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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 劉貞佑(Liu Chen-Yu) | |
dc.contributor.author | FRAN SISCA | en |
dc.contributor.author | 曾紫蕾 | zh_TW |
dc.date.accessioned | 2021-06-17T02:48:24Z | - |
dc.date.available | 2022-08-18 | |
dc.date.copyright | 2017-09-14 | |
dc.date.issued | 2017 | |
dc.date.submitted | 2017-08-15 | |
dc.identifier.citation | 1. Epigenetics. Environmental Health Perspectives. March 2006;114:8.
2. Bestor TH. The DNA methyltransferasea of mammals. Human Molecular Genetics. 2000;9:8. 3. Suzuki MM, Bird A. DNA methylation landscapes: provocative insights from epigenomics. Nat Rev Genet. Jun 2008;9(6):465-476. 4. Watkins DJ, Wellenius GA, Butler RA, Bartell SM, Fletcher T, Kelsey KT. Associations between serum perfluoroalkyl acids and LINE-1 DNA methylation. Environ Int. Feb 2014;63:71-76. 5. Hsu JY, Hsu JF, Ho HH, Chiang CF, Liao PC. Background levels of persistent organic pollutants in humans from Taiwan: perfluorooctane sulfonate and perfluorooctanoic acid. Chemosphere. Sep 2013;93(3):532-537. 6. ATSDR. PERFLUOROALKYLS 2009. 7. Haug LS, Salihovic S, Jogsten IE, et al. Levels in food and beverages and daily intake of perfluorinated compounds in Norway. Chemosphere. Aug 2010;80(10):1137-1143. 8. Haug LS, Thomsen C, Brantsaeter AL, et al. Diet and particularly seafood are major sources of perfluorinated compounds in humans. Environ Int. Oct 2010;36(7):772-778. 9. Lien GW, Huang CC, Wu KY, et al. Neonatal-maternal factors and perfluoroalkyl substances in cord blood. Chemosphere. Aug 2013;92(7):843-850. 10. Javins B, Hobbs G, Ducatman AM, Pilkerton C, Tacker D, Knox SS. Circulating maternal perfluoroalkyl substances during pregnancy in the C8 Health Study. Environ Sci Technol. Feb 5 2013;47(3):1606-1613. 11. Luebker DJ, York RG, Hansen KJ, Moore JA, Butenhoff JL. Neonatal mortality from in utero exposure to perfluorooctanesulfonate (PFOS) in Sprague-Dawley rats: dose-response, and biochemical and pharamacokinetic parameters. Toxicology. Nov 5 2005;215(1-2):149-169. 12. Apelberg BJ, Witter FR, Herbstman JB, et al. Cord serum concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) in relation to weight and size at birth. Environ Health Perspect. Nov 2007;115(11):1670-1676. 13. Guerrero-Preston R, Goldman LR, Brebi-Mieville P, et al. Global DNA hypomethylation is associated with in utero exposure to cotinine and perfluorinated alkyl compounds. Epigenetics. 2014;5(6):539-546. 14. Granum B, Haug LS, Namork E, et al. Pre-natal exposure to perfluoroalkyl substances may be associated with altered vaccine antibody levels and immune-related health outcomes in early childhood. J Immunotoxicol. Oct-Dec 2013;10(4):373-379. 15. Jin B, Li Y, Robertson KD. DNA methylation: superior or subordinate in the epigenetic hierarchy? Genes Cancer. Jun 2011;2(6):607-617. 16. Takacs ML, Abbott BD. Activation of mouse and human peroxisome proliferator-activated receptors (alpha, beta/delta, gamma) by perfluorooctanoic acid and perfluorooctane sulfonate. Toxicol Sci. Jan 2007;95(1):108-117. 17. Fournier T, Tsatsaris V, Handschuh K, Evain-Brion D. PPARs and the placenta. Placenta. Feb-Mar 2007;28(2-3):65-76. 18. Parast MM, Yu H, Ciric A, Salata MW, Davis V, Milstone DS. PPARgamma regulates trophoblast proliferation and promotes labyrinthine trilineage differentiation. PLoS One. Nov 30 2009;4(11):e8055. 19. Schaiff WT, Barak Y, Sadovsky Y. The pleiotropic function of PPAR gamma in the placenta. Mol Cell Endocrinol. Apr 25 2006;249(1-2):10-15. 20. Holdsworth-Carson SJ, Lim R, Mitton A, et al. Peroxisome proliferator-activated receptors are altered in pathologies of the human placenta: gestational diabetes mellitus, intrauterine growth restriction and preeclampsia. Placenta. Mar 2010;31(3):222-229. 21. Toth B, Bastug M, Mylonas I, et al. Peroxisome proliferator-activated receptor-gamma in normal human pregnancy and miscarriage. Acta Histochem. 2009;111(4):372-378. 22. Guruge KS, Yeung LWY, Yamanaka N, et al. Gene Expression Profiles in Rat Liver Treated With Perfluorooctanoic Acid (PFOA). Toxicological Sciences. 2006;89(1):93-107. 23. Wang L, Wang Y, Liang Y, et al. Specific accumulation of lipid droplets in hepatocyte nuclei of PFOA-exposed BALB/c mice. Sci Rep. 2013;3:2174. 24. Vanden Heuvel JP, Thompson JT, Frame SR, Gillies PJ. Differential Activation of Nuclear Receptors by Perfluorinated Fatty Acid Analogs and Natural Fatty Acids: A Comparison of Human, Mouse, and Rat Peroxisome Proliferator-Activated Receptor-α, -β, and -γ, Liver X Receptor-β, and Retinoid X Receptor-α. Toxicological Sciences. 2006;92(2):476-489. 25. Maccani MA, Marsit CJ. Epigenetics in the placenta. Am J Reprod Immunol. Aug 2009;62(2):78-89. 26. Cross JC. Formation of the Placenta and Extraembryonic Membranes. Annals of the New York Academy of Sciences. 1998;857(1):23-32. 27. Regnault TR, Galan HL, Parker TA, Anthony RV. Placental development in normal and compromised pregnancies-- a review. Placenta. Apr 2002;23 Suppl A:S119-129. 28. Pollheimer J, Knofler M. The role of the invasive, placental trophoblast in human pregnancy. Wien Med Wochenschr. May 2012;162(9-10):187-190. 29. Diaz M, Bassols J, Lopez-Bermejo A, Gomez-Roig MD, de Zegher F, Ibanez L. Placental expression of peroxisome proliferator-activated receptor gamma (PPARgamma): relation to placental and fetal growth. J Clin Endocrinol Metab. Aug 2012;97(8):E1468-1472. 30. Hsieh CJ, Hsieh WS, Su YN, et al. The Taiwan Birth Panel Study: a prospective cohort study for environmentally- related child health. BMC Res Notes. 2011;4:291. 31. Lien GW, Wen TW, Hsieh WS, Wu KY, Chen CY, Chen PC. Analysis of perfluorinated chemicals in umbilical cord blood by ultra-high performance liquid chromatography/tandem mass spectrometry. J Chromatogr B Analyt Technol Biomed Life Sci. Mar 15 2011;879(9-10):641-646. 32. WHO U. Low Birthweight Switzerland 2004. 33. Tucker J, McGuire W. Epidemiology of preterm birth. BMJ : British Medical Journal. 2004;329(7467):675-678. 34. Desjardins P, Conklin D. NanoDrop microvolume quantitation of nucleic acids. J Vis Exp. Nov 22 2010(45). 35. Piperi C, Farmaki E, Vlastos F, Papavassiliou AG, Martinet N. DNA Methylation Signature Analysis: How Easy Is It to Perform? Journal of Biomolecular Techniques : JBT. 2008;19(5):281-284. 36. Hayatsu H. Discovery of bisulfite-mediated cytosine conversion to uracil, the key reaction for DNA methylation analysis--a personal account. Proc Jpn Acad Ser B Phys Biol Sci. 2008;84(8):321-330. 37. Parrish RR, Day JJ, Lubin FD. Direct bisulfite sequencing for examination of DNA methylation with gene and nucleotide resolution from brain tissues. Curr Protoc Neurosci. Jul 2012;Chapter 7:Unit 7 24. 38. Dave V, Yousefi P, Huen K, Volberg V, Holland N. Relationship between expression and methylation of obesity-related genes in children. Mutagenesis. May 2015;30(3):411-420. 39. Kelstrup L, Hjort L, Houshmand-Oeregaard A, et al. Gene expression and DNA methylation of <em>PPARGC1A</em> in Muscle and Adipose Tissue from Adult Offspring of Women with Diabetes in Pregnancy. Diabetes. 2016. 40. Ronaghi M. Pyrosequencing sheds light on DNA sequencing. Genome research. 2001;11(1):3-11. 41. Tost J, Gut IG. DNA methylation analysis by pyrosequencing. Nat. Protocols. 09//print 2007;2(9):2265-2275. 42. Chen MH, Ha EH, Wen TW, et al. Perfluorinated compounds in umbilical cord blood and adverse birth outcomes. PLoS One. 2012;7(8):e42474. 43. Fei C, McLaughlin JK, Tarone RE, Olsen J. Perfluorinated chemicals and fetal growth: a study within the Danish National Birth Cohort. Environ Health Perspect. Nov 2007;115(11):1677-1682. 44. Stein CR, Savitz DA, Dougan M. Serum levels of perfluorooctanoic acid and perfluorooctane sulfonate and pregnancy outcome. Am J Epidemiol. Oct 01 2009;170(7):837-846. 45. Lee ES, Han S, Oh JE. Association between perfluorinated compound concentrations in cord serum and birth weight using multiple regression models. Reprod Toxicol. Jan 2016;59:53-59. 46. Bach CC, Bech BH, Nohr EA, et al. Perfluoroalkyl Acids in Maternal Serum and Indices of Fetal Growth: The Aarhus Birth Cohort. Environmental Health Perspectives. 10/23 04/07/received 10/09/accepted 2016;124(6):848-854. 47. Rappazzo KM, Coffman E, Hines EP. Exposure to Perfluorinated Alkyl Substances and Health Outcomes in Children: A Systematic Review of the Epidemiologic Literature. Int J Environ Res Public Health. Jun 27 2017;14(7). 48. Lopez-Espinosa MJ, Fletcher T, Armstrong B, et al. Association of Perfluorooctanoic Acid (PFOA) and Perfluorooctane Sulfonate (PFOS) with age of puberty among children living near a chemical plant. Environ Sci Technol. Oct 01 2011;45(19):8160-8166. 49. McCormick MC, Brooks-Gunn J, Buka SL, et al. Early intervention in low birth weight premature infants: results at 18 years of age for the Infant Health and Development Program. Pediatrics. Mar 2006;117(3):771-780. 50. Hack M, Flannery DJ, Schluchter M, Cartar L, Borawski E, Klein N. Outcomes in Young Adulthood for Very-Low-Birth-Weight Infants. New England Journal of Medicine. 2002/01/17 2002;346(3):149-157. 51. Lindley AA, Benson JE, Grimes C, Cole Iii TM, Herman AA. The relationship in neonates between clinically measured head circumference and brain volume estimated from head CT-scans. Early Human Development. 9// 1999;56(1):17-29. 52. Miller HC, Hassanein K. Maternal Smoking and Fetal Growth of Full Term Infants. Pediatr Res. 12//print 1974;8(12):960-963. 53. Reeves S, Bernstein I. Effects of maternal tobacco-smoke exposure on fetal growth and neonatal size. Expert Rev Obstet Gynecol. Nov 01 2008;3(6):719-730. 54. Fan Z, Zhang ZX, Li Y, et al. Relationship between birth size and coronary heart disease in China. Ann Med. Dec 2010;42(8):596-602. 55. Lahti J, Raikkonen K, Kajantie E, et al. Small body size at birth and behavioural symptoms of ADHD in children aged five to six years. J Child Psychol Psychiatry. Nov 2006;47(11):1167-1174. 56. Jarvelin MR, Sovio U, King V, et al. Early life factors and blood pressure at age 31 years in the 1966 northern Finland birth cohort. Hypertension. Dec 2004;44(6):838-846. 57. Loaiza S, Coustasse A, Urrutia-Rojas X, Atalah E. Birth weight and obesity risk at first grade in a cohort of Chilean children. Nutrición Hospitalaria. 2011;26:214-219. 58. Boekelheide K, Blumberg B, Chapin RE, et al. Predicting Later-Life Outcomes of Early-Life Exposures. Environmental Health Perspectives. 06/06 01/07/received 06/06/accepted 2012;120(10):1353-1361. 59. Apelberg BJ, Goldman LR, Calafat AM, et al. Determinants of Fetal Exposure to Polyfluoroalkyl Compounds in Baltimore, Maryland. Environmental Science & Technology. 2007/06/01 2007;41(11):3891-3897. 60. Inoue K, Okada F, Ito R, et al. Perfluorooctane Sulfonate (PFOS) and Related Perfluorinated Compounds in Human Maternal and Cord Blood Samples: Assessment of PFOS Exposure in a Susceptible Population during Pregnancy. Environmental Health Perspectives. 2004;112(11):1204-1207. 61. Midasch O, Drexler H, Hart N, Beckmann MW, Angerer J. Transplacental exposure of neonates to perfluorooctanesulfonate and perfluorooctanoate: a pilot study. Int Arch Occup Environ Health. Jul 2007;80(7):643-648. 62. Lau C, Anitole K, Hodes C, Lai D, Pfahles-Hutchens A, Seed J. Perfluoroalkyl acids: a review of monitoring and toxicological findings. Toxicol Sci. Oct 2007;99(2):366-394. 63. Steenland K, Fletcher T, Savitz DA. Epidemiologic evidence on the health effects of perfluorooctanoic acid (PFOA). Environ Health Perspect. Aug 2010;118(8):1100-1108. 64. Kennedy GL, Butenhoff JL, Olsen GW, et al. The Toxicology of Perfluorooctanoate. Critical Reviews in Toxicology. 2010;34(4):351-384. 65. Nelson HH, Marsit CJ, Kelsey KT. Global methylation in exposure biology and translational medical science. Environ Health Perspect. Nov 2011;119(11):1528-1533. 66. Abbott BD. Review of the expression of peroxisome proliferator-activated receptors alpha (PPAR alpha), beta (PPAR beta), and gamma (PPAR gamma) in rodent and human development. Reprod Toxicol. Jun 2009;27(3-4):246-257. 67. Maloney EK, Waxman DJ. trans-Activation of PPARα and PPARγ by Structurally Diverse Environmental Chemicals. Toxicology and Applied Pharmacology. 1999/12/01/ 1999;161(2):209-218. 68. Abbott BD, Wood CR, Watkins AM, Tatum-Gibbs K, Das KP, Lau C. Effects of perfluorooctanoic acid (PFOA) on expression of peroxisome proliferator-activated receptors (PPAR) and nuclear receptor-regulated genes in fetal and postnatal CD-1 mouse tissues. Reprod Toxicol. Jul 2012;33(4):491-505. 69. Lin CY, Wen LL, Lin LY, et al. The associations between serum perfluorinated chemicals and thyroid function in adolescents and young adults. J Hazard Mater. Jan 15 2013;244-245:637-644. 70. Haug LS, Thomsen C, Brantsæter AL, et al. Diet and particularly seafood are major sources of perfluorinated compounds in humans. Environment International. 2010/10/01/ 2010;36(7):772-778. 71. Chu T, Handley D, Bunce K, Surti U, Hogge WA, Peters DG. Structural and regulatory characterization of the placental epigenome at its maternal interface. PLoS One. Feb 23 2011;6(2):e14723. 72. Novakovic B, Yuen RK, Gordon L, et al. Evidence for widespread changes in promoter methylation profile in human placenta in response to increasing gestational age and environmental/stochastic factors. BMC Genomics. October 28 2011;12(1):529. 73. Xu Y, Wang Q, Cook TJ, Knipp GT. Effect of placental fatty acid metabolism and regulation by peroxisome proliferator activated receptor on pregnancy and fetal outcomes. J Pharm Sci. Oct 2007;96(10):2582-2606. 74. Shekhawat PS, Matern D, Strauss AW. Fetal fatty acid oxidation disorders, their effect on maternal health and neonatal outcome: impact of expanded newborn screening on their diagnosis and management. Pediatr Res. May 2005;57(5 Pt 2):78R-86R. 75. Eriksson JG. Early growth, and coronary heart disease and type 2 diabetes: experiences from the Helsinki Birth Cohort Studies. Int J Obes (Lond). Dec 2006;30 Suppl 4:S18-22. 76. Eriksson JG, Lindi V, Uusitupa M, et al. The Effects of the Pro12Ala Polymorphism of the Peroxisome Proliferator-Activated Receptor-γ2 Gene on Insulin Sensitivity and Insulin Metabolism Interact With Size at Birth. Diabetes. 2002;51(7):2321-2324. 77. Robins JC, Marsit CJ, Padbury JF, Sharma SS. ENDOCRINE DISRUPTORS, ENVIRONMENTAL OXYGEN, EPIGENETICS AND PREGNANCY. Frontiers in bioscience (Elite edition). 01/01 2011;3:690-700. 78. Rodie VA, Young A, Jordan F, Sattar N, Greer IA, Freeman DJ. Human Placental Peroxisome Proliferator-Activated Receptor δ and γ Expression in Healthy Pregnancy and in Preeclampsia and Intrauterine Growth Restriction. Journal of the Society for Gynecologic Investigation. 2005/07/01 2005;12(5):320-329. 79. Desai M, Guang H, Ferelli M, Kallichanda N, Lane RH. Programmed upregulation of adipogenic transcription factors in intrauterine growth-restricted offspring. Reprod Sci. Oct 2008;15(8):785-796. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/69036 | - |
dc.description.abstract | 背景: DNA甲基化是表基因調控的一種,這個過程會導致基因的表現產生改變,但基因序列不變。DNA甲基化也是胚胎發育過程中重要的機制之一。胎兒容易受環境因素的影響,特別是在發育期間,此期間的任何缺陷可能會增加疾病發生的風險。環境改變為基因調控的重要因子,產前暴露全氟碳化物可能連結到新生兒一些不良的健康結果,但機制尚未清楚。過氧化物酶體增殖物活化受體γ(peroxisome proliferator-activator receptor gamma)基因會在胎盤中表現,特別是滋養層,其功能為負責母親和胎兒之間的血液、營養和脂肪酸運送,而新生兒的不良健康結果也與滋養層的失調有相關。
目的: 研究全氟碳化物對於 peroxisome proliferator-activator receptor gamma 的甲基化程度影響。觀察在這個過程中甲基化的程度改變時候是不是會影響新生兒的出生結果。 方法 : 本次研究對象來自於台灣出生世代研究(Taiwan Birth Panel Study),於 2004年4月至2005年1月招募收試者。透過極致液相層析/串聯式質譜儀 (ultra-high-performance liquid chromatography/tandem mass spectrometry)分析臍帶血中的全氟烷基物質,包括全氟辛酸(PFOA)、全氟辛烷磺酸(PFOS)、全氟壬酸(PFNA)、全氟癸酸(PFUA)。經由亞硫酸氫鈉處理之胎盤 DNA 藉由焦磷酸定序(pyrosequencing) 方法分析PPARγ 基因在胎盤的甲基化程度。 結果: 我們有發現一些新生兒健康效應與全氟碳化物暴露存在相關,同時有性別上的差異。LnPFNA 與身長在女孩中有顯著正相關關係。但在男孩中沒有。LnPFOA和LnPFUA與男孩的嬰兒重量指標有顯著負相關。只有 PFUA 產前暴露與PPARγ DNA甲基化有顯著相關 [原始模式: β (95% CI) = -0.95 (-1.9, -0.03), p=0.04; 多重校正 β (95% CI) = -1.1 (-2.1, -0.11), p=0.02] 。進一步將 PFUA 暴露資料分組後,發現和PPARγ DNA甲基化程度呈現劑量效應關係 (ptrend = 0.02) 。與最低PFUA暴露組(<25百分位數)相比,最高PFUA暴(≥75百分位數)露與PPARγ DNA甲基化有顯著相關 [多重校正: β (95% CI) = -3.75 (-7.1, -0.76)] 。在原始或校正模型,PPARγ DNA甲基化程度與新生兒健康效應皆無顯著相關性。 結論: 我們的研究結果指出產前暴露到全氟碳化物可能導致幾個不利的新生兒健康效應。除此之外,產前全氟碳化物暴露與胎盤中PPARγ基因甲基化呈現負相關。我們的研究結果支持全氟碳化物暴露會影響表基因的調控,並在兒童的未來造成一些不良的後果。 | zh_TW |
dc.description.abstract | Background: DNA methylation is one of the epigenetics modification that allow gene expression changes changes without changing the DNA sequence. DNA methylation is also one of the important mechanisms take part during embryonic development. Fetus are more vulnerable to environmental substances especially during development period, any defects during this period could increase the risk in disease development later. Prenatal exposure to perfluoroalkyl substances can be linked to several adverse health outcomes to newborns, but the mechanisms still remains unclear. Peroxisome proliferator-activator receptor gamma (PPARγ) is expressed in placenta, especially trophoblast, which is responsible for the blood, nutrients and fatty acid transfer between mother and fetus. Several adverse health outcomes of newborns also have been linked to trophoblast dysregulation.
Objective: To investigate the association between exposure effects of perfluoroalkyl substances and PPARγ gene methylation level and study whether the PPARγ methylation changes could be associated with newborn’s birth outcomes. Methods: The study subjects were from the Taiwan Birth Panel Study. The participants were enrolled from April 2004 to January 2005. The exposure level of perfluoroalkyl substances, including perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA), perfluoroundecanoic acid (PFUA) were measured by ultra-high-performance liquid chromatography/tandem mass spectrometry by using cord blood. The DNA methylation of peroxisome proliferator-activator receptor gamma in placenta were quantified using pyrosequencing method. The results were analyzed using statistical method adjusted for potential confounder in multiple regression model. Result: Some birth outcomes were associated with perfluoroalkyl substances in sex-specific pattern. We observed LnPFNA has significant positive relationship with birth length in girls but not in boys. LnPFOA and LnPFUA were significant negatively associated with ponderal index in boys (p for interaction = 0.36 and 0.8 respectively). Only prenatal exposure to PFUA in natural log transformed were correlated with PPARγ DNA methylation levels in crude and adjusted model [crude: β (95% CI) = -0.95 (-1.9, -0.03), p=0.04; adjusted: β (95% CI) = -1.1 (-2.1, -0.11), p=0.02]. PFUA show a dose-response relationship with PPARγ DNA methylation levels (ptrend = 0.02) in categorized group. Compare to the lowest PFUA exposure group, the highest (≥75th percentile) PFUA expoure was associated with PPARγ DNA methylation levels [adjusted β (95% CI) = -3.75 (-7.1, -0.76)]. PPARγ DNA methylation levels were not significantly associated with birth outcomes, in either crude nor adjusted models. Conclusion: Our results suggest that prenatal exposure to perfluoroalkyl substances might resulted in several adverse birth outcomes. Other than that, perfluoroalkyl substances were associated with decrease PPARγ methylation level in placenta. Our findings support the hypothesis that perfluoroalkyl substances may generate epigenetics changes and cause some disease outcome later in life. | en |
dc.description.provenance | Made available in DSpace on 2021-06-17T02:48:24Z (GMT). No. of bitstreams: 1 ntu-106-R04844016-1.pdf: 1590063 bytes, checksum: 53684a9d4c5c3c34e4b943636ea4bee8 (MD5) Previous issue date: 2017 | en |
dc.description.tableofcontents | Acknowledgements………………………………………………………………i
中文摘要…………………………………………………………………………..ii Abstract…………………………………………………………………………...iv Contents…………………………………………………………………………..vi List of Tables……………………………………………………………………..vii List of Figures…………………………………………………………………….x Chapter 1. Introduction………………………………………………………….1 1.1 DNA Methylation……………………………………………….……………2 1.2 Perfluoroalkyl Substances (PFASs)………………………….…………...2 1.3 Peroxisome Proliferator-Activator Receptor Gamma…………………...4 1.4 Placenta……………………………………………………………………...6 1.5 Study Objective……………………………………………………………...7 Chapter 2. Materials and Methods………………………………….…………9 2.1 Study Subjects………………………………………….…………………...9 2.2 Analysis of Perfluoroalkyl Substances…………………………………....10 2.3 Birth Outcomes…………………………………….…………………….….11 2.4 DNA Methylation Analysis………………………….……………………....12 2.5 Statistical analysis…………………………….………………………..…...16 Chapter 3. Results………………………………………………………….…...18 Chapter 4. Discussion……………………………………………………….…..23 4.1 PFASs and Birth Outcomes………………………………………………...23 4.2 PFASs and DNA Methylation Levels…………………………………..…..26 4.3 DNA Methylation Levels and Birth Outcomes…………………………….28 4.4 Strengths………………………………………………………………….…..29 4.5 Limitations………………………………………………………………..…...30 Chapter 5. Conclusion……………………………………………………….…...31 References………………………………………………………………………...32 Appendix……………………………………………………………………..…….61 | |
dc.language.iso | en | |
dc.title | 產前全氟碳化物暴露對於PPARγ基因甲基化程度和新生兒的影響 | zh_TW |
dc.title | Prenatal Perfluoroalkyl Substances Exposures in Association with Peroxisome Proliferator-Activator Receptor Gamma Gene Methylation Levels and Birth Outcomes | en |
dc.type | Thesis | |
dc.date.schoolyear | 105-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 陳美蓮(Chen Mei-Lien),于明暉(Yu Ming-Whei),陳美惠(Chen Mei-Huei) | |
dc.subject.keyword | 基因甲基化,胎盤,全氟碳化物,PPARγ,產前暴露,新生兒健康效應, | zh_TW |
dc.subject.keyword | DNA methylation,placenta,perfluoroalkyl substances,PPARγ,prenatal exposure,birth outcomes, | en |
dc.relation.page | 73 | |
dc.identifier.doi | 10.6342/NTU201703211 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2017-08-16 | |
dc.contributor.author-college | 公共衛生學院 | zh_TW |
dc.contributor.author-dept | 環境衛生研究所 | zh_TW |
顯示於系所單位: | 環境衛生研究所 |
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