APE

  • 文章类型: Journal Article
    目的:这项研究的目的是检查1990年至2019年中国因颗粒物(PM2.5)污染引起的肺癌疾病负担。
    方法:来自2019年全球疾病负担研究的数据用于估计气管的疾病负担,在中国,支气管和肺癌归因于PM2.5。
    方法:将Joinpoint回归模型应用于残疾调整生命年(DALYs),以评估时间趋势并估计PM2.5对肺癌总体疾病负担的影响。此外,进行了年龄-时期-队列模型,以评估归因于PM2.5暴露的肺癌DALYs与年龄之间的关系,1990年至2019年中国的日历期和出生队列趋势。
    结果:由于固体燃料造成的家庭空气污染导致的肺癌DALYs下降,平均每年变化(AAPC)为每100,000人口2.9%,在过去的30年中,由于环境特殊物质污染(APE)而增加(AAPC:每100,000人口-4.7%)。男性的DALYs肺癌负担高于女性,它显示了年龄依赖性的增长。周期和队列效应也对APE引起的肺癌的DALYs发生率产生重大影响,表明每年所有年龄组的肺癌DALYs总体增加。
    结论:这项研究强调了需要有效的策略来减少中国的PM2.5暴露,特别是从户外来源。性别差异和年龄,研究中观察到的周期效应和队列效应为PM2.5引起的肺癌负担的长期趋势提供了有价值的见解.
    OBJECTIVE: The aim of this study was to examine the disease burden of lung cancer attributable to particulate matter (PM2.5) pollution in China from 1990 to 2019.
    METHODS: Data from the Global Burden of Disease Study 2019 were used to estimate the disease burden of tracheal, bronchus and lung cancer attributed to PM2.5 over time in China.
    METHODS: Joinpoint regression models were applied to disability-adjusted life years (DALYs) to assess the time trends and estimate the impact of PM2.5 on the overall disease burden of lung cancer. Furthermore, age-period-cohort models were conducted to assess the relationships between lung cancer DALYs attributed to PM2.5 exposure and age, calendar period and birth cohort trends in China from 1990 to 2019.
    RESULTS: Lung cancer DALYs attributable to household air pollution from solid fuels decreased with an average annual percent change (AAPC) of 2.9 % per 100,000 population, while those attributable to ambient particular matter pollution (APE) increased (AAPC: -4.7 % per 100,000 population) over the past 30 years. The burden of lung cancer in terms of DALYs in males was higher than in females, and it demonstrated an age-dependent increase. The period and cohort effects also had significant impacts on the DALYs rates of lung cancer attributable to APE, indicating an overall increase in lung cancer DALYs for all age groups in each year.
    CONCLUSIONS: This study highlights the need for effective strategies to reduce PM2.5 exposure in China, particularly from outdoor sources. Gender differences and age, period and cohort effects observed in the study provide valuable insights into long-term trends of lung cancer burden attributed to PM2.5.
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  • 文章类型: Journal Article
    OBJECTIVE: The purpose of the present study was to assess, compare, and identify factors of importance for long-term overall (OS) and disease-free (DFS) survival after conventional (cAPE) and extralevator abdominoperineal excision (ELAPE) on a nationwide basis.
    METHODS: This was a database study based on data from a nationwide colorectal cancer database. Patients undergoing surgery for rectal cancer in the period January 1, 2009 to August 31, 2012 were examined. Factors of importance for disease-free and overall survival were identified by multivariate Cox regressions.
    RESULTS: Five hundred patients were included in the final population. Two hundred seventy-six were operated by ELAPE and 224 by APE. Disease-free and overall survival did not differ between groups (4-year DFS 67 and 66 % after cAPE and ELAPE, respectively, (log-rank p = 0.82); 4-year OS 74 and 77 % after cAPE and ELAPE, respectively, (log-rank p = 0.59)). In Cox regression, the type of procedure did not affect DFS or OS. Factors of importance for DFS included increasing age, ypN-positive disease and neoadjuvant chemoradiation therapy. Factors of importance for OS included increasing age, circumferential resection margin (CRM) positivity, fixation of the tumor, blood transfusion, and increasing American Society of Anesthesiologists (ASA) score.
    CONCLUSIONS: In this nationwide study, we did not find any differences in DFS or OS after extralevator versus conventional abdominal perineal excision, and the type of procedure did not affect survival after adjusted analyses.
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  • 文章类型: Journal Article
    背景:硫氧还蛋白系统通过硫氧还蛋白和硫氧还蛋白还原酶的作用维持氧化还原平衡。硫氧还蛋白调节各种底物的活性,包括那些能抵消细胞氧化应激的.这些包括过氧化物酶,甲硫氨酸亚砜还原酶A和特异性转录因子。特别相关的是氧化还原因子-1,其进而激活其他氧化还原调节的转录因子。
    方法:讨论了人类硫氧还蛋白和硫氧还蛋白还原酶基因启动子中实验定义的转录因子结合位点以及参与调节细胞氧化还原状态的主要硫氧还蛋白系统底物的启动子。使用计算机模拟方法来鉴定所有这些启动子中这些转录因子的潜在推定结合位点。
    结论:我们的分析表明许多氧化还原基因启动子含有相同的转录因子结合位点。这些转录因子中的几个依次是氧化还原调节的。ARE存在于这些启动子中的几个中,并且在各种氧化应激刺激期间被Nrf2结合以上调基因表达。在相同的氧化应激刺激过程中,其他转录因子也与这些启动子结合,这种冗余支持了抗氧化反应的重要性。推定的转录因子位点在计算机中鉴定,结合该基因启动子的特定调控知识,可以为未来的实验提供信息。
    结论:氧化还原蛋白参与许多细胞信号通路,异常表达可导致疾病或其他病理状况。因此,理解它们的表达如何被调节对于开发靶向这些途径的治疗剂是相关的。
    BACKGROUND: The thioredoxin system maintains redox balance through the action of thioredoxin and thioredoxin reductase. Thioredoxin regulates the activity of various substrates, including those that function to counteract cellular oxidative stress. These include the peroxiredoxins, methionine sulfoxide reductase A and specific transcription factors. Of particular relevance is Redox Factor-1, which in turn activates other redox-regulated transcription factors.
    METHODS: Experimentally defined transcription factor binding sites in the human thioredoxin and thioredoxin reductase gene promoters together with promoters of the major thioredoxin system substrates involved in regulating cellular redox status are discussed. An in silico approach was used to identify potential putative binding sites for these transcription factors in all of these promoters.
    CONCLUSIONS: Our analysis reveals that many redox gene promoters contain the same transcription factor binding sites. Several of these transcription factors are in turn redox regulated. The ARE is present in several of these promoters and is bound by Nrf2 during various oxidative stress stimuli to upregulate gene expression. Other transcription factors also bind to these promoters during the same oxidative stress stimuli, with this redundancy supporting the importance of the antioxidant response. Putative transcription factor sites were identified in silico, which in combination with specific regulatory knowledge for that gene promoter may inform future experiments.
    CONCLUSIONS: Redox proteins are involved in many cellular signalling pathways and aberrant expression can lead to disease or other pathological conditions. Therefore understanding how their expression is regulated is relevant for developing therapeutic agents that target these pathways.
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