Pub Date : 2018-09-15DOI: 10.1183/13993003.CONGRESS-2018.PA1268
S. Anthérieu, B. Leclercq, L. Alleman, E. Perdrix, P. Coddeville, J. Lo-Guidice, G. Garçon
Background: The chronic exposure to air pollution-derived fine particulate matter (PM2.5) is suspected of exacerbating and even causing chronic inflammatory lung diseases. However, the knowledge of the underlying mechanisms is still incomplete. Objectives: To assess transcriptomic alterations in human bronchial epithelial cells exposed to PM2.5 and better understand how this exposure may lead to a shift from healthy to COPD phenotype. Methods: Normal human bronchial epithelial (NHBE) or COPD cells were differentiated at the air-liquid interface and repeatedly exposed to PM2.5 for 72h. Their transcriptomes were analyzed using human pangenomic microarrays. Results: Basal transcriptomes of both control cell phenotypes were first compared and 1280 transcripts were significantly deregulated in COPD vs NHBE cells. The transcription of 1168 genes was significantly altered by PM2.5 exposure in NHBE cells. Interestingly, among these deregulated mRNA, a large number (679) were in common with those found in shift from NHBE to COPD phenotype. Indeed, within this set of genes, we observed increased expression of genes involved in inflammation (e.g. TGF-b, IL-17, IL-33, CXCL1, CXCL3, CXCL6, CXCL8, CXCL14, CCL20), as well as genes associated with extracellular matrix remodeling (e.g. EGF, FGF1, KRT4, MMP9, MMP 13, TIMP-1). By contrast, only 107 transcripts were modulated by PM2.5 in COPD cells, evidencing an exacerbation of COPD. These alterations were validated by RTqPCR and at functional protein level. Conclusions: Overall these results showed that the transcriptomic alterations induced by PM2.5 exposure deregulated key pathways involved in COPD pathogenesis.
{"title":"Transcriptomic alterations induced by air pollution-derived PM2.5 reflect the shift from healthy to COPD-diseased human bronchial epithelium","authors":"S. Anthérieu, B. Leclercq, L. Alleman, E. Perdrix, P. Coddeville, J. Lo-Guidice, G. Garçon","doi":"10.1183/13993003.CONGRESS-2018.PA1268","DOIUrl":"https://doi.org/10.1183/13993003.CONGRESS-2018.PA1268","url":null,"abstract":"Background: The chronic exposure to air pollution-derived fine particulate matter (PM2.5) is suspected of exacerbating and even causing chronic inflammatory lung diseases. However, the knowledge of the underlying mechanisms is still incomplete. Objectives: To assess transcriptomic alterations in human bronchial epithelial cells exposed to PM2.5 and better understand how this exposure may lead to a shift from healthy to COPD phenotype. Methods: Normal human bronchial epithelial (NHBE) or COPD cells were differentiated at the air-liquid interface and repeatedly exposed to PM2.5 for 72h. Their transcriptomes were analyzed using human pangenomic microarrays. Results: Basal transcriptomes of both control cell phenotypes were first compared and 1280 transcripts were significantly deregulated in COPD vs NHBE cells. The transcription of 1168 genes was significantly altered by PM2.5 exposure in NHBE cells. Interestingly, among these deregulated mRNA, a large number (679) were in common with those found in shift from NHBE to COPD phenotype. Indeed, within this set of genes, we observed increased expression of genes involved in inflammation (e.g. TGF-b, IL-17, IL-33, CXCL1, CXCL3, CXCL6, CXCL8, CXCL14, CCL20), as well as genes associated with extracellular matrix remodeling (e.g. EGF, FGF1, KRT4, MMP9, MMP 13, TIMP-1). By contrast, only 107 transcripts were modulated by PM2.5 in COPD cells, evidencing an exacerbation of COPD. These alterations were validated by RTqPCR and at functional protein level. Conclusions: Overall these results showed that the transcriptomic alterations induced by PM2.5 exposure deregulated key pathways involved in COPD pathogenesis.","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"1 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2018-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42167940","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 : 2018-09-15DOI: 10.1183/13993003.CONGRESS-2018.PA1276
A. Amaral, M. Imboden, M. Wielscher, F. Rezwan, C. Minelli, J. Garcia-Aymerich, G. Peralta, J. Auvinen, A. Jeong, Emmanuel Schaffner, A. Beckmeyer-Borowko, J. Holloway, M. Järvelin, N. Probst-Hensch, D. Jarvis
Background: A Mendelian randomisation (MR) study and longitudinal studies have reported the association of lung function with body mass index (BMI). Aim: To investigate whether the association of lung function with BMI is mediated by DNA methylation. Methods: Using data from population-based cohorts (ECRHS, NFBC, SAPALDIA) from the Ageing Lungs in European Cohorts (ALEC) consortium and summary data from published studies, we assessed the mediating role of DNA methylation in the association of lung function with BMI using a 2-step epigenetic MR approach. In step 1 MR, we estimated the causal effect of BMI on peripheral blood DNA methylation (measured at genome-wide level, i.e. >450k CpGs), using 97 BMI-associated SNPs as instrumental variables for BMI in 2,134 participants. In step 2 MR, we estimated the causal effect of DNA methylation on FEV1, FVC, and FEV1/FVC in 7,577 participants (not included in the 1st step) from the same cohorts. As instrumental variables, in this step, we used independent SNPs occurring close (in cis) to 2 CpGs identified in the first step. MR estimates were derived using the Wald ratio, with standard error from the delta method. Results: In step 1, we found that BMI has a small causal effect on DNA methylation levels (less than 1% change in methylation per 1-unit increase in BMI) at 17 CpGs. Of these CpGs, just two were significantly associated with cis-SNPs. In step 2, we found little evidence of a causal effect of DNA methylation at these two sites on lung function. Conclusion: Our findings do not support a mediating effect of DNA methylation in the association of lung function with BMI. However, we were underpowered to detect small effects. Funding: EU H2020 #633212
{"title":"Body mass index and lung function: A two-step epigenetic Mendelian randomization study","authors":"A. Amaral, M. Imboden, M. Wielscher, F. Rezwan, C. Minelli, J. Garcia-Aymerich, G. Peralta, J. Auvinen, A. Jeong, Emmanuel Schaffner, A. Beckmeyer-Borowko, J. Holloway, M. Järvelin, N. Probst-Hensch, D. Jarvis","doi":"10.1183/13993003.CONGRESS-2018.PA1276","DOIUrl":"https://doi.org/10.1183/13993003.CONGRESS-2018.PA1276","url":null,"abstract":"Background: A Mendelian randomisation (MR) study and longitudinal studies have reported the association of lung function with body mass index (BMI). Aim: To investigate whether the association of lung function with BMI is mediated by DNA methylation. Methods: Using data from population-based cohorts (ECRHS, NFBC, SAPALDIA) from the Ageing Lungs in European Cohorts (ALEC) consortium and summary data from published studies, we assessed the mediating role of DNA methylation in the association of lung function with BMI using a 2-step epigenetic MR approach. In step 1 MR, we estimated the causal effect of BMI on peripheral blood DNA methylation (measured at genome-wide level, i.e. >450k CpGs), using 97 BMI-associated SNPs as instrumental variables for BMI in 2,134 participants. In step 2 MR, we estimated the causal effect of DNA methylation on FEV1, FVC, and FEV1/FVC in 7,577 participants (not included in the 1st step) from the same cohorts. As instrumental variables, in this step, we used independent SNPs occurring close (in cis) to 2 CpGs identified in the first step. MR estimates were derived using the Wald ratio, with standard error from the delta method. Results: In step 1, we found that BMI has a small causal effect on DNA methylation levels (less than 1% change in methylation per 1-unit increase in BMI) at 17 CpGs. Of these CpGs, just two were significantly associated with cis-SNPs. In step 2, we found little evidence of a causal effect of DNA methylation at these two sites on lung function. Conclusion: Our findings do not support a mediating effect of DNA methylation in the association of lung function with BMI. However, we were underpowered to detect small effects. Funding: EU H2020 #633212","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2018-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46398093","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 : 2018-09-15DOI: 10.1183/13993003.CONGRESS-2018.PA1262
T. Guo, Z. Tan, H. Luo
Purpose: Patients with Primary Ciliary Dyskinesia (PCD) have been rarely reported in China, and few studies are currently available to characterize the genetic basis of PCD in Chinese families. To identify the potential causative gene in a patient with PCD, who is from a consanguineous Chinese family. Methods: Runs of homozygosity and whole-exome sequencing were conducted on the family. Sanger sequencing was conducted to validate the candidate mutations and familial segregation. Real-time QPCR was used to measure the expression level of the possible causative gene. Zebrafish experiments were performed for candidate gene function verification. Results: A homozygous change in BRWD1, an important developmental gene, that resulted in a missense mutation in the WD-repeat domain of the protein and cosegregated with PCD phenotypes in the family. This mutation in BRWD1 was predicted to be highly deleterious, and qPCR analysis showed a significant and extreme decrease in the expression level of the mutant gene in the affected individual. Morpholino knockdown of brwd1 in zebrafish embryos resulted in situs inversus totalis (a typical phenotype of PCD) and abnormal cardiac looping. Conclusions: BRWD1 was therefore implicated as a novel causative gene for Primary Ciliary Dyskinesia. This homozygous variant was not reported before.
{"title":"Late Breaking Abstract - Mutations of BRWD1 may be associated with Primary Ciliary Dyskinesia","authors":"T. Guo, Z. Tan, H. Luo","doi":"10.1183/13993003.CONGRESS-2018.PA1262","DOIUrl":"https://doi.org/10.1183/13993003.CONGRESS-2018.PA1262","url":null,"abstract":"Purpose: Patients with Primary Ciliary Dyskinesia (PCD) have been rarely reported in China, and few studies are currently available to characterize the genetic basis of PCD in Chinese families. To identify the potential causative gene in a patient with PCD, who is from a consanguineous Chinese family. Methods: Runs of homozygosity and whole-exome sequencing were conducted on the family. Sanger sequencing was conducted to validate the candidate mutations and familial segregation. Real-time QPCR was used to measure the expression level of the possible causative gene. Zebrafish experiments were performed for candidate gene function verification. Results: A homozygous change in BRWD1, an important developmental gene, that resulted in a missense mutation in the WD-repeat domain of the protein and cosegregated with PCD phenotypes in the family. This mutation in BRWD1 was predicted to be highly deleterious, and qPCR analysis showed a significant and extreme decrease in the expression level of the mutant gene in the affected individual. Morpholino knockdown of brwd1 in zebrafish embryos resulted in situs inversus totalis (a typical phenotype of PCD) and abnormal cardiac looping. Conclusions: BRWD1 was therefore implicated as a novel causative gene for Primary Ciliary Dyskinesia. This homozygous variant was not reported before.","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2018-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46497554","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 : 2018-09-15DOI: 10.1183/13993003.CONGRESS-2018.OA2193
M. D. Vries, D. V. D. Plaat, I. Nedeljkovic, K. V. D. Velde, N. Amin, C. Duijn, J. Vonk, H. Boezen, C. V. Diemen
There are large differences in individual susceptibility to develop COPD, which cannot be explained by common genetic variants. Rare genetic variants, occurring in <1% of the general population, can potentially explain this individual risk to develop COPD. Here, we aim to identify rare genetic variants associated with COPD. Whole genome sequencing was performed on 36 subjects with COPD (FEV 1 /FVC<70% and FEV 1 %pred<90) from the LifeLines general population cohort who had never smoked and were not exposed to environmental smoke or occupational exposures. Rare genetic variants in coding regions with predicted pathogenic effect were selected with the GAVIN algorithm. Variants present in ≥3 subjects were compared with healthy, non-exposed subjects (N=1846) within LifeLines (GoNL imputed data), using a chi 2 test. Next, frequencies of significant variants were further tested in the general population, irrespective of exposures, between healthy (N=10,560) and COPD subjects (N=2,101) from the LifeLines cohort and replicated in the Rotterdam Study (10,897 healthy and 599 COPD subjects). We identified 7,357 predicted pathogenic variants in 5,196 unique genes of which 318 rare genetic variants were carried by ≥3 subjects. 127 of the 318 variants could be imputed in LifeLines and the frequency of 45 variants was significantly different between non-exposed COPD versus non-exposed healthy controls. Next, 5 variants were significantly associated with COPD in the LifeLines population and 2 of these variants, present in ARAP3 and KIF27 , were replicated in the Rotterdam study. Our study is the first to identify rare genetic variants associated with COPD in the general population
{"title":"Identification of novel rare genetic variants associated with COPD in the general population","authors":"M. D. Vries, D. V. D. Plaat, I. Nedeljkovic, K. V. D. Velde, N. Amin, C. Duijn, J. Vonk, H. Boezen, C. V. Diemen","doi":"10.1183/13993003.CONGRESS-2018.OA2193","DOIUrl":"https://doi.org/10.1183/13993003.CONGRESS-2018.OA2193","url":null,"abstract":"There are large differences in individual susceptibility to develop COPD, which cannot be explained by common genetic variants. Rare genetic variants, occurring in <1% of the general population, can potentially explain this individual risk to develop COPD. Here, we aim to identify rare genetic variants associated with COPD. Whole genome sequencing was performed on 36 subjects with COPD (FEV 1 /FVC<70% and FEV 1 %pred<90) from the LifeLines general population cohort who had never smoked and were not exposed to environmental smoke or occupational exposures. Rare genetic variants in coding regions with predicted pathogenic effect were selected with the GAVIN algorithm. Variants present in ≥3 subjects were compared with healthy, non-exposed subjects (N=1846) within LifeLines (GoNL imputed data), using a chi 2 test. Next, frequencies of significant variants were further tested in the general population, irrespective of exposures, between healthy (N=10,560) and COPD subjects (N=2,101) from the LifeLines cohort and replicated in the Rotterdam Study (10,897 healthy and 599 COPD subjects). We identified 7,357 predicted pathogenic variants in 5,196 unique genes of which 318 rare genetic variants were carried by ≥3 subjects. 127 of the 318 variants could be imputed in LifeLines and the frequency of 45 variants was significantly different between non-exposed COPD versus non-exposed healthy controls. Next, 5 variants were significantly associated with COPD in the LifeLines population and 2 of these variants, present in ARAP3 and KIF27 , were replicated in the Rotterdam study. Our study is the first to identify rare genetic variants associated with COPD in the general population","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2018-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42876464","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 : 2017-11-01DOI: 10.1186/s41021-017-0086-8
K. Masumura, S. Masuda
{"title":"Research on environmental mutagenesis from young scientists – the open symposium of the Japanese Environmental Mutagen Society (JEMS) in 2017","authors":"K. Masumura, S. Masuda","doi":"10.1186/s41021-017-0086-8","DOIUrl":"https://doi.org/10.1186/s41021-017-0086-8","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-017-0086-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46357687","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}
Rats are a standard experimental animal for cancer bioassay and toxicological research for chemicals. Although the genetic analyses were behind mice, rats have been more frequently used for toxicological research than mice. This is partly because they live longer than mice and induce a wider variety of tumors, which are morphologically similar to those in humans. The body mass is larger than mice, which enables to take samples from organs for studies on pharmacokinetics or toxicokinetics. In addition, there are a number of chemicals that exhibit marked species differences in the carcinogenicity. These compounds are carcinogenic in rats but not in mice. Such examples are aflatoxin B1 and tamoxifen, both are carcinogenic to humans. Therefore, negative mutagenic/carcinogenic responses in mice do not guarantee that the chemical is not mutagenic/carcinogenic to rats or perhaps to humans. To facilitate research on in vivo mutagenesis and carcinogenesis, several transgenic rat models have been established. In general, the transgenic rats for mutagenesis are treated with chemicals longer than transgenic mice for more exact examination of the relationship between mutagenesis and carcinogenesis. Transgenic rat models for carcinogenesis are engineered mostly to understand mechanisms underlying chemical carcinogenesis. Here, we review papers dealing with the transgenic rat models for mutagenesis and carcinogenesis, and discuss the future perspective.
{"title":"Transgenic rat models for mutagenesis and carcinogenesis.","authors":"Takehiko Nohmi, Kenichi Masumura, Naomi Toyoda-Hokaiwado","doi":"10.1186/s41021-016-0072-6","DOIUrl":"https://doi.org/10.1186/s41021-016-0072-6","url":null,"abstract":"<p><p>Rats are a standard experimental animal for cancer bioassay and toxicological research for chemicals. Although the genetic analyses were behind mice, rats have been more frequently used for toxicological research than mice. This is partly because they live longer than mice and induce a wider variety of tumors, which are morphologically similar to those in humans. The body mass is larger than mice, which enables to take samples from organs for studies on pharmacokinetics or toxicokinetics. In addition, there are a number of chemicals that exhibit marked species differences in the carcinogenicity. These compounds are carcinogenic in rats but not in mice. Such examples are aflatoxin B<sub>1</sub> and tamoxifen, both are carcinogenic to humans. Therefore, negative mutagenic/carcinogenic responses in mice do not guarantee that the chemical is not mutagenic/carcinogenic to rats or perhaps to humans. To facilitate research on in vivo mutagenesis and carcinogenesis, several transgenic rat models have been established. In general, the transgenic rats for mutagenesis are treated with chemicals longer than transgenic mice for more exact examination of the relationship between mutagenesis and carcinogenesis. Transgenic rat models for carcinogenesis are engineered mostly to understand mechanisms underlying chemical carcinogenesis. Here, we review papers dealing with the transgenic rat models for mutagenesis and carcinogenesis, and discuss the future perspective.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"39 ","pages":"11"},"PeriodicalIF":1.7,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-016-0072-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89717879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-06DOI: 10.1186/s41021-016-0068-2
K. Inami, Y. Mine, J. Tatsuzaki, C. Mori, M. Mochizuki
{"title":"Isolation and characterization of antimutagenic components of Glycyrrhiza aspera against N-methyl-N-nitrosourea","authors":"K. Inami, Y. Mine, J. Tatsuzaki, C. Mori, M. Mochizuki","doi":"10.1186/s41021-016-0068-2","DOIUrl":"https://doi.org/10.1186/s41021-016-0068-2","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"53 ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-016-0068-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41273479","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 : 2017-01-06DOI: 10.1186/s41021-016-0065-5
Katsuyoshi Horibata, Akiko Ukai, A. Ogata, D. Nakae, H. Ando, Y. Kubo, A. Nagasawa, K. Yuzawa, M. Honma
{"title":"Absence of in vivo mutagenicity of multi-walled carbon nanotubes in single intratracheal instillation study using F344 gpt delta rats","authors":"Katsuyoshi Horibata, Akiko Ukai, A. Ogata, D. Nakae, H. Ando, Y. Kubo, A. Nagasawa, K. Yuzawa, M. Honma","doi":"10.1186/s41021-016-0065-5","DOIUrl":"https://doi.org/10.1186/s41021-016-0065-5","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"49 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-016-0065-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65773459","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 : 2016-12-01DOI: 10.1186/s41021-016-0054-8
Y. Oda
{"title":"Development and progress for three decades in umu test systems","authors":"Y. Oda","doi":"10.1186/s41021-016-0054-8","DOIUrl":"https://doi.org/10.1186/s41021-016-0054-8","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"38 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-016-0054-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65773416","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 : 2016-12-01DOI: 10.1186/s41021-016-0051-y
Tetsuya Suzuki, H. Kamiya
{"title":"Mutations induced by 8-hydroxyguanine (8-oxo-7,8-dihydroguanine), a representative oxidized base, in mammalian cells","authors":"Tetsuya Suzuki, H. Kamiya","doi":"10.1186/s41021-016-0051-y","DOIUrl":"https://doi.org/10.1186/s41021-016-0051-y","url":null,"abstract":"","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"39 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41021-016-0051-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65773848","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}
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