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  • In our recent work we established

    2020-08-03

    In our recent work, we established a different and new strategy to overcome the immunogenicity problem. We showed that isolation of a novel form of the protein used with different epitops could also minimize the patient immune response. We showed that the antibody of one form of the enzyme does not neutralize the other form (Fig. 7) [10]. We therefore proposed that the two forms of the proteins or the x gal receptor could be used consecutively instead of using one form of the enzyme.
    Conclusions
    Conflict of interest statement
    Acknowledgements QNRF grant number NPRP6-065-3-012, Qatar National Research Fund, Doha Qatar for funding this work with grant number NPRP No.: NPRP6-065-3-012.
    Introduction Fetal growth restriction (FGR) occurs as a consequence of fetal environmental deterioration. It results in small for gestational age (SGA) newborns who are smaller in size than expected, with birth weight (BW) more than two standard deviations (SDs) below the mean BW of newborns of the same gestational age.2, 3 The number of low BW infants has recently risen in Japan because of increases in FGR, and children born SGA have an increased risk of developing adult non-communicable diseases such as developmental origins of health and disease (DOHaD).1, 5 Therefore, an understanding of the pathophysiology of FGR and the introduction of preventative strategies are urgently needed. In animal studies, intrauterine undernutrition was shown to result in low BW and the development of postnatal obesity, which were associated with altered gene expression in adipose tissue. Epigenetic regulation was recently proposed to be a major link between postconceptional fetal stress and gene expression changes. Moreover, in humans, the epigenetic changes caused by FGR were also suggested to affect postnatal growth; however, the evidence for this is limited. Placental insufficiency is regarded as the main etiology for FGR. Placental development is highly unique in eutherians and is regulated by numerous factors. For example, the novel retrotransposon-derived gene retrotransposon-like 1 (RTL1) was recently shown to play a key role in placental development.11, 12, 13 RTL1 is a paternally expressed imprinted gene located on human chromosome 14, which is highly expressed during late pregnancy in both the fetus and placenta. Intriguingly, RTL1 expression levels are regulated by DNA methylation in its promoter regions. In this study, we hypothesized that the DNA methylation status of RTL1 promoter regions would vary between healthy placentas and those of non-syndromic severe SGA fetuses.
    Materials and methods
    Discussion Although the development of SGA caused by FGR is strongly associated with placental insufficiencies such as aberrant vasculature and malpositioning, the etiology and severity of SGA is heterogeneous and varied. Moreover, the definition of SGA is also variously defined as a BW below the 10th percentile and more than −1.5 SD of the AGA. In this study, we postulated that placental insufficiency caused by aberrant RTL1 expression might result in marked FGR. To exclude incidental or non-pathologic SGA, we selected strict inclusion criteria of more than –2SD of the mean BW, and we defined severe SGA as more than –3SD of the mean BW. Interestingly, the incidence of pregnancy-induced hypertension was higher in the SGA group than in the severe SGA group, suggesting that the etiology of the latter is associated with placental pathologic conditions rather than complications of maternal hypertensive disorders.