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Effect of abnormal GpG methylation in the second trimester of pregnancy on adverse health risk of offspring

机译:妊娠中期GpG甲基化异常对子代不良健康风险的影响

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摘要

Effect of abnormal GpG methylation in amniotic fluid cells during the second trimester of pregnancy on adverse health risk of offspring was investigated. In total, 237 sets of amniotic fluid cells were collected from patients who received prenatal diagnosis in the Third Affiliated Hospital of Guangzhou Medical University (Guangzhou, China) from April 2010 to October 2011. Among them, 156 sets were from singleton and 81 sets were from twins. H19 gene was amplified by PCR, and the product was purified and pyrosequencing was used to detect the DNA methylation level of GapG. Follow-up records of the birth outcomes of pregnant women's offspring were collected. Positive rate of DNA amplification in 200 cases of amniotic fluid cells was 84.4% (200/237). Average age of singleton pregnancies was higher than that of twins (P<0.05), and no significant differences were found in gestational age and PCR amplification rate (P>0.05). There was no difference in the methylation level of GapG between singleton and twins (P>0.05), but the abnormal methylation rate of GapG1 in twin fetuses was significantly higher than that of singleton (20.3 vs. 3.6%, χ2=8.364, P=0.004). Offspring sex, singleton or twins, mode of delivery, time of pregnancy, and low birth weight showed no significant effect on GapG methylation level of H19 in the second trimester of pregnancy. No offspring deformities were found regardless of the increased or decreased degree of methylation (P>0.05). The number of fetuses born may cause abnormal GapG1 methylation, but no effect of GapG methylation on the adverse health risk of offspring was found.
机译:研究了妊娠中期妊娠期羊水细胞中异常GpG甲基化对后代不利健康风险的影响。 2010年4月至2011年10月,在广州医科大学第三附属医院收集了237例产前诊断的羊水细胞,其中单胎156例,单胎81例。从双胞胎。通过PCR扩增H19基因,纯化产物,并通过焦磷酸测序检测GapG的DNA甲基化水平。收集了孕妇后代的生育结果的后续记录。 200例羊水细胞中DNA扩增的阳性率为84.4%(200/237)。单胎妊娠的平均年龄高于双胎(P <0.05),胎龄和PCR扩增率均无显着性差异(P> 0.05)。单胎和双胞胎之间的GapG甲基化水平没有差异(P> 0.05),但双胎胎儿中GapG1的异常甲基化率显着高于单胎(20.3 vs. 3.6%,χ 2 < /sup>=8.364,P=0.004)。后代性别,单胎或双胞胎,分娩方式,怀孕时间和低出生体重对怀孕中期的H19的GapG甲基化水平无明显影响。无论甲基化程度增高或降低,均未发现后代畸形(P> 0.05)。出生的胎儿数量可能导致异常的GapG1甲基化,但未发现GapG甲基化对后代不利健康风险的影响。

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