%,11.5%和15.0%;P＜0.05).非条件Logistic回归显示,癌组织p16基因甲基化与年龄和病例组织类型有关(P＜0.05);癌组织DAPK基因甲基化与年龄、性别、临床分类有关(P＜0.05);而癌组织RARβ基因甲基化与临床分类和TNM(tumor node metastasis)分期相关(P＜0.05).癌组织p16基因甲基化与DAPK基因甲基化之间存在交互作用(OR=1.987,95%CI:1.055～3.743).吸烟者癌组织p16和DAPK基因甲基化的OR值分别为3.139(95%CI:1.046～9.419)和3.585(95%CI:1.270～10.123),未发现癌组织RARβ基因甲基化与吸烟有关.结论 p16,DAPK和RARβ甲基化与NSCIC患者临床特征关系密切.吸烟与p16和DAPK基因甲基化有关.

Abstract：

Objective To investigate the effects of promoter methylation of p16 , death-associated protein kinase (DAPK) and retinoic acid receptor-β (RARβ) genes on clinical data in non-small cell lung cancers, and to study the effect of smoking on the risk of gene methylation. Methods The promoter methylation of p16 , DAPK and RARβ genes in 200 primary non-small cell lung cancers and the corresponding nonmalignant lung tissues were determined by methylation-specific PCR. Results Methylation in the tumor tissues was detected in 51.0% for p16 , 60.0% for DAPK, and 58. 0% for RARβ gene, with significant differences (P ＜ 0. 05) when compared with those in the corresponding nonmalignant tissues (12. 5%,11.5% and 15.0%) respectively. p16 gene methylation in tumor tissue was associated with age significantly in unconditional logistic regression analysis (P＜0.01) and histologic type (P＜0. 05). DAPK gene methylation in tumor tissue was associated significantly with age (P＜0. 05), gender (P＜0.05) and clinical type (P＜ 0.05 ). RARβ gene methylation in tumor tissue was associated with clinical type (P＜0. 05) and tumor stage (P＜0. 05) significantly. The interaction odds ratio (OR) for the gene-gene interaction in tumor tissue between p16 and DAPK was 1. 987 (95%CI: 1. 055-3. 743). The results of the gene-smoking analyses revealed that a relationship existed between cigarette smoking and p16 gene methylation (OR= 3. 139, 95 % CI: 1. 046-9. 419), the OR for the relationship of DAPK gene methylation and cigarette smoking was 3. 585(95%CI: 1. 270-10. 123)in tumor tissue. The RARβ gene methylation did not differ based on the smoking status of patients in tumor tissue. Conclusion Thep16 , DAPK and RARβ genes methylation are strongly associated with clinical data of non-small cell lung cancer, and methylation of p16 and DAPK genes are associated with tobacco smoking.