首页> 外文期刊>Mutation research. Genetic toxicology testing >INTRAUTERINE GROWTH RETARDATION AS AN ENDPOINT IN MUTATION EPIDEMIOLOGY - AN EVALUATION BASED ON PATERNAL AGE
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INTRAUTERINE GROWTH RETARDATION AS AN ENDPOINT IN MUTATION EPIDEMIOLOGY - AN EVALUATION BASED ON PATERNAL AGE

机译:子宫内生长迟缓作为突变流行病学的终点-基于母体年龄的评价

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Czeizel recently suggested that intrauterine growth retardation might be of value as a phenotypic endpoint in mutation epidemiology. We hypothesized that if some fraction of small-for-gestational age (SGA) births are due to new germinal mutations, then an association with advanced paternal age should be present. We evaluated the relation between paternal age and SGA, low birthweight, and preterm births using a large sample of births (n = 254,892) from North Carolina. The analyses were restricted to births of mothers aged 20-34 years and adjusted for maternal age, race, education, marital status, gravidity, and smoking. No material increase in the risk of SGA, low birthweight, and preterm delivery was found for fathers in any age category. For example, odds ratios for SGA ranged from 0.87 (fathers aged 50 years or greater) to 1.13 (fathers aged 45-49 years). The results indicate no discernable relationship between SGA and related endpoints and the increase in increase of mutations that accompany advanced paternal age.
机译:Czeizel最近提出,子宫内生长迟缓可能是突变流行病学中的一个表型终点。我们假设如果小胎龄(SGA)出生是由于新的生发突变引起的,则应与父本高龄相关。我们使用来自北卡罗来纳州的大量出生样本(n = 254,892)评估了父亲年龄与SGA,低出生体重和早产之间的关系。这些分析仅限于20-34岁的母亲的出生,并根据母亲的年龄,种族,教育程度,婚姻状况,妊娠和吸烟情况进行了调整。对于任何年龄段的父亲,均未发现SGA,低出生体重和早产的风险有实质性增加。例如,SGA的优势比范围从0.87(年龄在50岁或以上的父亲)到1.13(年龄在45-49岁的父亲)。结果表明,SGA和相关终点之间没有可辨别的关系,而伴随着较高的父亲年龄的突变增加也没有增加。

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