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<title>American Journal of Epidemiology - current issue</title>
<link>http://aje.oxfordjournals.org</link>
<description>American Journal of Epidemiology - RSS feed of current issue</description>
<prism:eIssn>1476-6256</prism:eIssn>
<prism:coverDisplayDate>1 January 2009</prism:coverDisplayDate>
<prism:publicationName>American Journal of Epidemiology</prism:publicationName>
<prism:issn>0002-9262</prism:issn>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/1?rss=1">
<title><![CDATA[Spousal Concordance for Major Coronary Risk Factors: A Systematic Review and Meta-Analysis]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/1?rss=1</link>
<description><![CDATA[
<p>Spousal pairs permit assessment of determinants of diseases related to environment, because they share the same lifestyle and environment. The authors reviewed spouses' concordance for the major coronary risk factors. A search of the MEDLINE, PubMed, and EMBASE databases was performed. Seventy-one papers were selected for a total of 207 cohorts of pairs and 424,613 correlations in more than 100,000 couples. The most strongly correlated within-pairs factors were smoking and body mass index, with overall correlations of 0.23 (95% confidence interval: 0.12, 0.36) and 0.15 (95% confidence interval: 0.05, 0.25), respectively. Statistically significant positive correlations were also found for diastolic blood pressure, triglycerides, total and low density lipoprotein cholesterol, weight, and the waist/hip ratio. The overall odds ratios for concordance in hypertension, smoking, diabetes, and obesity were all statistically significant, ranging from 1.16 to 3.25. Assortative mating influenced concordance for blood pressure, smoking, glucose, low density lipoprotein cholesterol, weight, body mass index, and waist circumference. This systematic review shows a statistically significant positive spousal concordance for the majority of main coronary risk factors. However, the strength of the concordance was markedly different among factors and appeared to be quite modest for all of them. Interventions to reduce cardiovascular risk factors should be addressed jointly to both members of a marital couple.</p>
]]></description>
<dc:creator><![CDATA[Di Castelnuovo, A., Quacquaruccio, G., Donati, M. B., de Gaetano, G., Iacoviello, L.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn234</dc:identifier>
<dc:title><![CDATA[Spousal Concordance for Major Coronary Risk Factors: A Systematic Review and Meta-Analysis]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>8</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>1</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/9?rss=1">
<title><![CDATA[Neural Tube Defects and Maternal Folate Intake Among Pregnancies Conceived After Folic Acid Fortification in the United States]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/9?rss=1</link>
<description><![CDATA[
<p>Rates of neural tube defects have decreased since folic acid fortification of the food supply in the United States. The authors&rsquo; objective was to evaluate the associations between neural tube defects and maternal folic acid intake among pregnancies conceived after fortification. This is a multicenter, case-control study that uses data from the National Birth Defects Prevention Study, 1998&ndash;2003. Logistic regression was used to compute crude and adjusted odds ratios between cases and controls assessing maternal periconceptional use of folic acid and intake of dietary folic acid. Among 180 anencephalic cases, 385 spina bifida cases, and 3, 963 controls, 21.1%, 25.2%, and 26.1%, respectively, reported periconceptional use of folic acid supplements. Periconceptional supplement use did not reduce the risk of having a pregnancy affected by a neural tube defect. Maternal intake of dietary folate was not significantly associated with neural tube defects. In this study conducted among pregnancies conceived after mandatory folic acid fortification, the authors found little evidence of an association between neural tube defects and maternal folic acid intake. A possible explanation is that folic acid fortification reduced the occurrence of folic acid-sensitive neural tube defects. Further investigation is warranted to possibly identify women who remain at increased risk of preventable neural tube defects.</p>
]]></description>
<dc:creator><![CDATA[Mosley, B. S., Cleves, M. A., Siega-Riz, A. M., Shaw, G. M., Canfield, M. A., Waller, D. K., Werler, M. M., Hobbs, C. A., for the National Birth Defects Prevention Study]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn331</dc:identifier>
<dc:title><![CDATA[Neural Tube Defects and Maternal Folate Intake Among Pregnancies Conceived After Folic Acid Fortification in the United States]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>17</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>9</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/18?rss=1">
<title><![CDATA[Invited Commentary: Preventing Neural Tube Defects and More via Food Fortification?]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/18?rss=1</link>
<description><![CDATA[
<p>Many neural tube defects can be prevented if women take folic acid around the time of conception. However, the majority of women do not take folic acid at the critical time, so the US government required that food be fortified with folic acid effective January 1, 1998. Whether the amount being added was sufficient to prevent all folate-related neural tube defects has been hotly debated. Mosley et al. (<I>Am J Epidemiol.</I> 2008;169(1):9&ndash;17) found no evidence that folic acid supplement use or dietary folate intake was related to neural tube defects, indicating that fortified food is probably providing sufficient folic acid to prevent folate-related defects. Because data on the effectiveness of fortification in the United States are scarce, this is an important contribution. There is great interest in the other effects of fortification. Folic acid reduces homocysteine levels, and homocysteine has been linked to cardiovascular disease and cancer. On the basis of current evidence, however, it seems unlikely that fortification will reduce cardiovascular disease rates. Its effect on cancer remains unclear. Folic acid may be useful in primary prevention but may also stimulate the growth of existing malignancies or premalignant lesions. Although these issues remain unresolved, Mosley et al. have provided important data to address the primary question: Does fortification prevent folate-related neural tube defects?</p>
]]></description>
<dc:creator><![CDATA[Mills, J. L., Carter, T. C.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn329</dc:identifier>
<dc:title><![CDATA[Invited Commentary: Preventing Neural Tube Defects and More via Food Fortification?]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>21</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>18</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/22?rss=1">
<title><![CDATA[Mosley and Hobbs Respond to "Folic Acid Fortification and Neural Tube Defects"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/22?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mosley, B. S., Hobbs, C. A.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn320</dc:identifier>
<dc:title><![CDATA[Mosley and Hobbs Respond to "Folic Acid Fortification and Neural Tube Defects"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>23</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>22</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/24?rss=1">
<title><![CDATA[Distinct Trajectories of Perinatal Depressive Symptomatology: Evidence From Growth Mixture Modeling]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/24?rss=1</link>
<description><![CDATA[
<p>Although heterogeneity in the timing and persistence of maternal depressive symptomatology has implications for screening and treatment as well as associated maternal and child health outcomes, little is known about this variability. A prospective observational study of 1,735 low-income, multiethnic, inner-city women recruited in pregnancy from 2000 to 2002 and followed prospectively until 2004 (1 prenatal and 3 postpartum interviews) was used to determine whether distinct trajectories of depressive symptomatology can be defined from pregnancy through 2 years postpartum. Analysis was carried out through general growth mixture modeling. A model with 5 trajectory classes characterized the heterogeneity seen in the timing and magnitude of depressive symptoms among the study participants from Philadelphia, Pennsylvania. These classes included the following: 1) always or <I>chronic</I> depressive symptomatology (7%); 2) <I>antepartum</I> only (6%); 3) <I>postpartum</I>, which resolves after the first year postpartum (9%); 4) <I>late,</I> present at 25 months postpartum (7%); and 5) <I>never</I> having depressive symptomatology (71%). Women in these trajectory classes differed in demographic (nativity, education, race, parity) health, health behavior, and psychosocial characteristics (ambivalence about pregnancy and high objective stress). This heterogeneity should be considered in maternal depression programs. Additional research is needed to determine the association of these trajectory classes with maternal and child health outcomes.</p>
]]></description>
<dc:creator><![CDATA[Mora, P. A., Bennett, I. M., Elo, I. T., Mathew, L., Coyne, J. C., Culhane, J. F.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn283</dc:identifier>
<dc:title><![CDATA[Distinct Trajectories of Perinatal Depressive Symptomatology: Evidence From Growth Mixture Modeling]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>32</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>24</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/33?rss=1">
<title><![CDATA[Maternal Smoking, Preeclampsia, and Infant Health Outcomes in New York City, 1995-2003]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/33?rss=1</link>
<description><![CDATA[
<p>A number of previous studies have reported an inverse association between maternal smoking and preeclampsia. Additionally, some have suggested that smokers who develop preeclampsia have worse maternal and fetal outcomes than nonsmokers who develop preeclampsia. The authors examined the relation of smoking to preeclampsia among 674,250 singleton pregnancies in New York City between 1995 and 2003. Although smoking was associated with a reduced risk of preeclampsia overall (adjusted odds ratio = 0.88, 95% confidence interval: 0.82, 0.94), no association was found for preeclampsia superimposed on chronic hypertension (adjusted odds ratio = 1.04, 95% confidence interval: 0.90, 1.21). Furthermore, the apparent protection conferred by maternal smoking was restricted to women aged &le;30 years. Contrary to previous reports, the authors found evidence of a negative interaction between smoking and preeclampsia with respect to preterm delivery and birth weight; smokers who developed preeclampsia had a lower risk of preterm delivery, and a lower adjusted mean difference in birth weight, than would have been expected based on the independent effects of smoking and preeclampsia. These data suggest that smoking is only protective against preeclampsia without pregestational hypertension, and even then principally among younger women. Additionally, smokers who develop these disorders have no increased risk of adverse birth outcomes relative to nonsmokers who develop the same conditions.</p>
]]></description>
<dc:creator><![CDATA[Engel, S. M., Janevic, T. M., Stein, C. R., Savitz, D. A.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn293</dc:identifier>
<dc:title><![CDATA[Maternal Smoking, Preeclampsia, and Infant Health Outcomes in New York City, 1995-2003]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>40</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>33</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/41?rss=1">
<title><![CDATA[Study of Nevi in Children (SONIC): Baseline Findings and Predictors of Nevus Count]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/41?rss=1</link>
<description><![CDATA[
<p>The authors report baseline findings and predictors of nevus count (log total nevi) at the completion of year 1 (2004) of the first known population-based, prospective study of nevi in a US cohort of children. Overall, 64% (<I>n</I> = 443/691) of grade 5 students and their parents in Framingham, Massachusetts, completed surveys and underwent digital photography. Total nevus count was associated with skin and hair color and tendency to burn, as measured by a sun sensitivity index. In multivariate analyses, male gender (rate ratio (RR) = 1.38, 95% confidence interval (CI): 1.22, 1.55; <I>P</I> &lt; 0.0001), spending 5&ndash;6 weekly hours outdoors between 10 <scp>AM</scp> and 4 <scp>PM</scp> (RR = 1.13, 95% CI: 1.00, 1.28; <I>P</I> = 0.051), getting a painful sunburn once (RR = 1.24, 95% CI: 0.98, 1.57; <I>P</I> = 0.073) and at least twice (RR = 1.34, 95% CI: 0.99, 1.82; <I>P</I> = 0.061), and wearing a shirt at the beach or pool rarely (RR = 1.29, 95% CI: 1.08, 1.54; <I>P</I> = 0.005), sometimes (RR = 1.26, 95% CI: 1.01, 1.57; <I>P</I> = 0.041), and often and always (RR = 1.32, 95% CI: 1.13, 1.54; <I>P</I> = 0.001) were associated with increased number of nevi. Identifying factors that predict the development of nevi will improve primary prevention efforts during early life.</p>
]]></description>
<dc:creator><![CDATA[Oliveria, S. A., Satagopan, J. M., Geller, A. C., Dusza, S. W., Weinstock, M. A., Berwick, M., Bishop, M., Heneghan, M. K., Halpern, A. C.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn289</dc:identifier>
<dc:title><![CDATA[Study of Nevi in Children (SONIC): Baseline Findings and Predictors of Nevus Count]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>53</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>41</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/54?rss=1">
<title><![CDATA[Prevalence in the United States of Selected Candidate Gene Variants: Third National Health and Nutrition Examination Survey, 1991-1994]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/54?rss=1</link>
<description><![CDATA[
<p>Population-based allele frequencies and genotype prevalence are important for measuring the contribution of genetic variation to human disease susceptibility, progression, and outcomes. Population-based prevalence estimates also provide the basis for epidemiologic studies of gene&ndash;disease associations, for estimating population attributable risk, and for informing health policy and clinical and public health practice. However, such prevalence estimates for genotypes important to public health remain undetermined for the major racial and ethnic groups in the US population. DNA was collected from 7,159 participants aged 12 years or older in Phase 2 (1991&ndash;1994) of the Third National Health and Nutrition Examination Survey (NHANES III). Certain age and minority groups were oversampled in this weighted, population-based US survey. Estimates of allele frequency and genotype prevalence for 90 variants in 50 genes chosen for their potential public health significance were calculated by age, sex, and race/ethnicity among non-Hispanic whites, non-Hispanic blacks, and Mexican Americans. These nationally representative data on allele frequency and genotype prevalence provide a valuable resource for future epidemiologic studies in public health in the United States.</p>
]]></description>
<dc:creator><![CDATA[Chang, M.-h., Lindegren, M. L., Butler, M. A., Chanock, S. J., Dowling, N. F., Gallagher, M., Moonesinghe, R., Moore, C. A., Ned, R. M., Reichler, M. R., Sanders, C. L., Welch, R., Yesupriya, A., Khoury, M. J., for the CDC/NCI NHANES III Genomics Working Group]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn286</dc:identifier>
<dc:title><![CDATA[Prevalence in the United States of Selected Candidate Gene Variants: Third National Health and Nutrition Examination Survey, 1991-1994]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>66</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>54</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/67?rss=1">
<title><![CDATA[Investigation of Gender Heterogeneity in the Associations of Serum Phosphorus With Incident Coronary Artery Disease and All-Cause Mortality]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/67?rss=1</link>
<description><![CDATA[
<p>Serum phosphorus levels in the general population have been reported to be associated with cardiovascular morbidity and mortality and increased carotid intima-media thickness. The authors examined gender heterogeneity in the association of phosphorus with all-cause mortality and incident coronary artery disease using data from the Atherosclerosis Risk in Communities Study (1987&ndash;2001). Baseline phosphorus levels were higher in women and were associated differently among men and women with traditional atherosclerosis risk factors such as age, low density lipoprotein cholesterol, diabetes mellitus, and hypertension. In a multivariable-adjusted model, men in the highest quintile of serum phosphorus level (&gt;3.8 mg/dL) had an increased mortality rate (hazard ratio = 1.45, 95% confidence interval: 1.12, 1.88), while women did not (hazard ratio = 1.18, 95% confidence interval: 0.89, 1.57). The multivariable likelihood ratio test of effect modification by gender was significant at  = 0.1 (<I>P</I> = 0.085) for all-cause mortality. Although the associations of phosphorus with coronary artery disease also appeared to differ substantially by gender, the multivariable test for effect modification suggested that the difference was consistent with random variation (<I>P</I> = 0.195). These results suggest the need for further investigation into gender differences in the contribution of mineral metabolism to cardiovascular disease in the general population.</p>
]]></description>
<dc:creator><![CDATA[Onufrak, S. J., Bellasi, A., Cardarelli, F., Vaccarino, V., Muntner, P., Shaw, L. J., Raggi, P.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn285</dc:identifier>
<dc:title><![CDATA[Investigation of Gender Heterogeneity in the Associations of Serum Phosphorus With Incident Coronary Artery Disease and All-Cause Mortality]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>77</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>67</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/78?rss=1">
<title><![CDATA[Multistage Modeling of Leukemia in Benzene Workers: A Simple Approach to Fitting the 2-Stage Clonal Expansion Model]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/78?rss=1</link>
<description><![CDATA[
<p>A simple SAS software program (SAS Institute, Inc., Cary, North Carolina) was developed for fitting an exact formulation of the 2-stage clonal expansion model accommodating piecewise constant exposures and left and right censoring of observations. Data on leukemia mortality and occupational exposure to benzene among rubber hydrochloride production workers in Ohio (1940&ndash;1996) were analyzed by using this approach. A model in which benzene exposure increased clonal expansion fit these data well; little evidence of an association between benzene exposure and initiation of leukemia was found. The estimated exposure-response association increased in magnitude with age at exposure and decreased with time since exposure. This analysis shows that the 2-stage clonal expansion model can be readily fit to epidemiologic cohort data by using a simple SAS program. The illustrative analyses of leukemia mortality among rubber hydrochloride workers suggest that the effect of benzene on leukemia risk is due to an exposure-induced increase in the proliferation of initiated cells.</p>
]]></description>
<dc:creator><![CDATA[Richardson, D. B.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn284</dc:identifier>
<dc:title><![CDATA[Multistage Modeling of Leukemia in Benzene Workers: A Simple Approach to Fitting the 2-Stage Clonal Expansion Model]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>85</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>78</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/86?rss=1">
<title><![CDATA[Mortality After Exposure to Polychlorinated Biphenyls and Polychlorinated Dibenzofurans: A 40-Year Follow-up Study of Yusho Patients]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/86?rss=1</link>
<description><![CDATA[
<p>A 40-year follow-up study was conducted to examine mortality among 1,664 patients in Japan suffering from "Yusho," a disease caused by ingestion of rice oil contaminated with polychlorinated biphenyls and polychlorinated dibenzofurans. To evaluate the effects of exposure on mortality, the authors calculated standardized mortality ratios. National mortality rates for major causes of death were used as reference points. A total of 1,596 Yusho patients (95.9%) were followed until death or the end of the study (December 31, 2007). The standardized mortality ratios for most major causes of death were not significantly elevated, with the exceptions of all types of cancer (standardized mortality ratio (SMR) = 1.37, 95% confidence interval (CI): 1.11, 1.66), liver cancer (SMR = 1.82, 95% CI: 1.06, 2.91), and lung cancer (SMR = 1.75, 95% CI: 1.14, 2.57) in males. In addition, the standardized mortality ratios for all cancers, liver cancer, and lung cancer among males tended to decrease over time. Results from this study suggest that the carcinogenicity of polychlorinated biphenyls and polychlorinated dibenzofurans must be taken into account when evaluating mortality risk.</p>
]]></description>
<dc:creator><![CDATA[Onozuka, D., Yoshimura, T., Kaneko, S., Furue, M.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn295</dc:identifier>
<dc:title><![CDATA[Mortality After Exposure to Polychlorinated Biphenyls and Polychlorinated Dibenzofurans: A 40-Year Follow-up Study of Yusho Patients]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>95</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>86</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/96?rss=1">
<title><![CDATA[Light to Moderate Alcohol Consumption and Disability: Variable Benefits by Health Status]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/96?rss=1</link>
<description><![CDATA[
<p>In adults, light to moderate alcohol consumption is associated with lower risks for heart disease, diabetes, and mortality. This study examined whether light to moderate alcohol use is also associated with lower risk of incident physical disability over two 5-year periods in 4,276 noninstitutionalized adults in the United States, aged 50 years or older, by using data from 3 waves of the National Health and Nutrition Examination Survey Epidemiologic Follow-up Study surveys from 1982 to 1992. Light/moderate drinking (&lt;15 drinks per week and &lt;5 per drinking day or 4 per drinking day for women) was associated with reduced risk for incident disability or death over 5 years, compared with abstention (adjusted odds ratio = 0.77; <I>P</I> = 0.008). Among survivors, light/moderate drinking was associated with lower risk for incident disability, compared with abstention (adjusted odds ratio = 0.75; <I>P</I> = 0.009). In stratified analyses, disability risk decreased with light/moderate drinking in a dose-dependent fashion in men and women with good or better self-reported health but not in men or women with fair or worse self-reported health. Alcohol consumption in moderation might reduce the risk of developing physical disability in older adults in good health but not in those in poor health.</p>
]]></description>
<dc:creator><![CDATA[Karlamangla, A. S., Sarkisian, C. A., Kado, D. M., Dedes, H., Liao, D. H., Kim, S., Reuben, D. B., Greendale, G. A., Moore, A. A.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn294</dc:identifier>
<dc:title><![CDATA[Light to Moderate Alcohol Consumption and Disability: Variable Benefits by Health Status]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>104</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>96</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/105?rss=1">
<title><![CDATA[Timing Clinic Visits to Phases of the Menstrual Cycle by Using a Fertility Monitor: The BioCycle Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/105?rss=1</link>
<description><![CDATA[
<p>Planning study visits during specific menstrual cycle phases is important if the exposure or outcome is influenced by hormonal variation. However, hormone profiles differ across cycles and across women. The value of using fertility monitors to time clinic visits was evaluated in the BioCycle Study (2005&ndash;2007). Women aged 18&ndash;44 years (mean, 27.4) with self-reported menstrual cycle lengths of 21&ndash;35 days were recruited in Buffalo, New York, for 2 cycles (<I>n</I> = 250). Participants were provided with home fertility monitors that measured urinary estrone-3-glucuronide and luteinizing hormone (LH). The women were instructed to visit the clinic for a blood draw when the monitor indicated an LH surge. The monitor recorded a surge during 76% of the first cycles and 78% of the second cycles. Scheduling visits by using set cycle days or algorithms based on cycle length, such as a midcycle window or a window determined by assuming a fixed luteal phase length, would be simpler. However, even with perfect attendance in a 3-day window, these methods would have performed poorly, capturing the monitor-detected LH surge only 37%&ndash;57% of the time. Fertility monitors appear to be useful in timing clinic visits in a compliant population with flexible schedules.</p>
]]></description>
<dc:creator><![CDATA[Howards, P. P., Schisterman, E. F., Wactawski-Wende, J., Reschke, J. E., Frazer, A. A., Hovey, K. M.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn287</dc:identifier>
<dc:title><![CDATA[Timing Clinic Visits to Phases of the Menstrual Cycle by Using a Fertility Monitor: The BioCycle Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>112</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>105</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/113?rss=1">
<title><![CDATA[Fractional Polynomials and Model Selection in Generalized Estimating Equations Analysis, With an Application to a Longitudinal Epidemiologic Study in Australia]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/113?rss=1</link>
<description><![CDATA[
<p>In epidemiologic studies, researchers often need to establish a nonlinear exposure-response relation between a continuous risk factor and a health outcome. Furthermore, periodic interviews are often conducted to take repeated measurements from an individual. The authors proposed to use fractional polynomial models to jointly analyze the effects of 2 continuous risk factors on a health outcome. This method was applied to an analysis of the effects of age and cumulative fluoride exposure on forced vital capacity in a longitudinal study of lung function carried out among aluminum workers in Australia (1995&ndash;2003). Generalized estimating equations and the quasi-likelihood under the independence model criterion were used. The authors found that the second-degree fractional polynomial models for age and fluoride fitted the data best. The best model for age was robust across different models for fluoride, and the best model for fluoride was also robust. No evidence was found to suggest that the effects of smoking and cumulative fluoride exposure on change in forced vital capacity over time were significant. The trend 1 model, which included the unexposed persons in the analysis of trend in forced vital capacity over tertiles of fluoride exposure, did not fit the data well, and caution should be exercised when this method is used.</p>
]]></description>
<dc:creator><![CDATA[Cui, J., de Klerk, N., Abramson, M., Del Monaco, A., Benke, G., Dennekamp, M., Musk, A. W., Sim, M.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn292</dc:identifier>
<dc:title><![CDATA[Fractional Polynomials and Model Selection in Generalized Estimating Equations Analysis, With an Application to a Longitudinal Epidemiologic Study in Australia]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>121</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>113</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/122?rss=1">
<title><![CDATA[RE: "WATER DISINFECTION BY-PRODUCTS AND PRELABOR RUPTURE OF MEMBRANES"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/122?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Heitz, A., Kristiana, I.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn377</dc:identifier>
<dc:title><![CDATA[RE: "WATER DISINFECTION BY-PRODUCTS AND PRELABOR RUPTURE OF MEMBRANES"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>123</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>122</prism:startingPage>
<prism:section>LETTER</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/169/1/124?rss=1">
<title><![CDATA[Environmental Epidemiology: Principles and Methods: By Ray M. Merrill]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/169/1/124?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Checkoway, H.]]></dc:creator>
<dc:date>2008-12-29</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn373</dc:identifier>
<dc:title><![CDATA[Environmental Epidemiology: Principles and Methods: By Ray M. Merrill]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>169</prism:volume>
<prism:endingPage>125</prism:endingPage>
<prism:publicationDate>2009-01-01</prism:publicationDate>
<prism:startingPage>124</prism:startingPage>
<prism:section>BOOK-REVIEW</prism:section>
</item>

</rdf:RDF>