E. Barrón-Cabrera, O. Ramos-López, Karina González-Becerra, J. Riezu-Boj, F. Milagro, E. Martínez-López, J. A. Martínez
Background: Chronic diseases arise as a consequence of an unhealthy lifestyle primarily characterized by physical inactivity and unbalanced diets. Regular physical activity can improve health, and there is consistent evidence that these improvements may be the result of epigenetic modifications. Objective: To identify epigenetic modificationsas outcomes of exercise interventions related to specific metabolic alterations. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) methodology for manuscript research and preparation was followed using PubMed and EBSCO databases for literature review. Out of 2,638 articles identified, only 34 articles met the inclusion criteria. Results: The sections of the review were organized by metabolic alterations in which studies were grouped according to healthy, diseased, and trained individuals. Resistance exercise in humans induced epigenetic changes in pathways associated with energy metabolism and insulin sensitivity, contributing to healthy skeletal muscle. Endurance exercise also caused modifications in biomarkers associated to metabolic alterations through changes in DNA methylation and the expression of specific miRNAs. However, both resistance and endurance exercise are necessary to obtain a better physiological adaptation and a combination of both seems to be needed to properly tackle the increasing prevalence of non-communicable pathologies. Conclusion: Given the heterogeneity and complexity of the existing literature, it is currently not possible to propose a specific recommendation about the type, intensity, or duration of exercise that could be beneficial for different subsets of the population (healthy, diseased, and/or trained). Nevertheless, this review highlights the importance of exercise for health and shows the need to perform more research in this emerging area to identify epigenetic biomarkers that could serve as indicators of exercise adaptations.
{"title":"Epigenetic Modifications as Outcomes of Exercise Interventions Related to Specific Metabolic Alterations: A Systematic Review","authors":"E. Barrón-Cabrera, O. Ramos-López, Karina González-Becerra, J. Riezu-Boj, F. Milagro, E. Martínez-López, J. A. Martínez","doi":"10.1159/000503289","DOIUrl":"https://doi.org/10.1159/000503289","url":null,"abstract":"Background: Chronic diseases arise as a consequence of an unhealthy lifestyle primarily characterized by physical inactivity and unbalanced diets. Regular physical activity can improve health, and there is consistent evidence that these improvements may be the result of epigenetic modifications. Objective: To identify epigenetic modificationsas outcomes of exercise interventions related to specific metabolic alterations. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) methodology for manuscript research and preparation was followed using PubMed and EBSCO databases for literature review. Out of 2,638 articles identified, only 34 articles met the inclusion criteria. Results: The sections of the review were organized by metabolic alterations in which studies were grouped according to healthy, diseased, and trained individuals. Resistance exercise in humans induced epigenetic changes in pathways associated with energy metabolism and insulin sensitivity, contributing to healthy skeletal muscle. Endurance exercise also caused modifications in biomarkers associated to metabolic alterations through changes in DNA methylation and the expression of specific miRNAs. However, both resistance and endurance exercise are necessary to obtain a better physiological adaptation and a combination of both seems to be needed to properly tackle the increasing prevalence of non-communicable pathologies. Conclusion: Given the heterogeneity and complexity of the existing literature, it is currently not possible to propose a specific recommendation about the type, intensity, or duration of exercise that could be beneficial for different subsets of the population (healthy, diseased, and/or trained). Nevertheless, this review highlights the importance of exercise for health and shows the need to perform more research in this emerging area to identify epigenetic biomarkers that could serve as indicators of exercise adaptations.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"12 1","pages":"25 - 44"},"PeriodicalIF":2.6,"publicationDate":"2019-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503289","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42980300","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}
C. Kuttner, R. Mancina, G. Wagenpfeil, F. Lammert, C. Stokes
Background/Aims: The PNPLA3 loss-of-function variant p.I148M is a strong genetic determinant of nonalcoholic fatty liver disease. The PNPLA3 protein functions as an intracellular lipase in the liver, with a greater activity on unsaturated fatty acids. This study aimed to determine whether short-term supplementation with omega-3 fatty acids impacts hepatic steatosis differently in PNPLA3 p.148I wild-type individuals as compared to homozygous carriers of the PNPLA3 p.148M variant. Methods: Twenty subjects with hepatic steatosis (50% women, age 18–77 years) were included. Ten subjects homozygous for the PNPLA3 148M variant were matched to 10 wild-type individuals. The subjects received 4 g omega-3 fatty acids (1,840 mg eicosapentaenoic acid and 1,520 mg docosahexaenoic acid) a day for 4 weeks. Transient elastography with a controlled attenuation parameter (CAP) was used to quantify liver fat before and after the intervention. Body composition, fibrosis, liver function tests, serum free fatty acids (FFA) and glucose markers were compared. Results: Patients homozygous for the PNPLA3 p.148M variant (risk group) demonstrated no significant changes in CAP compared to baseline (284 ± 55 vs. 287 ± 65 dB/m) as did the control group (256 ± 56 vs. 262 ± 55 dB/m). While serum liver enzyme activities remained unchanged in both groups, the risk group displayed significantly (p = 0.02) lower baseline FFA concentrations (334.5 [range 281.0–431.0] vs. 564.5 [range 509.0–682.0] μmol/L), which markedly increased by 9.1% after the intervention. In contrast, FFA concentrations decreased significantly (p = 0.01) by 28.3% in the wild-type group. Conclusions: Short-term omega-3 fatty acid supplementation did not significantly alter hepatic steatosis. The nutrigenomic and metabolic effects of omega-3 fatty acids should be investigated further in carriers of the PNPLA3 148M risk variant.
{"title":"Four-Week Omega-3 Supplementation in Carriers of the Prosteatotic PNPLA3 p.I148M Genetic Variant: An Open-Label Study","authors":"C. Kuttner, R. Mancina, G. Wagenpfeil, F. Lammert, C. Stokes","doi":"10.1159/000502008","DOIUrl":"https://doi.org/10.1159/000502008","url":null,"abstract":"Background/Aims: The PNPLA3 loss-of-function variant p.I148M is a strong genetic determinant of nonalcoholic fatty liver disease. The PNPLA3 protein functions as an intracellular lipase in the liver, with a greater activity on unsaturated fatty acids. This study aimed to determine whether short-term supplementation with omega-3 fatty acids impacts hepatic steatosis differently in PNPLA3 p.148I wild-type individuals as compared to homozygous carriers of the PNPLA3 p.148M variant. Methods: Twenty subjects with hepatic steatosis (50% women, age 18–77 years) were included. Ten subjects homozygous for the PNPLA3 148M variant were matched to 10 wild-type individuals. The subjects received 4 g omega-3 fatty acids (1,840 mg eicosapentaenoic acid and 1,520 mg docosahexaenoic acid) a day for 4 weeks. Transient elastography with a controlled attenuation parameter (CAP) was used to quantify liver fat before and after the intervention. Body composition, fibrosis, liver function tests, serum free fatty acids (FFA) and glucose markers were compared. Results: Patients homozygous for the PNPLA3 p.148M variant (risk group) demonstrated no significant changes in CAP compared to baseline (284 ± 55 vs. 287 ± 65 dB/m) as did the control group (256 ± 56 vs. 262 ± 55 dB/m). While serum liver enzyme activities remained unchanged in both groups, the risk group displayed significantly (p = 0.02) lower baseline FFA concentrations (334.5 [range 281.0–431.0] vs. 564.5 [range 509.0–682.0] μmol/L), which markedly increased by 9.1% after the intervention. In contrast, FFA concentrations decreased significantly (p = 0.01) by 28.3% in the wild-type group. Conclusions: Short-term omega-3 fatty acid supplementation did not significantly alter hepatic steatosis. The nutrigenomic and metabolic effects of omega-3 fatty acids should be investigated further in carriers of the PNPLA3 148M risk variant.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"12 1","pages":"10 - 17"},"PeriodicalIF":2.6,"publicationDate":"2019-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000502008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42991143","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}
169 13th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN) July 12–13, 2019, Cambridge, UK Guest Editors: Kohlmeier, M. (Kannapolis, NC, USA); Chirita, A. (Timisoara, Romania); Beckett, E. (New Lambton Heights, NSW, Australia); Angelino, D. (Parma, Italy); Del Rio, D. (Parma, Italy); Niculescu, M. (Hillsborough, NC, USA) 168 Erratum 194
{"title":"Front & Back Matter","authors":"B. Koletzko, R. Shamir, D. Turck, M. Phillip","doi":"10.1159/000502462","DOIUrl":"https://doi.org/10.1159/000502462","url":null,"abstract":"169 13th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN) July 12–13, 2019, Cambridge, UK Guest Editors: Kohlmeier, M. (Kannapolis, NC, USA); Chirita, A. (Timisoara, Romania); Beckett, E. (New Lambton Heights, NSW, Australia); Angelino, D. (Parma, Italy); Del Rio, D. (Parma, Italy); Niculescu, M. (Hillsborough, NC, USA) 168 Erratum 194","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47535023","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}
Selected Abstracts from the 19 3rd European Summer School on Nutrigenomics Jesi, June 25–29, 2018
2018年6月25日至29日，第19届欧洲营养基因组学暑期学校节选
{"title":"Contents","authors":"Iwona Rudkowska, M. E. Tejero","doi":"10.1159/000502164","DOIUrl":"https://doi.org/10.1159/000502164","url":null,"abstract":"Selected Abstracts from the 19 3rd European Summer School on Nutrigenomics Jesi, June 25–29, 2018","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"11 1","pages":"I - IV"},"PeriodicalIF":2.6,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000502164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47353448","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}
E. Araújo, Luama Araujo dos Santos, Radamés Coutinho, Viviane Assis, N. Brandao, Daniela Almeida, G. Conceição, C. Figueredo, H. Fonseca, Maria de Lourdes Lima, D. Lemaire, D. Rios
Background/Aims: Metabolic syndrome (MetS) comprises a cluster of physiological and anthropometric abnormalities. MetS has been linked to lactose intolerance (LI). The aim of this study was to compare the sensitivity and specificity to detect LI using 2 different tests: (1) a genetic test and (2) an oral lactose tolerance test (OLTT). Methods: Two hundred and fifty-four MetS patients, ≥20 years of age, of both genders, were recruited for this comparative study. Nine single nucleotide polymorphisms (SNPs) were selected for genetic investigation: rs182549and rs4988235(both considered “gold standard”); rs56064699; rs148142676; rs562211644; rs59533246; rs3754689; rs2278544,and rs10552864(as potential novel SNPs). Sensitivity and specificity, as well as positive and negative predictive values, were calculated for each genotype using WINPEPI version 11.65. Differences between positive and negative OLTT groups were considered statistically significant when p ≤ 0.05. Results: Among the selected SNPs, only rs182549(p < 0.001) and rs4988235(p < 0.001) gave similar results compared to an OLTT. The sensitivity of both SNPs to detect LI was 87 and 86%, and specificity was 83 and 82.5%, respectively. Conclusion: Genetic tests using rs182549and rs4988235SNPs showed high agreement with OLTT. These genetic tests may be a good option to replace OLTT in MetS patients.
背景/目的:代谢综合征(MetS)包括一系列生理和人体测量异常。MetS与乳糖不耐症(LI)有关。本研究的目的是比较两种不同检测方法检测LI的敏感性和特异性:(1)基因检测和(2)口服乳糖耐量试验(OLTT)。方法:这项比较研究招募了254名年龄≥20岁的MetS患者，男女不限。选择9个单核苷酸多态性(snp)进行遗传研究:rs182549和rs4988235(均被认为是“金标准”);rs56064699;rs148142676;rs562211644;rs59533246;rs3754689;rs2278544和rs10552864(作为潜在的新snp)。使用WINPEPI version 11.65计算每种基因型的敏感性和特异性以及阳性和阴性预测值。当p≤0.05时，认为OLTT阳性组与阴性组之间差异有统计学意义。结果:在所选snp中，只有rs182549(p < 0.001)和rs4988235(p < 0.001)的结果与OLTT相似。两种snp检测LI的敏感性分别为87%和86%，特异性分别为83%和82.5%。结论:rs182549和rs4988235snp基因检测结果与OLTT高度一致。在met患者中，这些基因检测可能是替代OLTT的一个很好的选择。
{"title":"Genetic and Oral Tests for the Diagnosis of Lactose Intolerance in Mixed-Ancestry Brazilians with Metabolic Syndrome","authors":"E. Araújo, Luama Araujo dos Santos, Radamés Coutinho, Viviane Assis, N. Brandao, Daniela Almeida, G. Conceição, C. Figueredo, H. Fonseca, Maria de Lourdes Lima, D. Lemaire, D. Rios","doi":"10.1159/000501690","DOIUrl":"https://doi.org/10.1159/000501690","url":null,"abstract":"Background/Aims: Metabolic syndrome (MetS) comprises a cluster of physiological and anthropometric abnormalities. MetS has been linked to lactose intolerance (LI). The aim of this study was to compare the sensitivity and specificity to detect LI using 2 different tests: (1) a genetic test and (2) an oral lactose tolerance test (OLTT). Methods: Two hundred and fifty-four MetS patients, ≥20 years of age, of both genders, were recruited for this comparative study. Nine single nucleotide polymorphisms (SNPs) were selected for genetic investigation: rs182549and rs4988235(both considered “gold standard”); rs56064699; rs148142676; rs562211644; rs59533246; rs3754689; rs2278544,and rs10552864(as potential novel SNPs). Sensitivity and specificity, as well as positive and negative predictive values, were calculated for each genotype using WINPEPI version 11.65. Differences between positive and negative OLTT groups were considered statistically significant when p ≤ 0.05. Results: Among the selected SNPs, only rs182549(p < 0.001) and rs4988235(p < 0.001) gave similar results compared to an OLTT. The sensitivity of both SNPs to detect LI was 87 and 86%, and specificity was 83 and 82.5%, respectively. Conclusion: Genetic tests using rs182549and rs4988235SNPs showed high agreement with OLTT. These genetic tests may be a good option to replace OLTT in MetS patients.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"12 1","pages":"1 - 9"},"PeriodicalIF":2.6,"publicationDate":"2019-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000501690","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48587958","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}
109 12th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN) September 30 to October 3, 2018, Winnipeg, MB, Canada Guest Editors: Jones, P.J.H.; Myrie, S. (Winnipeg, MB) (available online only)
{"title":"Front & Back Matter","authors":"María Elizabeth Tejero Barrera","doi":"10.1159/000499123","DOIUrl":"https://doi.org/10.1159/000499123","url":null,"abstract":"109 12th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN) September 30 to October 3, 2018, Winnipeg, MB, Canada Guest Editors: Jones, P.J.H.; Myrie, S. (Winnipeg, MB) (available online only)","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"11 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47460883","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 : 2019-01-01Epub Date: 2019-09-11DOI: 10.1159/000502356
Vincent Rioux, Philippe Legrand
In mammalian species, the Fatty Acid Desaturase (FADS) gene cluster includes FADS1 (∆5-desaturase), FADS2 (∆6-desaturase), and a third gene member, named FADS3. According to its high degree of nucleotide sequence homology with both FADS1and FADS2, FADS3 was promptly suspected by researchers in the field to code for a new mammalian membrane-bound fatty acid desaturase. However, no catalytic activity was attributed to the FADS3 protein for a decade, until the rat FADS3 protein was shown in vitro to be able to catalyze the unexpected ∆13-desaturation of trans-vaccenic acid, producing the trans11,cis13-conjugated linoleic acid isomer. This review summarizes the recent investigations establishing the FADS3 enzyme as a reliable mammalian trans-vaccenate ∆13-desaturase in vivo and tries to identify further unresolved issues that need to be addressed.
{"title":"Fatty Acid Desaturase 3 (FADS3) Is a Specific ∆13-Desaturase of Ruminant trans-Vaccenic Acid.","authors":"Vincent Rioux, Philippe Legrand","doi":"10.1159/000502356","DOIUrl":"https://doi.org/10.1159/000502356","url":null,"abstract":"<p><p>In mammalian species, the Fatty Acid Desaturase (FADS) gene cluster includes FADS1 (∆5-desaturase), FADS2 (∆6-desaturase), and a third gene member, named FADS3. According to its high degree of nucleotide sequence homology with both FADS1and FADS2, FADS3 was promptly suspected by researchers in the field to code for a new mammalian membrane-bound fatty acid desaturase. However, no catalytic activity was attributed to the FADS3 protein for a decade, until the rat FADS3 protein was shown in vitro to be able to catalyze the unexpected ∆13-desaturation of trans-vaccenic acid, producing the trans11,cis13-conjugated linoleic acid isomer. This review summarizes the recent investigations establishing the FADS3 enzyme as a reliable mammalian trans-vaccenate ∆13-desaturase in vivo and tries to identify further unresolved issues that need to be addressed.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"12 1-6","pages":"18-24"},"PeriodicalIF":2.6,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000502356","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38364423","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}
Selected Abstracts from the 19 3rd European Summer School on Nutrigenomics Jesi, June 25–29, 2018 Research Articles 40 Serum Lipid Concentrations and FADS Genetic Variants in Young Mexican College Students: The UP-AMIGOS Cohort Study Vazquez-Vidal, I. (Urbana, IL/Kannapolis, NC); Voruganti, V.S. (Kannapolis, NC); Hannon, B.A. (Urbana, IL); Andrade, F.C.D. (Champaign, IL); Aradillas-García, C. (San Luis Potosí); Nakamura, M.T.; Terán-García, M. (Urbana, IL) 49 A Systematic Review of Genetic Testing and Lifestyle Behaviour Change: Are We Using High-Quality Genetic Interventions and Considering Behaviour Change Theory? Horne, J.; Madill, J.; O’Connor, C.; Shelley, J.; Gilliland, J. (London, ON) 64 A High-Protein/Low-Fat Diet May Interact with Vitamin D-Binding Protein Gene Variants to Moderate the Risk of Depression in Apparently Healthy Adults Pooyan, S.; Rahimi, M.H.; Mollahosseini, M.; Khorrami-Nezhad, L.; Nasir, Y.; Maghbooli, Z.; Mirzaei, K. (Tehran)
{"title":"Front & Back Matter","authors":"María Elizabeth Tejero Barrera","doi":"10.1159/000494150","DOIUrl":"https://doi.org/10.1159/000494150","url":null,"abstract":"Selected Abstracts from the 19 3rd European Summer School on Nutrigenomics Jesi, June 25–29, 2018 Research Articles 40 Serum Lipid Concentrations and FADS Genetic Variants in Young Mexican College Students: The UP-AMIGOS Cohort Study Vazquez-Vidal, I. (Urbana, IL/Kannapolis, NC); Voruganti, V.S. (Kannapolis, NC); Hannon, B.A. (Urbana, IL); Andrade, F.C.D. (Champaign, IL); Aradillas-García, C. (San Luis Potosí); Nakamura, M.T.; Terán-García, M. (Urbana, IL) 49 A Systematic Review of Genetic Testing and Lifestyle Behaviour Change: Are We Using High-Quality Genetic Interventions and Considering Behaviour Change Theory? Horne, J.; Madill, J.; O’Connor, C.; Shelley, J.; Gilliland, J. (London, ON) 64 A High-Protein/Low-Fat Diet May Interact with Vitamin D-Binding Protein Gene Variants to Moderate the Risk of Depression in Apparently Healthy Adults Pooyan, S.; Rahimi, M.H.; Mollahosseini, M.; Khorrami-Nezhad, L.; Nasir, Y.; Maghbooli, Z.; Mirzaei, K. (Tehran)","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2018-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44294307","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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