Figure 1 depicts mean levels (and standard errors) of observed maternal sensitivity as a function of risk level (low, medium, and high) and the presence or absence of the DRD4-7R allele in the mothers.
One potential source of error is maternal microchimerism of beta cells arising from the maternal circulation before, or at the time of, birth.
In summary, our analysis of aneuploidy mechanisms demonstrates that most trisomies are maternal meiotic errors, and that the presence of maternal meiotic errors in a single blastomere is positively predictive of a fully aneuploid embryo.
Type III errors explained 5.35% of maternal autosome and 20.00% of chromosome X maternal allele recovery errors (Additional file 1, Table S5).
Errors in the process of maternal or paternal meiosis can lead to chromosome trisomies.
Potential information biases include misreporting of age or recall errors on the timing of maternal deaths, or even non-recognition of early pregnancy-related deaths.
This exercise showed that all fields used in the present study had less than 2% errors with the exception of maternal height (4.4%), estimated gestation (5.6%), and induction of labour (6.4%).
However, a high frequency of maternal meiotic errors alone did not explain the dominance of maternal trisomies, as the incidences of mitotic and meiotic trisomies were roughly equivalent (χ, P = 0.99).
There is a substantial body of evidence that premature separation of sister chromatids (PSSC rather than non-disjunction of homologous chromosomes is the primary cause of maternal meiotic errors resulting in embryonic aneuploidy in women of advanced reproductive age (Angell, 1991; Pellestor et al., 2003; Gabriel et al., 2011; Magli et al., 2012).
Many students (41%) demonstrated replication but with a number of errors, such as the fusion of maternal and paternal chromosomes (similar to the formation by fertilization misconception identified by Smith, 1991), the addition of extra arms on the acrocentric chromosomes, or end-to-end fusion of acrocentric chromosomes.
