Smoking has a complex impact on the immune system, affecting both innate and adaptive immunity. It can exacerbate pathogenic immune responses and attenuate defensive immunity, leading to a higher susceptibility to inf...Smoking has a complex impact on the immune system, affecting both innate and adaptive immunity. It can exacerbate pathogenic immune responses and attenuate defensive immunity, leading to a higher susceptibility to infections and certain diseases. The chemicals in cigarette smoke, such as nicotine and carbon monoxide, can alter immune cell functions and inflammatory responses. Smoking can also have long-term effects on the immune system, with some changes persisting even after quitting [1]. According to a Penn Medicine Physician, the Medical Oncologist Dr. David Porter, “People who are smokers tend to get sicker from infections”, “It may be that smoking impacts the immune system’s ability to respond appropriately”. Thus, such individuals within smoking exposure history might be considered as immunocompromised due to the altered and weakened immune system. Cigarette smoking is a prevalent habit with far-reaching health implications. Among its many adverse effects, smoking significantly alters the immune system’s functionality [1].展开更多
Currently,cigarette smoke(CS)remains a major contributor to disease morbidity and mortality.CS can be divided into cigarette mainstream smoke(CMS)and side-stream smoke,depending on where it is produced by burning toba...Currently,cigarette smoke(CS)remains a major contributor to disease morbidity and mortality.CS can be divided into cigarette mainstream smoke(CMS)and side-stream smoke,depending on where it is produced by burning tobacco^([1]).CMS is inhaled by smokers from the filter end during cigarette combustion and is strongly associated with the development of several diseases^([2-4]).展开更多
Objective: Utilizing Mendelian Randomization, this study employs Single Nucleotide Polymorphisms (SNPs) as instrumental variables to explore the causal relationships between bibulosity, smoking, and Primary Open Angle...Objective: Utilizing Mendelian Randomization, this study employs Single Nucleotide Polymorphisms (SNPs) as instrumental variables to explore the causal relationships between bibulosity, smoking, and Primary Open Angle Glaucoma (POAG). Methods: GWAS data for bibulosity, smoking, and POAG were obtained from the Social Science Genetic Association Consortium website and the IEU OpenGWAS Project website, respectively. Using a P-value threshold of −8, a linkage disequilibrium coefficient (r2) of 0.001, and a linkage disequilibrium region width of 10,000 kb, the data were aggregated, resulting in 6 SNPs for bibulosity and 253 SNPs for smoking. Three regression models, MR-Egger, Weighted Median Estimator (WME), and Random-Effects Inverse-Variance Weighted (IVW) were applied to analyze the causal impact of bibulosity and smoking on POAG. Results: The GWAS data for alcohol consumption and smoking were derived from European populations, while the GWAS data for Primary Open-Angle Glaucoma (POAG) were sourced from East Asian populations, with no gender restrictions. Analysis using three different regression models revealed that neither excessive alcohol consumption nor smoking significantly increased the risk of developing POAG. Specifically, the odds ratios with 95% confidence intervals for the alcohol consumption group were 0.854 (0.597 - 1.221) in MR-Egger regression, 0.922 (0.691 - 1.231) in WME regression, and 0.944 (0.711 - 1.252) in IVW regression. For the smoking group, the odds ratios were 1.146 (0.546 - 2.406) in MR-Egger regression, 0.850 (0.653 - 1.111) in WME regression, and 0.939 (0.780 - 1.131) in IVW regression. Given the significant heterogeneity in the SNPs associated with smoking, the focus was primarily on the results from the IVW regression model. Conclusion: Alcohol consumption and smoking are not significant risk factors for the development of POAG.展开更多
文摘目的检测PP1A与GSDME在结直肠癌组织中的表达与CD8^(+)T淋巴细胞丰度,探讨PP1A与GSDME介导焦亡的相关性和临床意义。方法应用GEPIA数据库分析PP1A与GSDME在结直肠癌组织与正常组织中mRNA的表达。采用Western blot法检测结直肠癌组织与对应癌旁正常黏膜中PP1A蛋白表达水平,运用免疫组化法检测107例结直肠癌与癌旁正常黏膜中PP1A、GSDME蛋白的表达和CD8^(+)T淋巴细胞丰度。利用Spearman等级相关性分析PP1A、GSDME和CD8^(+)T淋巴细胞丰度的相关性。结果GEPIA数据库检索显示,PP1A与GSDME的mRNA在结直肠癌组织和正常组织中的表达差异有统计学意义(P<0.05)。Western blot法检测结果显示,结直肠癌组织中PP1A相对表达量明显高于癌旁组织(0.937 vs 0.643,P<0.001)。免疫组化结果显示,结直肠癌组织中PP1A的表达明显高于正常黏膜,而GSDME的表达明显低于正常黏膜(P<0.05),GSDME表达与结直肠癌患者年龄、临床分期和错配修复蛋白密切相关(P<0.05);CD8^(+)T细胞在癌浸润前沿的分布明显高于癌旁正常黏膜,且CD8^(+)T细胞在癌组织中的分布与pT分期、临床分期及淋巴结转移相关。Spearman相关性分析显示,PP1A与GSDME表达呈负相关(r=-0.196,P<0.05)。PP1A阳性结直肠癌患者的总生存期低于PP1A阴性患者(P<0.05),患者预后与分化程度、淋巴结转移、pT分期和临床分期相关。PP1A表达、肿瘤分化程度、临床分期、pT分期和淋巴结转移均是影响结直肠癌患者预后的独立危险因素。结论PP1A在结直肠癌中高表达,与GSDME介导的细胞焦亡呈负相关,两者表达差异性与结直肠癌的发生、发展及预后均密切相关,可作为判断结直肠癌患者预后的潜在指标,CD8^(+)T细胞的差异性分布可能与GSDME介导的细胞焦亡及肿瘤的发展相关。
文摘Smoking has a complex impact on the immune system, affecting both innate and adaptive immunity. It can exacerbate pathogenic immune responses and attenuate defensive immunity, leading to a higher susceptibility to infections and certain diseases. The chemicals in cigarette smoke, such as nicotine and carbon monoxide, can alter immune cell functions and inflammatory responses. Smoking can also have long-term effects on the immune system, with some changes persisting even after quitting [1]. According to a Penn Medicine Physician, the Medical Oncologist Dr. David Porter, “People who are smokers tend to get sicker from infections”, “It may be that smoking impacts the immune system’s ability to respond appropriately”. Thus, such individuals within smoking exposure history might be considered as immunocompromised due to the altered and weakened immune system. Cigarette smoking is a prevalent habit with far-reaching health implications. Among its many adverse effects, smoking significantly alters the immune system’s functionality [1].
基金supported by the National Natural Science Foundation of China(Grant No.82060638)Academic and Technical Leaders of Major Disciplines in Jiangxi Province(Grant No.20194BCJ22032)
文摘Currently,cigarette smoke(CS)remains a major contributor to disease morbidity and mortality.CS can be divided into cigarette mainstream smoke(CMS)and side-stream smoke,depending on where it is produced by burning tobacco^([1]).CMS is inhaled by smokers from the filter end during cigarette combustion and is strongly associated with the development of several diseases^([2-4]).
文摘Objective: Utilizing Mendelian Randomization, this study employs Single Nucleotide Polymorphisms (SNPs) as instrumental variables to explore the causal relationships between bibulosity, smoking, and Primary Open Angle Glaucoma (POAG). Methods: GWAS data for bibulosity, smoking, and POAG were obtained from the Social Science Genetic Association Consortium website and the IEU OpenGWAS Project website, respectively. Using a P-value threshold of −8, a linkage disequilibrium coefficient (r2) of 0.001, and a linkage disequilibrium region width of 10,000 kb, the data were aggregated, resulting in 6 SNPs for bibulosity and 253 SNPs for smoking. Three regression models, MR-Egger, Weighted Median Estimator (WME), and Random-Effects Inverse-Variance Weighted (IVW) were applied to analyze the causal impact of bibulosity and smoking on POAG. Results: The GWAS data for alcohol consumption and smoking were derived from European populations, while the GWAS data for Primary Open-Angle Glaucoma (POAG) were sourced from East Asian populations, with no gender restrictions. Analysis using three different regression models revealed that neither excessive alcohol consumption nor smoking significantly increased the risk of developing POAG. Specifically, the odds ratios with 95% confidence intervals for the alcohol consumption group were 0.854 (0.597 - 1.221) in MR-Egger regression, 0.922 (0.691 - 1.231) in WME regression, and 0.944 (0.711 - 1.252) in IVW regression. For the smoking group, the odds ratios were 1.146 (0.546 - 2.406) in MR-Egger regression, 0.850 (0.653 - 1.111) in WME regression, and 0.939 (0.780 - 1.131) in IVW regression. Given the significant heterogeneity in the SNPs associated with smoking, the focus was primarily on the results from the IVW regression model. Conclusion: Alcohol consumption and smoking are not significant risk factors for the development of POAG.
