請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/27542
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳保中(Pau-Chung Chen) | |
dc.contributor.author | Chen-Chung Ko | en |
dc.contributor.author | 柯晨鍾 | zh_TW |
dc.date.accessioned | 2021-06-12T18:09:03Z | - |
dc.date.available | 2011-02-19 | |
dc.date.copyright | 2008-02-19 | |
dc.date.issued | 2007 | |
dc.date.submitted | 2007-11-27 | |
dc.identifier.citation | Arai H, Miyamoto K, Taketani Y, Yamamoto H, Iemori Y, Morita K, et al. 1997. A vitamin D receptor gene polymorphism in the translation initiation codon: effect on protein activity and relation to bone mineral density in Japanese women. Journal of Bone & Mineral Research 12(6): 915-921.
Bellinger DC, Stiles KM, Needleman HL. 1992. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study.[see comment]. Pediatrics 90(6): 855-861. Bradley RH, Caldwell BM. 1988. Using the home inventory to assess the family environment. Pediatric Nursing 14(2): 97-102. Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP. 2006. Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environ Health Perspect 114(12): 1904-1909. Canfield RL, Henderson CR, Jr., Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. 2003. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter.[see comment]. New England Journal of Medicine 348(16): 1517-1526. Chia SE, Yap E, Chia KS. 2004. Delta-aminolevulinic acid dehydratase (ALAD) polymorphism and susceptibility of workers exposed to inorganic lead and its effects on neurobehavioral functions. Neurotoxicology 25(6): 1041-1047. Chiodo LM, Jacobson SW, Jacobson JL. 2004. Neurodevelopmental effects of postnatal lead exposure at very low levels. Neurotoxicology & Teratology 26(3): 359-371. Clarkson TW, Nordberg GF, Sager PR. 1985. Reproductive and developmental toxicity of metals. Scandinavian Journal of Work, Environment & Health 11(3 Spec No): 145-154. Dietrich KN, Ris MD, Succop PA, Berger OG, Bornschein RL. 2001. Early exposure to lead and juvenile delinquency. Neurotoxicology & Teratology 23(6): 511-518. Dietrich KN, Berger OG, Succop PA, Hammond PB, Bornschein RL. 1993. The developmental consequences of low to moderate prenatal and postnatal lead exposure: intellectual attainment in the Cincinnati Lead Study Cohort following school entry. Neurotoxicology & Teratology 15(1): 37-44. Faraco JH, Morrison NA, Baker A, Shine J, Frossard PM. 1989. ApaI dimorphism at the human vitamin D receptor gene locus. Nucleic Acids Research 17(5): 2150. Fullmer CS. 1992. Intestinal interactions of lead and calcium. Neurotoxicology 13(4): 799-807. Godwin HA. 2001. The biological chemistry of lead. Current Opinion in Chemical Biology 5(2): 223-227. Gross C, Krishnan AV, Malloy PJ, Eccleshall TR, Zhao XY, Feldman D. 1998. The vitamin D receptor gene start codon polymorphism: a functional analysis of FokI variants. Journal of Bone & Mineral Research 13(11): 1691-1699. Haynes EN, Kalkwarf HJ, Hornung R, Wenstrup R, Dietrich K, Lanphear BP. 2003. Vitamin D receptor Fok1 polymorphism and blood lead concentration in children. Environmental Health Perspectives 111(13): 1665-1669. Hwang YH, Ko Y, Chiang CD, Hsu SP, Lee YH, Yu CH, et al. 2004. Transition of cord blood lead level, 1985-2002, in the Taipei area and its determinants after the cease of leaded gasoline use. Environmental Research 96(3): 274-282. Hsieh LL, Liou SH, Chen YH, Tsai LC, Yang T, Wu TN. 2000. Association between aminolevulinate dehydrogenase genotype and blood lead levels in Taiwan. Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 42(2): 151-155. Kuningas M, Mooijaart SP, Jolles J, Slagboom PE, Westendorp RG, van Heemst D. 2007. VDR gene variants associate with cognitive function and depressive symptoms in old age. Neurobiol Aging. Lanphear BP, Dietrich K, Auinger P, Cox C. 2000. Cognitive deficits associated with blood lead concentrations <10 microg/dL in US children and adolescents. Public Health Rep 115(6): 521-529. Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, et al. 2005. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis.[see comment]. Environmental Health Perspectives 113(7): 894-899. Liao HF, Wang TM, Yao G, Lee WT. 2005. Concurrent validity of the Comprehensive Developmental Inventory for Infants and Toddlers with the Bayley Scales of Infant Development-II in preterm infants. Journal of the Formosan Medical Association = Taiwan yi zhi 104(10): 731-737. Liao HF, Pan YL. 2005. Test-retest and inter-rater reliability for the Comprehensive Developmental Inventory for Infants and Toddlers diagnostic and screening tests. Early human development 81(11): 927-937. Mendelsohn AL, Dreyer BP, Fierman AH, Rosen CM, Legano LA, Kruger HA, et al. 1998. Low-level lead exposure and behavior in early childhood. Pediatrics 101(3): E10. Morgan AM, Koch V, Lee V, Aldag J. 1988. Neonatal neurobehavioral examination. A new instrument for quantitative analysis of neonatal neurological status. Phys Ther 68(9): 1352-1358. Morrison NA, Yeoman R, Kelly PJ, Eisman JA. 1992. Contribution of trans-acting factor alleles to normal physiological variability: vitamin D receptor gene polymorphism and circulating osteocalcin. Proceedings of the National Academy of Sciences of the United States of America 89(15): 6665-6669. Morrison NA, Qi JC, Tokita A, Kelly PJ, Crofts L, Nguyen TV, et al. 1994. Prediction of bone density from vitamin D receptor alleles.[see comment][erratum appears in Nature 1997 May 1;387(6628):106]. Wasserman GA, Musabegovic A, Liu X, Kline J, Factor-Litvak P, Graziano JH. 2000. Lead exposure and motor functioning in 4(1/2)-year-old children: the Yugoslavia prospective study. J Pediatr 137(4): 555-561. Nature 367(6460): 284-287. Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. 1996. Bone lead levels and delinquent behavior.[see comment]. JAMA 275(5): 363-369. Onalaja AO, Claudio L. 2000. Genetic susceptibility to lead poisoning. Environmental Health Perspectives 108 Suppl 1: 23-28. Orphanides G, Kimber I. 2003. Toxicogenetics: applications and opportunities. Toxicological Sciences 75(1): 1-6. Preston BL, Warren RC, Wooten SM, Gragg RD, 3rd, Walker B. 2001. Environmental health and antisocial behavior: implications for public policy. Journal of Environmental Health 63(9): 9-19; quiz 33-14. Rezende VB, Barbosa F, Jr., Montenegro MF, Sandrim VC, Gerlach RF, Tanus-Santos JE. 2007. Haplotypes of vitamin D receptor modulate the circulating levels of lead in exposed subjects. Arch Toxicol. Tellez-Rojo MM, Bellinger DC, Arroyo-Quiroz C, Lamadrid-Figueroa H, Mercado-Garcia A, Schnaas-Arrieta L, et al. 2006. Longitudinal associations between blood lead concentrations lower than 10 microg/dL and neurobehavioral development in environmentally exposed children in Mexico City. Pediatrics 118(2): e323-330. Wang TM, Su CW, Liao HF, Lin LY, Chou KS, SH L. 1998. The standardization of the comprehensive developmental inventory for infants and toddlers. Psychological Testing 45: 19-46. Wang HH, Liao HF, Hsieh CL. 2006. Reliability, sensitivity to change, and responsiveness of the peabody developmental motor scales-second edition for children with cerebral palsy. Phys Ther 86(10): 1351-1359. Yuan W, Holland SK, Cecil KM, Dietrich KN, Wessel SD, Altaye M, et al. 2006. The impact of early childhood lead exposure on brain organization: a functional magnetic resonance imaging study of language function. Pediatrics 118(3): 971-977. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/27542 | - |
dc.description.abstract | 鉛暴露會對兒童的成長發育造成影響,尤其是神經系統方面,而近年來在許多流行病學的研究中,也發覺到不同的基因多型性在暴露到疾病的發生之過程中扮演著關鍵的角色,但是對於基因易感受性族群,尤其是胎兒成長發育的研究仍然缺乏,本篇的研究目的是探討Vitamin D Receptor基因多型性在臍帶血鉛暴露與兒童早期神經行為發展的影響。本研究對象來自「台灣出生世代研究」中,於孕婦生產時蒐集孕婦的血液與新生兒臍帶血,利用感應耦合電漿質譜分析儀(ICP-MS)進行懷孕期間鉛的暴露評估,並以問卷調查相關的干擾因子。於出生6個月與24個月後利用「嬰幼兒綜合發展測驗」,來評估新生兒的神經行為發展,並利用家庭環境評估量表評估兒童教養環境。基因多型性的分析以鉛毒性相關的Vitamin D Receptor基因為研究重點,利用real-time-PCR方法分析其基因多型性。研究族群平均血鉛濃度1.3 ug/dl,而各VDR FokI基因比例,TT佔21%, CT 佔54%,CC佔25 %。統計分析結果發現,高血鉛暴露(> 1.64 ug/dl)時,幼兒2歲的認知發展分數比低血鉛暴露(<= 1.64 ug/dl)下降5.85分,而在基因多型性方面,高血鉛暴露且具VDR FokI基因多型性兒童的社會領域發展分數比低血鉛暴露且無VDR FokI基因多型性兒童低6.83分,而在語言領域發展,不論血鉛濃度高低,VDR FokI基因多型性都有影響。因此,VDR FokI基因多型性可能會使得兒童神經行為的發展對鉛毒性感受性產生差異。 | zh_TW |
dc.description.abstract | Lead may produce adverse effects on the nervous system and influence cognition, memory and intelligence. Even with low dose exposure, lead may still have adverse effects on humans, especially infants and pregnant women. Genetic polymorphism may play an important role in modulating the health effects, but there have been few studies about the relation between genetic polymorphism and infant neurobehavioral development. The objective of this study was to explore the modifier effect of VDR FokI polymorphism on lead exposure and early childhood neurodevelopment.
Our study subjects were pregnant women and their neonates in the pilot study of Taiwan Birth Panel Study (TBPS) conducted between April 2004 and January 2005. We collected neonatal umbilical cord blood at delivery for lead analysis. The cord blood lead concentration was detected by ICP-MS. We obtained information on relevant confounding factors by personal interview based on a structured questionnaire. The Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT) and Infant/Toddler HOME of Home Observation for Measurement of the Environment Inventory (IT-HOME) were used to evaluate infant neurobehavioral development at six months of age. The second evaluation was performed when children were twenty-four months of age. VDR genetic polymorphisms were analyzed by real-time PCR method. The mean cord blood lead levels was 1.3 ug/dl and the VDR FokI genetic type rates were 21% for TT, 54% for CT and 24% for CC. Subjects with high lead exposure (> 1.64 ug/dl) had lower 5.85 scores in cognitive domain than subjects with low lead exposure (<= 1.64 ug/dl). Further, our analyses suggest that as cord blood lead increased, the scores of children with CT and CC genotype declined significantly (6.83 scores) in social domain compared with children who carried TT genotype. However, language scores were significantly lower in children with VDR FokI polymorphism regardless of lead levels. Overall, VDR FokI polymorphism may have a modifier effect on the neurobehavioral development of children who have lead toxicity. | en |
dc.description.provenance | Made available in DSpace on 2021-06-12T18:09:03Z (GMT). No. of bitstreams: 1 ntu-96-R94841014-1.pdf: 456584 bytes, checksum: b2b47b2afa467447e71e13ef64064f7b (MD5) Previous issue date: 2007 | en |
dc.description.tableofcontents | 摘要 I
Abstract Ⅲ Contents Ⅴ List of table Ⅵ Introduction 1 Materials and Methods 4 Study design and population 4 Medical records and questionnaire data 5 Neurobehavioral development measurements 6 Laboratory analysis 8 Lead levels analysis 8 DNA preparation and genetic polymorphism analysis 8 Sequence analysis 10 Covariates 10 Statistical analysis 12 Results 14 Discussion 16 Conclusion 22 Reference 23 Appendix 38 Lead and neurobehavioral development 38 Lead and genetic polymorphism 44 | |
dc.language.iso | en | |
dc.title | 臍帶血鉛、VDR-FokI多型性與兒童兩歲的神經發展 | zh_TW |
dc.title | Lead in umbilical cord blood, VDR-FokI polymorphism and children’s neurodevelopment at the age of two years | en |
dc.type | Thesis | |
dc.date.schoolyear | 96-1 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 莊弘毅(Hung-Yi Chuang),黃耀輝(Yaw-Huei Hwang),謝武勳(Wu-Shiun Hsieh),廖華芳(Hua-Fang Liao) | |
dc.subject.keyword | 鉛,神經行為發展,嬰幼兒綜合發展測驗,real-time PCR, | zh_TW |
dc.subject.keyword | lead,neurobehavioral development,Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT),real-time PCR, | en |
dc.relation.page | 52 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2007-11-27 | |
dc.contributor.author-college | 公共衛生學院 | zh_TW |
dc.contributor.author-dept | 職業醫學與工業衛生研究所 | zh_TW |
顯示於系所單位: | 職業醫學與工業衛生研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-96-1.pdf 目前未授權公開取用 | 445.88 kB | Adobe PDF |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。