<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1111/(ISSN)1365-3016" xmlns="http://purl.org/rss/1.0/"><title>Paediatric and Perinatal Epidemiology</title><description> Wiley Online Library : Paediatric and Perinatal Epidemiology</description><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F%28ISSN%291365-3016</link><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc</dc:publisher><dc:language xmlns:dc="http://purl.org/dc/elements/1.1/">en</dc:language><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/">© Blackwell Publishing Ltd</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">0269-5022</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1365-3016</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">May 2013</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">27</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">3</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">227</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">311</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1111/ppe.2013.27.issue-3/asset/cover.gif?v=1&amp;s=93c1cf41bd92ce65e9c9f1e677d797e2a428a619"/><items><rdf:Seq><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12057"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12051"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12055"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12054"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12053"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12052"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12056"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12050"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12040"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12042"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12036"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12048"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12049"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12043"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12044"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12046"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12045"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12047"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12057" xmlns="http://purl.org/rss/1.0/"><title>The Association between a Medical History of Depression and Gestational Diabetes in a Large Multi-ethnic Cohort in the United States</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12057</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Association between a Medical History of Depression and Gestational Diabetes in a Large Multi-ethnic Cohort in the United States</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Katherine Bowers, S. Katherine Laughon, Sungduk Kim, Sunni L. Mumford, Jennifer Brite, Michele Kiely, Cuilin Zhang</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-09T05:34:57.74426-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12057</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12057</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12057</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12057-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Both major depression and gestational diabetes mellitus (GDM) are prevalent among women of reproductive age. Our objective was to determine whether a medical history of depression is related to subsequent development of GDM.</p></div></div>
<div class="section" id="ppe12057-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The Consortium on Safe Labor was a US retrospective cohort study of 228 562 births between 2002 and 2008. Exclusion criteria for the present analysis included multiple gestation pregnancies (<em>n</em> = 5059), pre-existing diabetes (<em>n</em> = 12 771), deliveries &lt;24 weeks (<em>n</em> = 395), site GDM prevalence (&lt;1%) (<em>n</em> = 20 721) and missing data on pre-pregnancy body mass index (BMI) (<em>n</em> = 61 321). Using generalised estimating equations, we estimated the association between a history of depression and a pregnancy complicated by GDM.</p></div></div>
<div class="section" id="ppe12057-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The final analytic population included 121 260 women contributing 128 295 pregnancies, of which 5606 were affected by GDM. A history of depression was significantly associated with an increased risk of developing GDM (multivariate odds ratio [aOR] = 1.42 [95% confidence interval (CI) 1.26, 1.60]). Adjusting for pre-pregnancy BMI and weight gain during pregnancy attenuated the association, although it remained statistically significant (aOR = 1.17 [95% CI 1.03, 1.33]).</p></div></div>
<div class="section" id="ppe12057-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>A history of depression was significantly associated with an increased GDM risk among a large multi-ethnic US cohort of women. If the association is confirmed, depression presents a potentially modifiable risk factor of GDM and provides additional clues to the underlying pathophysiology of GDM.</p></div></div>
]]></content:encoded><description>


Background
Both major depression and gestational diabetes mellitus (GDM) are prevalent among women of reproductive age. Our objective was to determine whether a medical history of depression is related to subsequent development of GDM.


Methods
The Consortium on Safe Labor was a US retrospective cohort study of 228 562 births between 2002 and 2008. Exclusion criteria for the present analysis included multiple gestation pregnancies (n = 5059), pre-existing diabetes (n = 12 771), deliveries &lt;24 weeks (n = 395), site GDM prevalence (&lt;1%) (n = 20 721) and missing data on pre-pregnancy body mass index (BMI) (n = 61 321). Using generalised estimating equations, we estimated the association between a history of depression and a pregnancy complicated by GDM.


Results
The final analytic population included 121 260 women contributing 128 295 pregnancies, of which 5606 were affected by GDM. A history of depression was significantly associated with an increased risk of developing GDM (multivariate odds ratio [aOR] = 1.42 [95% confidence interval (CI) 1.26, 1.60]). Adjusting for pre-pregnancy BMI and weight gain during pregnancy attenuated the association, although it remained statistically significant (aOR = 1.17 [95% CI 1.03, 1.33]).


Conclusions
A history of depression was significantly associated with an increased GDM risk among a large multi-ethnic US cohort of women. If the association is confirmed, depression presents a potentially modifiable risk factor of GDM and provides additional clues to the underlying pathophysiology of GDM.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12051" xmlns="http://purl.org/rss/1.0/"><title>How to Measure Prenatal Stress? A Systematic Review of Psychometric Instruments to Assess Psychosocial Stress during Pregnancy</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12051</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">How to Measure Prenatal Stress? A Systematic Review of Psychometric Instruments to Assess Psychosocial Stress during Pregnancy</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Irina Nast, Margarete Bolten, Gunther Meinlschmidt, Dirk H. Hellhammer</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-25T03:30:35.728351-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12051</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12051</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12051</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12051-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>A growing body of literature documents associations of maternal psychosocial stress during pregnancy with fetal, infant and child behaviour and development. However, findings across studies are often inconsistent, which may in part be due to differences in stress definitions and assessments.</p></div></div>
<div class="section" id="ppe12051-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We systematically reviewed methods applied to assess maternal psychosocial stress during pregnancy in studies looking at associations with biobehavioural outcomes in the offspring. A systematic literature search was performed on <em>Web of Science</em> and <em>PubMed</em> for the time period between January 1999 and October 2009. Psychometric instruments assessing maternal psychosocial stress during pregnancy were identified and described if data on psychometric properties were available.</p></div></div>
<div class="section" id="ppe12051-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We identified 115 publications that assessed psychosocial stress during pregnancy with validated methods. These publications applied overall 43 different instruments assessing constructs falling under seven categories, ordered according to their frequency of use: <em>anxiety, depression, daily hassles, aspects of psychological symptomatology (not reduced to anxiety or depression), life events, specific socio-environmental stressors</em> and <em>stress related to pregnancy and parenting</em>. If available, we provide information on validity and reliability of the instruments for samples of pregnant women.</p></div></div>
<div class="section" id="ppe12051-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Within the ‘prenatal stress’ research, a broad range of instruments is applied to assess psychosocial stress during pregnancy. Prenatal stress research should take into consideration that the variety of methods in use might hamper the comparability of stress research results. In each category of stress constructs, one instrument with good psychometric properties in pregnant women is highlighted as the best currently available measure.</p></div></div>
]]></content:encoded><description>


Background
A growing body of literature documents associations of maternal psychosocial stress during pregnancy with fetal, infant and child behaviour and development. However, findings across studies are often inconsistent, which may in part be due to differences in stress definitions and assessments.


Methods
We systematically reviewed methods applied to assess maternal psychosocial stress during pregnancy in studies looking at associations with biobehavioural outcomes in the offspring. A systematic literature search was performed on Web of Science and PubMed for the time period between January 1999 and October 2009. Psychometric instruments assessing maternal psychosocial stress during pregnancy were identified and described if data on psychometric properties were available.


Results
We identified 115 publications that assessed psychosocial stress during pregnancy with validated methods. These publications applied overall 43 different instruments assessing constructs falling under seven categories, ordered according to their frequency of use: anxiety, depression, daily hassles, aspects of psychological symptomatology (not reduced to anxiety or depression), life events, specific socio-environmental stressors and stress related to pregnancy and parenting. If available, we provide information on validity and reliability of the instruments for samples of pregnant women.


Conclusions
Within the ‘prenatal stress’ research, a broad range of instruments is applied to assess psychosocial stress during pregnancy. Prenatal stress research should take into consideration that the variety of methods in use might hamper the comparability of stress research results. In each category of stress constructs, one instrument with good psychometric properties in pregnant women is highlighted as the best currently available measure.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12055" xmlns="http://purl.org/rss/1.0/"><title>Ambient Air Pollution and Traffic Exposures and Congenital Heart Defects in the San Joaquin Valley of California</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12055</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Ambient Air Pollution and Traffic Exposures and Congenital Heart Defects in the San Joaquin Valley of California</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Amy M. Padula, Ira B. Tager, Suzan L. Carmichael, S. Katharine Hammond, Wei Yang, Frederick Lurmann, Gary M. Shaw</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-21T21:18:51.548609-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12055</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12055</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12055</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12055-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Congenital anomalies are a leading cause of infant morbidity and mortality. Studies suggest associations between environmental contaminants and some anomalies, although evidence is limited.</p></div></div>
<div class="section" id="ppe12055-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We used data from the California Center of the National Birth Defects Prevention Study and the Children's Health and Air Pollution Study to estimate the odds of 27 congenital heart defects with respect to quartiles of seven ambient air pollutant and traffic exposures in California during the first 2 months of pregnancy, 1997–2006 (<em>n</em> = 822 cases and <em>n</em> = 849 controls).</p></div></div>
<div class="section" id="ppe12055-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Particulate matter &lt; 10 microns (PM<sub>10</sub>) was associated with pulmonary valve stenosis [adjusted odds ratio (aOR)<sub>Fourth Quartile</sub> = 2.6] [95% confidence intervals (CI) 1.2, 5.7] and perimembranous ventricular septal defects (aOR<sub>Third Quartile</sub> = 2.1) [95% CI 1.1, 3.9] after adjusting for maternal race/ethnicity, education and multivitamin use. PM<sub>2.5</sub> was associated with transposition of the great arteries (aOR<sub>Third Quartile</sub> = 2.6) [95% CI 1.1, 6.5] and inversely associated with perimembranous ventricular septal defects (aOR<sub>Fourth Quartile</sub> = 0.5) [95% CI 0.2, 0.9]. Secundum atrial septal defects were inversely associated with carbon monoxide (aOR<sub>Fourth Quartile</sub> = 0.4) [95% CI 0.2, 0.8] and PM<sub>2.5</sub> (aOR<sub>Fourth Quartile</sub> = 0.5) [95% CI 0.3, 0.8]. Traffic density was associated with muscular ventricular septal defects (aOR<sub>Fourth Quartile</sub> = 3.0) [95% CI 1.2, 7.8] and perimembranous ventricular septal defects (aOR<sub>Third Quartile</sub> = 2.4) [95% CI 1.3, 4.6], and inversely associated with transposition of the great arteries (aOR<sub>Fourth Quartile</sub> = 0.3) [95% CI 0.1, 0.8].</p></div></div>
<div class="section" id="ppe12055-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>PM<sub>10</sub> and traffic density may contribute to the occurrence of pulmonary valve stenosis and ventricular septal defects, respectively. The results were mixed for other pollutants and had little consistency with previous studies.</p></div></div>
]]></content:encoded><description>


Background
Congenital anomalies are a leading cause of infant morbidity and mortality. Studies suggest associations between environmental contaminants and some anomalies, although evidence is limited.


Methods
We used data from the California Center of the National Birth Defects Prevention Study and the Children's Health and Air Pollution Study to estimate the odds of 27 congenital heart defects with respect to quartiles of seven ambient air pollutant and traffic exposures in California during the first 2 months of pregnancy, 1997–2006 (n = 822 cases and n = 849 controls).


Results
Particulate matter &lt; 10 microns (PM10) was associated with pulmonary valve stenosis [adjusted odds ratio (aOR)Fourth Quartile = 2.6] [95% confidence intervals (CI) 1.2, 5.7] and perimembranous ventricular septal defects (aORThird Quartile = 2.1) [95% CI 1.1, 3.9] after adjusting for maternal race/ethnicity, education and multivitamin use. PM2.5 was associated with transposition of the great arteries (aORThird Quartile = 2.6) [95% CI 1.1, 6.5] and inversely associated with perimembranous ventricular septal defects (aORFourth Quartile = 0.5) [95% CI 0.2, 0.9]. Secundum atrial septal defects were inversely associated with carbon monoxide (aORFourth Quartile = 0.4) [95% CI 0.2, 0.8] and PM2.5 (aORFourth Quartile = 0.5) [95% CI 0.3, 0.8]. Traffic density was associated with muscular ventricular septal defects (aORFourth Quartile = 3.0) [95% CI 1.2, 7.8] and perimembranous ventricular septal defects (aORThird Quartile = 2.4) [95% CI 1.3, 4.6], and inversely associated with transposition of the great arteries (aORFourth Quartile = 0.3) [95% CI 0.1, 0.8].


Conclusions
PM10 and traffic density may contribute to the occurrence of pulmonary valve stenosis and ventricular septal defects, respectively. The results were mixed for other pollutants and had little consistency with previous studies.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12054" xmlns="http://purl.org/rss/1.0/"><title>Social Modifications of the Multiple Birth Effect on IQ and Body Size: a Population-Based Study of Young Adult Males</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12054</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Social Modifications of the Multiple Birth Effect on IQ and Body Size: a Population-Based Study of Young Adult Males</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Karri Silventoinen, Mikko Myrskylä, Per Tynelius, Yoshie Yokoyama, Finn Rasmussen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-15T22:12:10.371575-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12054</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12054</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12054</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12054-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Twins and triplets fall behind singletons in cognitive and physical development. We analysed whether these differences are modified by family social position.</p></div></div>
<div class="section" id="ppe12054-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>IQ, height, body mass index (BMI) and elbow flexion, handgrip and knee extension strength were measured in Swedish men born between 1951 and 1976 during the conscription examination at 17 to 20 years of age. Information from Swedish registers on all siblings and parental socio-economic position were linked to these measures. Together, the measures were available for 1 140 329 singletons, 19 755 twins and 207 triplets. The data were analysed using regression analyses and fixed-effect models which compare twins and triplets with their singleton brothers.</p></div></div>
<div class="section" id="ppe12054-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Twins and triplets had slightly lower IQ, height, BMI and muscle strength than did singletons both at the population level as well as when compared with their singleton brothers. Although the differences between twins and triplets were small, they were largest in families with lower socio-economic position. We also found larger differences in IQ among the sons of mothers born before 1940.</p></div></div>
<div class="section" id="ppe12054-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Twins and triplets fall slightly behind singletons in cognitive and physical development, even in early adulthood, but twins and triplets show no major differences. These differences are largest in families in a low socio-economic position. Our results underscore the importance of the postnatal environment in the development of twins and triplets and suggest that their parents, especially those in a low socio-economic position, need special support.</p></div></div>
]]></content:encoded><description>


Background
Twins and triplets fall behind singletons in cognitive and physical development. We analysed whether these differences are modified by family social position.


Methods
IQ, height, body mass index (BMI) and elbow flexion, handgrip and knee extension strength were measured in Swedish men born between 1951 and 1976 during the conscription examination at 17 to 20 years of age. Information from Swedish registers on all siblings and parental socio-economic position were linked to these measures. Together, the measures were available for 1 140 329 singletons, 19 755 twins and 207 triplets. The data were analysed using regression analyses and fixed-effect models which compare twins and triplets with their singleton brothers.


Results
Twins and triplets had slightly lower IQ, height, BMI and muscle strength than did singletons both at the population level as well as when compared with their singleton brothers. Although the differences between twins and triplets were small, they were largest in families with lower socio-economic position. We also found larger differences in IQ among the sons of mothers born before 1940.


Conclusions
Twins and triplets fall slightly behind singletons in cognitive and physical development, even in early adulthood, but twins and triplets show no major differences. These differences are largest in families in a low socio-economic position. Our results underscore the importance of the postnatal environment in the development of twins and triplets and suggest that their parents, especially those in a low socio-economic position, need special support.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12053" xmlns="http://purl.org/rss/1.0/"><title>Modelling Time to Death or Discharge in Neonatal Care: An Application of Competing Risks</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12053</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Modelling Time to Death or Discharge in Neonatal Care: An Application of Competing Risks</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sally R. Hinchliffe, Sarah E. Seaton, Paul C. Lambert, Elizabeth S. Draper, David J. Field, Bradley N. Manktelow</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-15T22:12:04.466226-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12053</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12053</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12053</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Methodology Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12053-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Understanding length of stay for babies in neonatal care is vital for planning services and for counselling parents. While previous work has focused on the length of stay of babies who survive to discharge, when investigating resource use within neonatal care, it is important to also incorporate information on those babies who die while in care. We present an analysis using <em>competing risks methodology</em> which allows the simultaneous modelling of babies who die in neonatal care and those who survive to discharge.</p></div></div>
<div class="section" id="ppe12053-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Data were obtained on 2723 babies born at 24–28 weeks gestational age in 2006–10 and admitted to neonatal care. Death and discharge alive are two mutually exclusive events and can be treated as competing risks. A flexible parametric modelling approach was used to analyse these two competing events and obtain estimates of the absolute probabilities of death or discharge.</p></div></div>
<div class="section" id="ppe12053-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The absolute probabilities of death or discharge are presented in graphical form showing the cause-specific cumulative incidence over time by gender, gestational age and birthweight. The discharge of babies alive generally occurred over a longer time period for babies of lower gestational age and smaller birthweight than for bigger babies.</p></div></div>
<div class="section" id="ppe12053-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>This study has presented a useful statistical method for modelling the length of stay where there are significant rates of in-unit mortality. In health care systems that are increasingly focusing on costs and resource planning, it is essential to consider not only length of stay of survivors but also for those patients who die before discharge.</p></div></div>
]]></content:encoded><description>


Background
Understanding length of stay for babies in neonatal care is vital for planning services and for counselling parents. While previous work has focused on the length of stay of babies who survive to discharge, when investigating resource use within neonatal care, it is important to also incorporate information on those babies who die while in care. We present an analysis using competing risks methodology which allows the simultaneous modelling of babies who die in neonatal care and those who survive to discharge.


Methods
Data were obtained on 2723 babies born at 24–28 weeks gestational age in 2006–10 and admitted to neonatal care. Death and discharge alive are two mutually exclusive events and can be treated as competing risks. A flexible parametric modelling approach was used to analyse these two competing events and obtain estimates of the absolute probabilities of death or discharge.


Results
The absolute probabilities of death or discharge are presented in graphical form showing the cause-specific cumulative incidence over time by gender, gestational age and birthweight. The discharge of babies alive generally occurred over a longer time period for babies of lower gestational age and smaller birthweight than for bigger babies.


Conclusion
This study has presented a useful statistical method for modelling the length of stay where there are significant rates of in-unit mortality. In health care systems that are increasingly focusing on costs and resource planning, it is essential to consider not only length of stay of survivors but also for those patients who die before discharge.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12052" xmlns="http://purl.org/rss/1.0/"><title>Ethnic Differences in the Initiation and Duration of Breast Feeding – Results from the Born in Bradford Birth Cohort Study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12052</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Ethnic Differences in the Initiation and Duration of Breast Feeding – Results from the Born in Bradford Birth Cohort Study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gillian Santorelli, Emily Petherick, Dagmar Waiblinger, Baltica Cabieses, Lesley Fairley</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-15T22:12:00.309087-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12052</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12052</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12052</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12052-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Initiation of breast feeding and duration of any breast feeding are known to differ by ethnic group, but there are limited data on differences in exclusive breast feeding. This study aimed to determine if there are ethnic differences in the initiation and duration of any and exclusive breast feeding.</p></div></div>
<div class="section" id="ppe12052-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Breast-feeding data were obtained from a subsample of 1365 women recruited to a multi-ethnic cohort study (Born in Bradford) between August 2008 and March 2009. Poisson regression was used to investigate the impact of socio-economic, life style and birth factors on ethnic differences in the prevalence of breast feeding.</p></div></div>
<div class="section" id="ppe12052-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Compared with white British mothers, initiation of breast feeding was significantly higher in all ethnic groups and this persisted after adjustment for socio-economic, life style and birth factors [Pakistani: prevalence rate ratio (PRR) = 1.19 (95% confidence interval 1.10, 1.29); Other South Asian: PRR = 1.29 (1.18, 1.42); Other ethnicities: PRR = 1.33 (1.21, 1.46)]. There were no differences in exclusive breast feeding at 4 months [Pakistani: PRR = 0.77 (0.54, 1.09); Other South Asian: PRR = 1.55 (0.99, 2.43); Other ethnicities: PRR = 1.50 (0.88, 2.56)]. Any breast feeding at 4 months was significantly higher in mothers of all non-white British ethnicities [Pakistani: PRR = 1.27 (1.02, 1.58); Other South Asian: PRR = 1.99 (1.52, 2.62); Other ethnicities: 2.45 (1.86, 3.21)].</p></div></div>
<div class="section" id="ppe12052-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Whilst women of ethnic minority groups were significantly more likely to initiate breast feeding and continue any breast feeding for 4 months compared with white British women, the rates of exclusive breast feeding at 4 months were not significantly different once socio-economic, life style and birth factors were accounted for.</p></div></div>
]]></content:encoded><description>


Background
Initiation of breast feeding and duration of any breast feeding are known to differ by ethnic group, but there are limited data on differences in exclusive breast feeding. This study aimed to determine if there are ethnic differences in the initiation and duration of any and exclusive breast feeding.


Methods
Breast-feeding data were obtained from a subsample of 1365 women recruited to a multi-ethnic cohort study (Born in Bradford) between August 2008 and March 2009. Poisson regression was used to investigate the impact of socio-economic, life style and birth factors on ethnic differences in the prevalence of breast feeding.


Results
Compared with white British mothers, initiation of breast feeding was significantly higher in all ethnic groups and this persisted after adjustment for socio-economic, life style and birth factors [Pakistani: prevalence rate ratio (PRR) = 1.19 (95% confidence interval 1.10, 1.29); Other South Asian: PRR = 1.29 (1.18, 1.42); Other ethnicities: PRR = 1.33 (1.21, 1.46)]. There were no differences in exclusive breast feeding at 4 months [Pakistani: PRR = 0.77 (0.54, 1.09); Other South Asian: PRR = 1.55 (0.99, 2.43); Other ethnicities: PRR = 1.50 (0.88, 2.56)]. Any breast feeding at 4 months was significantly higher in mothers of all non-white British ethnicities [Pakistani: PRR = 1.27 (1.02, 1.58); Other South Asian: PRR = 1.99 (1.52, 2.62); Other ethnicities: 2.45 (1.86, 3.21)].


Conclusions
Whilst women of ethnic minority groups were significantly more likely to initiate breast feeding and continue any breast feeding for 4 months compared with white British women, the rates of exclusive breast feeding at 4 months were not significantly different once socio-economic, life style and birth factors were accounted for.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12056" xmlns="http://purl.org/rss/1.0/"><title>Moving Forward: a New Associate Editor for Paediatric and Child Health Epidemiology</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12056</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Moving Forward: a New Associate Editor for Paediatric and Child Health Epidemiology</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Cande V. Ananth</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12056</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12056</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12056</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Editorial</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">227</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">227</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12050" xmlns="http://purl.org/rss/1.0/"><title>Current Vision and Future Directions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12050</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Current Vision and Future Directions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kenneth C. Schoendorf</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12050</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12050</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12050</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Commentary</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">228</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">228</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12040" xmlns="http://purl.org/rss/1.0/"><title>The Exposome – Exciting Opportunities for Discoveries in Reproductive and Perinatal Epidemiology</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12040</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Exposome – Exciting Opportunities for Discoveries in Reproductive and Perinatal Epidemiology</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Germaine M. Buck Louis, Edwina Yeung, Rajeshwari Sundaram, S. Katherine Laughon, Cuilin Zhang</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-21T18:47:17.467774-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12040</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12040</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12040</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">For discussion</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">229</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">236</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Summary</h3>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>Understanding the mechanisms that underlie successful human reproduction and development is an ambitious goal, given the many unique methodological challenges surrounding such study. These challenges are well understood by reproductive and perinatal epidemiologists and include its conditional nature, unobservable yet informative outcomes such as conception, multi-scale missing data, correlated or non-independent outcomes, interval censoring and a hierarchical data structure. Novel methodologies for overcoming these challenges and for answering critical data gaps are needed if we are to better understand the inefficiency that currently characterises human reproduction with the goal of improving population health. The exposome is an emerging paradigm that offers promise for understanding the natural history of human reproduction and development, and its many associated impairments that develop later in child- or adulthood. This novel paradigm recognises the need to identify and measure the totality of environmental (non-genetic) exposures from preconception through sensitive windows, and to identify patterns associated with healthy and adverse outcomes. The exposome accommodates research focusing on unique subpopulations, such as couples undergoing assisted reproductive technologies, so that methodological limitations such as unobservable and conditional outcomes can be better addressed. Reproductive and perinatal epidemiology is uniquely suited for proof-of-concept exposome research, given the intricate relations between fecundity, gravid health and later onset disease and the narrow and interrelated sensitive windows that characterise the conditional nature of human reproduction and development. Bold new conceptual frameworks such as the exposome are needed for designing research that may lead to discovery and improve population health.</p></div>
]]></content:encoded><description>

Understanding the mechanisms that underlie successful human reproduction and development is an ambitious goal, given the many unique methodological challenges surrounding such study. These challenges are well understood by reproductive and perinatal epidemiologists and include its conditional nature, unobservable yet informative outcomes such as conception, multi-scale missing data, correlated or non-independent outcomes, interval censoring and a hierarchical data structure. Novel methodologies for overcoming these challenges and for answering critical data gaps are needed if we are to better understand the inefficiency that currently characterises human reproduction with the goal of improving population health. The exposome is an emerging paradigm that offers promise for understanding the natural history of human reproduction and development, and its many associated impairments that develop later in child- or adulthood. This novel paradigm recognises the need to identify and measure the totality of environmental (non-genetic) exposures from preconception through sensitive windows, and to identify patterns associated with healthy and adverse outcomes. The exposome accommodates research focusing on unique subpopulations, such as couples undergoing assisted reproductive technologies, so that methodological limitations such as unobservable and conditional outcomes can be better addressed. Reproductive and perinatal epidemiology is uniquely suited for proof-of-concept exposome research, given the intricate relations between fecundity, gravid health and later onset disease and the narrow and interrelated sensitive windows that characterise the conditional nature of human reproduction and development. Bold new conceptual frameworks such as the exposome are needed for designing research that may lead to discovery and improve population health.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12042" xmlns="http://purl.org/rss/1.0/"><title>Maternal Stress/Distress, Hormonal Pathways and Spontaneous Preterm Birth</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12042</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Maternal Stress/Distress, Hormonal Pathways and Spontaneous Preterm Birth</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael S. Kramer, John Lydon, Lise Goulet, Susan Kahn, Mourad Dahhou, Robert W. Platt, Shakti Sharma, Michael J. Meaney, Louise Séguin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-04T22:41:55.907502-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12042</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12042</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12042</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Preterm Delivery</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">237</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">246</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12042-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Although second-trimester blood corticotrophin-releasing hormone (CRH) levels are robustly associated with preterm birth, the findings with respect to cortisol have been inconsistent, as have been those relating stress hormones to measured stressors and maternal distress.</p></div></div>
<div class="section" id="ppe12042-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We measured plasma CRH, adrenocorticotrophic hormone (ACTH), cortisol, cortisol-binding globulin, oestradiol and progesterone at 24–26 weeks in a nested case–control study of 206 women who experienced spontaneous preterm birth and 442 term controls. We also related the hormonal levels to measures of environmental stressors, perceived stress and maternal distress (also assessed at 24–26 weeks) and to placental histopathology.</p></div></div>
<div class="section" id="ppe12042-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>With the exception of an unexpectedly low oestradiol : progesterone ratio among cases (adjusted odds ratio = 0.5 [95% confidence interval 0.3, 0.8] for ratios above the median in controls), none of the hormonal measures was independently associated with spontaneous preterm birth; placental histopathological evidence of infection/inflammation, infarction or decidual vasculopathy; or measures of maternal stress or distress. CRH levels were positively associated with cortisol, but not with ACTH, whereas ACTH was also positively associated with cortisol.</p></div></div>
<div class="section" id="ppe12042-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our findings suggest an intact pituitary–adrenal axis and confirm the positive feedback effect of cortisol on (placental) CRH. Neither of these hormonal pathways, however, was strongly linked to maternal stress/distress or to the risk of spontaneous preterm birth.</p></div></div>
]]></content:encoded><description>


Background
Although second-trimester blood corticotrophin-releasing hormone (CRH) levels are robustly associated with preterm birth, the findings with respect to cortisol have been inconsistent, as have been those relating stress hormones to measured stressors and maternal distress.


Methods
We measured plasma CRH, adrenocorticotrophic hormone (ACTH), cortisol, cortisol-binding globulin, oestradiol and progesterone at 24–26 weeks in a nested case–control study of 206 women who experienced spontaneous preterm birth and 442 term controls. We also related the hormonal levels to measures of environmental stressors, perceived stress and maternal distress (also assessed at 24–26 weeks) and to placental histopathology.


Results
With the exception of an unexpectedly low oestradiol : progesterone ratio among cases (adjusted odds ratio = 0.5 [95% confidence interval 0.3, 0.8] for ratios above the median in controls), none of the hormonal measures was independently associated with spontaneous preterm birth; placental histopathological evidence of infection/inflammation, infarction or decidual vasculopathy; or measures of maternal stress or distress. CRH levels were positively associated with cortisol, but not with ACTH, whereas ACTH was also positively associated with cortisol.


Conclusions
Our findings suggest an intact pituitary–adrenal axis and confirm the positive feedback effect of cortisol on (placental) CRH. Neither of these hormonal pathways, however, was strongly linked to maternal stress/distress or to the risk of spontaneous preterm birth.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12036" xmlns="http://purl.org/rss/1.0/"><title>Cell Phone Exposures and Hearing Loss in Children in the Danish National Birth Cohort</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12036</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cell Phone Exposures and Hearing Loss in Children in the Danish National Birth Cohort</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Madhuri Sudan, Leeka Kheifets, Onyebuchi A. Arah, Jorn Olsen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12036</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12036</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12036</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Infant Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">247</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">257</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12036-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Children today are exposed to cell phones early in life, and may be the most vulnerable if exposure is harmful to health. We investigated the association between cell phone use and hearing loss in children.</p></div></div>
<div class="section" id="ppe12036-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The Danish National Birth Cohort (DNBC) enrolled pregnant women between 1996 and 2002. Detailed interviews were conducted during gestation, and when the children were 6 months, 18 months and 7 years of age. We used multivariable-adjusted logistic regression, marginal structural models (MSM) with inverse-probability weighting, and doubly robust estimation (DRE) to relate hearing loss at age 18 months to cell phone use at age 7 years, and to investigate cell phone use reported at age 7 in relation to hearing loss at age 7.</p></div></div>
<div class="section" id="ppe12036-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Our analyses included data from 52 680 children. We observed weak associations between cell phone use and hearing loss at age 7, with odds ratios and 95% confidence intervals from the traditional logistic regression, MSM and DRE models being 1.21 [95% confidence interval [CI] 0.99, 1.46], 1.23 [95% CI 1.01, 1.49] and 1.22 [95% CI 1.00, 1.49], respectively.</p></div></div>
<div class="section" id="ppe12036-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our findings could have been affected by various biases and are not sufficient to conclude that cell phone exposures have an effect on hearing. This is the first large-scale epidemiologic study to investigate this potentially important association among children, and replication of these findings is needed.</p></div></div>
]]></content:encoded><description>


Background
Children today are exposed to cell phones early in life, and may be the most vulnerable if exposure is harmful to health. We investigated the association between cell phone use and hearing loss in children.


Methods
The Danish National Birth Cohort (DNBC) enrolled pregnant women between 1996 and 2002. Detailed interviews were conducted during gestation, and when the children were 6 months, 18 months and 7 years of age. We used multivariable-adjusted logistic regression, marginal structural models (MSM) with inverse-probability weighting, and doubly robust estimation (DRE) to relate hearing loss at age 18 months to cell phone use at age 7 years, and to investigate cell phone use reported at age 7 in relation to hearing loss at age 7.


Results
Our analyses included data from 52 680 children. We observed weak associations between cell phone use and hearing loss at age 7, with odds ratios and 95% confidence intervals from the traditional logistic regression, MSM and DRE models being 1.21 [95% confidence interval [CI] 0.99, 1.46], 1.23 [95% CI 1.01, 1.49] and 1.22 [95% CI 1.00, 1.49], respectively.


Conclusions
Our findings could have been affected by various biases and are not sufficient to conclude that cell phone exposures have an effect on hearing. This is the first large-scale epidemiologic study to investigate this potentially important association among children, and replication of these findings is needed.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12048" xmlns="http://purl.org/rss/1.0/"><title>A Time and Place for Causal Inference Methods in Perinatal and Paediatric Epidemiology</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12048</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A Time and Place for Causal Inference Methods in Perinatal and Paediatric Epidemiology</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Katherine A. Ahrens, Enrique F. Schisterman</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12048</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12048</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12048</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Commentary</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">258</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">262</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12049" xmlns="http://purl.org/rss/1.0/"><title>Marginal Structural Models, Doubly Robust Estimation, and Bias Analysis in Perinatal and Paediatric Epidemiology</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12049</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Marginal Structural Models, Doubly Robust Estimation, and Bias Analysis in Perinatal and Paediatric Epidemiology</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Onyebuchi A. Arah, Madhuri Sudan, Jørn Olsen, Leeka Kheifets</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12049</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12049</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12049</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Commentary</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">263</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">265</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12043" xmlns="http://purl.org/rss/1.0/"><title>Smoking during Pregnancy and Risk of Autism Spectrum Disorder in a Finnish National Birth Cohort</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12043</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Smoking during Pregnancy and Risk of Autism Spectrum Disorder in a Finnish National Birth Cohort</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Phuong Lien Tran, Venla Lehti, Katja M. Lampi, Hans Helenius, Auli Suominen, Mika Gissler, Alan S. Brown, Andre Sourander</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12043</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12043</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12043</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Infant Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">266</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">274</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12043-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Results of previous population-based studies examining associations between smoking during pregnancy and autism spectrum disorders (ASD) are contradictory. Furthermore, there is a lack of population-based studies examining the relationship between smoking during pregnancy and the main diagnostic subtypes of ASD.</p></div></div>
<div class="section" id="ppe12043-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We conducted a population-based nested case–control study based on the Finnish Prenatal Study of Autism (FIPS-A) among liveborn infants delivered in Finland between 1987 and 2005. Data on maternal smoking during pregnancy were available from the Finnish Medical Birth Register (FMBR) since October 1990. Data on ASD in the offspring were obtained from the Finnish Hospital Discharge Register (FHDR).</p></div></div>
<div class="section" id="ppe12043-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Among the three subtypes of ASD, maternal smoking during the whole pregnancy was associated with an increased risk of pervasive developmental disorder (PDD) (odds ratio 1.2, 95% confidence interval 1.0, 1.5). The increase in odds persisted after controlling for maternal age, mother's socio-economic and psychiatric status, and infant's weight for gestational age. However, smoking exposure limited to the first trimester was not associated with PDD or any of the other ASD subtypes.</p></div></div>
<div class="section" id="ppe12043-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Maternal smoking is related to a modest increase in risk of PDD, while no associations were observed for childhood autism and Asperger's syndrome.</p></div></div>
]]></content:encoded><description>


Background
Results of previous population-based studies examining associations between smoking during pregnancy and autism spectrum disorders (ASD) are contradictory. Furthermore, there is a lack of population-based studies examining the relationship between smoking during pregnancy and the main diagnostic subtypes of ASD.


Methods
We conducted a population-based nested case–control study based on the Finnish Prenatal Study of Autism (FIPS-A) among liveborn infants delivered in Finland between 1987 and 2005. Data on maternal smoking during pregnancy were available from the Finnish Medical Birth Register (FMBR) since October 1990. Data on ASD in the offspring were obtained from the Finnish Hospital Discharge Register (FHDR).


Results
Among the three subtypes of ASD, maternal smoking during the whole pregnancy was associated with an increased risk of pervasive developmental disorder (PDD) (odds ratio 1.2, 95% confidence interval 1.0, 1.5). The increase in odds persisted after controlling for maternal age, mother's socio-economic and psychiatric status, and infant's weight for gestational age. However, smoking exposure limited to the first trimester was not associated with PDD or any of the other ASD subtypes.


Conclusions
Maternal smoking is related to a modest increase in risk of PDD, while no associations were observed for childhood autism and Asperger's syndrome.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12044" xmlns="http://purl.org/rss/1.0/"><title>Maternal Smoking During Pregnancy and Failure of the Georgia First Grade Criterion-Referenced Competency Test</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12044</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Maternal Smoking During Pregnancy and Failure of the Georgia First Grade Criterion-Referenced Competency Test</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jia Feng, Michael R. Kramer, Bridget V. Dever, Anne L. Dunlop, Bryan Williams, Lucky Jain</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12044</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12044</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12044</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Infant Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">275</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">282</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12044-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Maternal smoking during pregnancy (MSDP) has been reported to be associated with impaired measures of cognitive function, but it remains unclear whether exposure to MSDP has an impact upon offspring school performance. We examined the association between MSDP and failure of the Criterion-Referenced Competency Tests (CRCT) among Georgia first grade students.</p></div></div>
<div class="section" id="ppe12044-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A retrospective cohort was created by deterministically linking 331 531 children born in Georgia from 1998 to 2002 (inclusive) to their individual CRCT education records from 2005 to 2009. We evaluated the association between MSDP (yes/no) and failure of the CRCT Reading, English/Language Arts (ELA), and Mathematics tests, with adjustment for maternal and child sociodemographic characteristics and birth outcomes. Log-binomial models estimated the risk ratios and 95% confidence intervals. Conditional models were fitted to paired sibling data.</p></div></div>
<div class="section" id="ppe12044-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>MSDP was associated with CRCT failure with an adjusted risk ratios for Reading: 1.16 [95% CI 1.12, 1.21]; ELA: 1.12 [95%CI 1.10, 1.15]; and Mathematics: 1.13 [95%CI 1.10, 1.16]. The association remained significant in paired sibling analyses.</p></div></div>
<div class="section" id="ppe12044-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>MSDP may have independent long-term effects on offspring school performance, which does not appear to be through smoking-related adverse birth outcomes.</p></div></div>
]]></content:encoded><description>


Background
Maternal smoking during pregnancy (MSDP) has been reported to be associated with impaired measures of cognitive function, but it remains unclear whether exposure to MSDP has an impact upon offspring school performance. We examined the association between MSDP and failure of the Criterion-Referenced Competency Tests (CRCT) among Georgia first grade students.


Methods
A retrospective cohort was created by deterministically linking 331 531 children born in Georgia from 1998 to 2002 (inclusive) to their individual CRCT education records from 2005 to 2009. We evaluated the association between MSDP (yes/no) and failure of the CRCT Reading, English/Language Arts (ELA), and Mathematics tests, with adjustment for maternal and child sociodemographic characteristics and birth outcomes. Log-binomial models estimated the risk ratios and 95% confidence intervals. Conditional models were fitted to paired sibling data.


Results
MSDP was associated with CRCT failure with an adjusted risk ratios for Reading: 1.16 [95% CI 1.12, 1.21]; ELA: 1.12 [95%CI 1.10, 1.15]; and Mathematics: 1.13 [95%CI 1.10, 1.16]. The association remained significant in paired sibling analyses.


Conclusions
MSDP may have independent long-term effects on offspring school performance, which does not appear to be through smoking-related adverse birth outcomes.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12046" xmlns="http://purl.org/rss/1.0/"><title>Physical Activity During Pregnancy and Language Development in the Offspring</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12046</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Physical Activity During Pregnancy and Language Development in the Offspring</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Anne Marie Z. Jukic, Debbie A. Lawlor, Mette Juhl, Katrine M. Owe, Barbara Lewis, Jihong Liu, Allen J. Wilcox, Matthew P. Longnecker</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12046</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12046</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12046</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Infant Outcomes</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">283</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">293</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12046-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>In rodents, physical activity during pregnancy has been associated with improved learning and memory in the offspring. We used data from the Avon Longitudinal Study of Parents and Children (born in 1991–92) to investigate maternal physical activity during pregnancy and offspring language development.</p></div></div>
<div class="section" id="ppe12046-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>At 18 weeks of gestation, women reported the hours per week they participated in 11 leisure-time physical activities and the hours per week spent in general physical activity (leisure, household and occupational). Caregivers completed a modified MacArthur Infant Communication scale at 15 months. Verbal intelligence quotient (IQ) was measured at age 8 years. Regression analysis was used to examine the associations of physical activity with MacArthur score (more than 75th percentile) and verbal IQ. The number of participants available for analyses ranged from 4529 to 7162.</p></div></div>
<div class="section" id="ppe12046-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Children of women in the two highest quintiles of leisure activity (compared with no leisure activity) were more likely to have high 15-month MacArthur scores (adjusted odds ratio 1.2 [95% confidence interval 0.9, 1.4] and adjusted odds ratio 1.4 [95% CI 1.1, 1.7], respectively). Leisure activity was not associated with IQ, while general physical activity was linked with lower verbal IQ (1 and 3 points lower for the two highest quintiles).</p></div></div>
<div class="section" id="ppe12046-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The most robust finding was a transient increase in offspring vocabulary score at young ages with maternal leisure activity. Differences in the associations with leisure-time physical activity compared with general physical activity need further exploration.</p></div></div>
]]></content:encoded><description>


Background
In rodents, physical activity during pregnancy has been associated with improved learning and memory in the offspring. We used data from the Avon Longitudinal Study of Parents and Children (born in 1991–92) to investigate maternal physical activity during pregnancy and offspring language development.


Methods
At 18 weeks of gestation, women reported the hours per week they participated in 11 leisure-time physical activities and the hours per week spent in general physical activity (leisure, household and occupational). Caregivers completed a modified MacArthur Infant Communication scale at 15 months. Verbal intelligence quotient (IQ) was measured at age 8 years. Regression analysis was used to examine the associations of physical activity with MacArthur score (more than 75th percentile) and verbal IQ. The number of participants available for analyses ranged from 4529 to 7162.


Results
Children of women in the two highest quintiles of leisure activity (compared with no leisure activity) were more likely to have high 15-month MacArthur scores (adjusted odds ratio 1.2 [95% confidence interval 0.9, 1.4] and adjusted odds ratio 1.4 [95% CI 1.1, 1.7], respectively). Leisure activity was not associated with IQ, while general physical activity was linked with lower verbal IQ (1 and 3 points lower for the two highest quintiles).


Conclusions
The most robust finding was a transient increase in offspring vocabulary score at young ages with maternal leisure activity. Differences in the associations with leisure-time physical activity compared with general physical activity need further exploration.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12045" xmlns="http://purl.org/rss/1.0/"><title>Direct and Proxy Recall of Childhood Socio-Economic Position and Health</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12045</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Direct and Proxy Recall of Childhood Socio-Economic Position and Health</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jennifer K. Straughen, Cleopatra H. Caldwell, Theresa L. Osypuk, Laura Helmkamp, Dawn P. Misra</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12045</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12045</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12045</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Methodology Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">294</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">302</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12045-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The utility of proxy reporting within the life course framework has not been adequately assessed; therefore we sought to assess the magnitude and type of agreement that exists between index and proxy reports for bodyweight, health, and socio-economic position (SEP) in childhood.</p></div></div>
<div class="section" id="ppe12045-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Participants were enrolled as part of an ongoing study of preterm birth in African American women in Metro Detroit. Post-partum women and their mothers (<em>n</em> = 333 pairs) provided retrospective reports about the woman's childhood bodyweight, health, and SEP. Agreement was assessed using kappa, weighted kappa (κ), and intraclass correlation coefficients (ICC). Log-linear models were used to describe the pattern of agreement for ordinal data.</p></div></div>
<div class="section" id="ppe12045-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Birthweight and weight at age 18 was reported with a high level of agreement (ICC = 0.86 and 0.71, respectively). Kappa indicated moderate agreement for early and late childhood/adolescent weight. Log-linear models suggested that there was diagonal agreement plus linear by linear association for early childhood weight and linear by linear association in late childhood/adolescence. Reports of childhood medical problems and hospitalisations had only moderate agreement. Agreement for SEP in both early (κ = 0.14) and late childhood/adolescence (κ = 0.20) was poor. Log-linear models suggest a linear by linear association, indicating a positive association between the responses.</p></div></div>
<div class="section" id="ppe12045-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Results suggest that proxy reports may be utilised in conjunction with an index report to provide an estimate of the accuracy of report or to more fully capture experiences over the life course. This may be particularly useful when multiple developmental periods are examined.</p></div></div>
]]></content:encoded><description>


Background
The utility of proxy reporting within the life course framework has not been adequately assessed; therefore we sought to assess the magnitude and type of agreement that exists between index and proxy reports for bodyweight, health, and socio-economic position (SEP) in childhood.


Methods
Participants were enrolled as part of an ongoing study of preterm birth in African American women in Metro Detroit. Post-partum women and their mothers (n = 333 pairs) provided retrospective reports about the woman's childhood bodyweight, health, and SEP. Agreement was assessed using kappa, weighted kappa (κ), and intraclass correlation coefficients (ICC). Log-linear models were used to describe the pattern of agreement for ordinal data.


Results
Birthweight and weight at age 18 was reported with a high level of agreement (ICC = 0.86 and 0.71, respectively). Kappa indicated moderate agreement for early and late childhood/adolescent weight. Log-linear models suggested that there was diagonal agreement plus linear by linear association for early childhood weight and linear by linear association in late childhood/adolescence. Reports of childhood medical problems and hospitalisations had only moderate agreement. Agreement for SEP in both early (κ = 0.14) and late childhood/adolescence (κ = 0.20) was poor. Log-linear models suggest a linear by linear association, indicating a positive association between the responses.


Conclusions
Results suggest that proxy reports may be utilised in conjunction with an index report to provide an estimate of the accuracy of report or to more fully capture experiences over the life course. This may be particularly useful when multiple developmental periods are examined.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12047" xmlns="http://purl.org/rss/1.0/"><title>Pregnancy Recruitment for Population Research: the National Children's Study Vanguard Experience in Wayne County, Michigan</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12047</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Pregnancy Recruitment for Population Research: the National Children's Study Vanguard Experience in Wayne County, Michigan</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jean M. Kerver, Michael R. Elliott, Gwendolyn S. Norman, Robert J. Sokol, Daniel P. Keating, Glenn E. Copeland, Christine C. Johnson, Kendall K. Cislo, Kirsten H. Alcser, Shonda R. Kruger-Ndiaye, Beth-Ellen Pennell, Shobha Mehta, Christine L. M. Joseph, Nigel Paneth, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-10T04:46:00.323148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ppe.12047</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ppe.12047</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fppe.12047</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Study Design Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">303</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">311</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3>
<div class="section" id="ppe12047-sec-0001" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>To obtain a probability sample of pregnancies, the National Children's Study conducted door-to-door recruitment in randomly selected neighbourhoods in randomly selected counties in 2009–10. In 2011, an experiment was conducted in 10 US counties, in which the two-stage geographic sample was maintained, but participants were recruited in prenatal care provider offices. We describe our experience recruiting pregnant women this way in Wayne County, Michigan, a county where geographically eligible women attended 147 prenatal care settings, and comprised just 2% of total county pregnancies.</p></div></div>
<div class="section" id="ppe12047-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>After screening for address eligibility in prenatal care offices, we used a three-part recruitment process: (1) providers obtained permission for us to contact eligible patients, (2) clinical research staff described the study to women in clinical settings, and (3) survey research staff visited the home to consent and interview eligible women.</p></div></div>
<div class="section" id="ppe12047-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We screened 34 065 addresses in 67 provider settings to find 215 eligible women. Providers obtained permission for research contact from 81.4% of eligible women, of whom 92.5% agreed to a home visit. All home-visited women consented, giving a net enrolment of 75%. From birth certificates, we estimate that 30% of eligible county pregnancies were enrolled, reaching 40–50% in the final recruitment months.</p></div></div>
<div class="section" id="ppe12047-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>We recruited a high fraction of pregnancies identified in a broad cross-section of provider offices. Nonetheless, because of time and resource constraints, we could enrol only a fraction of geographically eligible pregnancies. Our experience suggests that the probability sampling of pregnancies for research could be more efficiently achieved through sampling of providers rather than households.</p></div></div>
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Background
To obtain a probability sample of pregnancies, the National Children's Study conducted door-to-door recruitment in randomly selected neighbourhoods in randomly selected counties in 2009–10. In 2011, an experiment was conducted in 10 US counties, in which the two-stage geographic sample was maintained, but participants were recruited in prenatal care provider offices. We describe our experience recruiting pregnant women this way in Wayne County, Michigan, a county where geographically eligible women attended 147 prenatal care settings, and comprised just 2% of total county pregnancies.


Methods
After screening for address eligibility in prenatal care offices, we used a three-part recruitment process: (1) providers obtained permission for us to contact eligible patients, (2) clinical research staff described the study to women in clinical settings, and (3) survey research staff visited the home to consent and interview eligible women.


Results
We screened 34 065 addresses in 67 provider settings to find 215 eligible women. Providers obtained permission for research contact from 81.4% of eligible women, of whom 92.5% agreed to a home visit. All home-visited women consented, giving a net enrolment of 75%. From birth certificates, we estimate that 30% of eligible county pregnancies were enrolled, reaching 40–50% in the final recruitment months.


Conclusions
We recruited a high fraction of pregnancies identified in a broad cross-section of provider offices. Nonetheless, because of time and resource constraints, we could enrol only a fraction of geographically eligible pregnancies. Our experience suggests that the probability sampling of pregnancies for research could be more efficiently achieved through sampling of providers rather than households.

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