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<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/617?rss=1">
<title><![CDATA[Intergenerational influences on health: how far back do we have to go?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/617?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Smith, G. D.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp230</dc:identifier>
<dc:title><![CDATA[Intergenerational influences on health: how far back do we have to go?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>618</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>617</prism:startingPage>
<prism:section>Editor's Choice</prism:section>
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<title><![CDATA[Unravelling prenatal influences: the case of smoking in pregnancy]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/619?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Maughan, B.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp211</dc:identifier>
<dc:title><![CDATA[Unravelling prenatal influences: the case of smoking in pregnancy]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>621</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
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<prism:section>Editorial</prism:section>
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<title><![CDATA[The disappearance of the sick-man from medical cosmology, 1770-1870]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/622?rss=1</link>
<description><![CDATA[
<p>The sick-man may be said to have disappeared from medical cosmology in two related senses during the period 1770&ndash;1870. Firstly, as control over the means of production of medical knowledge shifted away from the sick towards medical investigators the universe of discourse of medical theory changed from that of an integrated conception of the whole person to that of a network of bonds between microscopical particles. Secondly, as control over the occupational group of medical investigators was centralized in the hands of its senior members the plethora of theories and therapies, which had previously afforded the sick-man the opportunity to negotiate his own treatment, were replaced by a monolithic consensus of opinion imposed from within the community of medical investigators.</p>
]]></description>
<dc:creator><![CDATA[Jewson, N.D.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp180</dc:identifier>
<dc:title><![CDATA[The disappearance of the sick-man from medical cosmology, 1770-1870]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>633</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>622</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
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<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/633?rss=1">
<title><![CDATA[Commentary: The appearance of new medical cosmologies and the re-appearance of sick and healthy men and women: a comment on the merits of social theorizing]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/633?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Nettleton, S.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp181</dc:identifier>
<dc:title><![CDATA[Commentary: The appearance of new medical cosmologies and the re-appearance of sick and healthy men and women: a comment on the merits of social theorizing]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>636</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>633</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
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<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/637?rss=1">
<title><![CDATA[Commentary: From sick men and women, to patients, and thence to clients and consumers--the structuring of the 'patient' in the modern world]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/637?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Prior, L.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp182</dc:identifier>
<dc:title><![CDATA[Commentary: From sick men and women, to patients, and thence to clients and consumers--the structuring of the 'patient' in the modern world]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>639</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>637</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
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<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/639?rss=1">
<title><![CDATA[Commentary: Nicholas Jewson and the disappearance of the sick man from medical cosmology, 1770-1870]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/639?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Nicolson, M.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp183</dc:identifier>
<dc:title><![CDATA[Commentary: Nicholas Jewson and the disappearance of the sick man from medical cosmology, 1770-1870]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>642</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>639</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
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<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/642?rss=1">
<title><![CDATA[Commentary: Indeterminate sick-men--a commentary on Jewson's 'Disappearance of the sick-man from medical cosmology']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/642?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Armstrong, D.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp184</dc:identifier>
<dc:title><![CDATA[Commentary: Indeterminate sick-men--a commentary on Jewson's 'Disappearance of the sick-man from medical cosmology']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>645</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>642</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/646?rss=1">
<title><![CDATA[Commentary: From history of medicine to a general history of 'working knowledges']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/646?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pickstone, J. V]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp185</dc:identifier>
<dc:title><![CDATA[Commentary: From history of medicine to a general history of 'working knowledges']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>649</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>646</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/650?rss=1">
<title><![CDATA[Cohort Profile: The STRIP Study (Special Turku Coronary Risk Factor Intervention Project), an Infancy-onset Dietary and Life-style Intervention Trial]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/650?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Simell, O., Niinikoski, H., Ronnemaa, T., Raitakari, O. T, Lagstrom, H., Laurinen, M., Aromaa, M., Hakala, P., Jula, A., Jokinen, E., Valimaki, I., Viikari, J., for the STRIP Study Group]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn072</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The STRIP Study (Special Turku Coronary Risk Factor Intervention Project), an Infancy-onset Dietary and Life-style Intervention Trial]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>655</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>650</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/656?rss=1">
<title><![CDATA[Cohort Profile: The Copenhagen School Health Records Register]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/656?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Baker, J. L, Olsen, L. W, Andersen, I., Pearson, S., Hansen, B., Sorensen, T. I.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn164</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Copenhagen School Health Records Register]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>662</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>656</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/663?rss=1">
<title><![CDATA[Cohort Profile: The 1969-73 Vellore birth cohort study in South India]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/663?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Antonisamy, B, Raghupathy, P, Christopher, S., Richard, J, Rao, P S S, Barker, D. J P, Fall, C. H D]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn159</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The 1969-73 Vellore birth cohort study in South India]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>669</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>663</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/670?rss=1">
<title><![CDATA[Cochrane Column]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/670?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Young, T., Volmink, J, Irlam, J, Visser, M E, Rollins, N, Siegfried, N, Mahlungulu, S, Grobler, L A, Visser, M E, Volmink, J, Abba, K, Sudarsanam, T D, Grobler, L, Volmink, J]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp140</dc:identifier>
<dc:title><![CDATA[Cochrane Column]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>674</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>670</prism:startingPage>
<prism:section>Cochrane Column</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/675?rss=1">
<title><![CDATA[Viewpoint: The skeptical epidemiologist]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/675?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Vineis, P.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn361</dc:identifier>
<dc:title><![CDATA[Viewpoint: The skeptical epidemiologist]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>677</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>675</prism:startingPage>
<prism:section>Cochrane Column</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/678?rss=1">
<title><![CDATA[Authors' Response: A further plea for adherence to the principles underlying science in general and the epidemiologic enterprise in particular]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/678?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Boffetta, P., McLaughlin, J. K, La Vecchia, C., Tarone, R. E, Lipworth, L., Blot, W. J]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn362</dc:identifier>
<dc:title><![CDATA[Authors' Response: A further plea for adherence to the principles underlying science in general and the epidemiologic enterprise in particular]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>679</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>678</prism:startingPage>
<prism:section>Cochrane Column</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/680?rss=1">
<title><![CDATA[Maternal smoking during pregnancy and child behaviour problems: the Generation R Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/680?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Several studies showed that maternal smoking in pregnancy is related to behavioural and emotional disorders in the offspring. It is unclear whether this is a causal association, or can be explained by other smoking-related vulnerability factors for child behavioural problems.</p>
<p><b>Methods</b> Within a population-based birth cohort, both mothers and fathers reported on their smoking habits at several time-points during pregnancy. Behavioural problems were measured with the Child Behavior Checklist in 4680 children at the age of 18 months.</p>
<p><b>Results</b> With adjustment for age and gender only, children of mothers who continued smoking during pregnancy had higher risk of Total Problems [odds ratio (OR) 1.59, 95% confidence interval (CI): 1.21&ndash;2.08] and Externalizing problems (OR 1.45, 95% CI: 1.15&ndash;1.84), compared with children of mothers who never smoked. Smoking by father when mother did not smoke, was also related to a higher risk of behavioural problems. The statistical association of parental smoking with behavioural problems was strongly confounded by parental characteristics, chiefly socioeconomic status and parental psychopathology; adjustment for these factors accounted entirely for the effect of both maternal and paternal smoking on child behavioural problems.</p>
<p><b>Conclusions</b> Maternal smoking during pregnancy, as well as paternal smoking, occurs in the context of other factors that place the child at increased developmental risk, but may not be causally related to the child's behaviour. It is essential to include sufficient information on parental psychiatric symptoms in studies exploring the association between pre-natal cigarette smoke exposure and behavioural disorders.</p>
]]></description>
<dc:creator><![CDATA[Roza, S. J, Verhulst, F. C, Jaddoe, V. W., Steegers, E. A., Mackenbach, J. P, Hofman, A., Tiemeier, H.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn163</dc:identifier>
<dc:title><![CDATA[Maternal smoking during pregnancy and child behaviour problems: the Generation R Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>689</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>680</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/690?rss=1">
<title><![CDATA[GSTM1 polymorphisms modify the effect of maternal smoking during pregnancy on cognitive functioning in preschoolers]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/690?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Maternal smoking during pregnancy is associated with cognitive deficits in children. Parental factors are proposed as an explanatory. We studied the influence of <I>GSTM1</I> and <I>GSTT1</I> polymorphisms on the cognition effects induced by active maternal smoking during pregnancy.</p>
<p><b>Methods</b> Children (<I>n</I> = 384) from a prospective population-based birth cohort were assessed at 4 years. The McCarthy Scales of Children's Abilities (MCSA) was administrated. Maternal smoking was measured by questionnaire. Genotyping was conducted for null alleles from <I>GSTM1</I> and <I>GSTT1</I>. Multivariable linear regression models were used to examine the association between active maternal smoking during pregnancy and MCSA outcomes by <I>GSTM1</I> and <I>GSTT1</I> genotypes.</p>
<p><b>Results</b> Maternal smoking during pregnancy (reporting, yes) was inversely associated with global cognitive score among children having null allele for <I>GSTM1</I> (<I>&beta;</I> = &ndash;4.73, 95% CI &ndash;9.45 to &ndash;0.02); but not among children with present allele (<I>&beta;</I> = &ndash;1.04, 95% CI &ndash;7.88 to 5.81) (<I>P</I> for interaction 0.089). The interaction remained after adjusting by post-natal maternal smoking (<I>P</I> = 0.081). The effect was stronger for perceptual-performance (<I>&beta;</I> = &ndash;3.68, 95% CI &ndash;8.39 to 1.03; <I>P</I> for interaction 0.087), quantitative (<I>&beta;</I> = &ndash;7.00, 95% CI &ndash;17.39 to 3.39; <I>P</I> for interaction 0.048), verbal (<I>&beta;</I> = &ndash;3.63, 95% CI &ndash;8.43 to 1.17; <I>P</I> for interaction 0.264) and executive function (<I>&beta;</I> = &ndash;4.87, 95% CI &ndash;9.55 to &ndash;0.20; <I>P</I> for interaction 0.127). No interaction was found for <I>GSTT1</I>.</p>
<p><b>Conclusions</b> <I>GSTM1</I> deficiency increases the adverse effects of active maternal smoking during pregnancy on cognition in preschoolers, suggesting a biological interaction between child metabolic genes and tobacco smoke components in detoxification process during foetal neurodevelopment.</p>
]]></description>
<dc:creator><![CDATA[Morales, E., Sunyer, J., Julvez, J., Castro-Giner, F., Estivill, X., Torrent, M., De Cid, R.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp141</dc:identifier>
<dc:title><![CDATA[GSTM1 polymorphisms modify the effect of maternal smoking during pregnancy on cognitive functioning in preschoolers]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>697</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>690</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/698?rss=1">
<title><![CDATA[Smoking during pregnancy and hyperactivity-inattention in the offspring--comparing results from three Nordic cohorts]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/698?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Prenatal exposure to smoking has been associated with Attention Deficit Hyperactivity Disorder (ADHD) in a number of epidemiological studies. However, mothers with the ADHD phenotype may &lsquo;treat&rsquo; their problem by smoking and therefore be more likely to smoke even in a society where smoking is not acceptable. This will cause genetic confounding if ADHD has a heritable component, especially in populations with low prevalence rates of smoking since this reason for smoking is expected to be proportionally more frequent in a population with few &lsquo;normal&rsquo; smokers. We compared the association in cohorts with different smoking frequencies.</p>
<p><b>Methods</b> A total of 20 936 women with singleton pregnancies were identified within three population-based pregnancy cohorts in Northern Finland (1985&ndash;1986) and in Denmark (1984&ndash;1987 and 1989&ndash;1991). We collected self-reported data on their pre-pregnancy and pregnancy smoking habits and followed the children to school age where teachers and parents rated hyperactivity and inattention symptoms.</p>
<p><b>Results</b> Children, whose mothers smoked during pregnancy, had an increased prevalence of a high hyperactivity-inattention score compared with children of nonsmokers in each of the cohorts after adjustment for confounders but we found no statistical significant difference between the associations across the cohorts.</p>
<p><b>Conclusion</b> The estimated association was not strongest in the population with the fewest smokers which does not support the hypothesis that the association is entirely due to genetic confounding.</p>
]]></description>
<dc:creator><![CDATA[Obel, C., Linnet, K. M., Henriksen, T. B., Rodriguez, A., Jarvelin, M. R., Kotimaa, A., Moilanen, I., Ebeling, H., Bilenberg, N., Taanila, A., Ye, G., Olsen, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dym290</dc:identifier>
<dc:title><![CDATA[Smoking during pregnancy and hyperactivity-inattention in the offspring--comparing results from three Nordic cohorts]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>705</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>698</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/706?rss=1">
<title><![CDATA[Use of acetaminophen during pregnancy and risk of adverse pregnancy outcomes]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/706?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Acetaminophen use during pregnancy has been associated with a reduced risk of stillbirth and preterm birth, but findings are based on few studies with small numbers of exposed women.</p>
<p><b>Methods</b> To examine whether prenatal exposure to acetaminophen reduces the risk of adverse pregnancy outcomes, we used data from the Danish National Birth Cohort. We also examined the combined potential effects of acetaminophen, coffee and tobacco use on pre-eclampsia and preterm birth. The study population consisted of women who provided information on acetaminophen use during pregnancy and gave birth to singletons (<I>n</I> = 98 140). The cohort was linked to the Danish National Hospital Registry and the Medical Birth Registry, which covers all Danish hospitals, miscarriages and births in Denmark.</p>
<p><b>Results</b> Women using acetaminophen during the third trimester of pregnancy had an increased risk of preterm birth [adjusted hazard ratio (HR) = 1.14, 95% CI: 1.03&ndash;1.26]. The risk of preterm birth was increased in mothers with pre-eclampsia (HR = 1.55, 95% CI: 1.16&ndash;2.07) but not in women without pre-eclampsia (HR = 1.08, 95% CI: 0.97&ndash;1.20). Tobacco smoking and coffee consumption did not modify the effect of acetaminophen in any consistent pattern. No association was found between acetaminophen use and risk of preterm complications, miscarriages, stillbirths, low birth weight or small size for gestational age.</p>
<p><b>Conclusion</b> Findings do not provide strong support for a change in clinical practice regarding use of acetaminophen during pregnancy, but the increased risk of preterm birth among women with pre-eclampsia should be further investigated.</p>
]]></description>
<dc:creator><![CDATA[Rebordosa, C., Kogevinas, M., Bech, B. H, Sorensen, H. T, Olsen, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp151</dc:identifier>
<dc:title><![CDATA[Use of acetaminophen during pregnancy and risk of adverse pregnancy outcomes]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>714</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>706</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/715?rss=1">
<title><![CDATA[Vasculopathic and thrombophilic risk factors for spontaneous preterm birth]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/715?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Mothers who give birth to preterm infants are at increased risk of mortality from coronary heart disease and stroke, but the biological pathways underlying these associations have not been explored.</p>
<p><b>Methods</b> We carried out a case&ndash;control study nested in a large (<I>n</I> = 5337) prospective, multicentre cohort. All cohort women had an interview, examination and venipuncture at 24&ndash;26 weeks. Frozen plasma samples in spontaneous preterm births (<I>n</I> = 207) and 444 term controls were analysed for plasma homocysteine, folate, cholesterol (total, low-density lipoprotein and high-density lipoprotein) and thrombin&ndash;antithrombin (TAT) complexes. DNA was extracted and analysed for seven gene polymorphisms involved in thrombophilia or folate or homocysteine metabolism. Fresh placentas were fixed, stained and blindly assessed for histologic evidence of infarction and decidual vasculopathy.</p>
<p><b>Results</b> High (above the median) plasma homocysteine and HDL cholesterol were significantly and independently associated with the risk of spontaneous preterm birth [adjusted odds ratios (OR)s = 1.9 (95% 1.1&ndash;3.3) and 0.5 (0.3&ndash;0.9), respectively]. A higher proportion of women with high homocysteine concentrations had decidual vasculopathy [(13.0 vs 6.8%; OR = 1.9 (1.1&ndash;3.5)], although the positive association between decidual vasculopathy and preterm birth did not achieve statistical significance [OR = 1.5 (0.9&ndash;2.7)]. No significant associations were observed with the DNA polymorphisms or with plasma TAT or folate levels.</p>
<p><b>Conclusions</b> Similar vasculopathic risk factors may underlie preterm birth and adult coronary heart disease and stroke.</p>
]]></description>
<dc:creator><![CDATA[Kramer, M. S, Kahn, S. R, Rozen, R., Evans, R., Platt, R. W, Chen, M. F., Goulet, L., Seguin, L., Dassa, C., Lydon, J., McNamara, H., Dahhou, M., Genest, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp167</dc:identifier>
<dc:title><![CDATA[Vasculopathic and thrombophilic risk factors for spontaneous preterm birth]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>723</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>715</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/724?rss=1">
<title><![CDATA[Intergenerational effect of weight gain in childhood on offspring birthweight]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/724?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Some studies suggest that weight gain in childhood may increase the risk of chronic diseases in adulthood, and recent studies have noticed that the timing of weight gain may be related to its long-term consequence. However, weight gain in childhood has clear short-term benefits, and the literature on the pro and cons of weight gain in childhood is limited.</p>
<p><b>Methods</b> In 1982, all 5914 hospital births (over 99% of all deliveries) occurring in Pelotas, Southern Brazil, were identified and studied prospectively on several occasions. In 2004&ndash;05, we attempted to trace the whole cohort and information on offspring birthweight was collected. Conditional growth modelling was used to assess the association between offspring birthweight and weight gain from birth to 20 months, and from 20 to 42 months.</p>
<p><b>Results</b> In 2004&ndash;05, we interviewed 4297 subjects, with a follow-up rate of 77.4%. This manuscript includes data from 848 women who had already delivered a child and 525 men who were fathers at the mean age of 23 years. Maternal birthweight, weight and length for age <I>Z</I>-score at 20 months of age were positively associated with next-generation birthweight, whereas paternal variables were not related to the outcome. Conditional growth modelling analyses showed that women whose weight gain in the first 20 months of life was faster than predicted had heavier babies, whereas paternal weight gain was not associated. The association was strongest for mothers whose birthweight for gestational age was in the lowest tertile.</p>
<p><b>Conclusion</b> Maternal, but not paternal birthweight and weight gain in early childhood are positively associated with next-generation birthweight.</p>
]]></description>
<dc:creator><![CDATA[Horta, B. L, Gigante, D. P, Osmond, C., Barros, F. C, Victora, C. G]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp168</dc:identifier>
<dc:title><![CDATA[Intergenerational effect of weight gain in childhood on offspring birthweight]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>732</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>724</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/733?rss=1">
<title><![CDATA[The long arm of the family: are parental and grandparental earnings related to young men's body mass index and cognitive ability?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/733?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The lasting impact of parents&rsquo; socioeconomic status on their children's social trajectories and health is well-established, but do such intergenerationally transmitted inequalities persist also into the third generation? This study investigates the importance of parental and grandparental earnings for young men's body mass index (BMI) and cognitive ability at military conscription.</p>
<p><b>Methods</b> The database used was UBCoS Multigen, which combines existing data on an Uppsala cohort born 1915&ndash;29 with information on several subsequent generations. We analysed young men in the third generation with complete information about the earnings of paternal (<I>n</I> = 3577) and maternal (<I>n</I> = 4142) ancestors of the two preceding generations using OLS-regression.</p>
<p><b>Results</b> On the paternal side, father's and grandfather's, but not grandmother's, earnings predicted cognitive ability and BMI. In the mutually adjusted models, the associations with cognitive ability largely remained for young men whose fathers [<I>b</I> = &ndash;0.96 (95% CI: &ndash;1.25, &ndash;0.66)] and grandfathers [<I>b</I> = &ndash;0.60 (&ndash;0.87, &ndash;0.33)] were poor rather than well-off, whereas for BMI, only the association with grandfather's earnings [<I>b</I> = 0.78 (0.37, 1.19)] persisted. On the maternal side, the mutually adjusted models indicated that the mother's [<I>b</I> = &ndash;0.89 (&ndash;1.14, &ndash;0.65)] and the grandfather's [<I>b</I> = &ndash;0.65 (&ndash;0.89, &ndash;0.41)], but not the grandmother's, earnings were predictive of cognitive ability, whereas only the grandfather's [<I>b</I> = 0.56 (0.18, 0.94)] earnings seemed to be important for BMI.</p>
<p><b>Conclusions</b> The results suggest that the long arm of the family reaches beyond the second generation in its effect on health. Although this study has only scratched the surface of how health inequalities is reproduced, it suggests that policies that reduce social inequalities may have ramifications across several generations.</p>
]]></description>
<dc:creator><![CDATA[Modin, B., Fritzell, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp001</dc:identifier>
<dc:title><![CDATA[The long arm of the family: are parental and grandparental earnings related to young men's body mass index and cognitive ability?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>744</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>733</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/744?rss=1">
<title><![CDATA[Commentary: Will the 'Long Arm of the Family' have legs?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/744?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Currie, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp154</dc:identifier>
<dc:title><![CDATA[Commentary: Will the 'Long Arm of the Family' have legs?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>745</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>744</prism:startingPage>
<prism:section>Intergenerational Influences on Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/746?rss=1">
<title><![CDATA[Adherence to first-line antiretroviral therapy affects non-virologic outcomes among patients on treatment for more than 12 months in Lusaka, Zambia]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/746?rss=1</link>
<description><![CDATA[
<p><b>Background</b> High-level adherence to antiretroviral therapy (ART) is associated with favourable patient outcomes. In resource-constrained settings, however, there are few validated measures. We examined the correlation between clinical outcomes and the medication possession ratio (MPR), a pharmacy-based measure of adherence.</p>
<p><b>Methods</b> We analysed data from a large programmatic cohort across 18 primary care centres providing ART in Lusaka, Zambia. Patients were stratified into three categories based on MPR-calculated adherence over the first 12 months: optimal (&ge;95%), suboptimal (80&ndash;94%) and poor (&lt;80%).</p>
<p><b>Results</b> Overall, 27 115 treatment-na&iuml;ve adults initiated and continued ART for &ge;12 months: 17 060 (62.9%) demonstrated optimal adherence, 7682 (28.3%) had suboptimal adherence and 2373 (8.8%) had poor adherence. When compared with those with optimal adherence, post-12-month mortality risk was similar among patients with sub-optimal adherence [adjusted hazard ratio (AHR) = 1.0; 95% CI: 0.9&ndash;1.2] but higher in patients with poor adherence (AHR = 1.7; 95% CI: 1.4&ndash;2.2). Those &lt;80% MPR also appeared to have an attenuated CD4 response at 18 months (185 cells/&micro;l vs 217 cells/&micro;l; <I>P</I> &lt; 0.001), 24 months (213 cells/&micro;l vs 246 cells/&micro;l; <I>P</I> &lt; 0.001), 30 months (226 cells/&micro;l vs 261 cells/&micro;l; <I>P</I> &lt; 0.001) and 36 months (245 cells/&micro;l vs 275 cells/&micro;l; <I>P</I> &lt; 0.01) when compared with those above this threshold.</p>
<p><b>Conclusions</b> MPR was predictive of clinical outcomes and immunologic response in this large public sector antiretroviral treatment program. This marker may have a role in guiding programmatic monitoring and clinical care in resource-constrained settings.</p>
]]></description>
<dc:creator><![CDATA[Chi, B. H, Cantrell, R. A, Zulu, I., Mulenga, L. B, Levy, J. W, Tambatamba, B. C, Reid, S., Mwango, A., Mwinga, A., Bulterys, M., Saag, M. S, Stringer, J. S.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp004</dc:identifier>
<dc:title><![CDATA[Adherence to first-line antiretroviral therapy affects non-virologic outcomes among patients on treatment for more than 12 months in Lusaka, Zambia]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>756</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>746</prism:startingPage>
<prism:section>Infectious Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/757?rss=1">
<title><![CDATA[Community transmission of hepatitis B virus in Egypt: results from a case-control study in Greater Cairo]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/757?rss=1</link>
<description><![CDATA[
<p><b>Background</b> To identify current risk factors for hepatitis B virus (HBV) transmission in Greater Cairo.</p>
<p><b>Methods</b> A 1:1 matched case&ndash;control study was conducted in two &lsquo;fever&rsquo; hospitals in Cairo. Acute hepatitis B cases were patients with acute hepatitis, positive HBs antigen, and high anti-HBc IgM titres. Control subjects were acute hepatitis A patients (positive anti-HAV IgM) or relatives of patients diagnosed with acute hepatitis C, identified at the same hospitals, with no past HBV infection (negative anti-HBc) and matched to cases on the same age and sex. Conditional logistic regression was used to identify factors associated with acute hepatitis B.</p>
<p><b>Results</b> Between April 2002 and June 2006, 233 cases and 233 controls were recruited to the study. In multivariate analysis, factors associated with an increased HBV risk in males were illiteracy [odds ratio (OR) = 6.1, 95% confidence interval (CI) = 2.8&ndash;13.1], shaving at barbers (OR = 2.1, 95% CI = 1.1&ndash;3.9) and injecting drug use (IDU) (OR = 3.4, 95% CI = 1.0&ndash;11.4). In females, factors associated with an increased HBV risk were illiteracy (OR = 2.2, 95% CI = 1.0&ndash;5.0), recent (&lt;1 year) marriage (OR = 42.0, 95% CI = 3.8&ndash;463.9 compared with single women) and giving birth (OR = 3.7, 95% CI = 1.0&ndash;13.9).</p>
<p><b>Conclusion</b> In this study, HBV transmission took place primarily in the community, whether as a result of recent marriage (presumably first sexual intercourse), shaving at barbershops or IDU, and was more common among illiterates. Health promotion campaigns should be carried out to increase awareness about community transmission of HBV. In addition to routine immunization for infants and other populations, premarital screening might be useful to identify at-risk spouses in order to propose targeted immunization.</p>
]]></description>
<dc:creator><![CDATA[Jimenez, A. P., El-Din, N. S., El-Hoseiny, M., El-Daly, M., Abdel-Hamid, M., El Aidi, S., Sultan, Y., El-Sayed, N., Mohamed, M. K., Fontanet, A.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp194</dc:identifier>
<dc:title><![CDATA[Community transmission of hepatitis B virus in Egypt: results from a case-control study in Greater Cairo]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>765</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>757</prism:startingPage>
<prism:section>Infectious Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/766?rss=1">
<title><![CDATA[Recent diarrhoeal illness and risk of lower respiratory infections in children under the age of 5 years]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/766?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Children in low-income settings suffering from frequent diarrhoea episodes are also at a high risk of acute lower respiratory infections (ALRI). We explored whether this is due to common risk factors for both conditions or whether diarrhoea can increase the risk of ALRI directly.</p>
<p><b>Methods</b> We used a dynamic time-to-event analysis of data from two large child studies in low-income settings in Ghana and Brazil, with the cumulative diarrhoea prevalence over 2 weeks as the exposure and severe ALRI as outcome. The analysis was adjusted for baseline risk of ALRI and diarrhoea, seasonality and age.</p>
<p><b>Results</b> The child population from Ghana had a much higher risk of diarrhoea, malnutrition and death than the children in Brazil. In the data from Ghana, every additional day of diarrhoea within 2 weeks increased the risk of ALRI by a factor of 1.08 (95% CI 1.00&ndash;1.15). In addition, we found a roughly linear relationship between the number of diarrhoea days over the last 28 days and the risk of ALRI. In the Ghana data, 26% of ALRI episodes may be due to recent exposure to diarrhoea. The Brazilian data gave no evidence for an association between diarrhoea and ALRI.</p>
<p><b>Conclusion</b> Diarrhoea may contribute substantially to the burden of ALRI in malnourished child populations.</p>
]]></description>
<dc:creator><![CDATA[Schmidt, W.-P., Cairncross, S., Barreto, M. L, Clasen, T., Genser, B.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp159</dc:identifier>
<dc:title><![CDATA[Recent diarrhoeal illness and risk of lower respiratory infections in children under the age of 5 years]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>772</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>766</prism:startingPage>
<prism:section>Infectious Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/772?rss=1">
<title><![CDATA[Commentary: What is the role of co-morbidity in child mortality?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/772?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Walker, C. L F., Black, R. E]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp170</dc:identifier>
<dc:title><![CDATA[Commentary: What is the role of co-morbidity in child mortality?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>774</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>772</prism:startingPage>
<prism:section>Infectious Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/775?rss=1">
<title><![CDATA[Persistent pathogens linking socioeconomic position and cardiovascular disease in the US]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/775?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Numerous studies have documented a strong inverse association between cardiovascular disease and socioeconomic position (SEP). Several infections are associated with both cardiovascular disease and SEP; hence infection may form an important link between SEP and cardiovascular disease. This study examines whether seropositivity to cytomegalovirus (CMV), to herpes simplex virus type-1 (HSV-1), and/or to both pathogens mediates the relationship between SEP and cardiovascular disease history in a nationally representative sample of the United States.</p>
<p><b>Methods</b> We conducted a cross-sectional study of subjects &ge;45 years of age, who were tested for seropositivity to CMV, HSV-1 or both pathogens and assessed for cardiovascular disease history in the National Health and Nutrition Examination Survey III. Cardiovascular disease history was defined as history of stroke, heart attack and/or congestive heart failure and SEP as education level.</p>
<p><b>Results</b> SEP was associated with CMV, HSV-1 and seropositivity to both pathogens. CMV seropositivity was associated with cardiovascular disease history even after adjusting for confounders as well as SEP. The odds of reporting a history of cardiovascular disease for those with less than a high school education compared with those with more than a high school education decreased by 7.7% after adjusting for CMV (Sobel mediation test for CMV, <I>P</I> = 0.0006). In contrast, neither seropositivity to HSV-1 nor to both pathogens was associated with cardiovascular disease history after adjusting for SEP.</p>
<p><b>Conclusions</b> Persistent pathogens such as CMV infection may explain a portion of the relationship between SEP and cardiovascular disease in the United States. Further studies examining additional pathogens and sociobiological mechanisms are warranted.</p>
]]></description>
<dc:creator><![CDATA[Simanek, A. M, Dowd, J. B., Aiello, A. E]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn273</dc:identifier>
<dc:title><![CDATA[Persistent pathogens linking socioeconomic position and cardiovascular disease in the US]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>787</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>775</prism:startingPage>
<prism:section>Infectious Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/787?rss=1">
<title><![CDATA[Commentary: Understanding the pathophysiology of poverty]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/787?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Nieto, F J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp187</dc:identifier>
<dc:title><![CDATA[Commentary: Understanding the pathophysiology of poverty]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>790</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>787</prism:startingPage>
<prism:section>Infectious Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/791?rss=1">
<title><![CDATA[Salt intakes around the world: implications for public health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/791?rss=1</link>
<description><![CDATA[
<p><b>Background</b> High levels of dietary sodium (consumed as common salt, sodium chloride) are associated with raised blood pressure and adverse cardiovascular health. Despite this, public health efforts to reduce sodium consumption remain limited to a few countries. Comprehensive, contemporaneous sodium intake data from around the world are needed to inform national/international public health initiatives to reduce sodium consumption.</p>
<p><b>Methods</b> Use of standardized 24-h sodium excretion estimates for adults from the international INTERSALT (1985&ndash;87) and INTERMAP (1996&ndash;99) studies, and recent dietary and urinary sodium data from observational or interventional studies&mdash;identified by a comprehensive search of peer-reviewed and &lsquo;grey&rsquo; literature&mdash;presented separately for adults and children. Review of methods for the estimation of sodium intake/excretion. Main food sources of sodium are presented for several Asian, European and Northern American countries, including previously unpublished INTERMAP data.</p>
<p><b>Results</b> Sodium intakes around the world are well in excess of physiological need (i.e. 10&ndash;20 mmol/day). Most adult populations have mean sodium intakes &gt;100 mmol/day, and for many (particularly the Asian countries) mean intakes are &gt;200 mmol/day. Possible exceptions include estimates from Cameroon, Ghana, Samoa, Spain, Taiwan, Tanzania, Uganda and Venezuela, though methodologies were sub-optimal and samples were not nationally representative. Sodium intakes were commonly &gt;100 mmol/day in children over 5 years old, and increased with age. In European and Northern American countries, sodium intake is dominated by sodium added in manufactured foods (~75% of intake). Cereals and baked goods were the single largest contributor to dietary sodium intake in UK and US adults. In Japan and China, salt added at home (in cooking and at the table) and soy sauce were the largest sources.</p>
<p><b>Conclusions</b> Unfavourably high sodium intakes remain prevalent around the world. Sources of dietary sodium vary largely worldwide. If policies for salt reduction at the population level are to be effective, policy development and implementation needs to target the main source of dietary sodium in the various populations.</p>
]]></description>
<dc:creator><![CDATA[Brown, I. J, Tzoulaki, I., Candeias, V., Elliott, P.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp139</dc:identifier>
<dc:title><![CDATA[Salt intakes around the world: implications for public health]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>813</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>791</prism:startingPage>
<prism:section>Global Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/814?rss=1">
<title><![CDATA[Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/814?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Melanoma risk is related to sun exposure; we have investigated risk variation by tumour site and latitude.</p>
<p><b>Methods</b> We performed a pooled analysis of 15 case&ndash;control studies (5700 melanoma cases and 7216 controls), correlating patterns of sun exposure, sunburn and solar keratoses (three studies) with melanoma risk. Pooled odds ratios (pORs) and 95% Bayesian confidence intervals (CIs) were estimated using Bayesian unconditional polytomous logistic random-coefficients models.</p>
<p><b>Results</b> Recreational sun exposure was a risk factor for melanoma on the trunk (pOR = 1.7; 95% CI: 1.4&ndash;2.2) and limbs (pOR = 1.4; 95% CI: 1.1&ndash;1.7), but not head and neck (pOR = 1.1; 95% CI: 0.8&ndash;1.4), across latitudes. Occupational sun exposure was associated with risk of melanoma on the head and neck at low latitudes (pOR = 1.7; 95% CI: 1.0&ndash;3.0). Total sun exposure was associated with increased risk of melanoma on the limbs at low latitudes (pOR = 1.5; 95% CI: 1.0&ndash;2.2), but not at other body sites or other latitudes. The pORs for sunburn in childhood were 1.5 (95% CI: 1.3&ndash;1.7), 1.5 (95% CI: 1.3&ndash;1.7) and 1.4 (95% CI: 1.1&ndash;1.7) for melanoma on the trunk, limbs, and head and neck, respectively, showing little variation across latitudes. The presence of head and neck solar keratoses was associated with increased risk of melanoma on the head and neck (pOR = 4.0; 95% CI: 1.7&ndash;9.1) and limbs (pOR = 4.0; 95% CI: 1.9&ndash;8.4).</p>
<p><b>Conclusion</b> Melanoma risk at different body sites is associated with different amounts and patterns of sun exposure. Recreational sun exposure and sunburn are strong predictors of melanoma at all latitudes, whereas measures of occupational and total sun exposure appear to predict melanoma predominately at low latitudes.</p>
]]></description>
<dc:creator><![CDATA[Chang, Y.-m., Barrett, J. H, Bishop, D T., Armstrong, B. K, Bataille, V., Bergman, W., Berwick, M., Bracci, P. M, Elwood, J M., Ernstoff, M. S, Gallagher, R. P, Green, A. C, Gruis, N. A, Holly, E. A, Ingvar, C., Kanetsky, P. A, Karagas, M. R, Lee, T. K, Le Marchand, L., Mackie, R. M, Olsson, H., Osterlind, A., Rebbeck, T. R, Sasieni, P., Siskind, V., Swerdlow, A. J, Titus-Ernstoff, L., Zens, M. S, Newton-Bishop, J. A]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp166</dc:identifier>
<dc:title><![CDATA[Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>830</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>814</prism:startingPage>
<prism:section>Global Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/831?rss=1">
<title><![CDATA[Non-response to baseline, non-response to follow-up and mortality in the Whitehall II cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/831?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Little is known about the associations between non-response to follow-up surveys and mortality, or differences in these associations by socioeconomic position in studies with repeat data collections.</p>
<p><b>Methods</b> The Whitehall II study of socioeconomic inequalities in health provided response status from five data collection surveys; Phase 1 (1985&ndash;88, <I>n</I> = 10 308), Phase 5 (1997&ndash;99, <I>n</I> = 6533), and all-cause mortality to 2006. Odd-numbered phases included a medical examination in addition to a questionnaire.</p>
<p><b>Results</b> Non-response to baseline and to follow-up phases that included a medical examination was associated with a doubling of the mortality hazard in analyses adjusted for age and sex. Compared with complete responders, responders who missed one or more phases, but completed the last possible phase before they died, had a 38% excess risk of mortality. However, those who missed one or more phases including the last possible phase before death had an excess risk of 127%. There was no evidence that these associations differed by socioeconomic position.</p>
<p><b>Conclusion</b> In studies with repeat data collections, non-response to follow-up is associated with the same doubling of the mortality risk as non-response to baseline; an association that is not modified by socioeconomic position.</p>
]]></description>
<dc:creator><![CDATA[Ferrie, J. E, Kivimaki, M., Singh-Manoux, A., Shortt, A., Martikainen, P., Head, J., Marmot, M., Gimeno, D., De Vogli, R., Elovainio, M., Shipley, M. J]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp153</dc:identifier>
<dc:title><![CDATA[Non-response to baseline, non-response to follow-up and mortality in the Whitehall II cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>837</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>831</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/838?rss=1">
<title><![CDATA[Opening the Black Box: a motivation for the assessment of mediation]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/838?rss=1</link>
<description><![CDATA[
<p>Recent criticism of epidemiologic methods has focused on the limitations of &lsquo;black box&rsquo; epidemiology, a pejorative label given to the simple identification of exposure&ndash;disease relationships. The assessment of mediation is an important tool for addressing this criticism. By using mediation analysis to open the black box, underlying mechanisms of the observed associations can be described and causal inference improved. An explicit theoretical motivation for such an analysis has been missing from the epidemiological literature. To provide this motivation, we integrate literature from epidemiology and other social sciences to describe the reasons that an investigator might want to assess mediation. We then describe the connections between these reasons and specific measures of indirect and direct effects that have been previously described.</p>
]]></description>
<dc:creator><![CDATA[Hafeman, D. M, Schwartz, S.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn372</dc:identifier>
<dc:title><![CDATA[Opening the Black Box: a motivation for the assessment of mediation]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>845</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>838</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/845?rss=1">
<title><![CDATA[Commentary: Gilding the black box]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/845?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kaufman, J. S]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp163</dc:identifier>
<dc:title><![CDATA[Commentary: Gilding the black box]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>847</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>845</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/848?rss=1">
<title><![CDATA[Rotating shift work and the metabolic syndrome: a prospective study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/848?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Several studies have documented on the elevated cardiovascular risk among shift workers. In order to further explore this relation, we aimed at assessing the association between rotating shift work and the incidence of the metabolic syndrome (MetS).</p>
<p><b>Methods</b> In this population-based prospective study, 1529 employees from several large Belgian companies were followed for a median observation period of 6.6 years with respect to the onset of the MetS and its separate components.</p>
<p><b>Results</b> At baseline, 309 men (20.2%) were rotating shift workers. The MetS incidence rate in these shift workers (60.6 per 1000 person-years) was increased in comparison with day workers (37.2 per 1000 person-years) with an odds ratio (95% CI) of 1.77 (1.34&ndash;2.32). Multivariate adjustment for potential lifestyle and work-related confounders did only marginally affect the strength of the association. The risk for the development of MetS gradually increased independently with accumulated years of shift work. Rotating shift work not only had an impact on MetS as a cluster of conditions but on each of its individual components as well.</p>
<p><b>Conclusions</b> Hence, prospective evidence was found that rotating shift work increases the risk for developing the MetS over a period of 6 years.</p>
]]></description>
<dc:creator><![CDATA[De Bacquer, D, Van Risseghem, M, Clays, E, Kittel, F, De Backer, G, Braeckman, L]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn360</dc:identifier>
<dc:title><![CDATA[Rotating shift work and the metabolic syndrome: a prospective study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>854</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>848</prism:startingPage>
<prism:section>Metabolic Syndrome</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/854?rss=1">
<title><![CDATA[Commentary: Metabolic syndrome as a result of shift work exposure?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/854?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Karlsson, B.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp190</dc:identifier>
<dc:title><![CDATA[Commentary: Metabolic syndrome as a result of shift work exposure?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>855</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>854</prism:startingPage>
<prism:section>Metabolic Syndrome</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/856?rss=1">
<title><![CDATA[Mediterranean diet and inflammatory response in myocardial infarction survivors]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/856?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Within the framework of the multi-centre AIRGENE project we studied the association of the Mediterranean diet on plasma levels of various inflammatory markers, in myocardial infarction (MI) survivors from six geographic areas in Europe.</p>
<p><b>Methods</b> From 2003 to 2004, 1003 patients were repeatedly clinically examined. On every clinical visit (on average 5.8 times), blood EDTA-plasma samples were collected. High sensitivity C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen concentrations were measured based on standardized procedures. Dietary habits were evaluated through a semi-quantitative Food Frequency Questionnaire (FFQ), whereas adherence to the Mediterranean diet was assessed by a diet score.</p>
<p><b>Results</b> A protective effect of adherence to the Mediterranean diet was found. For each unit of increasing adherence to the Mediterranean diet score there was a reduction of 3.1% in the average CRP levels (95% CI 0.5&ndash;5.7%) and of 1.9% in the average IL-6 levels (95% CI 0.5&ndash;3.4%) after adjusting for centre, age, sex, body mass index, physical activity, smoking status, diabetes and medication intake. No significant association was observed between the diet score and fibrinogen levels. Moderate intake of red wine (1&ndash;12 wine glasses per month) was associated with lower levels of CRP, IL-6 and fibrinogen.</p>
<p><b>Conclusions</b> Adherence to the traditional Mediterranean diet was associated with a reduction of the concentrations of inflammatory markers in MI survivors. This may, in part, explain the beneficial effects of this diet on various chronic diseases such as atherosclerosis and cancer, and expands its role to secondary prevention level.</p>
]]></description>
<dc:creator><![CDATA[Panagiotakos, D. B, Dimakopoulou, K., Katsouyanni, K., Bellander, T., Grau, M., Koenig, W., Lanki, T., Pistelli, R., Schneider, A., Peters, A., on behalf of the AIRGENE Study Group]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp142</dc:identifier>
<dc:title><![CDATA[Mediterranean diet and inflammatory response in myocardial infarction survivors]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>866</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>856</prism:startingPage>
<prism:section>Nutrition</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/867?rss=1">
<title><![CDATA[Lung function in mid-life compared with later life is a stronger predictor of arterial stiffness in men: The Caerphilly Prospective Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/867?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Increased arterial stiffness predicts future cardiovascular disease and in some cross-sectional studies it is related to worse lung function and obstructive pulmonary disease. We assessed the predictive value of lung function measured in mid-life as compared with later life on arterial stiffness in the Caerphilly Prospective Study (CaPS).</p>
<p><b>Methods</b> Men aged 47&ndash;67 years had lung function measured between 1984 and 1988 and repeated between 2002 and 2004 (<I>n</I> = 827) as well as having carotid-femoral pulse wave velocity (PWV) measured.</p>
<p><b>Results</b> Both forced expiratory volume in 1 s (FEV<SUB>1</SUB>) and forced vital capacity (FVC) in mid-life and later life were inversely associated with PWV (<I>P</I> &lt; 0.0001) but mid-life measures were stronger predictors. Only mid-life measures remained predictors after mutual adjustment (FEV<SUB>1</SUB> mid-life <I>&beta;</I> coeff. &ndash;0.65, 95% CI &ndash;1.04, &ndash;0.26, <I>P</I> &lt; 0.0001; FVC mid-life <I>&beta;</I> coeff. &ndash;0.52, 95% CI &ndash;0.82, &ndash;0.23, <I>P</I> &lt; 0.0001). Adjustment for smoking status, early life, inflammatory and metabolic factors in sub-groups did not markedly change the associations.</p>
<p><b>Conclusions</b> Mid-life lung function is a stronger risk factor than in later life for arterial stiffness in men. It is possible that developmental factors influence both lung function and arterial stiffness. Lung function assessment in mid-life may identify individuals at greater risk of their future cardiovascular disease.</p>
]]></description>
<dc:creator><![CDATA[Bolton, C. E, Cockcroft, J. R, Sabit, R., Munnery, M., McEniery, C. M, Wilkinson, I. B, Ebrahim, S., Gallacher, J. E, Shale, D. J, Ben-Shlomo, Y.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn374</dc:identifier>
<dc:title><![CDATA[Lung function in mid-life compared with later life is a stronger predictor of arterial stiffness in men: The Caerphilly Prospective Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>876</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>867</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/877?rss=1">
<title><![CDATA[Homelessness as an independent risk factor for mortality: results from a retrospective cohort study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/877?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Homelessness is associated with increased risks of mortality but it has not previously been possible to distinguish whether this is typical of other socio-economically deprived populations, the result of a higher prevalence of morbidity or an independent risk of homelessness itself. The aim of this study was to describe mortality among a cohort of homeless adults and adjust for the effects of morbidity and socio-economic deprivation.</p>
<p><b>Methods</b> Retrospective 5-year study of two fixed cohorts, homeless adults and an age- and sex-matched random sample of the local non-homeless population in Greater Glasgow National Health Service Board area for comparison.</p>
<p><b>Results</b> Over 5 years of observation, 1.7% (209/12 451) of the general population and 7.2% (457/6323) of the homeless cohort died. The hazard ratio of all-cause mortality in homeless compared with non-homeless cohorts was 4.4 (95% CI: 3.8&ndash;5.2). After adjustment for age, sex and previous hospitalization, homelessness was associated with an all-cause mortality hazard ratio of 1.6 (95% CI: 1.3&ndash;1.9). Homelessness had differential effects on cause-specific mortality. Among patients who had been hospitalized for drug-related conditions, the homeless cohort experienced a 7-fold increase in risk of death from drugs compared with the general population.</p>
<p><b>Conclusions</b> Homelessness is an independent risk factor for deaths from specific causes. Preventive programmes might be most effectively targeted at the homeless with these conditions.</p>
]]></description>
<dc:creator><![CDATA[Morrison, D. S]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp160</dc:identifier>
<dc:title><![CDATA[Homelessness as an independent risk factor for mortality: results from a retrospective cohort study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>883</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>877</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/884?rss=1">
<title><![CDATA[Food frequency questionnaires vs diet diaries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/884?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mcneill, G., Masson, L., Macdonald, H., Haggarty, P., Macdiarmid, J., Craig, L., Kyle, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn237</dc:identifier>
<dc:title><![CDATA[Food frequency questionnaires vs diet diaries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>884</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>884</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/885?rss=1">
<title><![CDATA[Author's Response: Associations between dietary methods and biomarkers, and between fruits and vegetables and risk of ischaemic heart disease, in the EPIC Norfolk Cohort Study: response to letter by McNeill et al.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/885?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bingham, S., Luben, R., Welch, A., Low, Y. L., Khaw, K. T., Wareham, N., Day, N.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn234</dc:identifier>
<dc:title><![CDATA[Author's Response: Associations between dietary methods and biomarkers, and between fruits and vegetables and risk of ischaemic heart disease, in the EPIC Norfolk Cohort Study: response to letter by McNeill et al.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>885</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>885</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/886?rss=1">
<title><![CDATA[Experience of famine and bone health in post-menopausal women]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/886?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Marcus, E.-L., Menczel, J.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn010</dc:identifier>
<dc:title><![CDATA[Experience of famine and bone health in post-menopausal women]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>886</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>886</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/887?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/887?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Chan, F., Wong, S., Leung, J., Leung, P., Woo, J]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn011</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>887</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>887</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/888?rss=1">
<title><![CDATA[A Farewell to Alms: A Brief Economic History of the World. Gregory Clark.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/888?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Engerman, S. L]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn074</dc:identifier>
<dc:title><![CDATA[A Farewell to Alms: A Brief Economic History of the World. Gregory Clark.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>889</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>888</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/889?rss=1">
<title><![CDATA[GI Epidemiology. Nicholas J Talley, G Richard Locke III, Yuri A Saito (eds).]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/889?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Langman, M.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn137</dc:identifier>
<dc:title><![CDATA[GI Epidemiology. Nicholas J Talley, G Richard Locke III, Yuri A Saito (eds).]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>889</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>889</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/890?rss=1">
<title><![CDATA[Erratum]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/890?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp206</dc:identifier>
<dc:title><![CDATA[Erratum]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>890</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>890</prism:startingPage>
<prism:section>Erratum</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/891?rss=1">
<title><![CDATA[Erratum]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/3/891?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Subramanian, S., Jones, K., Kaddour, A., Krieger, N.]]></dc:creator>
<dc:date>2009-06-02</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp209</dc:identifier>
<dc:title><![CDATA[Erratum]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>894</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>891</prism:startingPage>
<prism:section>Erratum</prism:section>
</item>

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