18 research outputs found

    The effect of maternal anxiety on child behavior problems at 1.5 and 5 years (full cohort).

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    The effect of maternal anxiety on child behavior problems at 1.5 and 5 years (full cohort).</p

    MOESM1 of Comparison of blood RNA isolation methods from samples stabilized in Tempus tubes and stored at a large human biobank

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    Additional file 1. Target abundance of RNA transcripts. Evaluation of target abundance; i.e., whether low abundant RNA transcripts (RNA transcripts with Cq-values above 30 cycles) could be detected in blood-RNA samples isolated using the five blood-RNA isolation protocols. Low abundant mRNA and miRNA transcripts were detected in all analyzed samples. The average of non-normalized raw Cq-values of all targets from all adult (n=11-12 Tempus tubes) and cord blood (n=3-6 Tempus tubes) samples collected in the Tempus tubes of the blood-RNA samples isolated using the five RNA isolation protocols

    Incidence rates of progressive childhood encephalopathy in Oslo, Norway: a population based study-0

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    <p><b>Copyright information:</b></p><p>Taken from "Incidence rates of progressive childhood encephalopathy in Oslo, Norway: a population based study"</p><p>http://www.biomedcentral.com/1471-2431/7/25</p><p>BMC Pediatrics 2007;7():25-25.</p><p>Published online 27 Jun 2007</p><p>PMCID:PMC1914055.</p><p></p>n included the complete age cohort between 0 and 15 years

    Additional file 3: Table S1. of Road traffic noise and children’s inattention

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    Main results of ipw analyses, showing effect estimates for road traffic noise with 95% CIs. Table S2. Results of weighted analysis including both postnatal and pregnancy road traffic noisea. (DOCX 56 kb

    Additional file 1 of Parental genetically predicted liability for coronary heart disease and risk of adverse pregnancy outcomes: a cohort study

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    Additional file 1: Table S1. Genetic variants used in the calculation of the genetic risk score for coronary heart disease. Table S2. Description of participants with and without genotype data in MoBa and HUNT. Table S3. Sample sizes. Figure S1. Associations between one SD higher maternal genetic risk score for coronary heart disease and adverse pregnancy outcomes (A) and between one SD higher paternal genetic risk score and adverse pregnancy outcomes in female partners (B), in MoBa and HUNT participants individually

    X-Chromosomal Maternal and Fetal SNPs and the Risk of Spontaneous Preterm Delivery in a Danish/Norwegian Genome-Wide Association Study

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    <div><p>Background</p><p>Recent epidemiological studies suggest that the maternal genome is an important contributor to spontaneous preterm delivery (PTD). There is also a significant excess of males among preterm born infants, which may imply an X-linked mode of inheritance for a subset of cases. To explore this, we examined the effect of maternal and fetal X-chromosomal single nucleotide polymorphisms (SNPs) on the risk of PTD in two independent genome-wide association studies and one replication study.</p><p>Methods</p><p>Participants were recruited from the Danish National Birth Cohort and the Norwegian Mother and Child cohort studies. Data from these two populations were first analyzed independently, and then combined in a meta-analysis. Overall, we evaluated 12,211 SNPs in 1,535 case-mother dyads and 1,487 control-mother dyads. Analyses were done using a hybrid design that combines case-mother dyads and control-mother dyads, as implemented in the Haplin statistical software package. A sex-stratified analysis was performed for the fetal SNPs. In the replication study, 10 maternal and 16 fetal SNPs were analyzed using case-parent triads from independent studies of PTD in the United States, Argentina and Denmark.</p><p>Results</p><p>In the meta-analysis, the G allele at the maternal SNP rs2747022 in the FERM domain containing 7 gene (<i>FRMD7</i>) increased the risk of spontaneous PTD by 1.2 (95% confidence interval (CI): 1.1, 1.4). Although an association with this SNP was confirmed in the replication study, it was no longer statistically significant after a Bonferroni correction for multiple testing.</p><p>Conclusion</p><p>We did not find strong evidence in our data to implicate X-chromosomal SNPs in the etiology of spontaneous PTD. Although non-significant after correction for multiple testing, the mother’s G allele at rs2747022 in <i>FRMD7</i> increased the risk of spontaneous PTD across all populations in this study, thus warranting further investigation in other populations.</p></div
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