Gestational age within normal range and infants’ health and temperament at 3-months of age

<p><b>Objective:</b> To examine the association between gestational age (GA) at birth across the normal GA spectrum (37–41 weeks) and the temperament and health of 3-month old infants.</p> <p><b>Methods:</b> The sample comprised 242 “low-risk” mothers and infants without chronic illnesses or severe pregnancy complications. Infant temperament was defined by three constructs: Negative Affectivity (NA), Extraversion, and Regulation, assessed by parents’ reports on the Infant Behavior Questionnaire. Infants’ health was defined as the number of nonroutine doctors’ visits attended by the infants since their release from the hospital after birth. Analyses employed a continuous measure of GA to assess outcomes across GAs and a categorical measure (37, 38, 39–41 weeks GA) to examine contrasts.</p> <p><b>Results:</b> Extraversion was positively related to GA primarily due to the <i>lower</i> scores of infants born at 37 weeks compared to infants born at 39–41 weeks GA. NA showed a similar effect. The odds of infants born at 37 weeks attending a nonroutine medical visit were 2.8 times that of infants born full-term.</p> <p><b>Discussion:</b> Infants born at 37 weeks GA express less affect and use more nonroutine medical services than do infants born at 39–41 weeks GA. The findings underscore the importance of considering the risks of pregnancy prolongation with the developmental risk associated with early-term delivery.</p

Correlations between Risk at Birth and Maternal Behavior as a Function of the Presence/Absence of Maternal DRD4-III 7-Repeat Allele.

<p>*<i>p</i><.05;</p><p>**<i>p</i><.01, 1-tailed.</p

Mean maternal sensitivity based on risk at birth and the presence/absence of maternal DRD4-III 7-repeat allele.

<p>Mean levels (and standard errors) of observed maternal sensitivity as a function of child risk at birth (low, medium, and high) and the presence or absence of maternal DRD4-7R allele. Mothers who are non-carriers of the 7 allele showed no difference in levels of sensitivity under conditions of high, medium, and low risk at birth. Mothers who are carriers of the 7 allele were more sensitive to low-risk children and less sensitive to high-risk children.</p

Means and Standard Deviations of Study Variables by the Presence and Absence of Maternal DRD4-III 7-Repeat Allele.

<p>Means and Standard Deviations of Study Variables by the Presence and Absence of Maternal DRD4-III 7-Repeat Allele.</p

Salivary cortisol levels following the TSST.

<p>Area under the curve following the TSST for males and females. The rise in salivary cortisol is significant (SPSS GLM repeated measures) for men (F = 22.32 p<0.001) and for females (F = 9.04 p<0.001).</p

Linear regression analysis (average % methylation).

<p>* p<0.05; **p<0.01; ***p<0.001.</p><p>The significance levels are from the Coefficient's Table from the linear regression output of SPSS. The numbers in parentheses are the SE of the unstandardized beta coefficients. Each column is a separate regression analysis representing the addition of the predictor (column 1 = sex+methylation; column 2 = only in females methylation; column 3 is methylation + serotonin transporter + ESR1 dummy variables).</p

Methylation levels of the GR exon 1F and NFGI-A CpG #12 by gender.

<p>Percentage methylation levels of exon 1F (A) and NFGI-A CpG #12 (B) for males and females.</p

GR exon 1F methylation and total cortisol output.

<p>Correlation between AUC and average percent methylation at GR exon 1F in female subjects.</p

Methylation levels across 39 CpG sites in exon 1F for each subject.

<p>Methylation level of GR exon 1F at individual CpG sites for females (n = 46) (2A) and males (n = 46) (2B). Each point in the figure represents a single individual's percentage methylation value for each of the 39 CpG sites that were analyzed by bisulfite pyrosequencing. The points were color coded by the graph option in Excel and each color and shape represents an individual subject. The graph illustrates the marked individual differences (indicated by the shape and color of markers) in percentage methylation at each CpG site. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0048597#pone-0048597-g002" target="_blank">Figure (2C</a>) presents the promoter sequence of exon 1F showing the CpG sites and their position. Highlighted regions represent known or putative canonical (italics) and noncanonical (not italics) NGFI-A–binding sites, with the shaded grey area indicating the beginning of the exon (following McGowan et al (23)).</p