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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>15 May 2008</prism:coverDisplayDate>
<prism:publicationName>American Journal of Epidemiology</prism:publicationName>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1143?rss=1">
<title><![CDATA[Low Workplace Social Capital as a Predictor of Depression: The Finnish Public Sector Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1143?rss=1</link>
<description><![CDATA[
<p>In a prospective cohort study of Finnish public sector employees, the authors examined the association between workplace social capital and depression. Data were obtained from 33,577 employees, who had no recent history of antidepressant treatment and who reported no history of physician-diagnosed depression at baseline in 2000&ndash;2002. Their risk of depression was measured with two indicators: recorded purchases of antidepressants until December 31, 2005, and self-reports of new-onset depression diagnosed by a physician in the follow-up survey in 2004&ndash;2005. Multilevel logistic regression analysis was used to explore whether self-reported and aggregate-level workplace social capital predicted indicators of depression at follow-up. The odds for antidepressant treatment and physician-diagnosed depression were 20&ndash;50% higher for employees with low self-reported social capital than for those reporting high social capital. These associations were not accounted for by sex, age, marital status, socioeconomic position, place of work, smoking, alcohol use, physical activity, and body mass index. The association between social capital and self-reported depression attenuated but remained significant after further adjustment for baseline psychological distress (a proxy for undiagnosed mental health problems). Aggregate-level social capital was not associated with subsequent depression.</p>
]]></description>
<dc:creator><![CDATA[Kouvonen, A., Oksanen, T., Vahtera, J., Stafford, M., Wilkinson, R., Schneider, J., Vaananen, A., Virtanen, M., Cox, S. J., Pentti, J., Elovainio, M., Kivimaki, M.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn067</dc:identifier>
<dc:title><![CDATA[Low Workplace Social Capital as a Predictor of Depression: The Finnish Public Sector Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1151</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1143</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1152?rss=1">
<title><![CDATA[Invited Commentary: Social Capital, Social Contexts, and Depression]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1152?rss=1</link>
<description><![CDATA[
<p>The literature concerning social capital and health has grown exponentially during the past somewhat more than 10 years. The study by Kouvonen et al. (<I>Am J Epidemiol</I> 2008;167:1143&ndash;1151) is a longitudinal multilevel analysis of 33,577 public sector employees in Finland. The study shows a significant association between workplace social capital and depression, which is an interesting finding in a very new field of the study of social capital and health. However, the study also serves as an inspiration for further studies in important research areas. Workplace social capital may be investigated according to both horizontal, that is, social contacts and level of trust in relation to coworkers, and vertical, that is, relation with employer/supervisor across power gradients, dimensions. The fact that workplace social capital may affect social capital outside work and vice versa is also of interest. It is also important to define and identify the social context level in a correct way in multilevel studies. In the study by Kouvonen et al., the social context is not a geographic entity but an entity defined according to place of work, and the definition of such a social context entails several difficulties. This study presents interesting findings and provides a basis for future studies.</p>
]]></description>
<dc:creator><![CDATA[Lindstrom, M.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn070</dc:identifier>
<dc:title><![CDATA[Invited Commentary: Social Capital, Social Contexts, and Depression]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1154</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1152</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1155?rss=1">
<title><![CDATA[Determinants and Outcomes of Serious Attempted Suicide: A Nationwide Study in Finland, 1996-2003]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1155?rss=1</link>
<description><![CDATA[
<p>Suicide is among the 10 leading causes of death. Attempted suicide is 10&ndash;40 times more frequent than completed suicide and is the strongest single predictor of subsequent suicide. The current study population included all persons in Finland who were hospitalized with a diagnosis of attempted suicide between 1996 and 2003 (<I>N</I> = 18,199). Information on background variables and mortality was obtained by register linkage. The risk of repeated attempted suicide was 30% and the risk of suicide was 10%. The risks of repeated attempted suicide, completed suicide, and death from any cause were high immediately after discharge from the hospital. Analysis of competing causes of death revealed that while alcohol-related disorder was not associated with suicide, it markedly increased the risk of other violent death: The subdistribution hazards rate (SHR) was 2.61 (95% confidence interval (CI): 2.12, 3.21). Schizophrenia-related disorders (SHR = 1.87, 95% CI: 1.57, 2.21) and mood disorders (SHR = 1.72, 95% CI: 1.47, 2.01) were associated with the risk of suicide. The risks of suicide and all-cause mortality were extremely high immediately after hospitalization for attempted suicide.</p>
]]></description>
<dc:creator><![CDATA[Haukka, J., Suominen, K., Partonen, T., Lonnqvist, J.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn017</dc:identifier>
<dc:title><![CDATA[Determinants and Outcomes of Serious Attempted Suicide: A Nationwide Study in Finland, 1996-2003]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1163</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1155</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1164?rss=1">
<title><![CDATA[Maternal Dietary Intake of Vitamin A and Risk of Orofacial Clefts: A Population-based Case-Control Study in Norway]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1164?rss=1</link>
<description><![CDATA[
<p>A population-based case-control study was carried out in Norway between 1996 and 2001. The aim was to evaluate the association between maternal intake of vitamin A from diet and supplements and risk of having a baby with an orofacial cleft. Data on maternal dietary intake were available from 535 cases (188 with cleft palate only and 347 with cleft lip with or without cleft palate) and 693 controls. The adjusted odds ratio for isolated cleft palate only was 0.47 (95% confidence interval: 0.24, 0.94) when comparing the fourth and first quartiles of maternal intake of total vitamin A. In contrast, there was no appreciable association of total vitamin A with isolated cleft lip with or without cleft palate. An intake of vitamin A above the 95th percentile was associated with a lower estimated risk of all isolated clefts compared with the 40th&ndash;60th percentile (adjusted odds ratio = 0.48, 95% confidence interval: 0.20, 1.14). Maternal intake of vitamin A is associated with reduced risk of cleft palate only, and there is no evidence of increased risk of clefts among women in our study with the highest 5% of vitamin A intake.</p>
]]></description>
<dc:creator><![CDATA[Johansen, A. M. W., Lie, R. T., Wilcox, A. J., Andersen, L. F., Drevon, C. A.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn035</dc:identifier>
<dc:title><![CDATA[Maternal Dietary Intake of Vitamin A and Risk of Orofacial Clefts: A Population-based Case-Control Study in Norway]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1170</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1164</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1171?rss=1">
<title><![CDATA[Maternal Fish Intake during Pregnancy, Blood Mercury Levels, and Child Cognition at Age 3 Years in a US Cohort]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1171?rss=1</link>
<description><![CDATA[
<p>The balance of contaminant risk and nutritional benefit from maternal prenatal fish consumption for child cognitive development is not known. Using data from a prospective cohort study of 341 mother-child pairs in Massachusetts enrolled in 1999&ndash;2002, the authors studied associations of maternal second-trimester fish intake and erythrocyte mercury levels with children's scores on the Peabody Picture Vocabulary Test (PPVT) and Wide Range Assessment of Visual Motor Abilities (WRAVMA) at age 3 years. Mean maternal total fish intake was 1.5 (standard deviation, 1.4) servings/week, and 40 (12%) mothers consumed &gt;2 servings/week. Mean maternal mercury level was 3.8 (standard deviation, 3.8) ng/g. After adjustment using multivariable linear regression, higher fish intake was associated with better child cognitive test performance, and higher mercury levels with poorer test scores. Associations strengthened with inclusion of both fish and mercury: effect estimates for fish intake of &gt;2 servings/week versus never were 2.2 (95% confidence interval (CI): &ndash;2.6, 7.0) for the PPVT and 6.4 (95% CI: 2.0, 10.8) for the WRAVMA; for mercury in the top decile, they were &ndash;4.5 (95% CI: &ndash;8.5, &ndash;0.4) for the PPVT and &ndash;4.6 (95% CI: &ndash;8.3, &ndash;0.9) for the WRAVMA. Fish consumption of &le;2 servings/week was not associated with a benefit. Dietary recommendations for pregnant women should incorporate the nutritional benefits as well as the risks of fish intake.</p>
]]></description>
<dc:creator><![CDATA[Oken, E., Radesky, J. S., Wright, R. O., Bellinger, D. C., Amarasiriwardena, C. J., Kleinman, K. P., Hu, H., Gillman, M. W.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn034</dc:identifier>
<dc:title><![CDATA[Maternal Fish Intake during Pregnancy, Blood Mercury Levels, and Child Cognition at Age 3 Years in a US Cohort]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1181</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1171</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1182?rss=1">
<title><![CDATA[Eczema, Birth Order, and Infection]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1182?rss=1</link>
<description><![CDATA[
<p>The association between infections occurring in the first 2 years of life and development of eczema was investigated in 1,782 control children from a national population-based case-control study in the United Kingdom conducted over the period 1991&ndash;1996. Dates of eczema and infectious diagnoses were ascertained from contemporaneously collected primary care records. Children diagnosed with eczema before the age of 2 years had more prior clinically diagnosed infections recorded than did children without eczema (rate ratio = 1.26, 95% confidence interval (CI): 1.18, 1.36). The difference in infection rates between children with and without eczema was apparent from birth and throughout the first 2 years of life. As expected, compared with children of second or higher birth order, those firstborn were at increased risk of eczema (<I>p</I> = 0.020); however, the relation between eczema and prior infection was evident only among children of second or higher birth order and not among firstborn children (rate ratio = 1.45, 95% CI: 1.32, 1.59, and rate ratio = 1.08, 95% CI: 0.98, 1.20, respectively). The authors' results are consistent with the notion that the association between birth order and eczema is unlikely to be attributable to variations in early infectious exposure.</p>
]]></description>
<dc:creator><![CDATA[Hughes, A. M., Crouch, S., Lightfoot, T., Ansell, P., Simpson, J., Roman, E.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn042</dc:identifier>
<dc:title><![CDATA[Eczema, Birth Order, and Infection]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1187</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1182</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1188?rss=1">
<title><![CDATA[Domestic Violence and Chronic Malnutrition among Women and Children in India]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1188?rss=1</link>
<description><![CDATA[
<p>Domestic violence has harmful physical and psychological health correlates, but there is little evidence regarding a relation between domestic violence and malnutrition. To investigate this relation, the authors analyzed data from 69,072 women aged 15&ndash;49 years and 14,552 children aged 12&ndash;35 months in the 1998&ndash;1999 Indian National Family Health Survey. Physical domestic violence victimization was self-reported by the women. Aspects of nutritional status included in this study were anemia and underweight. Anemia was measured with a blood test for hemoglobin. Underweight was calculated from anthropometric measurements and was determined as body mass index for women, and it included stunting and wasting for children. Results indicate associations of multiple incidents of domestic violence in the previous year with anemia (odds ratio = 1.11, 95% confidence interval: 1.04, 1.18) and underweight (odds ratio = 1.21, 95% confidence interval: 1.13, 1.29) in women and a suggested relation among children. Possible mechanisms for this relation include withholding of food as a form of abuse and stress-mediated influences of domestic violence on nutritional outcomes. These findings indicate that reducing domestic violence is important not only from a moral and intrinsic perspective but also because of the instrumental health benefits likely to accrue.</p>
]]></description>
<dc:creator><![CDATA[Ackerson, L. K., Subramanian, S. V.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn049</dc:identifier>
<dc:title><![CDATA[Domestic Violence and Chronic Malnutrition among Women and Children in India]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1196</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1188</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1197?rss=1">
<title><![CDATA[A Prospective Study of Multivitamin Supplement Use and Risk of Breast Cancer]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1197?rss=1</link>
<description><![CDATA[
<p>The authors evaluated the association between multivitamin supplement use and breast cancer risk in a completed trial. At baseline (1992&ndash;1995), 37,920 US women aged &ge;45 years and free of cancer provided detailed information on multivitamin supplement use. During an average of 10 years of follow-up, 1,171 cases of invasive breast cancer were documented. Multivitamin use was not significantly associated with overall risk of breast cancer. Compared with the risk for never users, the multivariable relative risks were 0.97 (95% confidence interval: 0.81, 1.16) for past users and 0.99 (95% confidence interval: 0.82, 1.19) for current users. Current multivitamin use for &ge;20 years or &ge;6 times/week was also not significantly associated with risk. Multivitamin use was nonsignificantly inversely associated with risk of breast cancer among women consuming &ge;10 g/day of alcohol and with risk of estrogen receptor negative&ndash;progesterone receptor negative breast cancer. Multivitamin use was nonsignificantly associated with a reduced risk of developing &le;2-cm breast tumors but an increased risk of &gt;2-cm tumors. The authors' data indicate no overall association between multivitamin use and breast cancer risk but suggest that multivitamin use might reduce risk for women consuming alcohol or decrease risk of estrogen receptor negative&ndash;progesterone receptor negative breast cancer.</p>
]]></description>
<dc:creator><![CDATA[Ishitani, K., Lin, J., Manson, J. E., Buring, J. E., Zhang, S. M.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn027</dc:identifier>
<dc:title><![CDATA[A Prospective Study of Multivitamin Supplement Use and Risk of Breast Cancer]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1206</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1197</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1207?rss=1">
<title><![CDATA[Estrogen Plus Progestin Therapy and Breast Cancer in Recently Postmenopausal Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1207?rss=1</link>
<description><![CDATA[
<p>The Women's Health Initiative trial found a modestly increased risk of invasive breast cancer with daily 0.625-mg conjugated equine estrogens plus 2.5-mg medroxyprogesterone acetate, with most evidence among women who had previously received postmenopausal hormone therapy. In comparison, observational studies mostly report a larger risk increase. To explain these patterns, the authors examined the effects of this regimen in relation to both prior hormone therapy and time from menopause to first use of postmenopausal hormone therapy ("gap time") in the Women's Health Initiative trial and in a corresponding subset of the Women's Health Initiative observational study. Postmenopausal women with a uterus enrolled at 40 US clinical centers during 1993&ndash;1998. The authors found that hazard ratios agreed between the two cohorts at a specified gap time and time from hormone therapy initiation. Combined trial and observational study data support an adverse effect on breast cancer risk. Women who initiate use soon after menopause, and continue for many years, appear to be at particularly high risk. For example, for a woman who starts soon after menopause and adheres to this regimen, estimated hazard ratios are 1.64 (95% confidence interval: 1.00, 2.68) over a 5-year period of use and 2.19 (95% confidence interval: 1.56, 3.08) over a 10-year period of use.</p>
]]></description>
<dc:creator><![CDATA[Prentice, R. L., Chlebowski, R. T., Stefanick, M. L., Manson, J. E., Pettinger, M., Hendrix, S. L., Hubbell, F. A., Kooperberg, C., Kuller, L. H., Lane, D. S., McTiernan, A., Jo O'Sullivan, M., Rossouw, J. E., Anderson, G. L.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn044</dc:identifier>
<dc:title><![CDATA[Estrogen Plus Progestin Therapy and Breast Cancer in Recently Postmenopausal Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1216</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1207</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1217?rss=1">
<title><![CDATA[Estrogen Receptor Alpha and Matrix Metalloproteinase 2 Polymorphisms and Age-related Maculopathy in Older Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1217?rss=1</link>
<description><![CDATA[
<p>In this study, the authors sought to determine whether single nucleotide polymorphisms in the estrogen receptor alpha (<I>ESR1</I>) and matrix metalloproteinase 2 (<I>MMP2</I>) genes are associated with age-related maculopathy (ARM) in older women. Subjects comprised a random sample of Caucasian women aged &ge;74 years participating in the Study of Osteoporotic Fractures year 10 follow-up (<I>n</I> = 906) in 1997&ndash;1998. Fundus photographs were graded for ARM using a modification of the Wisconsin Age-Related Maculopathy Grading System. The prevalences of early ARM and late ARM were 46% and 4%, respectively. The <I>MMP2 rs2287074</I> single nucleotide polymorphism (G-&gt;A) was associated with ARM. The A allele was present in 47%, 43%, and 30% of subjects with no, early, and late ARM, respectively (<I>p</I> = 0.01), and was associated with lower odds of any ARM (for AG vs. GG, odds ratio = 0.80, 95% confidence interval: 0.65, 0.99; for AA vs. GG, odds ratio = 0.64, 95% confidence interval: 0.42, 0.98). An interaction with use of postmenopausal hormone therapy was significant (<I>p</I> = 0.02). The <I>MMP2 rs2287074</I> A allele may be associated with a lower likelihood of ARM in older Caucasian women, particularly those who have never used hormone therapy. The role of <I>MMP2 rs2287074</I> in ARM should be further elucidated.</p>
]]></description>
<dc:creator><![CDATA[Seitzman, R. L., Mahajan, V. B., Mangione, C., Cauley, J. A., Ensrud, K. E., Stone, K. L., Cummings, S. R., Hochberg, M. C., Hillier, T. A., Sinsheimer, J. S., Yu, F., Coleman, A. L., for the Study of Osteoporotic Fractures Research Group]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn024</dc:identifier>
<dc:title><![CDATA[Estrogen Receptor Alpha and Matrix Metalloproteinase 2 Polymorphisms and Age-related Maculopathy in Older Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1225</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1217</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1226?rss=1">
<title><![CDATA[Glomerular Filtration Rate, Albuminuria, and Risk of Cardiovascular and All-Cause Mortality in the US Population]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1226?rss=1</link>
<description><![CDATA[
<p>Decreased glomerular filtration rate (GFR) and albuminuria are used in combination to define chronic kidney disease, but their separate and combined effects on cardiovascular and all-cause mortality have not been studied in the general population. The linked mortality file of the Third National Health and Nutrition Examination Survey includes data from 13 years of follow-up (1988&ndash;2000) for 14,586 US adults. The authors estimated GFR from standardized serum creatinine levels. Albuminuria was defined by the urinary albumin:creatinine ratio. Incidence rate ratios (IRRs) were adjusted for major cardiovascular disease risk factors and C-reactive protein. Lower estimated GFR was associated with higher risks of cardiovascular and all-cause mortality overall and within every albuminuria category. Likewise, increasing albuminuria was associated with higher risk of estimated GFR overall and within every category. When estimated GFR and albuminuria were examined simultaneously, a 10-ml/minute/1.73 m<sup>2</sup> lower estimated GFR (among persons with estimated GFR &lt;60 ml/minute/1.73 m<sup>2</sup>) was associated with an IRR of 1.29 (95% confidence interval: 1.06, 1.55) for cardiovascular mortality and a doubling of albuminuria was associated with an IRR of 1.06 (95% confidence interval: 1.04, 1.08) for cardiovascular mortality. The authors conclude that moderately decreased estimated GFR and albuminuria independently predict cardiovascular and all-cause mortality in the general population. These data support recent recommendations defining chronic kidney disease and stratifying subsequent risks based on both decreased GFR and albuminuria.</p>
]]></description>
<dc:creator><![CDATA[Astor, B. C., Hallan, S. I., Miller, E. R., Yeung, E., Coresh, J.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn033</dc:identifier>
<dc:title><![CDATA[Glomerular Filtration Rate, Albuminuria, and Risk of Cardiovascular and All-Cause Mortality in the US Population]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1234</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1226</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1235?rss=1">
<title><![CDATA[Incident Diabetes and Pesticide Exposure among Licensed Pesticide Applicators: Agricultural Health Study, 1993-2003]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1235?rss=1</link>
<description><![CDATA[
<p>Exposure to certain environmental toxicants may be associated with increased risk of developing diabetes. The authors' aim was to investigate the relation between lifetime exposure to specific agricultural pesticides and diabetes incidence among pesticide applicators. The study included 33,457 licensed applicators, predominantly non-Hispanic White males, enrolled in the Agricultural Health Study. Incident diabetes was self-reported in a 5-year follow-up interview (1999&ndash;2003), giving 1,176 diabetics and 30,611 nondiabetics for analysis. Lifetime exposure to pesticides and covariate information were reported by participants at enrollment (1993&ndash;1997). Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively. The observed association of organochlorine and organophosphate insecticides with diabetes is consistent with results from previous human and animal studies. Long-term exposure from handling certain pesticides, in particular, organochlorine and organophosphate insecticides, may be associated with increased risk of diabetes.</p>
]]></description>
<dc:creator><![CDATA[Montgomery, M. P., Kamel, F., Saldana, T. M., Alavanja, M. C. R., Sandler, D. P.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn028</dc:identifier>
<dc:title><![CDATA[Incident Diabetes and Pesticide Exposure among Licensed Pesticide Applicators: Agricultural Health Study, 1993-2003]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1246</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1235</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1247?rss=1">
<title><![CDATA[Use of Recovery Biomarkers to Calibrate Nutrient Consumption Self-Reports in the Women's Health Initiative]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1247?rss=1</link>
<description><![CDATA[
<p>Underreporting of energy consumption by self-report is well-recognized, but previous studies using recovery biomarkers have not been sufficiently large to establish whether participant characteristics predict misreporting. In 2004&ndash;2005, 544 participants in the Women's Health Initiative Dietary Modification Trial completed a doubly labeled water protocol (energy biomarker), 24-hour urine collection (protein biomarker), and self-reports of diet (assessed by food frequency questionnaire (FFQ)), exercise, and lifestyle habits; 111 women repeated all procedures after 6 months. Using linear regression, the authors estimated associations of participant characteristics with misreporting, defined as the extent to which the log ratio (self-reported FFQ/nutritional biomarker) was less than zero. Intervention women in the trial underreported energy intake by 32% (vs. 27% in the comparison arm) and protein intake by 15% (vs. 10%). Younger women had more underreporting of energy (<I>p</I> = 0.02) and protein (<I>p</I> = 0.001), while increasing body mass index predicted increased underreporting of energy and overreporting of percentage of energy derived from protein (<I>p</I> = 0.001 and <I>p</I> = 0.004, respectively). Blacks and Hispanics underreported more than did Caucasians. Correlations of initial measures with repeat measures (<I>n</I> = 111) were 0.72, 0.70, 0.46, and 0.64 for biomarker energy, FFQ energy, biomarker protein, and FFQ protein, respectively. Recovery biomarker data were used in regression equations to calibrate self-reports; the potential application of these equations to disease risk modeling is presented. The authors confirm the existence of systematic bias in dietary self-reports and provide methods of correcting for measurement error.</p>
]]></description>
<dc:creator><![CDATA[Neuhouser, M. L., Tinker, L., Shaw, P. A., Schoeller, D., Bingham, S. A., Horn, L. V., Beresford, S. A. A., Caan, B., Thomson, C., Satterfield, S., Kuller, L., Heiss, G., Smit, E., Sarto, G., Ockene, J., Stefanick, M. L., Assaf, A., Runswick, S., Prentice, R. L.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn026</dc:identifier>
<dc:title><![CDATA[Use of Recovery Biomarkers to Calibrate Nutrient Consumption Self-Reports in the Women's Health Initiative]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1259</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1247</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1260?rss=1">
<title><![CDATA[Buccal Swabs and Treated Cards: Methodological Considerations for Molecular Epidemiologic Studies Examining Pediatric Populations]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1260?rss=1</link>
<description><![CDATA[
<p>Self-collection of buccal cells provides a noninvasive method for obtaining biologic samples for genetic analyses in pediatric studies. Nevertheless, low yields, microbial contamination, and degradation of buccal samples present challenges for epidemiologic studies incorporating genetic investigations. The aims of this study were to compare the quality and yield of DNA extracted from buccal specimens with BuccalAmp swabs (Epicenter BioTechnologies, Madison, Wisconsin) or FTA cards (Whatman, Inc., Clifton, New Jersey) and to investigate the use of whole-genome amplification (WGA) for increasing DNA yields for single nucleotide polymorphism analyses. Buccal specimens were collected from 55 children with acute lymphoblastic leukemia and 52 control children without acute lymphoblastic leukemia in New South Wales, Australia, in 2003&ndash;2004. Real-time polymerase chain reaction was used to evaluate polymorphisms in the genes encoding the cytochrome p450 enzyme CYP3A4 (<I>CYP3A4</I> A392G, also known as <I>CYP3A4*1B</I>) and the steroid xenobiotic receptor (<I>SXR</I> C25385T). Results showed that DNA could be isolated from buccal specimens collected by use of both methods and that yields could be substantially improved with WGA without introducing genotyping error. However, DNA quality was poorer in samples collected by BuccalAmp swabs, and the presence of polymerase chain reaction inhibitors in these samples reduced the sensitivity of quantitative real-time PCR analysis. These findings show that different methods for collecting buccal samples impact on the downstream success of genetic investigations and influence DNA quality after WGA.</p>
]]></description>
<dc:creator><![CDATA[Beckett, S. M., Laughton, S. J., Pozza, L. D., McCowage, G. B., Marshall, G., Cohn, R. J., Milne, E., Ashton, L. J.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn012</dc:identifier>
<dc:title><![CDATA[Buccal Swabs and Treated Cards: Methodological Considerations for Molecular Epidemiologic Studies Examining Pediatric Populations]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1267</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1260</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/167/10/1268?rss=1">
<title><![CDATA[Epidemiological Methods in Life Course Research: Edited by Andrew Pickles, Barbara Maughan, and Michael Wadsworth]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/167/10/1268?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Faerstein, E.]]></dc:creator>
<dc:date>2008-05-09</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwn054</dc:identifier>
<dc:title><![CDATA[Epidemiological Methods in Life Course Research: Edited by Andrew Pickles, Barbara Maughan, and Michael Wadsworth]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>167</prism:volume>
<prism:endingPage>1268</prism:endingPage>
<prism:publicationDate>2008-05-15</prism:publicationDate>
<prism:startingPage>1268</prism:startingPage>
<prism:section>BOOK-REVIEW</prism:section>
</item>

</rdf:RDF>