Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5391
F. Dako, Huaqing Zhao, Alexandra Mulvenna, Seen Gupta, S. Simpson, F. Kueppers
Introduction: Alpha-1-antitrypsin deficiency (AATD), better known for its lung and liver disease manifestations, has also been linked to aneurysmal disease arising from increased elastin breakdown. Aim: To investigate the relationship between AATD and ascending aortic distention. Methods: This was a retrospective cohort study performed at a tertiary academic centre. Patients with computed tomography (CT) scans and panlobular emphysema due to AATD (AATD group) or non-AATD-associated emphysema (control group) were identified and patient demographics, including age and sex, were recorded. The diameter of the mid ascending aorta was measured from outer wall to outer wall using non-gated axial CT scans, with or without contrast. Mean diameter for each group was calculated and compared using a two-sample t-test. Pearson’s correlation coefficient was used to determine the relationship between ascending aortic diameter and age. Results: Patients with AATD (n=51) were approximately 10 years younger than those in the control group (n=96; mean age: 55±9.5 vs 65±7.2 years, respectively). There was no difference in mean aortic diameter (3.34±0.43 vs 3.37±0.39 cm; p=0.68), and no within gender difference in diameter (males: 3.49±0.45 vs 3.5±0.39 cm, p=0.9; females: 3.14±0.32 vs 3.18±0.31 cm, p=0.68) between the AATD and control groups, respectively. Aortic diameter significantly increased with age in the AATD group (r=0.43, p=0.0016); a relationship that was not seen in the control group (r=0.16; p=0.11). Conclusions: To the best of our knowledge, this is the first controlled study to assess the relationship between AATD and ascending aortic diameter, and suggests AATD is associated with accelerated aortic wall degeneration.
引言：α-1-抗胰蛋白酶缺乏症（AATD）以其肺部和肝脏疾病表现而闻名，也与弹性蛋白分解增加引起的动脉瘤性疾病有关。目的：探讨AATD与升主动脉扩张的关系。方法：这是一项在高等教育中心进行的回顾性队列研究。对因AATD（AATD组）或非AATD相关肺气肿（对照组）引起的计算机断层扫描（CT）扫描和全小叶肺气肿的患者进行了识别，并记录了患者的人口统计数据，包括年龄和性别。使用非门控轴向CT扫描从外壁到外壁测量升主动脉中部的直径，无论是否进行对比。计算各组的平均直径，并使用双样本t检验进行比较。Pearson相关系数用于确定升主动脉直径与年龄之间的关系。结果：AATD患者（n=51）比对照组（n=96；平均年龄分别为55±9.5和65±7.2岁）年轻约10岁。AATD组和对照组的平均主动脉直径无差异（3.34±0.43 vs 3.37±0.39 cm；p=0.68），直径无性别差异（男性：3.49±0.45 vs 3.5±0.39厘米，p=0.9；女性：3.14±0.32 vs 3.18±0.31厘米，p＝0.68）。AATD组的主动脉直径随着年龄的增长而显著增加（r=0.43，p=0.0016）；在对照组中没有发现这种关系（r=0.16；p=0.11）。结论：据我们所知，这是第一项评估AATD与升主动脉直径之间关系的对照研究，并表明AATD与加速主动脉壁退化有关。
{"title":"Relationship between alpha-1-antitrypsin deficiency and ascending aortic distention","authors":"F. Dako, Huaqing Zhao, Alexandra Mulvenna, Seen Gupta, S. Simpson, F. Kueppers","doi":"10.1183/13993003.congress-2019.pa5391","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5391","url":null,"abstract":"Introduction: Alpha-1-antitrypsin deficiency (AATD), better known for its lung and liver disease manifestations, has also been linked to aneurysmal disease arising from increased elastin breakdown. Aim: To investigate the relationship between AATD and ascending aortic distention. Methods: This was a retrospective cohort study performed at a tertiary academic centre. Patients with computed tomography (CT) scans and panlobular emphysema due to AATD (AATD group) or non-AATD-associated emphysema (control group) were identified and patient demographics, including age and sex, were recorded. The diameter of the mid ascending aorta was measured from outer wall to outer wall using non-gated axial CT scans, with or without contrast. Mean diameter for each group was calculated and compared using a two-sample t-test. Pearson’s correlation coefficient was used to determine the relationship between ascending aortic diameter and age. Results: Patients with AATD (n=51) were approximately 10 years younger than those in the control group (n=96; mean age: 55±9.5 vs 65±7.2 years, respectively). There was no difference in mean aortic diameter (3.34±0.43 vs 3.37±0.39 cm; p=0.68), and no within gender difference in diameter (males: 3.49±0.45 vs 3.5±0.39 cm, p=0.9; females: 3.14±0.32 vs 3.18±0.31 cm, p=0.68) between the AATD and control groups, respectively. Aortic diameter significantly increased with age in the AATD group (r=0.43, p=0.0016); a relationship that was not seen in the control group (r=0.16; p=0.11). Conclusions: To the best of our knowledge, this is the first controlled study to assess the relationship between AATD and ascending aortic diameter, and suggests AATD is associated with accelerated aortic wall degeneration.","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"1 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41849228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5392
D. Naumov, O. Kotova, D. Gassan, E. Afanas'eva, J. Perelman, V. Kolosov
Background: Airway hyperresponsiveness (AHR) to osmotic stimuli is common and clinically relevant in asthma. AQP5 is a membrane water channel that may be functionally implicated in airway inflammation and hypersecretion. Objectives: The aim was to assess the effect of AQP5 SNPs on osmotic AHR in asthma patients. Methods: The study enrolled 274 patients with mild-to-moderate asthma, mean age 36.2±0.67 years. The patients underwent bronchoprovocation with 3-min inhalation of distilled water (hypoosmotic stimulus) and hypertonic saline aerosol (hyperosmotic stimulus). Lung function was measured by spirometry before and after each challenge. AQP5 SNPs (rs3759129, rs3736309, rs296756, rs1964676) were genotyped by LATE-PCR. Results: Association with hypoosmotic AHR was found for rs3759129 and rs296756. C allele of rs3759129 was protective against hypoosmotic AHR as AC heterozygotes had less profound response to the challenge compared to AA carriers (ΔFEV1 -1.4 (-6.3; 2.33)% vs. -5.4 (-12.0; -1.0)%, p=0.001; ΔFEF25-75 -1.0 (-18.0; 14.0)% vs. -9.1 (-21.1; 1.2)%, p=0.009). G allele of rs296756 in homozygous state also had protective effect. AA and AG (but not GG) carriers showed marked reduction in airway patency (ΔFEV1 -5,5 (-12,0; -0,8)% vs. -0,2 (-4,5; 3,4)%, p=0.004; ΔFEF25-75 -9,6 (-22,0; 2,3)% vs. 2,0 (-8,9; 9,0)%, p=0.008, for AA and GG genotypes, respectively). rs3759129 also influenced hyperosmotic AHR: all patients with the AHR had AA genotype while 27% of patients without the AHR had AC genotype (p=0.006). Conclusions:AC genotype of rs3759129 and GG genotype of rs296756 exert a protective effect on hypoosmotic AHR. AC genotype of rs3759129 also protects asthma patients from hyperosmotic AHR.
{"title":"Association of AQP5 gene polymorphisms with osmotic airway hyperresponsiveness in asthma","authors":"D. Naumov, O. Kotova, D. Gassan, E. Afanas'eva, J. Perelman, V. Kolosov","doi":"10.1183/13993003.congress-2019.pa5392","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5392","url":null,"abstract":"Background: Airway hyperresponsiveness (AHR) to osmotic stimuli is common and clinically relevant in asthma. AQP5 is a membrane water channel that may be functionally implicated in airway inflammation and hypersecretion. Objectives: The aim was to assess the effect of AQP5 SNPs on osmotic AHR in asthma patients. Methods: The study enrolled 274 patients with mild-to-moderate asthma, mean age 36.2±0.67 years. The patients underwent bronchoprovocation with 3-min inhalation of distilled water (hypoosmotic stimulus) and hypertonic saline aerosol (hyperosmotic stimulus). Lung function was measured by spirometry before and after each challenge. AQP5 SNPs (rs3759129, rs3736309, rs296756, rs1964676) were genotyped by LATE-PCR. Results: Association with hypoosmotic AHR was found for rs3759129 and rs296756. C allele of rs3759129 was protective against hypoosmotic AHR as AC heterozygotes had less profound response to the challenge compared to AA carriers (ΔFEV1 -1.4 (-6.3; 2.33)% vs. -5.4 (-12.0; -1.0)%, p=0.001; ΔFEF25-75 -1.0 (-18.0; 14.0)% vs. -9.1 (-21.1; 1.2)%, p=0.009). G allele of rs296756 in homozygous state also had protective effect. AA and AG (but not GG) carriers showed marked reduction in airway patency (ΔFEV1 -5,5 (-12,0; -0,8)% vs. -0,2 (-4,5; 3,4)%, p=0.004; ΔFEF25-75 -9,6 (-22,0; 2,3)% vs. 2,0 (-8,9; 9,0)%, p=0.008, for AA and GG genotypes, respectively). rs3759129 also influenced hyperosmotic AHR: all patients with the AHR had AA genotype while 27% of patients without the AHR had AC genotype (p=0.006). Conclusions:AC genotype of rs3759129 and GG genotype of rs296756 exert a protective effect on hypoosmotic AHR. AC genotype of rs3759129 also protects asthma patients from hyperosmotic AHR.","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49175845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5389
Leila Karimi, L. Lahousse, M. Ghanbari, N. Terzikhan, A. Uitterlinden, J. Lei, G. Brusselle, B. Stricker, K. Verhamme
{"title":"ADRB2 polymorphisms and risk of COPD exacerbations: the Rotterdam Study","authors":"Leila Karimi, L. Lahousse, M. Ghanbari, N. Terzikhan, A. Uitterlinden, J. Lei, G. Brusselle, B. Stricker, K. Verhamme","doi":"10.1183/13993003.congress-2019.pa5389","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5389","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46135156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5398
M. D. Vries, J. Vonk, M. Boezen
Introduction: Genome wide association studies (GWAS) have identified genetic variants associated with the presence of airway obstruction and COPD. These cross-sectional studies did not do justice to the fact that different paths can lead to COPD development. One path is accelerated lung function decline in adulthood, which may be influenced by genetic make-up and smoking. In this study, we aimed to identify genetic variants and gene-by-smoking interactions with lung function decline in the general population based LifeLines cohort study. Methods: We performed a GWAS on FEV1 decline after age 30 in 8,274 Lifelines subjects. Annual FEV1 decline was defined over 4.5 years of follow up. The analysis was adjusted for age, gender, height and smoking status at baseline. Additionally, a SNP-by-smoking interaction study (GWIS) was performed, with similar adjustments. Results: We found 73 variants in 15 genetic loci significantly associated with FEV1 decline (p Conclusion: We identified novel genetic variants associated with FEV1 decline in a large homogeneous cohort. Investigation of the gene-by-smoking interaction resulted in the identification of other novel genetic variants. All variants have not been identified in previous studies on FEV1 decline, indicating that this phenotype is very heterogeneous.
{"title":"Genetic variants and lung function decline in the LifeLines cohort study","authors":"M. D. Vries, J. Vonk, M. Boezen","doi":"10.1183/13993003.congress-2019.pa5398","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5398","url":null,"abstract":"Introduction: Genome wide association studies (GWAS) have identified genetic variants associated with the presence of airway obstruction and COPD. These cross-sectional studies did not do justice to the fact that different paths can lead to COPD development. One path is accelerated lung function decline in adulthood, which may be influenced by genetic make-up and smoking. In this study, we aimed to identify genetic variants and gene-by-smoking interactions with lung function decline in the general population based LifeLines cohort study. Methods: We performed a GWAS on FEV1 decline after age 30 in 8,274 Lifelines subjects. Annual FEV1 decline was defined over 4.5 years of follow up. The analysis was adjusted for age, gender, height and smoking status at baseline. Additionally, a SNP-by-smoking interaction study (GWIS) was performed, with similar adjustments. Results: We found 73 variants in 15 genetic loci significantly associated with FEV1 decline (p Conclusion: We identified novel genetic variants associated with FEV1 decline in a large homogeneous cohort. Investigation of the gene-by-smoking interaction resulted in the identification of other novel genetic variants. All variants have not been identified in previous studies on FEV1 decline, indicating that this phenotype is very heterogeneous.","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48242978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5397
L. Horsfall, S. Burgess, I. Hall, I. Nazareth
Introduction: Levels of serum oxidants and antioxidants depend on genetic factors and environmental exposures, which may influence respiratory health. Aims and Objectives: We examined factors linked with oxidant-antioxidant balance and their relative relationship with lung function in a large cross-sectional sample of the UK population. Material and Methods: This research used unrelated participants of European ancestry from the UK Biobank Resource. Serum bilirubin is a strong endogenous antioxidant and people homozygous for the T allele of rs887829 have levels approximately twice as high as those without this genotype. We examined the relationship between rs887829 and lung function (FEV1 and FVC) using multivariable linear regression. We also examined environmental variables linked to oxidant-antioxidant balance and tested for interactions with rs887829. The analyses were adjusted for conventional risk factors. Results: We included 267222 participants (124170 men, average age 57 years). Increased fruit/vegetable intake, antioxidant supplements and lower pollution levels (PM10) were independently associated with improved FEV1 (p Conclusions: The results do not support serum bilirubin as a therapeutic target but do emphasise the importance of encouraging healthy diets and improving policies to reduce pollution exposure. Wellcome Trust funded: 209207/Z/17/Z
{"title":"Genetic and environmental factors linked with oxidant-antioxidant balance and their relationship with respiratory health in UK Biobank","authors":"L. Horsfall, S. Burgess, I. Hall, I. Nazareth","doi":"10.1183/13993003.congress-2019.pa5397","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5397","url":null,"abstract":"Introduction: Levels of serum oxidants and antioxidants depend on genetic factors and environmental exposures, which may influence respiratory health. Aims and Objectives: We examined factors linked with oxidant-antioxidant balance and their relative relationship with lung function in a large cross-sectional sample of the UK population. Material and Methods: This research used unrelated participants of European ancestry from the UK Biobank Resource. Serum bilirubin is a strong endogenous antioxidant and people homozygous for the T allele of rs887829 have levels approximately twice as high as those without this genotype. We examined the relationship between rs887829 and lung function (FEV1 and FVC) using multivariable linear regression. We also examined environmental variables linked to oxidant-antioxidant balance and tested for interactions with rs887829. The analyses were adjusted for conventional risk factors. Results: We included 267222 participants (124170 men, average age 57 years). Increased fruit/vegetable intake, antioxidant supplements and lower pollution levels (PM10) were independently associated with improved FEV1 (p Conclusions: The results do not support serum bilirubin as a therapeutic target but do emphasise the importance of encouraging healthy diets and improving policies to reduce pollution exposure. Wellcome Trust funded: 209207/Z/17/Z","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43796139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5390
D. V. D. Plaat, C. Minelli, D. Jarvis, J. Garcia-Aymerich, F. Gómez-Real, B. Leynaert
Polycystic ovary syndrome (PCOS) affects between 5-20% of women. Oligomenorrhea (long and/or irregular cycles) is a common PCOS symptom and has been associated with lower forced vital capacity (FVC). We aimed to estimate the effect of PCOS on lung function using Mendelian randomization (MR), an approach that uses genetic variants as proxies to overcome confounding and reverse causation. We used an inverse variance-weighted (IVW) MR method to estimate the causal effect of PCOS on spirometric restriction (FVC The MR estimate shows that PCOS is associated with a 10% higher risk of spirometric restriction (OR 1.10 [1.05 to 1.15]), with no indication of pleiotropy (Q test P= 0.86; I2= 0). Estimates were similar when using MR methods adjusting for pleiotropy and when limiting the analysis to non-asthmatics (OR 1.12 [1.06 to 1.18]) or SNPs significant in European women (OR 1.10 [1.04 to 1.16]). Effect estimates were similar in normal weight and overweight (>26 kg/m2) women (interaction P=0.89). There was no association between PCOS and airflow obstruction (OR 0.98 [0.94 to 1.02]). Our MR results suggest that PCOS increases the risk of spirometric restriction. Further studies are needed to investigate the possible underlying mechanism. (ALEC, EU Grant #633212)
多囊卵巢综合征(PCOS)影响了5-20%的女性。月经少(长周期和/或不规则周期)是PCOS的常见症状，并与较低的用力肺活量(FVC)有关。我们的目的是使用孟德尔随机化(MR)来估计PCOS对肺功能的影响，这是一种使用遗传变异作为替代来克服混杂和反向因果关系的方法。我们使用逆方差加权(IVW) MR方法来估计PCOS对肺活量限制(FVC)的因果关系，MR估计显示PCOS与肺活量限制(FVC)的风险增加10%相关(OR 1.10[1.05至1.15])，没有多效性的迹象(Q检验P= 0.86;当使用MR方法调整多效性和将分析限制在非哮喘患者(OR为1.12[1.06至1.18])或欧洲女性显著snp (OR为1.10[1.04至1.16])时，估计结果相似。在正常体重和超重(体重为26 kg/m2)的女性中，效果估计相似(相互作用P=0.89)。PCOS与气流阻塞无相关性(OR 0.98[0.94 ~ 1.02])。我们的磁共振结果表明，多囊卵巢综合征增加了肺活量限制的风险。需要进一步的研究来调查可能的潜在机制。(ALEC, EU Grant #633212)
{"title":"Polycystic ovary syndrome and lung function: a Mendelian randomization study","authors":"D. V. D. Plaat, C. Minelli, D. Jarvis, J. Garcia-Aymerich, F. Gómez-Real, B. Leynaert","doi":"10.1183/13993003.congress-2019.pa5390","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5390","url":null,"abstract":"Polycystic ovary syndrome (PCOS) affects between 5-20% of women. Oligomenorrhea (long and/or irregular cycles) is a common PCOS symptom and has been associated with lower forced vital capacity (FVC). We aimed to estimate the effect of PCOS on lung function using Mendelian randomization (MR), an approach that uses genetic variants as proxies to overcome confounding and reverse causation. We used an inverse variance-weighted (IVW) MR method to estimate the causal effect of PCOS on spirometric restriction (FVC The MR estimate shows that PCOS is associated with a 10% higher risk of spirometric restriction (OR 1.10 [1.05 to 1.15]), with no indication of pleiotropy (Q test P= 0.86; I2= 0). Estimates were similar when using MR methods adjusting for pleiotropy and when limiting the analysis to non-asthmatics (OR 1.12 [1.06 to 1.18]) or SNPs significant in European women (OR 1.10 [1.04 to 1.16]). Effect estimates were similar in normal weight and overweight (>26 kg/m2) women (interaction P=0.89). There was no association between PCOS and airflow obstruction (OR 0.98 [0.94 to 1.02]). Our MR results suggest that PCOS increases the risk of spirometric restriction. Further studies are needed to investigate the possible underlying mechanism. (ALEC, EU Grant #633212)","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"1 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65989269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-13DOI: 10.1186/s41021-019-0132-9
Katsuyoshi Horibata, Masashi Sekimoto, K. Sugiyama
{"title":"Comprehensive framework between environment and genomic stability: the open symposium of the Japanese Environmental Mutagen Society (JEMS) in 2019","authors":"Katsuyoshi Horibata, Masashi Sekimoto, K. Sugiyama","doi":"10.1186/s41021-019-0132-9","DOIUrl":"https://doi.org/10.1186/s41021-019-0132-9","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-019-0132-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44672659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-22DOI: 10.1186/s41021-019-0131-x
G. Shailender, Seema Kumari, P. Kiranmayi, R. Malla
{"title":"Effect of MMP-2 gene silencing on radiation-induced DNA damage in human normal dermal fibroblasts and breast cancer cells","authors":"G. Shailender, Seema Kumari, P. Kiranmayi, R. Malla","doi":"10.1186/s41021-019-0131-x","DOIUrl":"https://doi.org/10.1186/s41021-019-0131-x","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-019-0131-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45520234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-16DOI: 10.1186/s41021-019-0130-y
A. Sassa, T. Fukuda, Akiko Ukai, Maki Nakamura, Michihito Takabe, T. Takamura‐Enya, M. Honma, M. Yasui
{"title":"Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells","authors":"A. Sassa, T. Fukuda, Akiko Ukai, Maki Nakamura, Michihito Takabe, T. Takamura‐Enya, M. Honma, M. Yasui","doi":"10.1186/s41021-019-0130-y","DOIUrl":"https://doi.org/10.1186/s41021-019-0130-y","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2019-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-019-0130-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43947827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-02DOI: 10.1186/s41021-018-0111-6
M. Yasui, S. Muto, A. Sassa
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