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<title><![CDATA[Smoking and lung cancer: causality, Cornfield and an early observational meta-analysis]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1169?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Davey Smith, G.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:23 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp317</dc:identifier>
<dc:title><![CDATA[Smoking and lung cancer: causality, Cornfield and an early observational meta-analysis]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1171</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1169</prism:startingPage>
<prism:section>Editor's Choice</prism:section>
</item>

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<title><![CDATA[Hidden in plain sight]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1172?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bresnahan, M., Li, G., Susser, E.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp293</dc:identifier>
<dc:title><![CDATA[Hidden in plain sight]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1174</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
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<title><![CDATA[Smoking and lung cancer: recent evidence and a discussion of some questions]]></title>
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<description><![CDATA[
<p><b>Summary</b> This report reviews some of the more recent epidemiologic and experimental findings on the relationship of tobacco smoking to lung cancer, and discusses some criticisms directed against the conclusion that tobacco smoking, especially cigarettes, has a causal role in the increase in broncho-genic carcinoma. The magnitude of the excess lung-cancer risk among cigarette smokers is so great that the results can not be interpreted as arising from an indirect association of cigarette smoking with some other agent or characteristic, since this hypothetical agent would have to be at least as strongly associated with lung cancer as cigarette use; no such agent has been found or suggested. The consistency of all the epidemiologic and experimental evidence also supports the conclusion of a causal relationship with cigarette smoking, while there are serious inconsistencies in reconciling the evidence with other hypotheses which have been advanced. Unquestionably there are areas where more research is necessary, and, of course, no single cause accounts for all lung cancer. The information already available, however, is sufficient for planning and activating public health measures. &ndash; <I>J. Nat. Cancer Inst</I>. <b>22:</b>173&ndash;203, 1959.</p>
]]></description>
<dc:creator><![CDATA[Cornfield, J., Haenszel, W., Hammond, E. C., Lilienfeld, A. M., Shimkin, M. B., Wynder, E. L.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp289</dc:identifier>
<dc:title><![CDATA[Smoking and lung cancer: recent evidence and a discussion of some questions]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1191</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1175</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

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<title><![CDATA[Commentary: Smoking and lung cancer: reflections on a pioneering paper]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1192?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cox, D. R]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp290</dc:identifier>
<dc:title><![CDATA[Commentary: Smoking and lung cancer: reflections on a pioneering paper]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1193</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1192</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
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<title><![CDATA[Commentary: 'Smoking and lung cancer'--the embryogenesis of modern epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1193?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Vandenbroucke, J. P]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp292</dc:identifier>
<dc:title><![CDATA[Commentary: 'Smoking and lung cancer'--the embryogenesis of modern epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1196</prism:endingPage>
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<prism:section>Reprints and Reflections</prism:section>
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<title><![CDATA[Commentary: Cornfield on cigarette smoking and lung cancer and how to assess causality]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[Zwahlen, M.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp294</dc:identifier>
<dc:title><![CDATA[Commentary: Cornfield on cigarette smoking and lung cancer and how to assess causality]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
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<title><![CDATA[Commentary: Cornfield, Epidemiology and Causality]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[Greenhouse, J. B]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp299</dc:identifier>
<dc:title><![CDATA[Commentary: Cornfield, Epidemiology and Causality]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1201</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1199</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1202?rss=1">
<title><![CDATA[Cohort Profile: The Danish HIV Cohort Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1202?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Obel, N., Engsig, F. N, Rasmussen, L. D, Larsen, M. V, Omland, L. H, Sorensen, H. T]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn192</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Danish HIV Cohort Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1206</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1202</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1207?rss=1">
<title><![CDATA[Cohort Profile: NICHD International Site Development Initiative (NISDI): a prospective, observational study of HIV-exposed and HIV-infected children at clinical sites in Latin American and Caribbean countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1207?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hazra, R., Stoszek, S. K, Freimanis Hance, L., Pinto, J., Marques, H., Peixoto, M., Alarcon, J., Mussi-Pinhata, M., Serchuck, L., for the NISDI Pediatric Study Group 2008]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn239</dc:identifier>
<dc:title><![CDATA[Cohort Profile: NICHD International Site Development Initiative (NISDI): a prospective, observational study of HIV-exposed and HIV-infected children at clinical sites in Latin American and Caribbean countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1214</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1207</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1215?rss=1">
<title><![CDATA[Cohort Profile: West of Scotland Twenty-07 Study: Health in the Community]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1215?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Benzeval, M., Der, G., Ellaway, A., Hunt, K., Sweeting, H., West, P., Macintyre, S.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn213</dc:identifier>
<dc:title><![CDATA[Cohort Profile: West of Scotland Twenty-07 Study: Health in the Community]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1223</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1215</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1224?rss=1">
<title><![CDATA[Diagnostic change and the increased prevalence of autism]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1224?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Increased autism prevalence rates have generated considerable concern. However, the contribution of changes in diagnostic practices to increased prevalence rates has not been thoroughly examined. Debates over the role of diagnostic substitution also continue. California has been an important test case in these controversies. The objective of this study was to determine the extent to which the increased prevalence of autism in California has been driven by changes in diagnostic practices, diagnostic substitution and diagnostic accretion.</p>
<p><b>Methods</b> Retrospective case record examination of 7003 patients born before 1987 with autism who were enrolled with the California Department of Developmental Services between 1992 and 2005 was carried out. Of principal interest were 631 patients with a sole diagnosis of mental retardation (MR) who subsequently acquired a diagnosis of autism. The outcome of interest was the probability of acquiring a diagnosis of autism as a result of changes in diagnostic practices was calculated. The probability of diagnostic change is then used to model the proportion of the autism caseload arising from changing diagnostic practices.</p>
<p><b>Results</b> The odds of a patient acquiring an autism diagnosis were elevated in periods in which the practices for diagnosing autism changed. The odds of change in years in which diagnostic practices changed were 1.68 [95% confidence interval (CI) 1.11&ndash;2.54], 1.55 (95% CI 1.03&ndash;2.34), 1.58 (95% CI 1.05&ndash;2.39), 1.82 (95% CI 1.23&ndash;2.7) and 1.61 (95% CI 1.09&ndash;2.39). Using the probability of change between 1992 and 2005 to generalize to the population with autism, it is estimated that 26.4% (95% CI 16.25&ndash;36.48) of the increased autism caseload in California is uniquely associated with diagnostic change through a single pathway&mdash;individuals previously diagnosed with MR.</p>
<p><b>Conclusion</b> Changes in practices for diagnosing autism have had a substantial effect on autism caseloads, accounting for one-quarter of the observed increase in prevalence in California between 1992 and 2005.</p>
]]></description>
<dc:creator><![CDATA[King, M., Bearman, P.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp261</dc:identifier>
<dc:title><![CDATA[Diagnostic change and the increased prevalence of autism]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1234</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1224</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1234?rss=1">
<title><![CDATA[Commentary: Effects of diagnostic thresholds and research vs service and administrative diagnosis on autism prevalence]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1234?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Charman, T., Pickles, A., Chandler, S., Wing, L., Bryson, S., Simonoff, E., Loucas, T., Baird, G.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp256</dc:identifier>
<dc:title><![CDATA[Commentary: Effects of diagnostic thresholds and research vs service and administrative diagnosis on autism prevalence]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1238</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1234</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1238?rss=1">
<title><![CDATA[Commentary: Fact and artefact in the secular increase in the rate of autism]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1238?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rutter, M.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp257</dc:identifier>
<dc:title><![CDATA[Commentary: Fact and artefact in the secular increase in the rate of autism]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1239</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1238</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1239?rss=1">
<title><![CDATA[Commentary: Diagnostic change and the increased prevalence of autism]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1239?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hertz-Picciotto, I.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp258</dc:identifier>
<dc:title><![CDATA[Commentary: Diagnostic change and the increased prevalence of autism]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1241</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1239</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1241?rss=1">
<title><![CDATA[Commentary: On King and Bearman]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1241?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Fombonne, E.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp259</dc:identifier>
<dc:title><![CDATA[Commentary: On King and Bearman]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1242</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1241</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1243?rss=1">
<title><![CDATA[Author's Response Commentaries on diagnostic accretion and the increased prevalence of measured autism]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1243?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bearman, P., King, M.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp263</dc:identifier>
<dc:title><![CDATA[Author's Response Commentaries on diagnostic accretion and the increased prevalence of measured autism]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1244</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1243</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1245?rss=1">
<title><![CDATA[Autism spectrum disorders in young children: effect of changes in diagnostic practices]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1245?rss=1</link>
<description><![CDATA[
<p><b>Background</b> It is unclear whether the increase in autism over the past two decades is a real increase or due to changes in diagnosis and ascertainment of autism spectrum disorders (ASDs), which include autism, Asperger syndrome and pervasive developmental disorder not otherwise specified (PDD-NOS). The aim of this study was to examine the trends in ASD over time in Western Australia (WA) and the possible effects and contribution of changes in diagnostic criteria, age at diagnosis, eligibility for service provision based on ASD diagnoses and changes in diagnostic practices.</p>
<p><b>Methods</b> A population-based study was conducted among the cohort of children born in WA between 1983 and 1999 and diagnosed with ASD between the age of 2 and 8 years up to December 31, 2004. The trend in ASD diagnosis over the study period was assessed by investigating birth cohort and period effects, and examining whether these were modified by age of diagnosis. ASD diagnosis corresponding with changes in diagnostic criteria, funding and service provision over time were also investigated. A subgroup analysis of children aged &le;5 years was also conducted to examine trends in the incidence and age of diagnosis of ASD and intellectual disability (ID) and to investigate the role of changes in diagnostic practices.</p>
<p><b>Results</b> The overall prevalence of ASD among children born between 1983 and 1999 and diagnosed by age 8 was 30 per 10 000 births with the prevalence of autism comprising 21 per 10 000 births. The prevalence of ASD increased by 11.9% per annum, from 8 cases per 10 000 births in 1983 to 46 cases per 10 000 births in 1999. The annual incidence of ASD, based on newly diagnosed ASD cases in each year from 1985 to 2002, increased over the study period. The increase in incidence of ASD appeared to coincide with changes in diagnostic criteria and availability of funding and services in WA, particularly for children aged &lt;5 years. The age-specific rates of autism and PDD-NOS increased over time and the median age of diagnosis for autism decreased from 4 to 3 years of age throughout the 1990s. For children aged &le;5 years the incidence of ASD diagnosis increased significantly from 1992, with an average annual increase of 22%. Similar findings were found for autism. In the corresponding years the incidence of diagnosis of severe ID fell by 10% per annum and mild&ndash;moderate ID increased by 3% per annum.</p>
<p><b>Conclusions</b> The rise in incidence of all types of ASDs by year of diagnosis appears to be related to changes in diagnostic and service provision practices in WA. In children aged &le;5 years, diagnosis of severe ID decreased, but mild&ndash;moderate ID increased during the study period. A true increase in ASD cannot be ruled out.</p>
]]></description>
<dc:creator><![CDATA[Nassar, N., Dixon, G., Bourke, J., Bower, C., Glasson, E., de Klerk, N., Leonard, H.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp260</dc:identifier>
<dc:title><![CDATA[Autism spectrum disorders in young children: effect of changes in diagnostic practices]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1254</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1245</prism:startingPage>
<prism:section>Special Theme: Autism</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1255?rss=1">
<title><![CDATA[Is the incidence of psychotic disorder in decline? Epidemiological evidence from two decades of research]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1255?rss=1</link>
<description><![CDATA[
<p><b>Background</b> It is unclear whether the incidence of first episode psychoses is in decline. We had the opportunity to determine whether incidence had changed over a 20-year period in a single setting, and test whether this could be explained by demographic or clinical changes.</p>
<p><b>Methods</b> The entire population at-risk aged 16&ndash;54 in Nottingham over three time periods (1978&ndash;80, 1993&ndash;95 and 1997&ndash;99) were followed up. All participants presenting with an ICD-9/10 first episode psychosis were included. The remainder of the population at-risk formed the denominator. Standardized incidence rates were calculated at each time period with possible change over time assessed via Poisson regression. We studied six outcomes: substance-induced psychoses, schizophrenia, other non-affective psychoses, manic psychoses, depressive psychoses and all psychotic disorders combined.</p>
<p><b>Results</b> Three hundred and forty-seven participants with a first episode psychosis during 1.2 million person-years of follow-up over three time periods were identified. The incidence of non-affective or affective psychoses had not changed over time following standardization for age, sex and ethnicity. We observed a linear increase in the incidence of substance-induced psychosis, per annum, over time (incidence rate ratios: 1.15; 95% CI 1.05&ndash;1.25). This could not be explained by longitudinal changes in the age, sex and ethnic structure of the population at-risk.</p>
<p><b>Conclusions</b> Our findings suggest psychotic disorders are not in decline, though there has been a change in the syndromal presentation of non-affective disorders, away from schizophrenia towards other non-affective psychoses. The incidence of substance-induced psychosis has increased, consistent with increases in substance toxicity over time, rather than changes in the prevalence or vulnerability to substance misuse. Increased clinical and popular awareness of substance misuse could also not be excluded.</p>
]]></description>
<dc:creator><![CDATA[Kirkbride, J B, Croudace, T, Brewin, J, Donoghue, K, Mason, P, Glazebrook, C, Medley, I, Harrison, G, Cooper, J E, Doody, G A, Jones, P B]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn168</dc:identifier>
<dc:title><![CDATA[Is the incidence of psychotic disorder in decline? Epidemiological evidence from two decades of research]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1264</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1255</prism:startingPage>
<prism:section>Psychiatric Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1265?rss=1">
<title><![CDATA[Socioeconomic position, psychosocial work environment and cerebrovascular disease among women: the Finnish public sector study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1265?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The excess risk of fatal and non-fatal cerebrovascular disease in people from low socioeconomic positions is only partially explained by conventional cerebrovascular risk factors. This has led to the suggestion that poor psychosocial work environments provide important additional explanatory power. However, little evidence is available for women.</p>
<p><b>Methods</b> We examined whether job demands or job control contributed to the socioeconomic gradient in cerebrovascular disease among 48 361 women aged 18&ndash;65 years. Job demands, job control and behavioural risk factors were self-reported in 2000&ndash;2002; socioeconomic position (as indexed by occupational class) and all of the health measures were obtained from registers. The outcome was recorded hospitalization or death from cerebrovascular disease.</p>
<p><b>Results</b> During a mean follow-up of 3.4 years, 124 women had a new cerebrovascular disease event. The risk was 2.3 (95% CI 1.3&ndash;3.9) times higher among women in low vs high socioeconomic positions. Adjustment for conventional risk factors, such as prevalent hypertension, coronary heart disease, diabetes, smoking, heavy alcohol consumption, physical inactivity and obesity, attenuated this excess risk by 23%. In contrast, adjustment for job demands and job control actually amplified the gradient by 36% suggesting a suppression effect.</p>
<p><b>Conclusions</b> In this contemporary cohort of employed women, job demands&mdash;alone and in combination with job control&mdash;suppressed rather than explained socioeconomic differences in cerebrovascular disease.</p>
]]></description>
<dc:creator><![CDATA[Kivimaki, M., Gimeno, D., Ferrie, J. E, Batty, G D., Oksanen, T., Jokela, M., Virtanen, M., Salo, P., Akbaraly, T. N, Elovainio, M., Pentti, J., Vahtera, J.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn373</dc:identifier>
<dc:title><![CDATA[Socioeconomic position, psychosocial work environment and cerebrovascular disease among women: the Finnish public sector study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1271</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1265</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1272?rss=1">
<title><![CDATA[Material, psychosocial, behavioural and biomedical factors in the explanation of relative socio-economic inequalities in mortality: evidence from the HUNT study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1272?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Previous studies have assessed the relative importance of material, psychosocial and behavioural factors in the explanation of relative socio-economic inequalities in mortality, but research into the contribution of biomedical factors has been limited. Our study examines the relative contribution of (i) material, (ii) psychosocial, (iii) behavioural and (iv) biomedical factors in the explanation of relative socio-economic (educational and income) inequalities in mortality.</p>
<p><b>Methods</b> Cohort study&mdash;baseline data from the Norwegian total county population-based HUNT 2 study linked to mortality data (1995/97 to 2003). In this analysis, 18 247 men and 18 278 women aged 24&ndash;80 without severe chronic disease at baseline were eligible.</p>
<p><b>Results</b> No socio-economic inequalities in mortality among women were found. In men, educational- and income-related inequalities in mortality were found with a relative risk for the lowest educational group of 1.67 (1.29&ndash;2.15) and the lowest income quartile of 2.03 (1.57&ndash;2.70). Together, the four explanatory factors reduced the relative risk of mortality of the lowest educational group to 1.18 (0.90&ndash;1.55) and the relative risk of mortality in the lowest income quartile was attenuated to 1.17 (0.83&ndash;1.63). Known biomedical factors contributed least to both educational and income inequalities in mortality.</p>
<p><b>Conclusions</b> Material factors were the most important in explaining income inequalities in mortality amongst men, whereas psychosocial and behavioural factors were the most important in explaining educational inequalities. This suggests that improving the material, psychosocial and behavioural circumstances of men might bring more substantial reductions in relative socio-economic inequalities in mortality.</p>
]]></description>
<dc:creator><![CDATA[Skalicka, V., van Lenthe, F., Bambra, C., Krokstad, S., Mackenbach, J.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp262</dc:identifier>
<dc:title><![CDATA[Material, psychosocial, behavioural and biomedical factors in the explanation of relative socio-economic inequalities in mortality: evidence from the HUNT study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1284</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1272</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1285?rss=1">
<title><![CDATA[Is it better to be rich in a poor area or poor in a rich area? A multilevel analysis of a case-control study of social determinants of tuberculosis]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1285?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Tuberculosis is known to have socio-economic determinants at individual and at area levels, but it is not known whether they are independent, whether they interact and their relative contributions to the burden of tuberculosis.</p>
<p><b>Methods</b> A case&ndash;control study was conducted in Recife, Brazil, to investigate individual and area social determinants of tuberculosis, to explore the relationship between determinants at the two levels and to calculate their relative contribution to the burden of tuberculosis. It included 1452 cases of tuberculosis diagnosed by the tuberculosis services and 5808 controls selected at random from questionnaires completed for the demographic census. Exhaustive information on social factors was collected from cases, using the questionnaire used in the census. Socio-economic information for areas was downloaded from the census. Multilevel logistic regression investigated individual and area effects.</p>
<p><b>Results</b> There was a marked and independent influence of social variables on the risk of tuberculosis, both at individual and area levels. At individual level, being aged &ge;20, being male, being illiterate, not working in the previous 7 days and possessing few goods, all increased the risk of tuberculosis. At area level, living in an area with many illiterate people and where few households own a computer also increased this risk; individual and area levels did not appear to interact. Twice as many cases were attributable to social variables at individual level than at area level.</p>
<p><b>Conclusions</b> Although individual characteristics are the main contributor to the risk of tuberculosis, contextual characteristics make a substantial independent contribution.</p>
]]></description>
<dc:creator><![CDATA[de Alencar Ximenes, R. A., de Fatima Pessoa Militao de Albuquerque, M., Souza, W. V, Montarroyos, U. R, Diniz, G. T N, Luna, C. F, Rodrigues, L. C]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp224</dc:identifier>
<dc:title><![CDATA[Is it better to be rich in a poor area or poor in a rich area? A multilevel analysis of a case-control study of social determinants of tuberculosis]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1296</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1285</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1295?rss=1">
<title><![CDATA[Commentary: Socio-economic determinants of tuberculosis in Recife, Brazil]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1295?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Marks, S.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp284</dc:identifier>
<dc:title><![CDATA[Commentary: Socio-economic determinants of tuberculosis in Recife, Brazil]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1296</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1295</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1297?rss=1">
<title><![CDATA[Socio-economic status, cortisol and allostatic load: a review of the literature]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1297?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The notion that chronic stress contributes to health inequalities by socio-economic status (SES) through physiological wear and tear has received widespread attention. This article reviews the literature testing associations between SES and cortisol, an important biomarker of stress, as well as the summary index of allostatic load (AL).</p>
<p><b>Methods</b> A search of all published literature on the PubMed and ISI Web of Knowledge literature search engines was conducted using broad search terms. The authors reviewed abstracts and selected articles that met the inclusion criteria. A total of 26 published studies were included in the review.</p>
<p><b>Results</b> Overall, SES was not consistently related to cortisol. Although several studies found an association between lower SES and higher levels of cortisol, many found no association, with some finding the opposite relationship. Lower SES was more consistently related to a blunted pattern of diurnal cortisol secretion, but whether this corresponded to higher or lower overall cortisol exposure varied by study. Approaches to collecting and analysing cortisol varied widely, likely contributing to inconsistent results. Lower SES was more consistently related to higher levels of AL, but primarily via the cardiovascular and metabolic components of AL rather than the neuroendocrine markers.</p>
<p><b>Conclusions</b> Current empirical evidence linking SES to cortisol and AL is weak. Future work should standardize approaches to measuring SES, chronic stress and cortisol to better understand these relationships.</p>
]]></description>
<dc:creator><![CDATA[Dowd, J. B, Simanek, A. M, Aiello, A. E]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp277</dc:identifier>
<dc:title><![CDATA[Socio-economic status, cortisol and allostatic load: a review of the literature]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1309</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1297</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1310?rss=1">
<title><![CDATA[Is education causally related to better health? A twin fixed-effect study in the USA]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1310?rss=1</link>
<description><![CDATA[
<p><b>Background</b> More years of schooling is generally associated with better health. However, this association may be confounded by unobserved common prior causes such as inherited ability, personality such as patience, or early family circumstances. The twin fixed-effect approach can potentially address this problem by cancelling these factors between twin pairs. The purpose of this study is to identify the causal effects of education on health and health behaviours using a twin fixed-effect approach.</p>
<p><b>Methods</b> We used twin data from the National Survey of Midlife Development in the United States, 1995&ndash;1996. The study population included 302 male [55.6% monozygotic (MZ) and 44.4% dizygotic (DZ)] and 387 female twin pairs (47.3% MZ and 52.7% DZ). A range of health outcomes [perceived global, physical and mental health, body mass index (BMI), waist circumference, waist&ndash;hip ratio, number of depressive symptoms] and health behaviours (smoking and physical activity) were examined among twin pairs who were discordant on years of schooling.</p>
<p><b>Results</b> Among MZ twins, more years of education was associated with better perceived global health. For all other health outcomes/behaviours, the point estimates of the effect of education in the fixed-effect analyses suggested a weak protective association. Among DZ male twins, each additional year of schooling lowered the prevalence of smoking by 32% [odds ratio (OR): 0.68, 95% confidence interval (CI): 0.48&ndash;0.97] in the fixed-effect analysis.</p>
<p><b>Conclusion</b> The widely reported associations between schooling and health outcomes/behaviours may not reflect causal relationships in every instance. Although low statistical power may explain some of the null associations, our twin fixed-effect analyses suggest that at least some cases of the education/health relationship reflect confounding by unobserved third variables.</p>
]]></description>
<dc:creator><![CDATA[Fujiwara, T., Kawachi, I.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp226</dc:identifier>
<dc:title><![CDATA[Is education causally related to better health? A twin fixed-effect study in the USA]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1322</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1310</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1322?rss=1">
<title><![CDATA[Commentary: Strengths and limitations of the discordant twin-pair design in social epidemiology. Where do we go from here?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1322?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Madsen, M., Osler, M.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp264</dc:identifier>
<dc:title><![CDATA[Commentary: Strengths and limitations of the discordant twin-pair design in social epidemiology. Where do we go from here?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1323</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1322</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1324?rss=1">
<title><![CDATA[Modelling income group differences in the health and economic impacts of targeted food taxes and subsidies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1324?rss=1</link>
<description><![CDATA[
<p><b>Objective</b> To examine the effects, by income group, of targeted food taxes and subsidies on nutrition, health and expenditure in the UK.</p>
<p><b>Methods</b> A model based on consumption data and demand elasticity was constructed to predict the effects of four food taxation-subsidy regimens. Resulting changes in demand, expenditure, nutrition, cardiovascular disease (CVD) and cancer mortality were estimated.</p>
<p><b>Data</b> Expenditure data were taken from the Expenditure and Food Survey; estimates of price elasticities of demand for food were taken from a report based on the National Food Survey 1988&ndash;2000. Estimates of effect on CVD and cancer mortality of changing fat, salt, fruit and vegetable intake were taken from previous meta-analyses.</p>
<p><b>Results</b> (i) Taxing principal sources of dietary saturated fat is unlikely to reduce cardiovascular disease (CVD) or cancer mortality. (ii) Taxing &lsquo;less healthy&rsquo; foods (defined by the WXYfm nutrient profiling model) could increase CVD and cancer deaths by 35&ndash;1300 yearly. (iii) Taxing &lsquo;less healthy&rsquo; foods and subsidising fruits and vegetables by 17.5% could avert up to 2900 CVD and cancer deaths yearly. (iv) Taxing &lsquo;less healthy&rsquo; foods and using all tax revenue to subsidize fruits and vegetables could avert up to 6400 CVD and cancer deaths yearly. Few obesity-related CVD deaths are averted by any of the regimens. All four regimens would be economically regressive and positive health effects will not necessarily be greater in lower-income groups where the need for dietary improvement is higher.</p>
<p><b>Conclusions</b> A targeted food tax combined with the appropriate subsidy on fruits and vegetables could reduce deaths from CVD and cancer.</p>
]]></description>
<dc:creator><![CDATA[Nnoaham, K. E, Sacks, G., Rayner, M., Mytton, O., Gray, A.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp214</dc:identifier>
<dc:title><![CDATA[Modelling income group differences in the health and economic impacts of targeted food taxes and subsidies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1333</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1324</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1334?rss=1">
<title><![CDATA[School performance and hospital admissions due to self-inflicted injury: a Swedish national cohort study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1334?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Self-inflicted injury in youth has increased in many Western countries during recent decades. Education is the most influential societal determinant of living conditions in young people after early childhood. This study tested the hypothesis that school performance predicts self-inflicted injury.</p>
<p><b>Methods</b> A national cohort of 447 929 children born during 1973&ndash;77 was followed prospectively in the National Patient Discharge Register from the end of their ninth and last year of compulsory school until 2001. Multivariate Cox analyses of proportional hazards were used to test hypotheses regarding grades in ninth grade as predictors of hospital admission due to self-inflicted injury.</p>
<p><b>Results</b> The risk of hospital admission because of self-inflicted injury increased steeply in a step-wise manner with decreasing grade point average. Hazard ratios were 6.2 (95% confidence interval 5.5&ndash;7.0) in those with the lowest level of grade point average compared with the highest. The risks were similar for women and men. Adjustment for potential socio-economic confounders in a multivariate proportional hazards regression analysis attenuated this strong gradient only marginally.</p>
<p><b>Conclusion</b> School performance is a strong factor for predicting future mental ill-health as expressed by self-inflicted injury.</p>
]]></description>
<dc:creator><![CDATA[Jablonska, B., Lindberg, L., Lindblad, F., Rasmussen, F., Ostberg, V., Hjern, A.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp236</dc:identifier>
<dc:title><![CDATA[School performance and hospital admissions due to self-inflicted injury: a Swedish national cohort study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1341</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1334</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1342?rss=1">
<title><![CDATA[Maternal smoking, biofuel smoke exposure and child height-for-age in seven developing countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1342?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Children are at high risk of exposure to environmental tobacco smoke and biofuel smoke at home in developing countries. This study examines whether exposure to cigarette and biofuel smoke is associated with height-for-age of children (0&ndash;59 months) in seven developing countries.</p>
<p><b>Methods</b> The data are from Demographic and Health Surveys conducted in Cambodia, Dominican Republic, Haiti, Jordan, Moldova, Namibia and Nepal between 2005 and 2007. The respondents were women (15&ndash;49 years) and their children in seven countries (<I>n</I> = 28 439), and men (15&ndash;59 years) from four countries. The outcome is a physical measurement of child height-for-age in standard deviation units.</p>
<p><b>Results</b> Multilevel regression analysis showed that the country of residence modified the association between maternal smoking and child height-for-age. Exposure to maternal smoking was associated negatively with child height-for-age in Cambodia, Namibia and Nepal, whereas it was not in other countries. Multilevel regression analysis revealed that biofuel smoke exposure was associated with a decrease in child height-for-age [<I>b</I> = &ndash;0.13, 95% confidence interval (CI) = &ndash;0.19 to &ndash;0.07, <I>P</I> &lt; 0.001]. No interaction was found between country of residence and biofuel smoke exposure. Multinomial logistic regression results showed that biofuel smoke exposure was associated with both stunting [odds ratio (OR) = 1.25, 95% CI = 1.08&ndash;1.44, <I>P</I> = 0.002) and severe stunting (OR = 1.27, 95% CI = 1.02&ndash;1.59, <I>P</I> = 0.04), after controlling for covariates.</p>
<p><b>Conclusion</b> The findings suggest that exposure to maternal smoking and biofuel smoke may contribute to growth deficiencies in young children. Programmes are needed to ensure smoke-free home environments for children.</p>
]]></description>
<dc:creator><![CDATA[Kyu, H. H., Georgiades, K., Boyle, M. H]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp253</dc:identifier>
<dc:title><![CDATA[Maternal smoking, biofuel smoke exposure and child height-for-age in seven developing countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1350</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1342</prism:startingPage>
<prism:section>Environmental Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1351?rss=1">
<title><![CDATA[Exposure to indoor biomass fuel and tobacco smoke and risk of adverse reproductive outcomes, mortality, respiratory morbidity and growth among newborn infants in south India]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1351?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Exposure to indoor air pollution due to open burning of biomass fuel is common in low- and middle-income countries. Previous studies linked this exposure to an increased risk of respiratory illness, low birth weight (LBW) and other disorders. We assessed the association between exposure to biomass fuel sources and second-hand tobacco smoke (SHTS) in the home and adverse health outcomes in early infancy in a population in rural south India.</p>
<p><b>Methods</b> A population-based cohort of newborns was followed from birth through 6 months. Household characteristics were assessed during an enrolment interview including the primary type of cooking fuel and smoking behaviour of household residents. Follow-up visits for morbidity were carried out every 2 weeks after delivery. Infants were discharged at 6 months when anthropometric measurements were collected.</p>
<p><b>Results</b> 11 728 live-born infants were enrolled and followed, of whom 92.3% resided in households that used wood and/or dung as a primary source of fuel. Exposure to biomass fuel was associated with an adjusted 49% increased risk of LBW, a 34% increased incidence of respiratory illness and a 21% increased risk of 6-month infant mortality. Exposed infants also had 45 and 30% increased risks of underweight and stunting at 6 months. SHTS exposure was also associated with these adverse health outcomes except for attained growth.</p>
<p><b>Conclusions</b> Open burning of biomass fuel in the home is associated with significant health risks to the newborn child and young infant. Community-based trials are needed to clarify causal connections and identify effective approaches to reduce this burden of illnesses.</p>
]]></description>
<dc:creator><![CDATA[Tielsch, J. M, Katz, J., Thulasiraj, R. D, Coles, C. L, Sheeladevi, S, Yanik, E. L, Rahmathullah, L.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp286</dc:identifier>
<dc:title><![CDATA[Exposure to indoor biomass fuel and tobacco smoke and risk of adverse reproductive outcomes, mortality, respiratory morbidity and growth among newborn infants in south India]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1363</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1351</prism:startingPage>
<prism:section>Environmental Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1364?rss=1">
<title><![CDATA[Ranking of genome-wide association scan signals by different measures]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1364?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The <I>P</I>-value approach has been employed to prioritizing genome-wide association (GWA) scan signals, with a genome-wide significance defined by a prior <I>P</I>-value threshold, although this is not ideal. A rationale put forward is that the association signals rather should be expected to give less support for single nucleotide polymorphisms (SNPs) that are rare (with associated low-power tests) than for common SNPs with equivalent <I>P</I>-values, unless investigators believe, <I>a priori</I>, that rare causative variants contribute to the disease and have more pronounced effects.</p>
<p><b>Methods</b> Using data from a GWA scan for type 2 diabetes (1924 cases, 2938 controls, 393 453 SNPs), we compared <I>P</I>-values with four alternative signal measures: likelihood ratio (LR), Bayes factor (BF; with a specified prior distribution for true effects), &lsquo;frequentist factor&rsquo; (FF; reflecting the ratio between estimated&mdash;post-data&mdash; &lsquo;power&rsquo; and <I>P</I>-value) and probability of pronounced effect size (PrPES).</p>
<p><b>Results</b> The 19 common SNPs [minor allele frequency (MAF) among the controls &gt;29%] yielding strong <I>P</I>-value signals (<I>P</I> &lt; 5 <FONT FACE="arial,helvetica">x</FONT> 10<sup>&ndash;7</sup>) were also top ranked by the other approaches. There was a strong similarity between the <I>P</I>-values, LR and BF signals, in terms of ranking SNPs. In contrast, FF and PrPES signals down-weighted rare SNPs (control MAF &lt;10%) with low <I>P</I>-values.</p>
<p><b>Conclusions</b> For prioritization of signals that do not achieve compelling levels of evidence for association, the main driving force behind observed differences between the various association signals appears to be SNP MAF. The statistical power afforded by follow-up samples for establishing replication should be taken into account when tailoring the signal selection strategy.</p>
]]></description>
<dc:creator><![CDATA[Stromberg, U., Bjork, J., Vineis, P., Broberg, K., Zeggini, E.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp285</dc:identifier>
<dc:title><![CDATA[Ranking of genome-wide association scan signals by different measures]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1373</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1364</prism:startingPage>
<prism:section>Genetic Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1374?rss=1">
<title><![CDATA[The paraoxonase (PON1) Q192R polymorphism is not associated with poor health status or depression in the ELSA or INCHIANTI studies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1374?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The human paraoxonase (PON1) protein detoxifies certain organophosphates, and the <I>PON1</I> Q192R polymorphism (rs662) affects PON1 activity. Groups with higher dose exposure to organophosphate sheep dips or first Gulf War nerve toxins reported poorer health if they had 192R, and these associations have been used to exemplify Mendelian randomization analysis. However, a reported association of 192R with depression in a population-based study of older women recently cast doubt on the specificity of the higher dose findings. We aimed to examine associations between the <I>PON1</I> Q192R polymorphism and self-reported poor health and depression in two independent population-based studies.</p>
<p><b>Methods</b> We used logistic regression models to examine the associations in men and women aged 60&ndash;79 years from the English Longitudinal Study of Ageing (ELSA, <I>n</I> = 3158) and InCHIANTI (<I>n</I> = 761) population studies. Outcomes included the Center for Epidemiologic Studies Depression (CES-D) scale, self-rated general health status and (in ELSA only) diagnoses of depression.</p>
<p><b>Results</b> The <I>PON1</I> Q192R polymorphism was not associated with self-reported poor health {meta-analysis: odds ratio (OR) = 1.01 [confidence interval (CI) 0.91&ndash;1.13], <I>P</I> = 0.80} or depressive symptoms in either study or in meta-analyses [CES-D: OR = 1.01 (CI 0.87&ndash;1.17), <I>P</I> = 0.90]. There was also no association with histories of diagnosed depression in ELSA [OR = 1.03 (CI 0.82&ndash;1.30), <I>P</I> = 0.80].</p>
<p><b>Conclusions</b> We found no evidence of an association between the <I>PON1</I> Q192R polymorphism and poor general or mental health in two independent population-based studies. Neither the claimed Q192R association with depression in the general population nor its theoretical implications were supported.</p>
]]></description>
<dc:creator><![CDATA[Rice, N. E, Bandinelli, S., Corsi, A. M., Ferrucci, L., Guralnik, J. M, Miller, M. A, Kumari, M., Murray, A., Frayling, T. M, Melzer, D.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp265</dc:identifier>
<dc:title><![CDATA[The paraoxonase (PON1) Q192R polymorphism is not associated with poor health status or depression in the ELSA or INCHIANTI studies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1379</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1374</prism:startingPage>
<prism:section>Genetic Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1380?rss=1">
<title><![CDATA[Maternal anaemia and preterm birth: a prospective cohort study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1380?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The role of maternal anaemia in preterm birth remains poorly defined, and the association between anaemia and preterm birth clinical subtypes remain unclear. We examined if maternal anaemia exposure both within and across trimesters during gestation is associated with preterm birth.</p>
<p><b>Methods</b> This was a secondary analysis of data from a population-based prospective cohort study in 13 counties of East China (1993&ndash;96). All singleton live births delivered at 20&ndash;44 weeks to women with at least one haemoglobin measure during pregnancy were included (<I>n</I> = 160 700). Risk of preterm birth (&lt;37 weeks) was examined by clinical subtypes, namely, preterm premature rupture of membranes (PROM), spontaneous preterm labour and medically indicated preterm birth. Haemoglobin changes across trimesters were assessed as proxy of haemo-dilution and haemo-concentration. Multivariable Cox proportional hazards regression models were fitted.</p>
<p><b>Results</b> Preterm birth rates of preterm birth were 4.1% for anaemic and 5% for non-anaemic women (<I>P</I> &lt; 0.05). Compared with haemoglobin of 11 g/dl (reference), values &le;5 g/dl in the first trimester were associated with increased risk for preterm PROM [hazard ratio (HR) 3.3, 95% confidence interval (CI) 1.4&ndash;7.7], whereas low haemoglobin in the third trimester was associated with reduced risk of spontaneous preterm labour. Haemodilution was associated with reduced risk for preterm birth.</p>
<p><b>Conclusions</b> Anaemia in early pregnancy was found to be associated with increased risk for preterm PROM, whereas exposure in late pregnancy was associated with reduced risk for spontaneous preterm labour.</p>
]]></description>
<dc:creator><![CDATA[Zhang, Q., Ananth, C. V, Li, Z., Smulian, J. C]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp243</dc:identifier>
<dc:title><![CDATA[Maternal anaemia and preterm birth: a prospective cohort study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1389</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1380</prism:startingPage>
<prism:section>Perinatal Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1390?rss=1">
<title><![CDATA[Fetal growth and behaviour problems in early adolescence: findings from the Mater University Study of Pregnancy]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1390?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The nature of the association between birth weight and behavioural problems in adolescence is unclear. Recent studies are limited by their capacity to adjust for important obstetric and measurement issues.</p>
<p><b>Aim</b> To examine the nature of the association between birth weight and a range of behavioural symptoms, including anxiety/depression and social problems, in adolescence.</p>
<p><b>Methods</b> Data from 4971 mothers and their children participating in the Mater University Study of Pregnancy (MUSP), a prospective, population-based birth cohort, are presented. This study commenced in Brisbane, Australia, in 1981. Mothers and their children were followed up at 3&ndash;5 days post-birth, and 6 months, 5 years and 14 years after the initial interview. Internalizing and externalizing behaviour problems, social problems and anxiety/depressive symptoms were assessed using Achenbach's Youth Self Report (YSR) of the Child Behaviour Check List (CBCL).</p>
<p><b>Results</b> There was no evidence of a linear association between birth weight and behavioural symptoms, when birth weight <I>z</I>-scores were examined as a continuous variable. However, a non-linear association was identified when birth weight <I>z</I>-scores were categorized into quintiles. Children in the lowest and highest quintiles were at higher risk of increased anxiety/depressive and social problems symptoms. After adjustment for potential confounders, birth weight showed a non-linear association with the log odds of social problems {Quintile 1 odds ratio (OR) 1.59 [95% confidence interval (CI) 1.13, 2.23] Quintile 5 OR 1.57 (95% CI 1.12, 2.20)}.</p>
<p><b>Conclusions</b> Our findings provide further support for an association between birth weight and some adolescent behaviour problems. This association is likely to be non-linear, affecting babies at both the lower and higher ends of the birth weight distribution.</p>
]]></description>
<dc:creator><![CDATA[Alati, R., Najman, J. M, O'Callaghan, M., Bor, W., Williams, G. M, Clavarino, A.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp252</dc:identifier>
<dc:title><![CDATA[Fetal growth and behaviour problems in early adolescence: findings from the Mater University Study of Pregnancy]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1400</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1390</prism:startingPage>
<prism:section>Perinatal Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1401?rss=1">
<title><![CDATA[Enhanced post-natal growth is associated with elevated blood pressure in young Senegalese adults]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1401?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Evidence suggests that intrauterine growth restriction followed by rapid post-natal growth is associated with high blood pressure. We assessed the effect of early size and post-natal growth on blood pressure in a population from West Africa, where fetal growth retardation and childhood malnutrition are common.</p>
<p><b>Methods</b> A total of 1288 Senegalese subjects were followed from infancy to young adulthood (mean age 17.9 years). Adult systolic blood pressure (SBP) was regressed on infant and adult anthropometric characteristics.</p>
<p><b>Results</b> In unadjusted analyses, infant size was positively associated with adult SBP (1.1 &plusmn; 0.3; <I>P</I> = 0.001 for weight; 0.7 &plusmn; 0.3; <I>P</I> = 0.04 for length). With adjustment for current size, the regression coefficients for infant size were reversed (&ndash;0.2 &plusmn; 0.3; <I>P</I> = 0.51 for weight; &ndash;0.3 &plusmn; 0.3; <I>P</I> = 0.35 for length). SBP increased by 4.1 and 2.9 mmHg for 1 standard deviation (SD) increase in current weight or height, respectively. No interaction between infant size and current size was found in the overall models (<I>P</I> = 0.11 for weight, <I>P</I> = 0.95 for height), but this term interacted with sex for weight effect. A negative interaction was found in males (&ndash;0.9 &plusmn; 0.4; <I>P</I> = 0.02) but not in females (0.3 &plusmn; 0.4; <I>P</I> = 0.46). The association of current weight with SBP was stronger in lighter weight male infants.</p>
<p><b>Conclusions</b> These findings support the hypothesis that subjects who were small in early life and experienced enhanced post-natal growth have higher levels of SBP, even in low-income settings.</p>
]]></description>
<dc:creator><![CDATA[Cournil, A., Coly, A. N., Diallo, A., Simondon, K. B.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp255</dc:identifier>
<dc:title><![CDATA[Enhanced post-natal growth is associated with elevated blood pressure in young Senegalese adults]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1410</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1401</prism:startingPage>
<prism:section>Perinatal Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1411?rss=1">
<title><![CDATA[Author's Response Comments on the study of McGeoghegan et al.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1411?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McGeoghegan, D., Binks, K., Gillies, M., Jones, S., Whalley, S.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn123</dc:identifier>
<dc:title><![CDATA[Author's Response Comments on the study of McGeoghegan et al.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1411</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1411</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1412?rss=1">
<title><![CDATA[Exposure to alcohol use in motion pictures and teen drinking in Germany]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1412?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dinani, N., Wood, N. R, Robbe, I. J]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn053</dc:identifier>
<dc:title><![CDATA[Exposure to alcohol use in motion pictures and teen drinking in Germany]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1412</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1412</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1413?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1413?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hanewinkel, R., Tanski, S. E, Sargent, J. D]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn054</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1414</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1413</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1415?rss=1">
<title><![CDATA[Defeating Autism: A Damaging Delusion. Michael Fitzpatrick.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1415?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Grinker, R. R.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp242</dc:identifier>
<dc:title><![CDATA[Defeating Autism: A Damaging Delusion. Michael Fitzpatrick.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1417</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1415</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1417?rss=1">
<title><![CDATA[Autism's False Prophets. Paul Offit.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1417?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stein, Z.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp267</dc:identifier>
<dc:title><![CDATA[Autism's False Prophets. Paul Offit.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1419</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1417</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1419?rss=1">
<title><![CDATA[Population and Disease: Transforming English Society, 1550-1850. Peter Razzell.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1419?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Truelsen, T.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn175</dc:identifier>
<dc:title><![CDATA[Population and Disease: Transforming English Society, 1550-1850. Peter Razzell.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1420</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1419</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1420?rss=1">
<title><![CDATA[Survival Analysis for Epidemiologic and Medical Research. Steve Selvin.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1420?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kim, L.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn190</dc:identifier>
<dc:title><![CDATA[Survival Analysis for Epidemiologic and Medical Research. Steve Selvin.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1421</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1420</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1422?rss=1">
<title><![CDATA[Improving epidemiological surveys of sexual behaviour conducted by telephone]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1422?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Turner, C. F, Al-Tayyib, A., Rogers, S. M, Eggleston, E., Villarroel, M. A, Roman, A. M, Chromy, J. R, Cooley, P. C]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp302</dc:identifier>
<dc:title><![CDATA[Improving epidemiological surveys of sexual behaviour conducted by telephone]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1422</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1422</prism:startingPage>
<prism:section>Erratum</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/895?rss=1">
<title><![CDATA[Ideology with evidence: global warming, maps and ethics]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/895?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ebrahim, S.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp268</dc:identifier>
<dc:title><![CDATA[Ideology with evidence: global warming, maps and ethics]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>896</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>895</prism:startingPage>
<prism:section>Editor's Choice</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/897?rss=1">
<title><![CDATA[Birth cohort studies: past, present and future]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/897?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lawlor, D. A, Andersen, A.-M. N., Batty, G D.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp240</dc:identifier>
<dc:title><![CDATA[Birth cohort studies: past, present and future]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>902</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>897</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/903?rss=1">
<title><![CDATA[Facts, opinions and affaires du couer]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/903?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Marmot, M.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp234</dc:identifier>
<dc:title><![CDATA[Facts, opinions and affaires du couer]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>907</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>903</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/908?rss=1">
<title><![CDATA[Commentary: A continued affair with science and judgements]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/908?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Marmot, M.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp246</dc:identifier>
<dc:title><![CDATA[Commentary: A continued affair with science and judgements]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>910</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>908</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/911?rss=1">
<title><![CDATA[Commentary: Making risk factors more cost-effective predictors of disease]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/911?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rothstein, W. G]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp231</dc:identifier>
<dc:title><![CDATA[Commentary: Making risk factors more cost-effective predictors of disease]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>913</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>911</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/914?rss=1">
<title><![CDATA[Commentary: Facts, opinions and affaires du coeur]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/914?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Carter, S.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp232</dc:identifier>
<dc:title><![CDATA[Commentary: Facts, opinions and affaires du coeur]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>916</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>914</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/917?rss=1">
<title><![CDATA[Born in Bradford: Madonna and child or?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/917?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Beesley, I.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp219</dc:identifier>
<dc:title><![CDATA[Born in Bradford: Madonna and child or?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>920</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>917</prism:startingPage>
<prism:section>Photoessay</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/921?rss=1">
<title><![CDATA[Born in Bradford]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/921?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McMillan, I.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp270</dc:identifier>
<dc:title><![CDATA[Born in Bradford]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>921</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>921</prism:startingPage>
<prism:section>Diversion</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/922?rss=1">
<title><![CDATA[Cohort Profile: The Swiss Inflammatory Bowel Disease Cohort Study (SIBDCS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/922?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pittet, V., Juillerat, P., Mottet, C., Felley, C., Ballabeni, P., Burnand, B., Michetti, P., Vader, J.-P., the Swiss IBD Cohort Study Group]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn180</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Swiss Inflammatory Bowel Disease Cohort Study (SIBDCS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>931</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>922</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/932?rss=1">
<title><![CDATA[Cohort Profile: The Newcastle Thousand Families 1947 Birth Cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/932?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pearce, M. S, Unwin, N. C, Parker, L., Craft, A. W]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn184</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Newcastle Thousand Families 1947 Birth Cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>937</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>932</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/938?rss=1">
<title><![CDATA[Cohort Profile: The Danish Web-based Pregnancy Planning Study--'Snart-Gravid']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/938?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mikkelsen, E. M, Hatch, E. E, Wise, L. A, Rothman, K. J, Riis, A., Sorensen, H. T.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn191</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Danish Web-based Pregnancy Planning Study--'Snart-Gravid']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>943</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>938</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/944?rss=1">
<title><![CDATA[Low birthweight and subsequent emotional and behavioural outcomes in 12-year-old children in Soweto, South Africa: findings from Birth to Twenty]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/944?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The fetal origins hypothesis suggests that an adverse prenatal environment, indexed by low birthweight (LBW), may increase the risk of developing later disease. Recently the hypothesis has been extended to psychological outcomes, especially depression. The aim of this analysis was to test, for the first time in a developing country setting, the association between LBW and psychological symptoms, in Soweto, South Africa.</p>
<p><b>Methods</b> A sample of 1029 children was drawn from Birth to Twenty, a longitudinal cohort followed from pregnancy to young adulthood. This sample completed the Youth Self Report at age 12 years, a validated psychological measure of behavioural and emotional adjustment. Scores were compared between LBW (&lt;2500 g) and normal birthweight children using multivariate analysis with adjustment for potential birth and life events confounding factors.</p>
<p><b>Results</b> No associations were found between LBW and total [adjusted odds ratio (OR) 1.09, 95% confidence interval (CI) 0.69&ndash;1.74], internalizing (adjusted OR 0.81, 95% CI 0.52&ndash;1.28) or externalizing profiles (adjusted OR 0.81, 95% CI 0.49&ndash;1.36). The only difference detected was for the internalizing sub-profile of Somatic Complaints (adjusted OR 2.02, 95% CI 1.21&ndash;3.38), which on subgroup analysis was greatest among females.</p>
<p><b>Conclusions</b> We found no convincing evidence of an association between LBW and emotional and behavioural outcomes in 12-year olds in this sample in urban South Africa. To our knowledge, this is the first published assessment of this association in a developing world context.</p>
]]></description>
<dc:creator><![CDATA[Sabet, F., Richter, L. M, Ramchandani, P. G, Stein, A., Quigley, M. A, Norris, S. A]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp204</dc:identifier>
<dc:title><![CDATA[Low birthweight and subsequent emotional and behavioural outcomes in 12-year-old children in Soweto, South Africa: findings from Birth to Twenty]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>954</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>944</prism:startingPage>
<prism:section>Life Course Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/955?rss=1">
<title><![CDATA[Head size at birth and long-term mortality from coronary heart disease]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/955?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Many studies have shown that low birthweight is associated with increased risk of heart disease in adulthood. It is controversial whether this association is caused by genetic or non-genetic factors, and whether life course exposures, such as adult overweight, could modify the association. We have studied the association of head circumference at birth with later deaths from coronary heart disease (CHD), and assessed whether maternal height and adult body mass could modify the association.</p>
<p><b>Methods</b> Population-based cohort study of 35 846 men and women born between 1920 and 1959 with mortality follow-up from 1961 to 2005.</p>
<p><b>Results</b> During follow-up, 630 people died from CHD and there was an inverse association of head circumference with deaths from CHD (<I>P</I><SUB>trend</SUB> = 0.010). The association was modified by maternal height (<I>P</I><SUB>interaction</SUB> = 0.01) and by adult body mass (<I>P</I><SUB>interaction</SUB> = 0.05). People in the lowest third of head circumference, who had a tall mother or a high body mass index in adulthood, were at the highest risk of death from CHD.</p>
<p><b>Conclusions</b> Head circumference at birth was inversely associated with deaths from CHD, and the combination of small head and tall mother, or small head and high adult body mass, was associated with the highest risk. These findings suggest that combined effects of genetic factors (growth potential and intrauterine growth) and non-genetic factors acting throughout the life course (intrauterine growth restriction and later weight gain) could mediate the effects of birth size on adult heart disease.</p>
]]></description>
<dc:creator><![CDATA[Risnes, K. R, Nilsen, T. I L, Romundstad, P. R, Vatten, L. J]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp169</dc:identifier>
<dc:title><![CDATA[Head size at birth and long-term mortality from coronary heart disease]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>962</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>955</prism:startingPage>
<prism:section>Life Course Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/963?rss=1">
<title><![CDATA[Light-at-night, circadian disruption and breast cancer: assessment of existing evidence]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/963?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Breast cancer incidence is increasing globally for largely unknown reasons. The possibility that a portion of the breast cancer burden might be explained by the introduction and increasing use of electricity to light the night was suggested &gt;20 years ago.</p>
<p><b>Methods</b> The theory is based on nocturnal light-induced disruption of circadian rhythms, notably reduction of melatonin synthesis. It has formed the basis for a series of predictions including that non-day shift work would increase risk, blind women would be at lower risk, long sleep duration would lower risk and community nighttime light level would co-distribute with breast cancer incidence on the population level.</p>
<p><b>Results</b> Accumulation of epidemiological evidence has accelerated in recent years, reflected in an International Agency for Research on Cancer (IARC) classification of shift work as a probable human carcinogen (2A). There is also a strong rodent model in support of the light-at-night (LAN) idea.</p>
<p><b>Conclusion</b> If a consensus eventually emerges that LAN does increase risk, then the mechanisms for the effect are important to elucidate for intervention and mitigation. The basic understanding of phototransduction for the circadian system, and of the molecular genetics of circadian rhythm generation are both advancing rapidly, and will provide for the development of lighting technologies at home and at work that minimize circadian disruption, while maintaining visual efficiency and aesthetics. In the interim, there are strategies now available to reduce the potential for circadian disruption, which include extending the daily dark period, appreciate nocturnal awakening in the dark, using dim red light for nighttime necessities, and unless recommended by a physician, not taking melatonin tablets.</p>
]]></description>
<dc:creator><![CDATA[Stevens, R. G]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp178</dc:identifier>
<dc:title><![CDATA[Light-at-night, circadian disruption and breast cancer: assessment of existing evidence]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>970</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>963</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/971?rss=1">
<title><![CDATA[Obesity and cancer: Mendelian randomization approach utilizing the FTO genotype]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/971?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Obesity is a risk factor for several cancers although appears to have an inverse association with cancers strongly related to tobacco. Studying obesity is difficult due to numerous biases and confounding.</p>
<p><b>Methods</b> To avoid these biases we used a Mendelian randomization approach incorporating an analysis of variants in the <I>FTO</I> gene that are strongly associated with BMI levels among 7000 subjects from a study of lung, kidney and upper-aerodigestive cancer.</p>
<p><b>Results</b> The <I>FTO</I> A allele which is linked with increased BMI was associated with a decreased risk of lung cancer (allelic odds ratio (OR) = 0.92, 95% confidence interval (CI) 0.84&ndash;1.00). It was also associated with a weak increased risk of kidney cancer, which was more apparent before the age of 50 (OR = 1.44, CI 1.09&ndash;1.90).</p>
<p><b>Conclusion</b> Our results highlight the potential for genetic variation to act as an unconfounded marker of environmentally modifiable factors, and offer the potential to obtain estimates of the causal effect of obesity. However, far larger sample sizes than studied here will be required to undertake this with precision.</p>
]]></description>
<dc:creator><![CDATA[Brennan, P., McKay, J., Moore, L., Zaridze, D., Mukeria, A., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Mates, D., Bencko, V., Foretova, L., Janout, V., Chow, W.-H., Rothman, N., Chabrier, A., Gaborieau, V., Timpson, N., Hung, R. J, Smith, G. D.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp162</dc:identifier>
<dc:title><![CDATA[Obesity and cancer: Mendelian randomization approach utilizing the FTO genotype]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>975</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>971</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/975?rss=1">
<title><![CDATA[Commentary: A new dawn for genetic epidemiology?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/975?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Frayling, T. M]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp228</dc:identifier>
<dc:title><![CDATA[Commentary: A new dawn for genetic epidemiology?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>977</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>975</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/978?rss=1">
<title><![CDATA[Socio-economic status and oesophageal cancer: results from a population-based case-control study in a high-risk area]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/978?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Cancer registries in the 1970s showed that parts of Golestan Province in Iran had the highest rate of oesophageal squamous cell carcinoma (OSCC) in the world. More recent studies have shown that while rates are still high, they are approximately half of what they were before, which might be attributable to improved socio-economic status (SES) and living conditions in this area. We examined a wide range of SES indicators to investigate the association between different SES components and risk of OSCC in the region.</p>
<p><b>Methods</b> Data were obtained from a population-based case&ndash;control study conducted between 2003 and 2007 with 300 histologically proven OSCC cases and 571 matched neighbourhood controls. We used conditional logistic regression to compare cases and controls for individual SES indicators, for a composite wealth score constructed using multiple correspondence analysis, and for factors obtained from factors analysis.</p>
<p><b>Results</b> We found that various dimensions of SES, such as education, wealth and being married were all inversely related to OSCC. The strongest inverse association was found with education. Compared with no education, the adjusted odds ratios (95% confidence intervals) for primary education and high school or beyond were 0.52 (0.27&ndash;0.98) and 0.20 (0.06&ndash;0.65), respectively.</p>
<p><b>Conclusions</b> The strong association of SES with OSCC after adjustment for known risk factors implies the presence of yet unidentified risk factors that are correlated with our SES measures; identification of these factors could be the target of future studies. Our results also emphasize the importance of using multiple SES measures in epidemiological studies.</p>
]]></description>
<dc:creator><![CDATA[Islami, F., Kamangar, F., Nasrollahzadeh, D., Aghcheli, K., Sotoudeh, M., Abedi-Ardekani, B., Merat, S., Nasseri-Moghaddam, S., Semnani, S., Sepehr, A., Wakefield, J., Moller, H., Abnet, C. C, Dawsey, S. M, Boffetta, P., Malekzadeh, R.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp195</dc:identifier>
<dc:title><![CDATA[Socio-economic status and oesophageal cancer: results from a population-based case-control study in a high-risk area]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>988</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>978</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/989?rss=1">
<title><![CDATA[Environmental risk factors for lung cancer in Iran: a case-control study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/989?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Lung cancer remains the leading cause of cancer death in the world. In Iran, lung cancer is one of the five leading tumours and its incidence has been increasing steadily in both men and women. There is a paucity of data from Iran on risk factors for lung cancer. We evaluated environmental risk factors for lung cancer in a case&ndash;control study in five hospitals of Tehran.</p>
<p><b>Methods</b> Between October 2002 and October 2005, 242 (178 male, 64 female) patients with histologically confirmed lung cancer and two controls for each patient (242 hospital controls and 242 visiting healthy controls) matched for age, sex and place of residence were interviewed using a structured questionnaire on potential risk factors for lung cancer, including environmental and occupational exposures. Associations between risk factors and lung cancer were assessed using conditional logistic regression.</p>
<p><b>Results</b> Smokers were 66.5% of all cases (85.4% of men and 14.1% of women) and smoking was the strongest correlate of lung cancer in multivariate analysis [odds ratio (OR) 5.4, 95% confidence interval (CI) 3.2&ndash;8.9]. Occupational exposures to inorganic dusts (OR 4.2, 95% CI 2.8&ndash;6.7), chemical compounds (OR = 3.4, 95% CI 2.1&ndash;5.6) and heavy metals (OR 3.0, 95% CI 1.3&ndash;7.0) were also independent risk factors for lung cancer.</p>
<p><b>Conclusions</b> In our study, smoking was the principal risk factor for lung cancer. However, preventable exposures in the environment, including occupational settings, should not be ignored.</p>
]]></description>
<dc:creator><![CDATA[Hosseini, M., Naghan, P. A., Karimi, S., SeyedAlinaghi, S., Bahadori, M., Khodadad, K., Mohammadi, F., Keynama, K., Masjedi, M. R.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp218</dc:identifier>
<dc:title><![CDATA[Environmental risk factors for lung cancer in Iran: a case-control study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>996</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>989</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/997?rss=1">
<title><![CDATA[Unprotected sex following HIV testing among women in Uganda and Zimbabwe: short- and long-term comparisons with pre-test behaviour]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/997?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Despite widespread condom promotion for HIV prevention, prospective measurement of condom use before and after HIV testing is infrequent.</p>
<p><b>Methods</b> We analysed data from a prospective study of hormonal contraception and HIV acquisition among Zimbabwean and Ugandan women (1999&ndash;2004), in which HIV testing and counselling were performed approximately every 3 months. We used zero-inflated negative binomial (ZINB) models to examine the number and proportion of unprotected sex acts, comparing behaviour reported 2&ndash;6 months before HIV testing with behaviour reported both 2&ndash;6 months (short-term analysis) and 12&ndash;16 months (long-term analysis) after HIV testing.</p>
<p><b>Results</b> Short- and long-term analyses were similar, so we present only long-term findings from 151 HIV-infected and 650 uninfected participants. The proportion of HIV-infected women reporting any unprotected acts in a typical month declined from 74% (pre-infection behaviour) to 56% (12&ndash;16 months after HIV diagnosis). In multivariable models, HIV-infected women were twice as likely to report that all sex acts were protected by condoms after diagnosis compared with beforehand [adjusted odds ratio (aOR): 1.99, 95% confidence interval (CI): 1.12&ndash;3.53]; uninfected women were somewhat less likely to report that all acts were protected (aOR: 0.82, 95% CI: 0.64&ndash;1.04). HIV-infected women also reduced their number of unprotected acts by 38% (95% CI: &ndash;16 to &ndash;55%). However, their proportion of unprotected acts changed little (7% reduction, 95% CI: &ndash;18 to + 6%). Uninfected women reported little change in number or proportion of unprotected acts over the same time period.</p>
<p><b>Conclusions</b> HIV-infected women reduced the number, but not the proportion, of unprotected acts. HIV-negative women did not increase condom use after testing and counselling, but neither did they decrease condom use, suggesting that testing negative was not interpreted as endorsement of risky behaviour.</p>
]]></description>
<dc:creator><![CDATA[Turner, A. N., Miller, W. C, Padian, N. S, Kaufman, J. S, Behets, F. M, Chipato, T., Mmiro, F. A, Salata, R. A, Morrison, C. S]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp171</dc:identifier>
<dc:title><![CDATA[Unprotected sex following HIV testing among women in Uganda and Zimbabwe: short- and long-term comparisons with pre-test behaviour]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1007</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>997</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1008?rss=1">
<title><![CDATA[Localized spatial clustering of HIV infections in a widely disseminated rural South African epidemic]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1008?rss=1</link>
<description><![CDATA[
<p><b>Background</b> South Africa contains more than one in seven of the world's HIV-positive population. Knowledge of local variation in levels of HIV infection is important for prioritization of areas for intervention. We apply two spatial analytical techniques to investigate the micro-geographical patterns and clustering of HIV infections in a high prevalence, rural population in KwaZulu-Natal, South Africa.</p>
<p><b>Methods</b> All 12 221 participants who consented to an HIV test in a population under continuous demographical surveillance were linked to their homesteads and geo-located in a geographical information system (accuracy of &lt;2 m). We then used a two-dimensional Gaussian kernel of radius 3 km to produce robust estimates of HIV prevalence that vary across continuous geographical space. We also applied a Kulldorff spatial scan statistic (Bernoulli model) to formally identify clusters of infections (<I>P</I> &lt; 0.05).</p>
<p><b>Results</b> The results reveal considerable geographical variation in local HIV prevalence (range = 6&ndash;36%) within this relatively homogenous population and provide clear empirical evidence for the localized clustering of HIV infections. Three high-risk, overlapping spatial clusters [Relative Risk (RR) = 1.34&ndash;1.62] were identified by the Kulldorff statistic along the National Road (<I>P</I> &le; 0.01), whereas three low risk clusters (RR = 0.2&ndash;0.38) were identified elsewhere in the study area (<I>P</I> &le; 0.017).</p>
<p><b>Conclusions</b> The findings show the existence of several localized HIV epidemics of varying intensity that are partly contained within geographically defined communities. Despite the overall high prevalence of HIV in many rural South African settings, the results support the need for interventions that target socio-geographic spaces (communities) at greatest risk to supplement measures aimed at the general population.</p>
]]></description>
<dc:creator><![CDATA[Tanser, F., Barnighausen, T., Cooke, G. S, Newell, M.-L.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp148</dc:identifier>
<dc:title><![CDATA[Localized spatial clustering of HIV infections in a widely disseminated rural South African epidemic]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1016</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1008</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1016?rss=1">
<title><![CDATA[Commentary: Spatial clustering of HIV infection: providing clues for effective HIV prevention]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1016?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Karim, S. S A.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp201</dc:identifier>
<dc:title><![CDATA[Commentary: Spatial clustering of HIV infection: providing clues for effective HIV prevention]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1017</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1016</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1018?rss=1">
<title><![CDATA[Smoking, drinking and incident tuberculosis in rural India: population-based case-control study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1018?rss=1</link>
<description><![CDATA[
<p><b>Background</b> To investigate the extent to which smoking and/or drinking can increase the incidence of pulmonary tuberculosis (TB), a population-based case&ndash;control study was conducted in rural south India.</p>
<p><b>Methods</b> A total of 1839 males and 870 females treated in 2000&ndash;03 by state TB clinics were interviewed at home in 2004&ndash;05 about their education, smoking and drinking habits before disease onset. As controls, 2134 men and 2119 women without TB were randomly chosen from case villages and interviewed. Incidence rate ratios (RRs) are from logistic regression, adjusted for age and education.</p>
<p><b>Results</b> No women smoked or drank. The main analyses are of men aged 35&ndash;64 years, 949 cases treated for new pulmonary TB and 1963 controls. In the study, 81.5% of the cases and 55.2% of the controls had ever smoked, yielding a standardized ever- vs never-smoker TB incidence RR of 2.7 [95% confidence interval (CI) 2.2&ndash;3.3, <I>P</I> &lt; 0.00001). Among control ever-smokers 96% still smoked, 71% used only bidis (mean 17 per day) and 28% used only cigarettes (mean 7 per day). After additional adjustment for alcohol, this RR was 2.2 (95% CI 1.7&ndash;2.7, <I>P</I> &lt; 0.00001), but even among those who had never drunk alcohol the standardized ever- vs never-smoker RR was 2.6 (95% CI 2.0&ndash;3.6, <I>P</I> &lt; 0.00001). The corresponding RRs for ever- vs never-drinking were somewhat less extreme: 2.2 (95% CI 1.8&ndash;2.6, <I>P</I> &lt; 0.00001) without adjustment for smoking, 1.5 (95% CI 1.2&ndash;1.9, <I>P</I> = 0.00004) with adjustment for smoking and 2.1 (95% CI 1.4&ndash;3.0, 2<I>P</I> = 0.0001) among those who had never smoked. Among control ever-drinkers, 96% still drank and 99% used only spirits (mean 0.3 l/week).</p>
<p><b>Conclusions</b> This study of reliably confirmed disease (by the criteria of state TB clinics) demonstrates an increased incidence of pulmonary TB among those who smoke and among those who drink. The effects of smoking after adjustment for drinking were more definite than those of drinking after adjustment for smoking.</p>
]]></description>
<dc:creator><![CDATA[Gajalakshmi, V., Peto, R.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp225</dc:identifier>
<dc:title><![CDATA[Smoking, drinking and incident tuberculosis in rural India: population-based case-control study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1025</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1018</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1026?rss=1">
<title><![CDATA[Prevalence of pulmonary tuberculosis amongst the tribal population of Madhya Pradesh, central India]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1026?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This was a prevalence survey of pulmonary tuberculosis (PTB) disease in the tribal population of Madhya Pradesh state, central India.</p>
<p><b>Methods</b> A community-based cross-sectional tuberculosis (TB) disease prevalence survey was undertaken among adults aged &ge;15 years in the tribal population of Madhya Pradesh. A multistage stratified cluster sampling was adopted. A representative random sample of villages predominated by tribal populations was selected from 11 districts. All eligible individuals were questioned for chest symptoms relating to TB. Sputum samples were collected from all eligible individuals, transported to the laboratory, and examined by Ziehl&ndash;Neelsen (ZN) smear microscopy and solid media culture methods.</p>
<p><b>Results</b> Of the 23 411 individuals eligible for screening, 22 270 (95.1%) were screened for symptoms. The overall proportion of symptomatic individuals was 7.9%. Overall prevalence (culture and/or smear positive) of PTB was 387 [95% confidence interval (CI): 273&ndash;502] per 100 000 population. The prevalence increased with age and was also significantly higher among males (554/100 000; 95% CI: 415&ndash;693) as compared with females (233/100 000; 95% CI: 101&ndash;364) (<I>P</I> &lt; 0.001).</p>
<p><b>Conclusion</b> The findings suggest that the TB situation amongst the tribal population is not that different from the situation among the non-tribal population in the country. However, TB remains a major public health problem amongst the tribal population and there is a need to maintain and further strengthen TB control measures on a sustained and long-term basis.</p>
]]></description>
<dc:creator><![CDATA[Bhat, J., Rao, V. G, Gopi, P. G., Yadav, R., Selvakumar, N., Tiwari, B., Gadge, V., Bhondeley, M. K, Wares, F.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp222</dc:identifier>
<dc:title><![CDATA[Prevalence of pulmonary tuberculosis amongst the tribal population of Madhya Pradesh, central India]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1032</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1026</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1033?rss=1">
<title><![CDATA[Post-traumatic stress reactions among Rwandan children and adolescents in the early aftermath of genocide]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1033?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Epidemiological investigations of post-traumatic stress reactions in Sub-Saharan Africa, where atrocious violence against civilians is endemic, are rare. This article is the first complete report of the key community-based findings of a 1995 psychiatric epidemiological survey of young survivors of the 1994 Rwandan Genocide.</p>
<p><b>Methods</b> The National Trauma Survey (NTS) of Rwandans aged 8&ndash;19 measured traumatic exposures using an inventory of possible war time experiences and post-traumatic stress reactions with a checklist of symptoms of Post-traumatic stress disorder (PTSD). Individuals meeting assessed PTSD diagnostic criteria are classified as cases of &lsquo;probable PTSD&rsquo;. The NTS interviewed youth residing in the community and others institutionalized in unaccompanied children's centres; the former (<I>n</I> = 1547) are the subject of the present report. Instrument change midway into the study divides respondents into two samples.</p>
<p><b>Results</b> Among respondents, over 90% witnessed killings and had their lives threatened; 35% lost immediate family members; 30% witnessed rape or sexual mutilation; 15% hid under corpses. In Sample 1, 95% of respondents reported one or more re-experiencing symptom, 95% reported three or more avoidance/blunting symptoms and 63% reported two or more arousal symptoms; in Sample 2, these figures were 96%, 95% and 56%, respectively. The overall rate of &lsquo;probable PTSD&rsquo; was 62% and 54% in Samples 1 and 2, respectively, and exhibited a dose&ndash;response relationship with exposure. Among the most heavily exposed individuals the rate was 100%. Rates of &lsquo;probable PTSD&rsquo; were higher among females than among males. Results for age were inconsistent.</p>
<p><b>Conclusion</b> In industrialized societies, most survivors of traumatizing violence experience symptoms only transiently. In the Rwanda survey, symptom levels and rates of &lsquo;probable PTSD&rsquo; were exceptionally elevated, suggesting that at the limits of catastrophic man-made violence, psychological resilience among youth is all but extinguished.</p>
]]></description>
<dc:creator><![CDATA[Neugebauer, R., Fisher, P. W, Turner, J B., Yamabe, S., Sarsfield, J. A, Stehling-Ariza, T.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn375</dc:identifier>
<dc:title><![CDATA[Post-traumatic stress reactions among Rwandan children and adolescents in the early aftermath of genocide]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1045</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1033</prism:startingPage>
<prism:section>Mental Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1045?rss=1">
<title><![CDATA[Commentary: Explaining enormous variations in rates of disorder in trauma-focused psychiatric epidemiology after major emergencies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1045?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rodin, D., van Ommeren, M.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp203</dc:identifier>
<dc:title><![CDATA[Commentary: Explaining enormous variations in rates of disorder in trauma-focused psychiatric epidemiology after major emergencies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1048</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1045</prism:startingPage>
<prism:section>Mental Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1049?rss=1">
<title><![CDATA[Polymorphisms of the CRP gene inhibit inflammatory response and increase susceptibility to depression: The Health in Men Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1049?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Depression has been associated with chronic changes in the serum concentration of C-reactive protein (CRP) in observational studies, but it is unclear if this association is causal or is due to confounding and bias. Genetic studies are less subject to this type of error and offer an opportunity to investigate if CRP is causally linked to depression, particularly because known polymorphisms of the <I>CRP</I> gene have been associated with high- and low-basal serum concentrations of CRP [single nucleotide polymorphisms (SNPs) rs1130864 and rs1205, respectively]. The aim of this study is to determine if polymorphisms of SNPs rs1130864 and rs1205 are associated with prevalent depression.</p>
<p><b>Methods</b> We completed a cross-sectional study of a community sample of 3700 men aged &ge;70 years, and used the 15-item Geriatric Depression Scale (GDS-15) to assess depressive symptoms. A GDS-15 score 7 or more indicates the presence of clinically significant depressive symptoms. Physical morbidity was assessed with the physical component summary score (PCS) of the SF-36 Health Survey. We collected fasting blood samples to measure high sensitivity CRP and to extract DNA for the genotyping of SNPs rs1130864 and rs1205 of the <I>CRP</I> gene.</p>
<p><b>Results</b> One hundred and eighty-two men were depressed (4.9%). The odds of depression increased by 2% (95% CI = 1&ndash;4%) for every unit (mg/l) increase of CRP and nearly doubled for men with CRP &ge; 3 mg/l vs &lt;1 mg/l [odds ratio (OR) = 1.95, 95% confidence interval (CI) = 1.27&ndash;2.98]. However, the association between high CRP (&ge;3 mg/l) and depression was no longer significant after the analyses were adjusted for smoking, age, body mass index (BMI) and PCS. Men with the CT and TT genotypes of rs1130864 had 1.36 (95% CI = 1.13&ndash;1.63) and 2.31 (95% CI = 1.65&ndash;3.24) greater odds of CRP &ge;3 mg/l than CC carriers, but there was no association between this polymorphism and the presence of prevalent depression. The G &gt; A polymorphism of SNP rs1205 was associated with 24% (95% CI = 16&ndash;32%) lower concentration of CRP compared with other genotypes. Men with the rs1205 AA genotype had 1.66 (95% CI = 1.07&ndash;2.57) and 1.67 (95% CI = 1.08&ndash;2.58) greater odds of having clinically significant depression than participants with the GA and GG genotypes, respectively.</p>
<p><b>Conclusion</b> Our study shows that clinically significant depressive symptoms in later life are unlikely to be caused by an increase in the serum concentration of CRP. Instead, we found that the risk of depression was greater amongst people who carry the rs1205 G &gt; A genetic polymorphism of the <I>CRP</I> gene, which was associated with ~20% lower serum concentration of CRP compared with other genotypes. This suggests that CRP may be a compensatory response to external insults that predispose to depression, and that an increase in the concentration of CRP might be adaptive.</p>
]]></description>
<dc:creator><![CDATA[Almeida, O. P, Norman, P. E, Allcock, R., Bockxmeer, F. v., Hankey, G. J, Jamrozik, K., Flicker, L.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp199</dc:identifier>
<dc:title><![CDATA[Polymorphisms of the CRP gene inhibit inflammatory response and increase susceptibility to depression: The Health in Men Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1059</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1049</prism:startingPage>
<prism:section>Mental Health</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1060?rss=1">
<title><![CDATA[Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1060?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In Caucasian populations, adult height is inversely associated with cardiovascular disease (CVD) risk and positively related to some cancers. However, there are few data from Asian populations and from women. We sought to determine the sex- and region-specific associations between height and cardiovascular outcomes, and deaths due to cancer, respiratory and injury in populations from the Asia-Pacific region.</p>
<p><b>Methods</b> Thirty-nine studies from the Asia Pacific Cohort Studies Collaboration database were included. We used Cox proportional hazard regression models to estimate the associations between height and pre-specified outcomes.</p>
<p><b>Results</b> A total of 510 800 participants with 21 623 deaths were included. Amongst men, inverse linear associations were observed between height and coronary heart disease (CHD), stroke, CVD, injury and total mortality. The hazard ratios [95% confidence intervals, (CI)] for a 1-SD (= 6 cm) increment in height ranged from 0.85 (0.80&ndash;0.91) for injury to 0.97 (0.95&ndash;0.98) for total mortality. Similar trends were found between height and CHD, haemorrhagic stroke and CVD in women. A positive linear association was observed between height and cancer mortality. For each standard deviation greater height, the risk of cancer was increased by 5% (2&ndash;8%) and 9% (5&ndash;14%) in men and women, respectively. No regional difference was observed between Asian and Australasian cohorts. Adjusting for markers of education did not alter the results.</p>
<p><b>Conclusions</b> The opposing relationships of height with CVD and cancer suggest that care is required in setting national policies on childhood nutrition lest they have unintended consequences on the incidence of major non-communicable diseases.</p>
]]></description>
<dc:creator><![CDATA[Lee, C. M. Y., Barzi, F., Woodward, M., Batty, G D., Giles, G. G, Wong, J. W., Jamrozik, K., Lam, T. H., Ueshima, H., Kim, H. C., Gu, D. F., Schooling, M., Huxley, R. R, for The Asia Pacific Cohort Studies Collaboration]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp150</dc:identifier>
<dc:title><![CDATA[Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1071</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1060</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1072?rss=1">
<title><![CDATA[Could mitochondrial efficiency explain the susceptibility to adiposity, metabolic syndrome, diabetes and cardiovascular diseases in South Asian populations?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1072?rss=1</link>
<description><![CDATA[
<p><b>Background</b> South Asians are susceptible to cardiovascular disease (CVD), especially after migration to affluent countries. Contributing factors include high prevalence of diabetes, and possibly insulin resistance. Excess adiposity centrally may underlie such metabolic disturbances. The thrifty genotype, thrifty phenotype, adipose tissue compartment and variable disease selection hypotheses are among the explanations posed.</p>
<p><b>Methods</b> Data from individual studies and review articles known to the authors were examined. A Medline bibliographic database search was also performed. Reference lists were reviewed to identify additional relevant data sources. Key references were examined by both authors. </p>
<p><b>Results</b> We propose, and evaluate, the evidence for a &lsquo;mitochondrial efficiency hypothesis&rsquo; i.e. that ancestral changes in mitochondrial coupling efficiency enhanced the successful adaptation of South Asians to environmental stressors by maximizing the conversion of energy to adenosine triphosphate (ATP) rather than heat. This adaptation may be disadvantageous when South Asians are physically inactive and consume high-caloric diets. There is evidence that common mitochondrial mutations vary geographically. Mutations, including those affecting the function of mitochondrial uncoupling proteins (UCPs), may influence the balance of energy and heat production. These may influence basal metabolic rate (BMR), energy efficiency, the tendency to gain weight and hence metabolic disease. UCP gene polymorphisms are related to differences in BMR between African-Americans and Europeans. Similar data for South Asians are lacking but the few studies comparing BMR indicate that South Asians have a lower BMR, which is explained by a lower lean body mass, and higher fat mass. Once adjusted for body composition, BMR is similar. A high fat mass, <I>per se</I>, is a strategy for reducing energy use while conserving body size. Indians in the USA had higher oxidative phosphorylation capacity than Northern European Americans.</p>
<p><b>Conclusion</b> The evidence justifies full exploration of this mitochondrial effeciency hypothesis in South Asians, which may also be relevant to other warm-climate adapted populations.</p>
]]></description>
<dc:creator><![CDATA[Bhopal, R. S, Rafnsson, S. B]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp202</dc:identifier>
<dc:title><![CDATA[Could mitochondrial efficiency explain the susceptibility to adiposity, metabolic syndrome, diabetes and cardiovascular diseases in South Asian populations?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1081</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1072</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1082?rss=1">
<title><![CDATA[Ethnic and gender differences in physical activity levels among 9-10-year-old children of white European, South Asian and African-Caribbean origin: the Child Heart Health Study in England (CHASE Study)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1082?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Ethnic differences in physical activity in children in the UK have not been accurately assessed. We made objective measurements of physical activity in 9&ndash;10-year-old British children of South Asian, black African&ndash;Caribbean and white European origin.</p>
<p><b>Methods</b> Cross-sectional study of urban primary school children (2006&ndash;07). Actigraph-GT1M activity monitors were worn by 2071 children during waking hours on at least 1 full day. Ethnic differences in mean daily activity [counts, counts per minute of registered time (CPM) and steps] were adjusted for age, gender, day of week and month. Multilevel modelling allowed for repeated days within individual and clustering within school.</p>
<p><b>Results</b> In white Europeans, mean daily counts, CPM and mean daily steps were 394 785, 498 and 10 220, respectively. South Asian and black Caribbean children recorded more registered time per day than white Europeans (34 and 36 min, respectively). Compared with white Europeans, South Asians recorded 18 789 fewer counts [95% confidence interval (CI) 6390&ndash;31 187], 41 fewer CPM 95% CI 26&ndash;57) and 905 fewer steps (95% CI 624&ndash;1187). Black African&ndash;Caribbeans recorded 25 359 more counts (95% CI 14 273&ndash;36 445), and similar CPM, but fewer steps than white Europeans. Girls recorded less activity than boys in all ethnic groups, with 74 782 fewer counts (95% CI 66 665&ndash;82 899), 84 fewer CPM (95% CI 74&ndash;95) and 1484 fewer steps (95% CI 1301&ndash;1668).</p>
<p><b>Conclusion</b> British South Asian children have lower objectively measured physical activity levels than European whites and black African&ndash;Caribbeans.</p>
]]></description>
<dc:creator><![CDATA[Owen, C. G, Nightingale, C. M, Rudnicka, A. R, Cook, D. G, Ekelund, U., Whincup, P. H]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp176</dc:identifier>
<dc:title><![CDATA[Ethnic and gender differences in physical activity levels among 9-10-year-old children of white European, South Asian and African-Caribbean origin: the Child Heart Health Study in England (CHASE Study)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1093</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1082</prism:startingPage>
<prism:section>Health Behaviours</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1094?rss=1">
<title><![CDATA[Seasonality in maternal intake and activity influence offspring's birth size among rural Indian mothers--Pune Maternal Nutrition Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1094?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Farming populations from developing countries are exposed to seasonal energy stress due to variations in food availability and energy output related to agricultural activities. This study aims to examine the impact of seasonality in maternal intake and activity on neonatal size.</p>
<p><b>Methods</b> Maternal anthropometry, dietary intakes (24-h recall and food-frequency questionnaire) and activity pattern (questionnaire) at 18 &plusmn; 2 and 28 &plusmn; 2 weeks gestation, and neonatal anthropometry, were measured in a prospective study of 797 rural Indian women.</p>
<p><b>Results</b> Maternal energy and protein intakes were inadequate (70% of recommended dietary allowance). Both intake and activity showed seasonal variation (<I>P</I> = 0.001), with peak values in winter i.e. during harvest, at 18 weeks (median energy 1863 kcal/day, protein 47.5 g/day) and 28 weeks (median energy 1687 kcal/day, protein 43.7 g/day), coinciding with the maximum maternal activity (median score 86.1 at 18 weeks and 79.5 at 28 weeks). Mean birth weight and length (adjusted for pre-pregnant weight, parity, gestation and sex) of babies was highest in summer (peak at February 2733 g, 48.6 cm, respectively) and lowest in winter (nadir at January 2591 g, 47.1 cm, respectively). Regression analysis showed that maternal intake at 18th week had a positive association (<I>P</I> = 0.05), maternal activity at 28th week had a negative association (<I>P</I> = 0.002) and exposure (in weeks) to winter during gestation had a positive association (<I>P</I> = 0.04) with birth size. Furthermore, higher maternal intakes, coupled with lower maternal activity in late gestation were associated with higher birth weight, especially during winter.</p>
<p><b>Conclusions</b> If causal, these observations indicate that complete exposure (16 weeks) to the winter season (harvest-time) in late gestation could increase birth weight by 90 g in poor farming communities in rural India, and the benefit would increase further by lowering maternal activity. Our results underscore the importance of considering seasonality in planning targeted intervention strategies in such settings.</p>
]]></description>
<dc:creator><![CDATA[Rao, S., Kanade, A. N, Yajnik, C. S, Fall, C. H D]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp223</dc:identifier>
<dc:title><![CDATA[Seasonality in maternal intake and activity influence offspring's birth size among rural Indian mothers--Pune Maternal Nutrition Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1103</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1094</prism:startingPage>
<prism:section>Health Behaviours</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1104?rss=1">
<title><![CDATA[Ethics and observational studies in medical research: various rules in a common framework]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1104?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Research ethics have become universal in their principles through international agreements. The standardization of regulations facilitates the internationalization of research concerning drugs. However, in so-called observational studies (i.e. from data collected retrospectively or prospectively, obtained without any additional therapy or monitoring procedure) the modalities used for applying the main principles vary from one country to another. This situation may entail problems for the conduct of multi-centric international studies, as well as for the publication of results if the authors and editors come from countries governed by different regulations. In particular, several French observational studies were rejected or retracted by US peer-reviewed journals, because their protocols have not been submitted to an Institutional Review Board/Independent Ethics Committee (IRB/IEC).</p>
<p><b>Methods</b> National legislation case analysis.</p>
<p><b>Results</b> In accordance with European regulation, French observational studies from data obtained without any additional therapy or monitoring procedure, do not need the approval of an IRB/IEC. Nevertheless, these studies are neither exempt from scientific opinion nor from ethical and legal authorization.</p>
<p><b>Conclusion</b> We wish to demonstrate through the study of this example that different bodies of law can provide equivalent levels of protection that respect the same ethical principles. Our purpose in writing this article was to encourage public bodies, scientific journals and researchers to gain a better understanding of the various sets of specific national regulations and to speak a common language.</p>
]]></description>
<dc:creator><![CDATA[Claudot, F., Alla, F., Fresson, J., Calvez, T., Coudane, H., Bonaiti-Pellie, C.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp164</dc:identifier>
<dc:title><![CDATA[Ethics and observational studies in medical research: various rules in a common framework]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1108</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1104</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1108?rss=1">
<title><![CDATA[Commentary: Can we facilitate the ethical approval of international observational studies?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1108?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cuttini, M., Saracci, R.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp238</dc:identifier>
<dc:title><![CDATA[Commentary: Can we facilitate the ethical approval of international observational studies?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1109</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1108</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1110?rss=1">
<title><![CDATA[Interpreting data in the face of competing explanations: assessing the hypothesis that observed spontaneous clearance of Helicobacter pylori was all measurement error]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1110?rss=1</link>
<description><![CDATA[
<p><b>Background</b> We previously reported frequent transient positive urea breath tests for <I>Helicobacter pylori</I> infection in a cohort study of young children, and interpreted this as evidence of frequent spontaneous clearance of this infection. In a commentary, Perry and Parsonnet suggested that all transient positive tests we observed could be false positives and thus the appearance of transient infection could be an artifact.</p>
<p><b>Methods</b> We address the logic of the implicit argument that the transient infections were an artifact and we demonstrate a simple likelihood calculation to assess the plausibility of competing explanations. We calculate the likelihood of observing our data based on a range of clearance and measurement error rates and then how this updates a set of prior beliefs.</p>
<p><b>Results</b> The likelihood calculations and resulting posterior probabilities show strong support for the hypothesis of spontaneous clearance, after allowing for measurement error, even starting with a very high prior probability of no spontaneous clearance. The scenario Perry and Parsonnet present is incompatible with our data, and thus not a plausible explanation for our observations. Attributing most observed transient infections to measurement error requires assuming a high false positive rate and a very low infection rate and/or a high false negative rate, alternatives that are not supported by evidence.</p>
<p><b>Conclusions</b> Acknowledgment of plausible levels of measurement error does not change the strong support our data provides for the hypothesis of frequent transient infection. Debate about competing explanations for observations should be accompanied by quantitative analysis that shows which is more plausible. We demonstrate one method for doing such analysis.</p>
]]></description>
<dc:creator><![CDATA[Phillips, C. V, Goodman, K. J]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp006</dc:identifier>
<dc:title><![CDATA[Interpreting data in the face of competing explanations: assessing the hypothesis that observed spontaneous clearance of Helicobacter pylori was all measurement error]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1117</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1110</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1118?rss=1">
<title><![CDATA[Improving epidemiological surveys of sexual behaviour conducted by telephone]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1118?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This study assesses the impact of Telephone Audio Computer-Assisted Self-Interviewing (T-ACASI) on the reporting of sensitive (mainly heterosexual) behaviours.</p>
<p><b>Methods</b> A randomized experiment was embedded in a telephone survey that drew probability samples of the populations of the USA (<I>N</I> = 1543) and Baltimore city (<I>N</I> = 744). Respondents were randomly assigned to have questions asked either by a T-ACASI computer or by a human telephone interviewer.</p>
<p><b>Results</b> Compared with interviewer-administered telephone surveys, T-ACASI obtained more frequent reporting of a range of mainly heterosexual behaviours that were presumed to be sensitive, including recency of anal sex [adjusted odds ratio (A-OR) = 2.00, <I>P</I> &lt; 0.001), sex during menstrual period (A-OR = 1.49, <I>P</I> &lt; 0.001), giving oral sex (A-OR = 1.40, <I>P</I> = 0.001) and receiving oral sex (A-OR = 1.36, <I>P</I> = 0.002), and sexual difficulties for the respondent (A-OR = 1.45, <I>P</I> = 0.034) and their main sex partner (A-OR = 1.48, <I>P</I> = 0.0). T-ACASI also obtained less frequent reporting that respondent had a &lsquo;main sex partner&rsquo; (A-OR = 0.56, <I>P</I> = 0.011) and discussed contraception prior to first sex with that sex partner (A-OR = 0.82, <I>P</I> = 0.094). For both males and females, T-ACASI obtained more frequent reports of first vaginal sex occurring at early ages (before ages 12 through 15). &lsquo;For males only&rsquo;, T-ACASI also elicited more frequent reports that first vaginal sex had &lsquo;not&rsquo; occurred at later ages (i.e. by ages 20 through 24).</p>
<p><b>Conclusion</b> T-ACASI increases the likelihood that survey respondents will report sensitive heterosexual behaviours.</p>
]]></description>
<dc:creator><![CDATA[Turner, C. F, Al-Tayyib, A., Rogers, S. M, Eggleston, E., Villarroel, M. A, Roman, A. M, Chromy, J. R, Cooley, P. C]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp210</dc:identifier>
<dc:title><![CDATA[Improving epidemiological surveys of sexual behaviour conducted by telephone]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1127</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1118</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1128?rss=1">
<title><![CDATA[Association of age, sex and seat belt use with the risk of early death in drivers of passenger cars involved in traffic crashes]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1128?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This study was designed to break down the association of age, sex and seat belt use with risk of death for drivers of automobiles involved in a crash into two theoretical components: intrinsic severity of the crash and occupant resilience.</p>
<p><b>Methods</b> We studied all 84 338 pairs of drivers and front-seat passengers aged &gt;=18 years in passenger cars involved in traffic crashes with victims recorded in the Spanish traffic crash registry between 2000 and 2004. Relative risks (RR) for the association of age, male sex and non-seat belt use with risk of death were calculated with Poisson conditional and unconditional multiple regression models.</p>
<p><b>Results</b> For drivers, the risk of death associated with severity of the crash was slightly higher in men (RR = 1.18), and decreased with age (RR = 0.993 per year). However, resilience-dependent risk of death increased with age (RR = 1.028 per year), and especially among unbelted occupants (RR = 4.02).</p>
<p><b>Conclusions</b> We conclude that in drivers involved in traffic crashes the association of age, sex and seat belt use with risk of death depends on the component of risk considered: severity of the crash or the occupant's resilience to energy.</p>
]]></description>
<dc:creator><![CDATA[Lardelli-Claret, P., Espigares-Rodriguez, E., Amezcua-Prieto, C., Jimenez-Moleon, J. J., de Dios Luna-del-Castillo, J., Bueno-Cavanillas, A.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp143</dc:identifier>
<dc:title><![CDATA[Association of age, sex and seat belt use with the risk of early death in drivers of passenger cars involved in traffic crashes]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1134</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1128</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1134?rss=1">
<title><![CDATA[Commentary: Causal pathways of relative motor vehicle crash fatality risk are hard to estimate from police records]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1134?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Zador, P. L]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp227</dc:identifier>
<dc:title><![CDATA[Commentary: Causal pathways of relative motor vehicle crash fatality risk are hard to estimate from police records]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1136</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1134</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1137?rss=1">
<title><![CDATA[Population adiposity and climate change]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1137?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The increasing global prevalence of overweight and obesity has serious implications for the environment, as well as for health. We estimate the impact on greenhouse gas emissions of increases in the population distribution of body mass index (BMI).</p>
<p><b>Methods</b> We estimated the food energy required to maintain basal metabolic rate in two hypothetical adult populations using the Schofield equations for males and females. Additional greenhouse gas emissions due to higher fuel energy use for transporting a heavier population were estimated.</p>
<p><b>Results</b> Compared with a normal population distribution of BMI, a population with 40% obese requires 19% more food energy for its total energy expenditure. Greenhouse gas emissions from food production and car travel due to increases in adiposity in a population of 1 billion are estimated to be between 0.4 Giga tonnes (GT) and 1.0 GT of carbon dioxide equivalents per year.</p>
<p><b>Conclusions</b> The maintenance of a healthy BMI has important environmental benefits in terms of lower greenhouse gas emissions.</p>
]]></description>
<dc:creator><![CDATA[Edwards, P., Roberts, I.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp172</dc:identifier>
<dc:title><![CDATA[Population adiposity and climate change]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1140</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1137</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1141?rss=1">
<title><![CDATA[Commentary: Why diets need to change to avert harm from global warming]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1141?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Powles, J.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp247</dc:identifier>
<dc:title><![CDATA[Commentary: Why diets need to change to avert harm from global warming]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1142</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1141</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1143?rss=1">
<title><![CDATA[Endometriosis risk in relation to naevi, freckles and skin sensitivity to sun exposure: the French E3N cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1143?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Endometriosis is an important women's health issue, however its aetiology remains unknown. An association between endometriosis and cutaneous melanoma was described, possibly explained through common genetic features. To further investigate this association, we assessed the link between phenotypic traits predisposing to melanoma and the risk of endometriosis.</p>
<p><b>Methods</b> Using a case&ndash;control design, we analysed data from 97 215 women of the Etude Epid&eacute;miologique aupr&egrave;s de femmes de l&rsquo;Education Nationale study, a cohort of 98 995 French women insured by a national health&nbsp;scheme&nbsp;mostly covering teachers, and aged 40&ndash;65 years at inclusion in 1990. Risk estimates were computed using unconditional logistic regression models.</p>
<p><b>Results</b> After adjustment for potential confounding factors, there was a positive dose&ndash;effect relationship between risk of endometriosis (reported as surgically ascertained, <I>n</I> = 4241) and skin sensitivity to sun exposure [moderate: odds ratio (OR) 1.09, 95% confidence interval (CI) 0.99&ndash;1.19; high: OR 1.22; 95% CI 1.10&ndash;1.36; compared with none; <I>P</I><SUB>trend</SUB> &lt; 0.0001], number of naevi (few: OR 1.19, 95% CI 1.05&ndash;1.35; many: OR 1.37, 95% CI 1.21&ndash;1.55; very many: OR 1.59, 95% CI 1.37&ndash;1.83; compared with none; <I>P</I><SUB>trend</SUB> &lt; 0.0001) and number of freckles (few: OR 1.08, 95% CI 1.00&ndash;1.17; very many/many: OR 1.11, 95% CI 1.03&ndash;1.20; compared with none; <I>P</I><SUB>trend</SUB> = 0.005).</p>
<p><b>Conclusion</b> This study is, to our knowledge, the first to report a positive dose&ndash;effect relationship between the risk of endometriosis and skin sensitivity to sun exposure, and number of naevi and freckles. These data suggest that endometriosis and melanoma may share some genetic features.</p>
]]></description>
<dc:creator><![CDATA[Kvaskoff, M., Mesrine, S., Clavel-Chapelon, F., Boutron-Ruault, M.-C.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp175</dc:identifier>
<dc:title><![CDATA[Endometriosis risk in relation to naevi, freckles and skin sensitivity to sun exposure: the French E3N cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1153</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1143</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1154?rss=1">
<title><![CDATA[Commentary: Endometriosis--epidemiologic considerations for a potentially 'high-risk' population]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1154?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Missmer, S. A]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp249</dc:identifier>
<dc:title><![CDATA[Commentary: Endometriosis--epidemiologic considerations for a potentially 'high-risk' population]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1155</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1154</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1156?rss=1">
<title><![CDATA[Effect on response rates of stamps vs a pre-printed business reply envelope in a mailed follow-up survey among middle-aged Danish men]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1156?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Osler, M., Juhl, M., Lund, R., Andersen, A.-M. N., Kriegbaum, M., Christensen, U.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn044</dc:identifier>
<dc:title><![CDATA[Effect on response rates of stamps vs a pre-printed business reply envelope in a mailed follow-up survey among middle-aged Danish men]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1157</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1156</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1157?rss=1">
<title><![CDATA[Response to 'Cancer incidence rates among South Asians in four geographic regions: India, Singapore, UK and US']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1157?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Babu, G. R]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn119</dc:identifier>
<dc:title><![CDATA[Response to 'Cancer incidence rates among South Asians in four geographic regions: India, Singapore, UK and US']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1158</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1157</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1158?rss=1">
<title><![CDATA[Author's response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1158?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sinha, R., Devesa, S., Rastogi, T., Mathew, A.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn120</dc:identifier>
<dc:title><![CDATA[Author's response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1159</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1158</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1159?rss=1">
<title><![CDATA[Comments: The non-cancer mortality experience of male workers at British Nuclear Fuels plc, 1946-2005]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1159?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Little, M P, Tawn, E J, Tzoulaki, I, Wakeford, R, Hildebrandt, G, Tapio, S, Elliott, P]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn122</dc:identifier>
<dc:title><![CDATA[Comments: The non-cancer mortality experience of male workers at British Nuclear Fuels plc, 1946-2005]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1164</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1159</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1165?rss=1">
<title><![CDATA[Marketing Health: Smoking and the Discourse of Public Health in Britain 1945-2000.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1165?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Clancy, L.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn142</dc:identifier>
<dc:title><![CDATA[Marketing Health: Smoking and the Discourse of Public Health in Britain 1945-2000.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1166</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1165</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1166?rss=1">
<title><![CDATA[Public health: ethical issues.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1166?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kar-Purkayastha, I.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn150</dc:identifier>
<dc:title><![CDATA[Public health: ethical issues.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1167</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1166</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/4/1168?rss=1">
<title><![CDATA[Books Received]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/4/1168?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 12:49:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp254</dc:identifier>
<dc:title><![CDATA[Books Received]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1168</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1168</prism:startingPage>
<prism:section>Books Received</prism:section>
</item>

<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>Tue, 02 Jun 2009 02:11:42 PDT</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>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/619?rss=1">
<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>Tue, 02 Jun 2009 02:11:42 PDT</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>
<prism:startingPage>619</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/3/622?rss=1">
<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>Tue, 02 Jun 2009 02:11:42 PDT</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>
</item>

<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>Tue, 02 Jun 2009 02:11:42 PDT</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>
</item>

<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>Tue, 02 Jun 2009 02:11:42 PDT</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>
</item>

<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>Tue, 02 Jun 2009 02:11:42 PDT</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>
</item>

<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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:42 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>Tue, 02 Jun 2009 02:11:43 PDT</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>

</rdf:RDF>