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<title>International Journal of Epidemiology - Advance Access</title>
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<title><![CDATA[Marriages between first cousins in England and their effects]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp335v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Darwin, G. H]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 04:57:08 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp335</dc:identifier>
<dc:title><![CDATA[Marriages between first cousins in England and their effects]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Reprints and Reiterations</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp334v1?rss=1">
<title><![CDATA[Illustrating bias due to conditioning on a collider]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp334v1?rss=1</link>
<description><![CDATA[
<p>That conditioning on a common effect of exposure and outcome may cause selection, or collider-stratification, bias is not intuitive. We provide two hypothetical examples to convey concepts underlying bias due to conditioning on a collider. In the first example, fever is a common effect of influenza and consumption of a tainted egg-salad sandwich. In the second example, case-status is a common effect of a genotype and an environmental factor. In both examples, conditioning on the common effect imparts an association between two otherwise independent variables; we call this selection bias.</p>
]]></description>
<dc:creator><![CDATA[Cole, S. R, Platt, R. W, Schisterman, E. F, Chu, H., Westreich, D., Richardson, D., Poole, C.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 04:57:08 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp334</dc:identifier>
<dc:title><![CDATA[Illustrating bias due to conditioning on a collider]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp329v1?rss=1">
<title><![CDATA[Comparative appraisal of educational inequalities in overweight and obesity among adults in 19 European countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp329v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In Western societies, a lower educational level is often associated with a higher prevalence of overweight and obesity. However, there may be important international differences in the strength and direction of this relationship, perhaps in respect of differing levels of socio-economic development. We aimed to describe educational inequalities in overweight and obesity across Europe, and to explore the contribution of level of socio-economic development to cross-national differences in educational inequalities in overweight and obese adults in Europe.</p>
<p><b>Methods</b> Cross-sectional data, based on self-reports, were derived from national health interview surveys from 19 European countries (<I>N</I> = 127 018; age range = 25&ndash;44 years). Height and weight data were used to calculate the body mass index (BMI). Multivariate regression analysis was employed to measure educational inequalities in overweight and obesity, based on BMI. Gross domestic product (GDP) per capita was used as a measure of level of socio-economic development.</p>
<p><b>Results</b> Inverse educational gradients in overweight and obesity (i.e. higher education, less overweight and obesity) are a generalized phenomenon among European men and even more so among women. Baltic and eastern European men were the exceptions, with weak positive associations between education and overweight and obesity. Educational inequalities in overweight and obesity were largest in Mediterranean women. A 10 000-euro increase in GDP was related to a 3% increase in overweight and obesity for low-educated men, but a 4% decrease for high-educated men. No associations with GDP were observed for women.</p>
<p><b>Conclusion</b> In most European countries, people of lower educational attainment are now most likely to be overweight or obese. An increasing level of socio-economic development was associated with an emergence of inequalities among men, and a persistence of these inequalities among women.</p>
]]></description>
<dc:creator><![CDATA[Roskam, A.-J. R, Kunst, A. E, Van Oyen, H., Demarest, S., Klumbiene, J., Regidor, E., Helmert, U., Jusot, F., Dzurova, D., Mackenbach, J. P, for additional participants to the study]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 04:57:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp329</dc:identifier>
<dc:title><![CDATA[Comparative appraisal of educational inequalities in overweight and obesity among adults in 19 European countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp313v1?rss=1">
<title><![CDATA[Commentary: The background and outcomes of the first-cousin marriage controversy in Great Britain]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp313v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bittles, A H]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 04:57:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp313</dc:identifier>
<dc:title><![CDATA[Commentary: The background and outcomes of the first-cousin marriage controversy in Great Britain]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp312v1?rss=1">
<title><![CDATA[Commentary: Of the same blood]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp312v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stoltenberg, C.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 04:57:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp312</dc:identifier>
<dc:title><![CDATA[Commentary: Of the same blood]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp311v1?rss=1">
<title><![CDATA[Commentary: Darwin's Origin: the Irish connection]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp311v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Evans, A.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 04:57:05 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp311</dc:identifier>
<dc:title><![CDATA[Commentary: Darwin's Origin: the Irish connection]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp340v1?rss=1">
<title><![CDATA[Paternal involvement in childcare and unintentional injury of young children: a population-based cohort study in Japan]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp340v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Unintentional injury is the leading cause of death in young children. A previous study reported the protective effect of maternal parenting on young childhood injury; however, few studies have shown an association between paternal involvement in childcare and young childhood injury. The purpose of this study is to investigate the impact of paternal involvement in childcare to reduce the likelihood of childhood injury.</p>
<p><b>Methods</b> A population-based birth cohort study in Japan (2001&ndash;02), the &lsquo;Longitudinal Survey of Babies Born in 21st Century&rsquo;, was used (<I>n</I> = 42 144). The impact of paternal involvement in childcare of 6-month-old infants (feeding, diaper change, bathing, putting the child to sleep, playing, taking a walk) on the incidence of young childhood injury (fall, near-drowning, accidental ingestion or burn) until 18 months of age was analysed by multiple logistic regression.</p>
<p><b>Results</b> Infants who received a high degree of paternal involvement in childcare at 6 months were less likely to suffer from all unintentional injuries at 18 months than those who received a low degree of paternal involvement in childcare (adjusted odds ratio 0.91, 95% confidence interval 0.85&ndash;0.98). Taking the child for a walk by the father strongly prevented all unintentional injuries, and there were dose&ndash;effect relationships (<I>P</I><SUB>trend</SUB> &lt; 0.001).</p>
<p><b>Conclusions</b> Paternal involvement in childcare at 6 months of age prevented childhood injury at 18 months of age. Paternal involvement in childcare might be a useful indicator for predicting childhood injury.</p>
]]></description>
<dc:creator><![CDATA[Fujiwara, T., Okuyama, M., Takahashi, K.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 07:03:33 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp340</dc:identifier>
<dc:title><![CDATA[Paternal involvement in childcare and unintentional injury of young children: a population-based cohort study in Japan]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp320v2?rss=1">
<title><![CDATA[Abdominal aortic aneurysms, or a relatively large diameter of non-aneurysmal aortas, increase total and cardiovascular mortality: the Tromso study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp320v2?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In a population-based study in Troms&oslash;, Norway, the authors assessed whether an abdominal aortic aneurysm (AAA) or the maximal infrarenal aortic diameter in a non-aneurismal aorta influence total and cardiovascular disease (CVD) mortality.</p>
<p><b>Methods</b> A total of 6640 men and women, aged 25&ndash;84 years, were included in a 10-year mortality follow-up: 345 subjects with a diagnosed AAA and 6295 subjects with a non-aneurismal aorta. Non-aneurismal aortic diameter and prevalent AAAs were categorized into seven groups.</p>
<p><b>Results</b> In subjects without an AAA, an aortic diameter &ge;30 mm increased age- and sex-adjusted total mortality [mortality rate ratio (MRR) = 3.73, 95% confidence interval (CI) 1.77&ndash;7.89] and CVD mortality (MRR = 9.24, 95% CI 4.07&ndash;20.97) compared with subjects with aortic diameter of 21&ndash;23 mm. An AAA at screening was strongly associated with deaths from aortic aneurysm and was associated with total (MRR = 1.60, 95% CI 1.31&ndash;1.96) and CVD mortality (MRR = 2.41, 95% CI 1.81&ndash;3.21). This was not explained by deaths due to an AAA. Adjustments for CVD risk factors could fully explain the increased total, but not CVD mortality in subjects with an AAA.</p>
<p><b>Conclusions</b> An AAA increases total and CVD mortality. In the large majority of subjects with a non-aneurysmal aorta, the diameter does not influence total or CVD mortality. However, in individuals with a maximal diameter &gt;26 mm (2% of the population), a positive relationship is found.</p>
]]></description>
<dc:creator><![CDATA[Forsdahl, S. H., Solberg, S., Singh, K., Jacobsen, B. K]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 06:42:21 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp320</dc:identifier>
<dc:title><![CDATA[Abdominal aortic aneurysms, or a relatively large diameter of non-aneurysmal aortas, increase total and cardiovascular mortality: the Tromso study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp342v1?rss=1">
<title><![CDATA[Commentary: Treated HIV infection is a chronic disease: the case against cause of death analyses]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp342v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Justice, A. C]]></dc:creator>
<dc:date>Mon, 09 Nov 2009 02:36:45 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp342</dc:identifier>
<dc:title><![CDATA[Commentary: Treated HIV infection is a chronic disease: the case against cause of death analyses]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-09</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp327v1?rss=1">
<title><![CDATA[Daytime napping and mortality, with a special reference to cardiovascular disease: the JACC study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp327v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Daytime napping is associated with elevated risk of all-cause mortality in the elderly. However, the association with cardiovascular disease (CVD) risk is inconsistent.</p>
<p><b>Methods</b> From 1988 to 1990, a total of 67 129 Japanese non-workers or daytime workers (27 755 men and 39 374 women) aged 40&ndash;79 years, without a history of stroke, heart disease or cancer, completed a lifestyle questionnaire. They were followed for mortality until the end of 2003.</p>
<p><b>Results</b> During the 879 244 person-year follow-up, 9643 deaths (2852 from CVD, 3643 from cancer, 2392 from other internal causes, 738 from external causes and 18 from unspecified causes) were observed. After adjustment for possible confounders, subjects with a daytime napping habit had elevated hazard ratios (HRs) for mortality from all causes [HR 1.19, 95% confidence interval (CI) 1.14&ndash;1.24, <I>P</I> &lt; 0.001], CVD (HR 1.31, 95% CI 1.22&ndash;1.42, <I>P</I> &lt; 0.001), non-cardiovascular/non-cancer internal diseases (HR 1.26, 95% CI 1.16&ndash;1.37, <I>P</I> &lt; 0.001) and external causes (HR 1.28, 95% CI 1.10&ndash;1.50, <I>P</I> = 0.001), but not for cancer death (HR 1.03, 95% CI 0.96&ndash;1.10, <I>P</I> = 0.400). The risk of CVD mortality associated with daytime napping was diminished among overweight subjects, but pronounced in those with weight loss after age 20 years, with non-regular employment, with lower education level and with a follow-up period &lt;5 years.</p>
<p><b>Conclusions</b> Daytime napping is associated with elevated risk of CVD mortality as well as non-cardiovascular/non-cancer and external deaths. Daytime napping may elevate risk of CVD death through some biological effects but, to a larger extent, some comorbid disorders causing weight loss or associated with non-regular employment and low education level could explain this association.</p>
]]></description>
<dc:creator><![CDATA[Tanabe, N., Iso, H., Seki, N., Suzuki, H., Yatsuya, H., Toyoshima, H., Tamakoshi, A., for the JACC Study Group]]></dc:creator>
<dc:date>Mon, 09 Nov 2009 02:36:45 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp327</dc:identifier>
<dc:title><![CDATA[Daytime napping and mortality, with a special reference to cardiovascular disease: the JACC study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-09</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp319v1?rss=1">
<title><![CDATA[Risk of injury according to participation in specific physical activities: a 6-year follow-up of 14 356 participants of the SUN cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp319v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Physical activity is generally accepted as a healthy habit. Nevertheless, its associated risk to cause injuries has not been sufficiently evaluated. Measuring this risk more precisely would contribute to giving more accurate health advice to the general population.</p>
<p><b>Methods</b> Data are from participants (60% women, mean age 38 years) in a cohort of university graduates in Spain (1999&ndash;2008). Among other exposures and outcomes, they self report on frequency of participation in several physical activities over 1 year, and on incidence of sports-related injuries after 2, 4 or 6 years follow-up. Participation in 17 physical activities was categorized as a dichotomous variable (yes/no) and also according to average time per week spent in each one. Proportional hazards regression was used to estimate the adjusted relative risks [hazard ratios (HRs)] of incident injury associated with each specific physical activity or with total weekly energy expenditure in leisure-time activity [metabolic equivalents (METs)-h/week]. Statistical analyses were stratified by sex.</p>
<p><b>Results</b> We identified 1658 incident sports-related injuries among 14 356 participants after a median follow-up of 4.6 years. When we adjusted for overall energy expenditure (METs-h/week) in other activities, age and body mass index (BMI), a higher risk of injury was associated with participation in soccer, other team sports, skiing, tennis, running and athletics (HRs ranging from 1.50 to 1.86) among men. With the exception of soccer (rarely practiced by women in Spain), similar results were found for women (HRs ranging from 1.61 to 2.04). Walking, gymnastics, swimming, mountain hiking and gardening were associated with a low injury risk.</p>
<p><b>Conclusions</b> Despite the healthy effects of physical activity, we consider that the higher risk for injuries related to soccer, team sports, skiing, tennis, running or athletics should be taken into consideration when advice for more physical activity is given to the general population. Daily routine physical activities such as walking or gardening should be encouraged.</p>
]]></description>
<dc:creator><![CDATA[Pons-Villanueva, J., Segui-Gomez, M., Martinez-Gonzalez, M. A]]></dc:creator>
<dc:date>Fri, 06 Nov 2009 06:50:47 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp319</dc:identifier>
<dc:title><![CDATA[Risk of injury according to participation in specific physical activities: a 6-year follow-up of 14 356 participants of the SUN cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-06</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp326v1?rss=1">
<title><![CDATA[Author's Response *  On the roles of skin type and sun exposure in the risk of endometriosis and melanoma]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp326v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kvaskoff, M., Mesrine, S., Clavel-Chapelon, F., Boutron-Ruault, M.-C.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 05:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp326</dc:identifier>
<dc:title><![CDATA[Author's Response *  On the roles of skin type and sun exposure in the risk of endometriosis and melanoma]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp324v1?rss=1">
<title><![CDATA[On the roles of skin type and sun exposure in the risk of endometriosis and melanoma]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp324v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Grant, W. B]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 05:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp324</dc:identifier>
<dc:title><![CDATA[On the roles of skin type and sun exposure in the risk of endometriosis and melanoma]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp323v1?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp323v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Schwartz, S., Hafeman, D., Campbell, U., Gatto, N.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 05:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp323</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp322v1?rss=1">
<title><![CDATA[Cohort Profile: The China Health and Nutrition Survey--monitoring and understanding socio-economic and health change in China, 1989-2011]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp322v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Popkin, B. M, Du, S., Zhai, F., Zhang, B.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 05:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp322</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The China Health and Nutrition Survey--monitoring and understanding socio-economic and health change in China, 1989-2011]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp315v1?rss=1">
<title><![CDATA[Rose's population strategy of prevention need not increase social inequalities in health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp315v1?rss=1</link>
<description><![CDATA[
<p> Geoffrey Rose's 1985 paper, <I>Sick individuals and sick populations</I>, continues to spark debate and discussion. Since this original publication, there have been two notable challenges to Rose's population strategy of prevention. First, identification of high-risk individuals has improved considerably in accuracy, which some believe obviates the need for population-wide prevention strategies. Secondly, and more recently, it has been suggested that population strategies of prevention may inadvertently worsen social inequalities in health. We argue that population prevention will not necessarily worsen social inequalities in health, and the likelihood of it doing so will depend on whether the prevention strategy is more structural (targets conditions in which behaviours occur) or agentic (targets behaviour change among individuals) in nature. Also, there are potential drawbacks of approaches that focus on discrete populations (i.e. high risk or vulnerable) that need to be considered when selecting a strategy. Although Rose's ideas need to be continually scrutinized, his population strategy of prevention still holds considerable merit for improving population health and narrowing social inequalities in health.</p>
]]></description>
<dc:creator><![CDATA[McLaren, L., McIntyre, L., Kirkpatrick, S.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 05:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp315</dc:identifier>
<dc:title><![CDATA[Rose's population strategy of prevention need not increase social inequalities in health]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp325v1?rss=1">
<title><![CDATA[Commentary: Heart rate and blood pressure: risk factors or risk markers?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp325v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Carnethon, M. R]]></dc:creator>
<dc:date>Wed, 28 Oct 2009 04:05:29 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp325</dc:identifier>
<dc:title><![CDATA[Commentary: Heart rate and blood pressure: risk factors or risk markers?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-28</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp318v1?rss=1">
<title><![CDATA[Commentary: Assessing the impact of breastfeeding on child health: where conventional methods alone fall short for reliably establishing causal inference]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp318v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Brion, M.-J.]]></dc:creator>
<dc:date>Wed, 28 Oct 2009 04:05:28 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp318</dc:identifier>
<dc:title><![CDATA[Commentary: Assessing the impact of breastfeeding on child health: where conventional methods alone fall short for reliably establishing causal inference]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-28</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp316v1?rss=1">
<title><![CDATA[Commentary: Early stimulation and child development]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp316v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Walker, S. P]]></dc:creator>
<dc:date>Wed, 28 Oct 2009 04:05:27 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp316</dc:identifier>
<dc:title><![CDATA[Commentary: Early stimulation and child development]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-28</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp314v1?rss=1">
<title><![CDATA[Education reduces the effects of genetic susceptibilities to poor physical health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp314v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Greater education is associated with better physical health. This has been of great concern to public health officials. Most demonstrations show that education influences mean levels of health. Little is known about the influence of education on variance in health status, or about how this influence may impact the underlying genetic and environmental sources of health problems. This study explored these influences.</p>
<p><b>Methods</b> In a 2002 postal questionnaire, 21 522 members of same-sex pairs in the Danish Twin Registry born between 1931 and 1982 reported physical health in the 12-item Short Form Health Survey. We used quantitative genetic models to examine how genetic and environmental variance in physical health differed with level of education, adjusting for birth-year effects.</p>
<p><b>Results and Conclusions</b> As expected, greater education was associated with better physical health. Greater education was also associated with smaller variance in health status. In both sexes, 2 standard deviations (SDs) above mean educational level, variance in physical health was only about half that among those 2 SDs below. This was because fewer highly educated people reported poor health. There was less total variance in health primarily because there was less genetic variance. Education apparently reduced expression of genetic susceptibilities to poor health. The patterns of genetic and environmental correlations suggested that this might take place because more educated people manage their environments to protect their health. If so, fostering the personal charactieristics associated with educational attainment could be important in reducing the education&ndash;health gradient.</p>
]]></description>
<dc:creator><![CDATA[Johnson, W., Kyvik, K. O., Mortensen, E. L, Skytthe, A., Batty, G D., Deary, I. J]]></dc:creator>
<dc:date>Tue, 27 Oct 2009 06:10:48 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp314</dc:identifier>
<dc:title><![CDATA[Education reduces the effects of genetic susceptibilities to poor physical health]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-27</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp309v1?rss=1">
<title><![CDATA[Modelling relative survival in the presence of incomplete data: a tutorial]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp309v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Missing data frequently create problems in the analysis of population-based data sets, such as those collected by cancer registries. Restriction of analysis to records with complete data may yield inferences that are substantially different from those that would have been obtained had no data been missing. &lsquo;Naive&rsquo; methods for handling missing data, such as restriction of the analysis to complete records or creation of a &lsquo;missing&rsquo; category, have drawbacks that can invalidate the conclusions from the analysis. We offer a tutorial on modern methods for handling missing data in relative survival analysis.</p>
<p><b>Methods</b> We estimated relative survival for 29 563 colorectal cancer patients who were diagnosed between 1997 and 2004 and registered in the North West Cancer Intelligence Service. The method of multiple imputation (MI) was applied to account for the common example of incomplete stage at diagnosis, under the missing at random (MAR) assumption. Multivariable regression with a generalized linear model and Poisson error structure was then used to estimate the excess hazard of death of the colorectal cancer patients, over and above the background mortality, adjusting for significant predictors of mortality.</p>
<p><b>Results</b> Incomplete information on stage, morphology and grade meant that only 55% of the data could be included in the &lsquo;complete-case&rsquo; analysis. All cases could be included after indicator method (IM) or MI method. Handling missing data by MI produced a significantly lower estimate of the excess mortality for stage, morphology and grade, with the largest reductions occurring for late-stage and high-grade tumours, when compared with the results of complete-case analysis.</p>
<p><b>Conclusion</b> In complete-case analysis, almost 50% of the information could not be included, and with the IM, all records with missing values for stage were combined into a single &lsquo;missing&rsquo; category. We show that MI methods greatly improved the results by exploiting all the information in the incomplete records. This method also helped to ensure efficient inferences about survival were made from the multivariate regression analyses.</p>
]]></description>
<dc:creator><![CDATA[Nur, U., Shack, L. G, Rachet, B., Carpenter, J. R, Coleman, M. P]]></dc:creator>
<dc:date>Sun, 25 Oct 2009 22:15:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp309</dc:identifier>
<dc:title><![CDATA[Modelling relative survival in the presence of incomplete data: a tutorial]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-25</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp304v1?rss=1">
<title><![CDATA[Bias correction of estimates of familial risk from population-based cohort studies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp304v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In addition to guiding molecular epidemiology investigations, estimates of the increased risk of disease in relatives of affected persons are also important for screening and counselling decisions. Since precise estimation of such familial risks (FRs) requires large sample sizes, many of the estimates in common use have been obtained from historical electronic records of disease in entire populations, where the relatives of affected and unaffected persons are compared. These estimates may be biased due to failure to identify relatives as affected if they are diagnosed before the start-up date of disease registration.</p>
<p><b>Methods</b> This article presents a method for correcting the bias in FR estimates from such misclassification of family history, using a simple formula that depends on the prevalence and sensitivity of the observed family history. The sensitivity is estimated by using the R package <I>poplab</I> to create realistic populations of related individuals and then imposing the start-up effect of disease registration.</p>
<p><b>Results</b> For a range of FRs, the truncation of family history is demonstrated to result in non-differential misclassification, and sensitivity that has little or no dependence on the FR. The bias is most pronounced for high FRs and for registers with a short life span, and increases with the age of the study cohort. In all the situations studied, the bias-corrected estimates are in excellent agreement with the true values.</p>
<p><b>Conclusions</b> In summary, our method can correct the inevitable bias in FRs induced by using electronic population data, and is a feasible alternative to the use of validation samples.</p>
]]></description>
<dc:creator><![CDATA[Leu, M., Czene, K., Reilly, M.]]></dc:creator>
<dc:date>Tue, 13 Oct 2009 07:44:15 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp304</dc:identifier>
<dc:title><![CDATA[Bias correction of estimates of familial risk from population-based cohort studies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-13</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp307v1?rss=1">
<title><![CDATA[Does BCG vaccination protect against the development of childhood asthma? A systematic review and meta-analysis of epidemiological studies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp307v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Results have been conflicting as to whether Bacillus Calmette-Gu&eacute;rin (BCG) vaccine, a non-specific stimulator of the immune function, protects, predisposes or is unrelated to the development of childhood asthma. In this systematic review and meta-analysis, we qualitatively and quantitatively appraised the epidemiological evidence.</p>
<p><b>Methods</b> Eligible studies were identified using a search strategy that included a computerized literature search and a manual search of each article's reference list, up to June 2008. A total of 23 studies were included (10 cohort, 5 case&ndash;control and 8 cross-sectional). Each study was summarized and rated for methodological quality. Pooled odds ratio (OR) estimates and 95% confidence intervals (CIs) were calculated using fixed-effects (FE) or random-effects (RE) models; if heterogeneity was present, the latter was used. Three indicators of BCG exposure were considered including BCG vaccination, tuberculin response and scar diameter.</p>
<p><b>Results</b> The pooled estimate of association for 23 studies reporting on any of the three indicators suggested a protective effect of BCG exposure on childhood asthma occurrence. The studies were heterogeneous, especially when tuberculin response was considered. Restriction to a subgroup of 16 studies that considered BCG vaccination indicated a protective effect with no evidence of heterogeneity. The overall pooled OR using an FE model was 0.86 (95% CI 0.79&ndash;0.93). Exclusion of three studies with the lowest quality scores showed a similar association.</p>
<p><b>Conclusion</b> These results strengthen the epidemiological evidence in support of the hypothesis that exposure to the BCG vaccine in early life prevents asthma, possibly through a modulation of the immune maturation process.</p>
]]></description>
<dc:creator><![CDATA[El-Zein, M., Parent, M.-E., Benedetti, A., Rousseau, M.-C.]]></dc:creator>
<dc:date>Mon, 12 Oct 2009 00:48:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp307</dc:identifier>
<dc:title><![CDATA[Does BCG vaccination protect against the development of childhood asthma? A systematic review and meta-analysis of epidemiological studies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-12</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp308v1?rss=1">
<title><![CDATA[A consistent log-linear relationship between tuberculosis incidence and body mass index]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp308v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Low weight for height is an established risk factor for tuberculosis (TB), and recent studies suggest that overweight is a protective factor. No previous systematic review has been done to explore the consistency and establish the gradient of this apparent &lsquo;dose&ndash;response&rsquo; relationship.</p>
<p><b>Methods</b> A systematic literature review was carried out to identify cohort studies that collected data on weight and height at baseline and that used a diagnosis of active TB as the study outcome. Weight-for-height measures used in the original studies were transformed into body mass index (BMI). Exponential trend lines were fitted to each data set.</p>
<p><b>Results</b> Six studies were included. In all of them, there was a log-linear inverse relationship between TB incidence and BMI, within the BMI range 18.5&ndash;30 kg/m<sup>2</sup>. The average slope gave a reduction in TB incidence of 13.8% [95% confidence interval 13.4&ndash;14.2] per unit increase in BMI. The dose&ndash;response relationship was less certain at BMI &lt;18.5 and &gt;30 kg/m<sup>2</sup>.</p>
<p><b>Conclusion</b> There is a strong and consistent log-linear relationship between TB incidence and BMI across a variety of settings with different levels of TB burden. More research is required to test the relationship at very low and very high BMI levels, to establish the biological mechanism linking BMI with risk of TB and to establish the potential impact on the global TB epidemic of changing nutritional status of populations.</p>
]]></description>
<dc:creator><![CDATA[Lonnroth, K., Williams, B. G, Cegielski, P., Dye, C.]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 08:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp308</dc:identifier>
<dc:title><![CDATA[A consistent log-linear relationship between tuberculosis incidence and body mass index]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp306v1?rss=1">
<title><![CDATA[Mortality of HIV-infected patients starting potent antiretroviral therapy: comparison with the general population in nine industrialized countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp306v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Mortality in HIV-infected patients has declined substantially with combination antiretroviral therapy (ART), but it is unclear whether it has reached that of the general population. We compared mortality in patients starting ART in nine countries of Europe and North America with the corresponding general population, taking into account their response to ART.</p>
<p><b>Methods</b> Eligible patients were enrolled in prospective cohort studies participating in the ART Cohort Collaboration. We calculated the ratio of observed to expected deaths from all causes [standardized mortality ratio (SMR)], measuring time from 6 months after starting ART, according to risk group, clinical stage at the start of ART and CD4 cell count and viral load at 6 months. Expected numbers of deaths were obtained from age-, sex- and country-specific mortality rates.</p>
<p><b>Results</b> Among 29 935 eligible patients, 1134 deaths were recorded in 131 510 person-years of follow-up. The median age was 37 years, 8162 (27%) patients were females, 4400 (15%) were injecting drug users (IDUs) and 6738 (23%) had AIDS when starting ART. At 6 months, 23 539 patients (79%) had viral load measurements &le;500 copies/ml. The lowest SMR, 1.05 [95% confidence interval (CI) 0.82&ndash;1.35] was found for men who have sex with men (MSM) who started ART free of AIDS, reached a CD4 cell count of &ge;350 cells/&micro;L and suppressed viral replication to &le;500 copies/ml by the sixth month. In contrast, the SMR was 73.7 (95% CI 46.4&ndash;116.9) in IDUs who failed to suppress viral replication and had CD4 cell counts &lt;50 cells/&micro;L at 6 months. The percentage of patients with SMRs &lt;2 was 46% for MSM, 42% for heterosexually infected patients and 0% for patients with a history of injection drug use. Corresponding percentages for SMRs &gt;10 were 4, 14 and 47%.</p>
<p><b>Conclusions</b> In industrialized countries, the mortality experience of HIV-infected patients who start ART and survive the first 6 months continues to be higher than in the general population, but for many patients excess mortality is moderate and comparable with patients having other chronic conditions. Much of the excess mortality might be prevented by earlier diagnosis of HIV followed by timely initiation of ART.</p>
]]></description>
<dc:creator><![CDATA[The Antiretroviral Therapy Cohort Collaboration]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 08:36:40 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp306</dc:identifier>
<dc:title><![CDATA[Mortality of HIV-infected patients starting potent antiretroviral therapy: comparison with the general population in nine industrialized countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp296v1?rss=1">
<title><![CDATA[Causal thinking and complex system approaches in epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp296v1?rss=1</link>
<description><![CDATA[
<p> Identifying biological and behavioural causes of diseases has been one of the central concerns of epidemiology for the past half century. This has led to the development of increasingly sophisticated conceptual and analytical approaches focused on the isolation of single causes of disease states. However, the growing recognition that (i) factors at multiple levels, including biological, behavioural and group levels may influence health and disease, and (ii) that the interrelation among these factors often includes dynamic feedback and changes over time challenges this dominant epidemiological paradigm. Using obesity as an example, we discuss how the adoption of complex systems dynamic models allows us to take into account the causes of disease at multiple levels, reciprocal relations and interrelation between causes that characterize the causation of obesity. We also discuss some of the key difficulties that the discipline faces in incorporating these methods into non-infectious disease epidemiology. We conclude with a discussion of a potential way forward.</p>
]]></description>
<dc:creator><![CDATA[Galea, S., Riddle, M., Kaplan, G. A]]></dc:creator>
<dc:date>Fri, 09 Oct 2009 08:36:39 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp296</dc:identifier>
<dc:title><![CDATA[Causal thinking and complex system approaches in epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-09</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp303v1?rss=1">
<title><![CDATA[Does screening history explain the ethnic differences in stage at diagnosis of cervical cancer in New Zealand?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp303v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> There are ethnic disparities in cervical cancer survival in New Zealand. The objectives of this study were to assess the associations of screening history, ethnicity, socio-economic status (SES) and rural residence with stage at diagnosis in women diagnosed with cervical cancer in New Zealand during 1994&ndash;2005.</p>
<p><b>Methods</b> The 2323 cases were categorized as &lsquo;ever screened&rsquo; if they had had at least one smear prior to 6 months before diagnosis, and as &lsquo;regular screening&rsquo; if they had had no more than 36 months between any two smears in the period 6&ndash;114 months before diagnosis. Logistic regression was used to estimate the associations of screening history, ethnicity, SES and urban/rural residence with stage at diagnosis.</p>
<p><b>Results</b> The percentages &lsquo;ever screened&rsquo; were 43.3% overall, 24.8% in Pacific, 30.5% in Asian, 40.6% in Maori and 46.1% in &lsquo;Other&rsquo; women. The corresponding estimates for &lsquo;regular screening&rsquo; were 14.0, 5.7, 7.8, 12.5 and 15.3%. Women with &lsquo;regular screening&rsquo; had a lower risk of late stage diagnosis [odds ratio (OR) 0.16, 95% confidence interval (CI) 0.10&ndash;0.26], and the effect was greater for squamous cell carcinoma (OR 0.12, 95% CI 0.07&ndash;0.23) than for adenocarcinoma (OR 0.32, 95% CI 0.13&ndash;0.82). The increased risk of late-stage diagnosis (OR 2.72, 95% CI 1.99&ndash;3.72) in Maori (compared with &lsquo;Other&rsquo;) women decreased only slightly when adjusted for screening history (OR 2.45, 95% CI 1.77&ndash;3.39).</p>
<p><b>Conclusions</b> Over half of cases had not been &lsquo;ever screened&rsquo;. Regular screening substantially lowered the risk of being diagnosed at a late stage. However, screening history does not appear to explain the ethnic differences in stage at diagnosis.</p>
]]></description>
<dc:creator><![CDATA[Brewer, N., Pearce, N., Jeffreys, M., Borman, B., Ellison-Loschmann, L.]]></dc:creator>
<dc:date>Tue, 06 Oct 2009 06:21:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp303</dc:identifier>
<dc:title><![CDATA[Does screening history explain the ethnic differences in stage at diagnosis of cervical cancer in New Zealand?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-06</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp310v1?rss=1">
<title><![CDATA[Commentary: A Darwin family concern]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp310v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kuper, A.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 07:42:22 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp310</dc:identifier>
<dc:title><![CDATA[Commentary: A Darwin family concern]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-05</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp300v1?rss=1">
<title><![CDATA[Causes of death in HIV-infected women: persistent role of AIDS. The 'Mortalite 2000 & 2005' Surveys (ANRS EN19)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp300v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Little is known about the causes of death in human immunodeficiency virus (HIV)-infected women in the era of combination antiretroviral therapy (ART).</p>
<p><b>Methods</b> In the French nationwide Mortalit&eacute; 2000 and 2005 surveys, physicians reported causes of deaths in HIV-infected adults in 2000 and 2005, using a standardized questionnaire. We used multivariate logistic regression models to study the association between gender and AIDS-defining causes of death, adjusting for other characteristics.</p>
<p><b>Results</b> Of the 1013 HIV-infected adults who died in 2005, 247 (24%) were women. Half of women were infected through heterosexual contacts, compared with 25% men. In 2005, the proportion of AIDS-defining causes of death was higher in women than in men (43 vs 34%; <I>P</I> = 0.01), whereas it had been the same in 2000 (47% in women and men). In 2005, women died less frequently than men from respiratory malignancies (lung, ear/nose/throat) and cardiovascular disease (9% of all causes of death in women compared with 16% in men; <I>P</I> = 0.004), and suicides or accidents (4 vs 9%; <I>P</I> = 0.02). Socio-economic precariousness, younger age, less alcohol and tobacco consumption and lack of prior ART explained the higher proportion of deaths from AIDS in women compared with men.</p>
<p><b>Conclusions</b> The higher proportion of AIDS-related deaths in women is probably explained by two factors: (i) some HIV-infected women, especially migrants in poor socio-economic conditions, may not have access to optimal care; and (ii) a lower prevalence of risk factors for respiratory, cardiovascular and violent deaths means that the risk of dying from non-AIDS causes may be lower in women.</p>
]]></description>
<dc:creator><![CDATA[Hessamfar-Bonarek, M., Morlat, P., Salmon, D., Cacoub, P., May, T., Bonnet, F., Rosenthal, E., Costagliola, D., Lewden, C., Chene, G., the Mortalite 2000 & 2005 Study Groups]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 07:42:21 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp300</dc:identifier>
<dc:title><![CDATA[Causes of death in HIV-infected women: persistent role of AIDS. The 'Mortalite 2000 & 2005' Surveys (ANRS EN19)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-05</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp291v1?rss=1">
<title><![CDATA[Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp291v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Quitting tobacco or alcohol use has been reported to reduce the head and neck cancer risk in previous studies. However, it is unclear how many years must pass following cessation of these habits before the risk is reduced, and whether the risk ultimately declines to the level of never smokers or never drinkers.</p>
<p><b>Methods</b> We pooled individual-level data from case&ndash;control studies in the International Head and Neck Cancer Epidemiology Consortium. Data were available from 13 studies on drinking cessation (9167 cases and 12 593 controls), and from 17 studies on smoking cessation (12 040 cases and 16 884 controls). We estimated the effect of quitting smoking and drinking on the risk of head and neck cancer and its subsites, by calculating odds ratios (ORs) using logistic regression models.</p>
<p><b>Results</b> Quitting tobacco smoking for 1&ndash;4 years resulted in a head and neck cancer risk reduction [OR 0.70, confidence interval (CI) 0.61&ndash;0.81 compared with current smoking], with the risk reduction due to smoking cessation after &ge;20 years (OR 0.23, CI 0.18&ndash;0.31), reaching the level of never smokers. For alcohol use, a beneficial effect on the risk of head and neck cancer was only observed after &ge;20 years of quitting (OR 0.60, CI 0.40&ndash;0.89 compared with current drinking), reaching the level of never drinkers.</p>
<p><b>Conclusions</b> Our results support that cessation of tobacco smoking and cessation of alcohol drinking protect against the development of head and neck cancer.</p>
]]></description>
<dc:creator><![CDATA[Marron, M., Boffetta, P., Zhang, Z.-F., Zaridze, D., Wunsch-Filho, V., Winn, D. M, Wei, Q., Talamini, R., Szeszenia-Dabrowska, N., Sturgis, E. M, Smith, E., Schwartz, S. M, Rudnai, P., Purdue, M. P, Olshan, A. F, Eluf-Neto, J., Muscat, J., Morgenstern, H., Menezes, A., McClean, M., Matos, E., Mates, I. N., Lissowska, J., Levi, F., Lazarus, P., Vecchia, C. L., Koifman, S., Kelsey, K., Herrero, R., Hayes, R. B, Franceschi, S., Fernandez, L., Fabianova, E., Daudt, A. W, Maso, L. D., Curado, M. P., Cadoni, G., Chen, C., Castellsague, X., Boccia, S., Benhamou, S., Ferro, G., Berthiller, J., Brennan, P., Moller, H., Hashibe, M.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 07:42:19 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp291</dc:identifier>
<dc:title><![CDATA[Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-05</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp298v1?rss=1">
<title><![CDATA[Commentary: Raising the bar on telomere epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp298v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Aviv, A.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 05:06:19 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp298</dc:identifier>
<dc:title><![CDATA[Commentary: Raising the bar on telomere epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp297v1?rss=1">
<title><![CDATA[Cohort Profile: The Canadian HIV-Hepatitis C Co-infection Cohort Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp297v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Klein, M. B, Saeed, S., Yang, H., Cohen, J., Conway, B., Cooper, C., Cote, P., Cox, J., Gill, J., Haase, D., Haider, S., Montaner, J., Pick, N., Rachlis, A., Rouleau, D., Sandre, R., Tyndall, M., Walmsley, S.]]></dc:creator>
<dc:date>Mon, 28 Sep 2009 04:12:12 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp297</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Canadian HIV-Hepatitis C Co-infection Cohort Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-28</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp305v1?rss=1">
<title><![CDATA[Commentary: External validity of results of randomized trials: disentangling a complex concept]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp305v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rothwell, P. M]]></dc:creator>
<dc:date>Wed, 23 Sep 2009 09:05:17 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp305</dc:identifier>
<dc:title><![CDATA[Commentary: External validity of results of randomized trials: disentangling a complex concept]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-23</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp295v1?rss=1">
<title><![CDATA[Commentary: Societal influences on cardiovascular disease: time to assess and act]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp295v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Prabhakaran, D., Roy, A.]]></dc:creator>
<dc:date>Wed, 23 Sep 2009 09:05:17 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp295</dc:identifier>
<dc:title><![CDATA[Commentary: Societal influences on cardiovascular disease: time to assess and act]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-23</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp288v1?rss=1">
<title><![CDATA[Association between a 15q25 gene variant, smoking quantity and tobacco-related cancers among 17 000 individuals]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp288v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Genetic variants in 15q25 have been identified as potential risk markers for lung cancer (LC), but controversy exists as to whether this is a direct association, or whether the 15q variant is simply a proxy for increased exposure to tobacco carcinogens.</p>
<p><b>Methods</b> We performed a detailed analysis of one 15q single nucleotide polymorphism (SNP) (rs16969968) with smoking behaviour and cancer risk in a total of 17 300 subjects from five LC studies and four upper aerodigestive tract (UADT) cancer studies.</p>
<p><b>Results</b> Subjects with one minor allele smoked on average 0.3 cigarettes per day (CPD) more, whereas subjects with the homozygous minor AA genotype smoked on average 1.2 CPD more than subjects with a GG genotype (<I>P</I> &lt; 0.001). The variant was associated with heavy smoking (&gt;20 CPD) [odds ratio (OR) = 1.13, 95% confidence interval (CI) 0.96&ndash;1.34, <I>P</I> = 0.13 for heterozygotes and 1.81, 95% CI 1.39&ndash;2.35 for homozygotes, <I>P</I> &lt; 0.0001]. The strong association between the variant and LC risk (OR = 1.30, 95% CI 1.23&ndash;1.38, <I>P</I> = 1 <FONT FACE="arial,helvetica">x</FONT> 10<sup>&ndash;18</sup>), was virtually unchanged after adjusting for this smoking association (smoking adjusted OR = 1.27, 95% CI 1.19&ndash;1.35, <I>P</I> = 5 <FONT FACE="arial,helvetica">x</FONT> 10<sup>&ndash;13</sup>). Furthermore, we found an association between the variant allele and an earlier age of LC onset (<I>P</I> = 0.02). The association was also noted in UADT cancers (OR = 1.08, 95% CI 1.01&ndash;1.15, <I>P</I> = 0.02). Genome wide association (GWA) analysis of over 300 000 SNPs on 11 219 subjects did not identify any additional variants related to smoking behaviour.</p>
<p><b>Conclusions</b> This study confirms the strong association between 15q gene variants and LC and shows an independent association with smoking quantity, as well as an association with UADT cancers.</p>
]]></description>
<dc:creator><![CDATA[Lips, E. H, Gaborieau, V., McKay, J. D, Chabrier, A., Hung, R. J, Boffetta, P., Hashibe, M., Zaridze, D., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Mates, D., Bencko, V., Foretova, L., Janout, V., Field, J. K, Liloglou, T., Xinarianos, G., McLaughlin, J., Liu, G., Skorpen, F., Elvestad, M. B., Hveem, K., Vatten, L., Study, E., Benhamou, S., Lagiou, P., Holcatova, I., Merletti, F., Kjaerheim, K., Agudo, A., Castellsague, X., Macfarlane, T. V, Barzan, L., Canova, C., Lowry, R., Conway, D. I, Znaor, A., Healy, C., Curado, M. P., Koifman, S., Eluf-Neto, J., Matos, E., Menezes, A., Fernandez, L., Metspalu, A., Heath, S., Lathrop, M., Brennan, P.]]></dc:creator>
<dc:date>Wed, 23 Sep 2009 09:05:16 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp288</dc:identifier>
<dc:title><![CDATA[Association between a 15q25 gene variant, smoking quantity and tobacco-related cancers among 17 000 individuals]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-23</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp287v1?rss=1">
<title><![CDATA[A systematic review and meta-analysis of perinatal variables in relation to the risk of testicular cancer--experiences of the mother]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp287v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> We undertook a systematic review and meta-analysis of perinatal variables in relation to testicular cancer risk, with a specific focus upon characteristics of the mother.</p>
<p><b>Methods</b> EMBASE, PubMed, Scopus and Web of Science databases were searched using sensitive search strategies. Meta-analysis was undertaken using STATA 10.</p>
<p><b>Results</b> A total of 5865 references were retrieved, of which 67 met the inclusion criteria and contributed data to at least one perinatal analysis. Random effects meta-analysis found maternal bleeding during pregnancy [odds ratio (OR) 1.33, 95% confidence interval (CI) 1.02&ndash;1.73], birth order (primiparous vs not, 1.08, 95% CI 1.01&ndash;1.16; second vs first, OR 0.94, 95% CI 0.88&ndash;0.99; third vs first, OR 0.91, 95% CI 0.83&ndash;1.01; fourth vs first, OR 0.80, 95% CI 0.69&ndash;0.94) and sibship size (2 vs 1, OR 0.93, 95% CI 0.75&ndash;1.15; 3 vs 1, OR 0.89, 95% CI 0.74&ndash;1.07; 4 vs 1, OR 0.75, 95% CI 0.62&ndash;0.90) to be associated with testicular cancer risk. Meta-analyses that produced summary estimates which indicated no association included maternal age, maternal nausea, maternal hypertension, pre-eclampsia, breech delivery and caesarean section. Meta-regression provided evidence that continent of study is important in the relationship between caesarean section and testicular cancer (<I>P</I> = 0.035), and a meta-analysis restricted to the three studies from the USA was suggestive of association (OR 1.67, 95% CI 1.07&ndash;2.56).</p>
<p><b>Conclusions</b> This systematic review and meta-analysis has found evidence for associations of maternal bleeding, birth order, sibship size and possibly caesarean section with risk of testicular cancer.</p>
]]></description>
<dc:creator><![CDATA[Cook, M. B, Akre, O., Forman, D., Madigan, M P., Richiardi, L., McGlynn, K. A]]></dc:creator>
<dc:date>Wed, 23 Sep 2009 09:05:14 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp287</dc:identifier>
<dc:title><![CDATA[A systematic review and meta-analysis of perinatal variables in relation to the risk of testicular cancer--experiences of the mother]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-23</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp282v1?rss=1">
<title><![CDATA[Increases in body mass index over a 7-year period and risk of cause-specific mortality in Korean men]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp282v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The association between increased body mass index (BMI) and subsequent mortality remains unclear in Asians. This study investigated the associations between BMI increases and cause-specific mortality in middle-aged Korean men.</p>
<p><b>Methods</b> We conducted a retrospective cohort study of 473 358 Korean men aged 30&ndash;64 years, who had undergone health examinations in both 1992 and 1998 and were followed up during 1998&ndash;2004. Cox proportional hazards for cause-specific 7-year mortality in relation to BMI changes after stratification of baseline BMI status were analysed.</p>
<p><b>Results</b> Mortality from cardiovascular disease (CVD) was associated with BMI in both 1992 and 1998. Non-CVD mortality was inversely associated with BMI in both 1992 and 1998. We cross-classified participants into groups based on their baseline BMI levels and percent BMI changes during follow-up; men with the lowest BMI level at baseline (BMI in 1992 &lt;21 kg/m<sup>2</sup>) and stable BMI during follow-up (percent change in BMI &lt;5%) were included in the reference category. Compared with the reference group, CVD mortality was higher in initially obese men (BMI in 1992 &ge;25 kg/m<sup>2</sup>) with any increase of BMI, and in initially lean men (BMI in 1992 &lt;21 kg/m<sup>2</sup>) or initially overweight men (BMI in 1992 23&ndash;24.9 kg/m<sup>2</sup>) with BMI increases of &ge;10%. BMI increases of 5.0&ndash;9.9% in men with baseline BMI &lt;25 kg/m<sup>2</sup> and stable BMI in men with baseline BMI &ge;21 kg/m<sup>2</sup> appeared to lower the risk for non-CVD or all-cause mortality, to below the levels seen in the reference group.</p>
<p><b>Conclusions</b> Among middle-aged Korean men, obesity or severe weight gain was detrimental to CVD mortality. An increase in BMI appeared to have a predictive value for CVD mortality, especially when used in combination with baseline BMI level. In contrast, moderate weight gain in non-obese men seemed to protect against non-CVD and all-cause mortality.</p>
]]></description>
<dc:creator><![CDATA[Yun, K. E., Park, H. S., Song, Y.-M., Cho, S.-I.]]></dc:creator>
<dc:date>Thu, 17 Sep 2009 07:39:00 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp282</dc:identifier>
<dc:title><![CDATA[Increases in body mass index over a 7-year period and risk of cause-specific mortality in Korean men]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-17</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp301v1?rss=1">
<title><![CDATA[Commentary: Reducing HIV-associated tuberculosis in children]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp301v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Boulle, A., Eley, B.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 07:48:47 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp301</dc:identifier>
<dc:title><![CDATA[Commentary: Reducing HIV-associated tuberculosis in children]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-15</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp283v1?rss=1">
<title><![CDATA[Risk of cancer among hairdressers and related workers: a meta-analysis]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp283v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Hairdressers and allied occupations represent a large and fast growing group of professionals. The fact that these professionals are chronically exposed to a large number of chemicals present in their work environment, including potential carcinogens contained in hair dyes, makes it necessary to carry out a systematic evaluation of the risk of cancer in this group.</p>
<p><b>Methods</b> We retrieved studies by systematically searching Medline and other computerized databases, and by manually examining the references of the original articles and monographs retrieved. We also contacted international researchers working on this or similar topics to complete our search. We included 247 studies reporting relative risk (RR) estimates of hairdresser occupation and cancer of different sites.</p>
<p><b>Results</b> Study-specific RRs were weighted by the inverse of their variance to obtain fixed and random effects pooled estimates. The pooled RR of occupational exposure as a hairdresser was 1.27 (95% CI 1.15&ndash;1.41) for lung cancer, 1.52 [95% confidence interval (CI) 1.11&ndash;2.08] for larynx cancer, 1.30 (95% CI 1.20&ndash;1.42) for bladder cancer and 1.62 (95% CI 1.22&ndash;2.14) for multiple myeloma. Data for other anatomic sites showed increases of smaller magnitude. The results restricted to those studies carried out before the ban of two major carcinogens from hair dyes in the mid-1970s were similar to the general results.</p>
<p><b>Conclusions</b> Hairdressers have a higher risk of cancer than the general population. Improvement of the ventilation system in the hairdresser salons and implementation of hygiene measures aimed at mitigating exposure to potential carcinogens at work may reduce the risk.</p>
]]></description>
<dc:creator><![CDATA[Takkouche, B., Regueira-Mendez, C., Montes-Martinez, A.]]></dc:creator>
<dc:date>Mon, 14 Sep 2009 22:21:04 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp283</dc:identifier>
<dc:title><![CDATA[Risk of cancer among hairdressers and related workers: a meta-analysis]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-14</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp276v1?rss=1">
<title><![CDATA[Cohort Profile: Research on Osteoarthritis/Osteoporosis Against Disability study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp276v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yoshimura, N., Muraki, S., Oka, H., Kawaguchi, H., Nakamura, K., Akune, T.]]></dc:creator>
<dc:date>Fri, 11 Sep 2009 07:36:04 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp276</dc:identifier>
<dc:title><![CDATA[Cohort Profile: Research on Osteoarthritis/Osteoporosis Against Disability study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-11</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp278v1?rss=1">
<title><![CDATA[Bayesian perspectives for epidemiologic research: III. Bias analysis via missing-data methods]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp278v1?rss=1</link>
<description><![CDATA[
<p> I present some extensions of Bayesian methods to situations in which biases are of concern. First, a basic misclassification problem is illustrated using data from a study of sudden infant death syndrome. Bayesian analyses are then given. These analyses can be conducted directly, or by converting actual-data records to incomplete records and prior distributions to complete-data records, then applying missing-data techniques to the augmented data set. The analyses can easily incorporate any complete (&lsquo;validation&rsquo; or second-stage) data that might be available, as well as adjustments for confounding and selection bias. The approach illustrates how conventional analyses depend on implicit certainty that bias parameters are null and how these implausible assumptions can be replaced by plausible priors for bias parameters.</p>
]]></description>
<dc:creator><![CDATA[Greenland, S.]]></dc:creator>
<dc:date>Wed, 09 Sep 2009 23:07:57 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp278</dc:identifier>
<dc:title><![CDATA[Bayesian perspectives for epidemiologic research: III. Bias analysis via missing-data methods]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-09</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp275v1?rss=1">
<title><![CDATA[Cohort Profile: The PROLIFE study in Kerala, India]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp275v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Soman, C. R., Shahulhameed, S., Ramankutty, V., Vijayakumar, K., Kunjukrishnapillai, R., Ajayan, K., Sajikumar, S., for the PROLIFE study group]]></dc:creator>
<dc:date>Tue, 08 Sep 2009 22:56:40 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp275</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The PROLIFE study in Kerala, India]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-09-08</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp280v1?rss=1">
<title><![CDATA[Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp280v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Whereas the International Agency for Research on Cancer (IARC) Monograph concluded that the evidence for the relationship between cigarette smoking and liver cancer is sufficient, the US Surgeon General's report summarized the data as suggestive but not sufficient.</p>
<p><b>Methods</b> A meta-analysis of previous epidemiologic studies may help to clarify the potential association. We identified 38 cohort studies and 58 case&ndash;control studies in a systematic literature search for studies on liver cancer and cigarette smoking. The meta-relative risk (mRR) of liver cancer and dose&ndash;response trends were calculated. Tests for heterogeneity, publication bias assessment and influence analyses were performed.</p>
<p><b>Results</b> Compared with never smokers, the adjusted mRR was 1.51 [95% confidence interval (CI) 1.37&ndash;1.67] for current smokers and 1.12 (95% CI 0.78&ndash;1.60) for former smokers. The increased liver cancer risk among current smokers appeared to be consistent in strata of different regions, study designs, study sample sizes and publication periods.</p>
<p><b>Conclusion</b> The results of our meta-analysis show that tobacco smoking is associated with liver cancer development, which supports the conclusion by the IARC Monograph. This conclusion has an important public health message for areas with high smoking prevalence and high liver cancer incidence such as China.</p>
]]></description>
<dc:creator><![CDATA[Lee, Y.-C. A., Cohet, C., Yang, Y.-C., Stayner, L., Hashibe, M., Straif, K.]]></dc:creator>
<dc:date>Mon, 31 Aug 2009 06:58:52 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp280</dc:identifier>
<dc:title><![CDATA[Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-31</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp272v1?rss=1">
<title><![CDATA[Child development in a birth cohort: effect of child stimulation is stronger in less educated mothers]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp272v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Child health has improved in many developing countries, bringing new challenges, including realization of the children's full physical and intellectual potential. This study explored child development within a birth cohort, its psychosocial determinants and interactions with maternal schooling and economic position.</p>
<p><b>Methods</b> All children born in Pelotas, Brazil, in 2004, were recruited to a birth cohort study. These children were assessed at birth and at 3, 12 and 24 months of age. In this last assessment involving 3869 children, detailed information on socio-economic and health characteristics was collected. Child development was assessed using the screening version of Battelle's Development Inventory. Five markers of cognitive stimulation and social interaction were recorded and summed to form a score ranging from 0&ndash;5. The outcomes studied were mean development score and low performance (less than 10th percentile of the sample).</p>
<p><b>Results</b> Child development was strongly associated with socio-economic position, maternal schooling and stimulation. Having been told a story and owning a book were the least frequent markers among children with score 1. These children were 8.3 times more likely to present low performance than those who scored 5. The effect of stimulation was much stronger among children from mothers with a low level of schooling&mdash;one additional point added 1.7 on the child's development for children of low-schooling mothers, whereas only 0.6 was added for children of high-schooling mothers.</p>
<p><b>Conclusions</b> Our stimulation markers cannot be directly translated into intervention strategies, but strongly suggest that suitably designed cognitive stimulation can have an important effect on children, especially those from mothers with low schooling.</p>
]]></description>
<dc:creator><![CDATA[Barros, A. J., Matijasevich, A., Santos, I. S, Halpern, R.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 06:24:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp272</dc:identifier>
<dc:title><![CDATA[Child development in a birth cohort: effect of child stimulation is stronger in less educated mothers]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-28</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp274v1?rss=1">
<title><![CDATA[Does breastfeeding protect against childhood overweight? Hong Kong's 'Children of 1997' birth cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp274v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Observational studies from mainly Western settings suggest breastfeeding may protect against childhood adiposity; however, breastfeeding and adiposity share social patterning potentially generating confounding, making evidence from other settings valuable.</p>
<p><b>Methods</b> We used multivariable linear regression to examine the prospective adjusted associations of breastfeeding with body mass index (BMI), height and weight <I>z</I>-scores at 7 years of age relative to the 2007 World Health Organization (WHO) growth reference, in a large (<I>n</I> = 8327), population-representative Hong Kong Chinese birth cohort, recruited between April and May 1997 with high follow-up (<I>n</I> = 7026).</p>
<p><b>Results</b> Low socio-economic position (SEP) was associated with never breastfeeding and with exclusive breastfeeding for &ge;3 months. We did not find any association between breastfeeding and BMI [<I>z</I>-score mean difference 0.07, 95% confidence interval (CI) &ndash;0.05 to 0.19], height (0.02, 95% CI &ndash;0.07 to 0.11) or weight (0.07, 95% CI &ndash;0.05 to 0.18), adjusted for sex, birth weight, gestational age, SEP, second-hand smoke (SHS) exposure, parity, mother's age at birth, mother's place of birth and serious infant morbidity.</p>
<p><b>Conclusions</b> In a non-European setting, breastfeeding was not associated with child adiposity, suggesting that observed protective effects may be due to socially patterned confounding by SEP, maternal adiposity and maternal smoking.</p>
]]></description>
<dc:creator><![CDATA[Kwok, M. K., Schooling, C M., Lam, T. H., Leung, G. M]]></dc:creator>
<dc:date>Thu, 20 Aug 2009 23:09:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp274</dc:identifier>
<dc:title><![CDATA[Does breastfeeding protect against childhood overweight? Hong Kong's 'Children of 1997' birth cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-20</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp281v1?rss=1">
<title><![CDATA[Author's Response Time to forget about obesity]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp281v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Roberts, I., Edwards, P.]]></dc:creator>
<dc:date>Mon, 17 Aug 2009 07:28:38 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp281</dc:identifier>
<dc:title><![CDATA[Author's Response Time to forget about obesity]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-17</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp279v1?rss=1">
<title><![CDATA[Obesity and climate change]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp279v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Gallar, M.]]></dc:creator>
<dc:date>Mon, 17 Aug 2009 07:28:38 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp279</dc:identifier>
<dc:title><![CDATA[Obesity and climate change]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-17</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp269v1?rss=1">
<title><![CDATA[Estimating the odds ratio when exposure has a limit of detection]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp269v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In epidemiologic research, little emphasis has been placed on methods to account for left-hand censoring of &lsquo;exposures&rsquo; due to a limit of detection (LOD).</p>
<p><b>Methods</b> We calculate the odds of anti-HIV therapy naivet&eacute; in 45 HIV-infected men as a function of measured log<SUB>10</SUB> plasma HIV RNA viral load using five approaches including <I>ad hoc</I> methods as well as a maximum likelihood estimate (MLE). We also generated simulations of a binary outcome with 10% incidence and a 1.5-fold increased odds per log increase in a log-normally distributed exposure with 25, 50 and 75% of exposure data below LOD. Simulated data were analysed using the same five methods, as well as the full data.</p>
<p><b>Results</b> In the example, the estimated odds ratio (OR) varied by 1.22-fold across methods, from 1.45 to 1.77 per log<SUB>10</SUB> copies of viral load and the standard error for the log OR varied by 1.52-fold across methods, from 0.31 to 0.47. In the simulations, use of full data or the MLE was unbiased with appropriate confidence interval (CI) coverage. However, as the proportion of exposure below LOD increased, substituting LOD, LOD/2 or LOD/2 was increasingly biased with increasingly inappropriate CI coverage. Finally, exclusion of values below LOD was unbiased but imprecise.</p>
<p><b>Conclusions</b> In this example and the settings explored by simulation, and among methods readily available to investigators (i.e. sans full data), the MLE provided an unbiased and appropriately precise estimate of the exposure&ndash;outcome OR.</p>
]]></description>
<dc:creator><![CDATA[Cole, S. R, Chu, H., Nie, L., Schisterman, E. F]]></dc:creator>
<dc:date>Mon, 10 Aug 2009 09:03:16 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp269</dc:identifier>
<dc:title><![CDATA[Estimating the odds ratio when exposure has a limit of detection]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-10</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp273v1?rss=1">
<title><![CDATA[Influences on the reduction of relative telomere length over 10 years in the population-based Bruneck Study: introduction of a well-controlled high-throughput assay]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp273v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Telomeres play a key role in the maintenance of chromosome integrity. Short telomeres are linked to age-associated diseases and cancer. Our aim was to determine the decrease rate of relative telomere length (RTL) over 10 years and whether this rate was influenced by age, sex and smoking behaviour.</p>
<p><b>Methods</b> We compared RTL in 510 sample pairs from the longitudinal population-based Bruneck Study, which were collected in 1995 and recollected in 2005, and additionally determined RTL from 159 participants who died during follow-up. RTL were determined by a high-throughput real-time PCR assay and by applying a mathematical model.</p>
<p><b>Results</b> The telomeres shortened, on average, by 455 bp over 10 years. The RTL shortening rate was highly correlated with baseline RTL (<I>r</I> = 0.674, <I>P</I> &lt; 0.001). Participants who died within the observed period had considerably shorter telomeres than those who survived (median RTL of 0.98 vs 1.49; <I>P</I> &lt; 0.001). In contrast to previous studies, smoking behaviour had no influence on RTL and on telomere shortening.</p>
<p><b>Conclusion</b> This is the first comprehensive longitudinal study of individuals who were, on average, 60 at baseline, and who were re-evaluated 10 years later. Our methodology proved to be a reliable tool for a rapid, accurate and cost-efficient determination of RTL with a low amount of DNA.</p>
]]></description>
<dc:creator><![CDATA[Ehrlenbach, S., Willeit, P., Kiechl, S., Willeit, J., Reindl, M., Schanda, K., Kronenberg, F., Brandstatter, A.]]></dc:creator>
<dc:date>Fri, 07 Aug 2009 07:42:59 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp273</dc:identifier>
<dc:title><![CDATA[Influences on the reduction of relative telomere length over 10 years in the population-based Bruneck Study: introduction of a well-controlled high-throughput assay]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-07</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp271v1?rss=1">
<title><![CDATA[Commentary: On Hashizume et al.'s 'The effect of temperature on mortality in rural Bangladesh']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp271v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dear, K.]]></dc:creator>
<dc:date>Fri, 07 Aug 2009 07:42:56 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp271</dc:identifier>
<dc:title><![CDATA[Commentary: On Hashizume et al.'s 'The effect of temperature on mortality in rural Bangladesh']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-07</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp266v1?rss=1">
<title><![CDATA[Genomes and What to Make of Them. Barry Barnes and John Dupre.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp266v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mclennan, G.]]></dc:creator>
<dc:date>Mon, 03 Aug 2009 08:05:00 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp266</dc:identifier>
<dc:title><![CDATA[Genomes and What to Make of Them. Barry Barnes and John Dupre.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-08-03</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp251v1?rss=1">
<title><![CDATA[Gains of stopping smoking: portraits of the dialogue between public health promotion, art and design]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp251v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Szklo, A. S, Coutinho, E. S F, Spitz, R., Gamba, N.]]></dc:creator>
<dc:date>Mon, 13 Jul 2009 08:17:08 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp251</dc:identifier>
<dc:title><![CDATA[Gains of stopping smoking: portraits of the dialogue between public health promotion, art and design]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-07-13</prism:publicationDate>
<prism:section>Photoessay</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp250v1?rss=1">
<title><![CDATA[Sibship size, Helicobacter pylori infection and chronic atrophic gastritis: a population-based study among 9444 older adults from Germany]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp250v1?rss=1</link>
<description><![CDATA[
<p><I><b>Background</b></I> Early-life social environment has been suggested to play an important role during the development of <I>Helicobacter pylori</I>-related gastric diseases. We aimed to assess the association of sibship size with <I>H. pylori</I> infection and chronic atrophic gastritis (CAG) in a population-based study from Germany.</p>
<p><I><b>Methods</b></I> In the baseline examination of ESTHER, a study conducted in Saarland, serological measurements of pepsinogen I and II and <I>H. pylori</I> antibodies were taken in 9444 participants aged 50&ndash;74 years. Information on potential risk factors and medical history were obtained by self-administered standardized questionnaire.</p>
<p><b>Results</b> A strong dose&ndash;response relationship between sibship size and <I>H. pylori</I> seroprevalence was observed (<I>P</I> &lt; 0.01). Adjusted odds ratios (ORs) 95% confidence interval (CI) for <I>H. pylori</I> seropositivity for subjects with 4, 5, 6 and 7 or more siblings compared with subjects without siblings were 1.45 (1.20&ndash;1.77), 1.83 (1.50&ndash;2.22) and 1.84 (1.47&ndash;2.31), respectively. A large sibship size was also associated with an increased risk of CAG with an adjusted OR of 1.42 (1.01&ndash;2.01) for 7 or more compared with less than or equal to 2 siblings. This association was attenuated but not entirely eliminated after additional adjustment for <I>H. pylori</I> infection. Notably, a significant association between large sibship size and CAG was also found among <I>H. pylori</I>-negative subjects.</p>
<p><I><b>Conclusions</b></I> Our results suggest that large sibship size is associated with increased <I>H. pylori</I> prevalence and CAG risk. The association with CAG risk may be mediated at least in part by <I>H. pylori</I> infection. However, mechanisms other than <I>H. pylori</I> infection may contribute to the &lsquo;sibling effect&rsquo; as well.</p>
]]></description>
<dc:creator><![CDATA[Gao, L., Weck, M. N, Raum, E., Stegmaier, C., Rothenbacher, D., Brenner, H.]]></dc:creator>
<dc:date>Mon, 13 Jul 2009 08:17:07 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp250</dc:identifier>
<dc:title><![CDATA[Sibship size, Helicobacter pylori infection and chronic atrophic gastritis: a population-based study among 9444 older adults from Germany]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-07-13</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp245v1?rss=1">
<title><![CDATA[Long-term association of routine blood count (Coulter) variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp245v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Since evidence of a long-term association between routine blood count (Coulter) variables and coronary heart disease (CHD) is inconsistent, the authors analysed white blood cell count (WBC), red blood cell count (RBC), haemoglobin (Hgb), packed cell volume (PCV) and platelet count for their long-term associations with CHD mortality in the first Northwick Park Heart Study (NPHS-I). NPHS-I has follow-up information for &gt;30 years on 2167 White men and 941 White women and holds entry and follow-up data on haematological variables and other known CHD risk factors.</p>
<p><b>Methods</b> Proportional hazards Cox models were fitted to estimate rate ratios (RRs) for the separate and joint effects of entry and follow-up Coulter variables.</p>
<p><b>Results</b> Entry RBC, PCV and Hgb were significant risk factors for CHD mortality after adjustment for gender but only PCV remained significant after adjustment for potential confounders [RR per 1 standard deviation (SD) increase = 1.17, 95% confidence interval (CI) 1.00&ndash;1.37]. This effect was partly reduced when the values of 6 years were analysed (RR per 1 SD increase = 1.10, 95% CI 0.93&ndash;1.30). No significant gender, smoking or age/time interactions were identified. PCV was the only significant predictor when all Coulter variables were studied jointly.</p>
<p><b>Conclusion</b> PCV was found to predict CHD mortality even after controlling for classical risk factors. This may give some insight into possible mechanisms, such as an influence on thrombin production.</p>
]]></description>
<dc:creator><![CDATA[Pizzi, C., De Stavola, B. L, Meade, T. W]]></dc:creator>
<dc:date>Mon, 13 Jul 2009 08:17:06 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp245</dc:identifier>
<dc:title><![CDATA[Long-term association of routine blood count (Coulter) variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-07-13</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp217v3?rss=1">
<title><![CDATA[Cohort Profile: The EPIC-NL study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp217v3?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Beulens, J. W J, Monninkhof, E. M, Verschuren, W M M., van der Schouw, Y. T, Smit, J., Ocke, M. C, Jansen, E. H J M, van Dieren, S., Grobbee, D. E, Peeters, P. H M, Bueno-de-Mesquita, H B.]]></dc:creator>
<dc:date>Wed, 08 Jul 2009 02:30:37 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp217</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The EPIC-NL study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-07-08</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp244v1?rss=1">
<title><![CDATA[Correlates of environmental factors and human plague: an ecological study in Vietnam]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp244v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Human plague caused by <I>Yersinia pestis</I> remains a public health threat in endemic countries, because the disease is associated with increased risk of mortality and severe economic and social consequences. During the past 10 years, outbreaks of plague have occasionally occurred in Vietnam's Central Highlands region. The present study sought to describe and analyse the occurrence of plague and its association with ecological factors.</p>
<p><b>Methods</b> The study included all 510 communes of the Central Highlands region (with a total population of ~4 million) where 95% of incidence of plague cases in Vietnam had been reported from 1997 through 2002. Plague was clinically ascertained by using a standard protocol by WHO. Data on domestic fleas and rodents were obtained by using traps and periodic surveillance in accordance with the WHO guidelines. Temperature, duration of sunshine, rainfall and humidity were recorded as monthly averages by local meteorological stations. The association between these ecological factors and plague was assessed by using the Poisson regression model.</p>
<p><b>Results</b> From 1997 through 2002, 472 cases of plague were reported, of whom 24 (5.1%) died. The incidence of plague peaked during the dry season, with ~63% of cases occurring from February through April. The risk of plague occurrence was associated with an increased monthly flea index (RR and 95% CI: 1.93; 1.61&ndash;2.33 for months with the flea index &gt;1) and increased rodent density (RR 1.23; 1.15&ndash;1.32 per each 3% increase in density). Moreover, the risk of plague increased during the dry season (RR 2.07; 1.64&ndash;2.62), when rainfall fell &lt;10 mm (RR 1.44; 1.17&ndash;1.77).</p>
<p><b>Conclusions</b> These data suggest that the flea index, rodent density and rainfall could be used as ecological indicators of plague risk in Vietnam. The data also suggest that the occurrence of plague in Vietnam's Central Highlands is likely resulted from multiple causes that remain to be delineated.</p>
]]></description>
<dc:creator><![CDATA[Pham, H. V, Dang, D. T, Tran Minh, N. N, Nguyen, N. D, Nguyen, T. V]]></dc:creator>
<dc:date>Tue, 07 Jul 2009 04:46:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp244</dc:identifier>
<dc:title><![CDATA[Correlates of environmental factors and human plague: an ecological study in Vietnam]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-07-07</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp241v1?rss=1">
<title><![CDATA[Evaluation of a pre-existing, 3-year household water treatment and handwashing intervention in rural Guatemala]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp241v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The promotion of household water treatment and handwashing with soap has led to large reductions in child diarrhoea in randomized efficacy trials. Currently, we know little about the health effectiveness of behaviour-based water and hygiene interventions after the conclusion of intervention activities.</p>
<p><b>Methods</b> We present an extension of previously published design (propensity score matching) and analysis (targeted maximum likelihood estimation) methods to evaluate the behavioural and health impacts of a pre-existing but non-randomized intervention (a 3-year, combined household water treatment and handwashing campaign in rural Guatemala). Six months after the intervention, we conducted a cross-sectional cohort study in 30 villages (15 intervention and 15 control) that included 600 households, and 929 children &lt;5 years of age.</p>
<p><b>Results</b> The study design created a sample of intervention and control villages that were comparable across more than 30 potentially confounding characteristics. The intervention led to modest gains in confirmed water treatment behaviour [risk difference = 0.05, 95% confidence interval (CI) 0.02&ndash;0.09]. We found, however, no difference between the intervention and control villages in self-reported handwashing behaviour, spot-check hygiene conditions, or the prevalence of child diarrhoea, clinical acute lower respiratory infections or child growth.</p>
<p><b>Conclusions</b> To our knowledge this is the first post-intervention follow-up study of a combined household water treatment and handwashing behaviour change intervention, and the first post-intervention follow-up of either intervention type to include child health measurement. The lack of child health impacts is consistent with unsustained behaviour adoption. Our findings highlight the difficulty of implementing behaviour-based household water treatment and handwashing outside of intensive efficacy trials.</p>
]]></description>
<dc:creator><![CDATA[Arnold, B., Arana, B., Mausezahl, D., Hubbard, A., Colford, J. M]]></dc:creator>
<dc:date>Thu, 02 Jul 2009 09:49:08 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp241</dc:identifier>
<dc:title><![CDATA[Evaluation of a pre-existing, 3-year household water treatment and handwashing intervention in rural Guatemala]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-07-02</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp248v1?rss=1">
<title><![CDATA[Commentary: Trends in indigenous inequalities in mortality in New Zealand]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp248v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Harper, S.]]></dc:creator>
<dc:date>Mon, 29 Jun 2009 07:08:56 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp248</dc:identifier>
<dc:title><![CDATA[Commentary: Trends in indigenous inequalities in mortality in New Zealand]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-29</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp237v1?rss=1">
<title><![CDATA[Predicting ambient ultraviolet from routine meteorological data; its potential use as an instrumental variable for vitamin D status in pregnancy in a longitudinal birth cohort in the UK]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp237v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Maternal vitamin D status in pregnancy has been postulated to have important effects on intrauterine development. UVB radiation is not commonly measured but is the prime determinant of circulating 25-hydroxyvitamin-D [25-(OH)D] and is highly dependent on regional weather including cloud cover, ozone and sunshine hours.</p>
<p><b>Methods</b> Using linear regression we described the relationship between estimated ambient-erythemal ultraviolet (eUV) exposure in Oxford (1990&ndash;95) and total hours of sunshine and month in order to forecast eUV in nearby regions, whilst adjusting for regional variations in weather. The forecast was validated with empirical data collected from Cornwall and then predicted for the Avon region. Total 98-day prenatal ambient-eUV was then predicted in 355 expectant mothers in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort and its relationship with maternal vitamin D status was determined.</p>
<p><b>Results</b> Estimated ambient-eUV was strongly associated with measured ambient-eUV (<I>r</I><sup>2</sup> = 0.989) with a near 1:1 prediction for the validation data set [<I>&beta;</I> = 0.99, 95% confidence interval (CI) 0.913, 1.067 <I>r</I><sup>2</sup> = 0.980]; strong seasonal associations were observed between eUV in the last trimester of pregnancy and maternal serum 25-(OH)D concentrations (<I>r</I><sup>2</sup> = 0.40).</p>
<p><b>Conclusion</b> This technique of prediction could be applied to existing cohorts allowing the relationship between maternal vitamin D status and the health of the offspring to be studied via instrumental variable analysis.</p>
]]></description>
<dc:creator><![CDATA[Sayers, A., Tilling, K., Boucher, B. J, Noonan, K., Tobias, J. H]]></dc:creator>
<dc:date>Mon, 29 Jun 2009 07:08:55 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp237</dc:identifier>
<dc:title><![CDATA[Predicting ambient ultraviolet from routine meteorological data; its potential use as an instrumental variable for vitamin D status in pregnancy in a longitudinal birth cohort in the UK]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-29</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp229v1?rss=1">
<title><![CDATA[Resting heart rate and blood pressure, independent of each other, proportionally raise the risk for type-2 diabetes mellitus]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp229v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Fast heart rate and high blood pressure (BP) at rest may raise risk for the development of type-2 diabetes mellitus (DM). We therefore investigated dose&ndash;response and interactive effects of resting heart rate and BP on the incidence of DM in a Japanese population.</p>
<p><b>Methods</b> A follow-up study was conducted for 16 828 men and 8368 women aged 30&ndash;59 years and apparently healthy at baseline. Incident DM was identified by &lsquo;fasting serum glucose &ge;7.00 mmol/l (126 mg/dl)&rsquo; or/and &lsquo;under medical treatment for DM&rsquo;. Using Cox proportional hazard models, hazard ratio (HR) for incident DM were estimated according to the quartiles of heart rate, systolic or diastolic BP (SBP, DBP), and its linear trends were checked by computing the three indices as continuous variables. Subsequently, interactive effects of slow/fast heart rate (dichotomized by the median) and low/high SBP or DBP (dichotomized by the median) on HR were examined. Baseline age, body mass index, smoking, drinking, exercise and education were computed as conventional confounders.</p>
<p><b>Results</b> During the follow-up of 125 106 person-years for men and 59 616 person-years for women, 869 men and 224 women developed DM. The multivariate-adjusted HR for incident DM increased across quartiles of heart rate, SBP and DBP in both sexes (linear trend <I>P</I>&lt;0.001 for all). Neither sex showed any significant interactive effects of heart rate and SBP or DBP on HR.</p>
<p><b>Conclusions</b> Resting heart rate and BP proportionally raise the risk for DM in middle-aged healthy men and women. Moreover, the adverse effects of fast heart rate and high BP are independent of each other as well as of the influences of conventional confounders.</p>
]]></description>
<dc:creator><![CDATA[Nagaya, T., Yoshida, H., Takahashi, H., Kawai, M.]]></dc:creator>
<dc:date>Mon, 29 Jun 2009 07:08:57 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp229</dc:identifier>
<dc:title><![CDATA[Resting heart rate and blood pressure, independent of each other, proportionally raise the risk for type-2 diabetes mellitus]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-29</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp233v1?rss=1">
<title><![CDATA[Cohort Profile: The Chinese national free antiretroviral treatment cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp233v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ma, Y., Zhang, F., Zhao, Y., Zang, C., Zhao, D., Dou, Z., Yu, L., Fang, H., Zhu, T. Y, Chen, R. Y]]></dc:creator>
<dc:date>Thu, 25 Jun 2009 05:24:22 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp233</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Chinese national free antiretroviral treatment cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-25</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp212v1?rss=1">
<title><![CDATA[Elevated serum creatine kinase predicts first-ever myocardial infarction: a 12-year population-based cohort study in Japan, the Suita study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp212v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In myocardial infarction (MI), it is well known that serum creatine kinase (s-CK) increases after onset, but it is unclear whether s-CK elevates before MI onset. The present analysis examined whether elevated s-CK levels predicted first-ever MI or stroke.</p>
<p><b>Methods</b> This study was a population-based cohort study in a Japanese urban area. Study subjects were comprised of 5026 initially healthy Japanese (2370 men and 2656 women, mean age: 54.5 years) without a history of MI or stroke. They were followed-up for 11.8 years on average, and 103 MIs (definite: 45; probable: 58) and 168 strokes (definite: 126; probable: 42) were observed. There was no subject who developed MI just at baseline (the follow-up period among those with definite MI was, at earliest, 0.20 years).</p>
<p><b>Results</b> The adjusted hazard ratio for definite MI was 4.18 (95% confidence interval 1.66&ndash;10.53) with s-CK levels of &ge;200 IU/l, compared with the reference category (s-CK levels of &le;99 IU/l), whereas no relationship was observed between s-CK levels and the risk for stroke. With regard to definite MI, an interaction between s-CK levels and dyslipidaemia was observed. Among subjects with hypercholesterolaemia, the hazard ratio linearly elevated with increased s-CK levels. On the other hand, no linear elevation was observed among subjects without hypercholesterolaemia (<I>P</I> for interaction = 0.011).</p>
<p><b>Conclusions</b> The present study suggested that screening for elevated s-CK levels in initially healthy Japanese subjects was useful to predict first-ever MI in the future, especially in subjects with dyslipidaemia.</p>
]]></description>
<dc:creator><![CDATA[Watanabe, M., Okamura, T., Kokubo, Y., Higashiyama, A., Okayama, A.]]></dc:creator>
<dc:date>Thu, 25 Jun 2009 05:24:21 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp212</dc:identifier>
<dc:title><![CDATA[Elevated serum creatine kinase predicts first-ever myocardial infarction: a 12-year population-based cohort study in Japan, the Suita study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-25</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp239v1?rss=1">
<title><![CDATA[Commentary: How does 'insurance' improve equity in health?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp239v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Starfield, B.]]></dc:creator>
<dc:date>Tue, 23 Jun 2009 22:42:18 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp239</dc:identifier>
<dc:title><![CDATA[Commentary: How does 'insurance' improve equity in health?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-23</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp235v1?rss=1">
<title><![CDATA[Commentary: Environmental determinants of dimorphic systemic mycoses--the macro and the micro]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp235v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Baumgardner, D. J]]></dc:creator>
<dc:date>Mon, 15 Jun 2009 06:06:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp235</dc:identifier>
<dc:title><![CDATA[Commentary: Environmental determinants of dimorphic systemic mycoses--the macro and the micro]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-15</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp216v1?rss=1">
<title><![CDATA[Cohort Profile: The German uranium miners cohort study (WISMUT cohort), 1946-2003]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp216v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kreuzer, M., Schnelzer, M., Tschense, A., Walsh, L., Grosche, B.]]></dc:creator>
<dc:date>Wed, 03 Jun 2009 10:13:54 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp216</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The German uranium miners cohort study (WISMUT cohort), 1946-2003]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-03</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp221v1?rss=1">
<title><![CDATA[Neighbourhood food environment and area deprivation: spatial accessibility to grocery stores selling fresh fruit and vegetables in urban and rural settings]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp221v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The &lsquo;deprivation amplification&rsquo; hypothesis suggests that residents of deprived neighbourhoods have universally poorer access to high-quality food environments, which in turn contributes to the development of spatial inequalities in diet and diet-related chronic disease. This paper presents results from a study that quantified access to grocery stores selling fresh fruit and vegetables in four environmental settings in Scotland, UK.</p>
<p><b>Methods</b> Spatial accessibility, as measured by network travel times, to 457 grocery stores located in 205 neighbourhoods in four environmental settings (island, rural, small town and urban) in Scotland was calculated using Geographical Information Systems. The distribution of accessibility by neighbourhood deprivation in each of these four settings was investigated.</p>
<p><b>Results</b> Overall, the most deprived neighbourhoods had the best access to grocery stores and grocery stores selling fresh produce. Stratified analysis by environmental setting suggests that the least deprived compared with the most deprived urban neighbourhoods have greater accessibility to grocery stores than their counterparts in island, rural and small town locations. Access to fresh produce is better in more deprived compared with less deprived urban and small town neighbourhoods, but poorest in the most affluent island communities with mixed results for rural settings.</p>
<p><b>Conclusions</b> The results presented here suggest that the assumption of a universal &lsquo;deprivation amplification&rsquo; hypothesis in studies of the neighbourhood food environment may be misguided. Associations between neighbourhood deprivation and grocery store accessibility vary by environmental setting. Theories and policies aimed at understanding and rectifying spatial inequalities in the distribution of neighbourhood exposures for poor diet need to be context specific.</p>
]]></description>
<dc:creator><![CDATA[Smith, D. M, Cummins, S., Taylor, M., Dawson, J., Marshall, D., Sparks, L., Anderson, A. S]]></dc:creator>
<dc:date>Tue, 02 Jun 2009 09:57:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp221</dc:identifier>
<dc:title><![CDATA[Neighbourhood food environment and area deprivation: spatial accessibility to grocery stores selling fresh fruit and vegetables in urban and rural settings]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-02</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp220v1?rss=1">
<title><![CDATA[Politics or policies vs politics and policies: a comment on Lundberg]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp220v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Muntaner, C., Borrell, C., Espelt, A., RodrIguez-sanz, M., PasarIn, M I., Benach, J, Navarro, V.]]></dc:creator>
<dc:date>Tue, 02 Jun 2009 09:57:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp220</dc:identifier>
<dc:title><![CDATA[Politics or policies vs politics and policies: a comment on Lundberg]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-02</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp213v1?rss=1">
<title><![CDATA[How willing are the public to pay for anti-hypertensive drugs for primary prevention of cardiovascular disease: a survey in a Chinese city]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp213v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Current recommendations on drug treatment of hypertension for primary prevention of cardiovascular disease are primarily determined by the evidence of effectiveness, disregard the resources available and values of people, and recommend a universally fixed risk cutoff for initiating drug treatment. The guidelines may have over-estimated the willingness of the public to accept and pay for these drugs and a fixed cutoff may not fit all populations. Moreover, the public may have been misinformed and are unable to make the right decision even if they are consulted. We conducted this study to address these issues and to describe the gap between current policy and what the public truly want.</p>
<p><b>Methods</b> A cross-sectional survey with face-to-face interviews of rural and urban residents in northern China. Before providing any information, we asked the residents whether they would accept drug treatment if they had hypertension and also asked them to estimate the 5-year cardiovascular risk in untreated hypertension and the benefits from anti-hypertensive drugs. We then informed the participants of necessary information and asked them above what benefit they would be willing to pay the current cost, and how much they would be willing to pay for the actual benefit, for anti-hypertensive drugs out of pocket.</p>
<p><b>Results</b> Eight hundred and eighty-seven rural residents and 921 urban residents were interviewed with a response rate of 97%. Ninety-five percent [95% confidence interval (CI) 94&ndash;96%] of the residents said they would take anti-hypertensive drugs if they had hypertension, although 91% (95% CI 89&ndash;92%) said they did not have sufficient knowledge to make a decision. Seventy-eight percent (95% CI 76&ndash;80%) believed that anti-hypertensive drugs were primarily to lower blood pressure or relieve symptoms. They over-estimated the cardiovascular risk of untreated hypertension by approximately 12 times and the absolute benefit of drug treatment by 20 times. Given the actual absolute benefit of the drugs, only 23% (95% CI 21&ndash;25%) were willing to pay the current annual cost of $500 Ren Min Bi (US$73.3, 54.8 as of 8 May 2009) for these drugs. Given the current cost, they were, on average, willing to pay for the drugs only when the 5-year cardiovascular disease risk was as high as 35% (95% CI 31&ndash;38%) or even higher.</p>
<p><b>Conclusion</b> The public in China are significantly misinformed and considerably over estimate the risk of hypertension and the benefit of treatment. The public's willingness to pay for anti-hypertensive drugs is much lower than the current guidelines implicitly assume. The willingness to pay should be considered, along with other factors, when prescribing anti-hypertensive drugs to an individual patient or making hypertension guidelines for a population.</p>
]]></description>
<dc:creator><![CDATA[Tang, J.-L., Wang, W.-Z., An, J.-G., Hu, Y.-H., Cheng, S.-H., Griffiths, S.]]></dc:creator>
<dc:date>Tue, 02 Jun 2009 09:57:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp213</dc:identifier>
<dc:title><![CDATA[How willing are the public to pay for anti-hypertensive drugs for primary prevention of cardiovascular disease: a survey in a Chinese city]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-02</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp215v1?rss=1">
<title><![CDATA[Cohort profile: Survey of Families, Income and Employment (SoFIE) and Health Extension (SoFIE-health)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp215v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Carter, K. N, Cronin, M., Blakely, T., Hayward, M., Richardson, K.]]></dc:creator>
<dc:date>Thu, 28 May 2009 09:21:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp215</dc:identifier>
<dc:title><![CDATA[Cohort profile: Survey of Families, Income and Employment (SoFIE) and Health Extension (SoFIE-health)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-28</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp205v2?rss=1">
<title><![CDATA[Cohort profile: The China Jintan Child Cohort Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp205v2?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Liu, J., McCauley, L. A, Zhao, Y., Zhang, H., Pinto-Martin, J., Jintan Cohort Study Group]]></dc:creator>
<dc:date>Mon, 18 May 2009 23:08:44 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp205</dc:identifier>
<dc:title><![CDATA[Cohort profile: The China Jintan Child Cohort Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-18</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp208v1?rss=1">
<title><![CDATA[Anti-retroviral therapy reduces incident tuberculosis in HIV-infected children]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp208v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> We aimed to estimate the effect of anti-retroviral therapy (ART) on incident tuberculosis (TB) in a cohort of HIV-infected children.</p>
<p><b>Methods</b> We analysed data from ART-na&iuml;ve, TB disease-free children enrolled between December 2004 and April 2008 into an HIV care program in Kinshasa, Democratic Republic of Congo. To estimate the effect of ART on TB incidence while accounting for time-dependent confounders affected by exposure, a Cox proportional hazards marginal structural model was used.</p>
<p><b>Results</b> 364 children contributed 596.0 person-years of follow-up. At baseline, the median age was 6.9 years; 163 (44.8%) were in HIV clinical stage 3 or 4. During follow-up, 242 (66.5%) children initiated ART and 81 (22.3%) developed TB. At TB diagnosis, 41 (50.6%) were receiving ART. The TB incidence rate in those receiving ART was 10.2 per 100 person-years [95% confidence interval (CI) 7.4&ndash;13.9] compared with 20.4 per 100 person-years (95% CI 14.6&ndash;27.8) in those receiving only primary HIV care. TB incidence decreased with time on ART, from 18.9 per 100 person-years in the first 6 months to 5.3 per 100 person-years after 12 months of ART. The model-estimated TB hazard ratio for ART was 0.51 (95% CI 0.27&ndash;0.94).</p>
<p><b>Conclusions</b> For HIV-infected children in TB-endemic areas, ART reduces the hazard of developing TB by 50%.</p>
]]></description>
<dc:creator><![CDATA[Edmonds, A., Lusiama, J., Napravnik, S., Kitetele, F., Van Rie, A., Behets, F.]]></dc:creator>
<dc:date>Fri, 15 May 2009 09:43:42 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp208</dc:identifier>
<dc:title><![CDATA[Anti-retroviral therapy reduces incident tuberculosis in HIV-infected children]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-15</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp207v1?rss=1">
<title><![CDATA[Climate and acute/subacute paracoccidioidomycosis in a hyper-endemic area in Brazil]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp207v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Paracoccidioidomycosis (PCM) is Latin America's most prevalent systemic mycosis, carrying an important social burden. Its agent, <I>Paracoccidioides brasiliensis</I>, has rarely been identified in nature. Studies characterizing acute/subacute PCM incidence and their relationship with climate variables are not available. This work analysed a series of acute/subacute cases that occurred in the Botucatu area, S&atilde;o Paulo State, Brazil, from 1969 to 1999, as an outcome of weather variability.</p>
<p><b>Methods</b> Stepwise regression of annual data was applied to model incidence, calculated based on 91 cases, from lagged variables: antecedent precipitation, air temperature, soil water storage, absolute and relative air humidity, and Southern Oscillation Index (SOI).</p>
<p><b>Results</b> Multiple regression analyses resulted in a model, which explains 49% of the incidence variance, taking into account the absolute air humidity in the year of exposure, soil water storage and SOI of the previous 2 years.</p>
<p><b>Conclusions</b> The correlations may reflect enhanced fungal growth after increase in soil water storage in the longer term and greater spore release with increase in absolute air humidity in the short term.</p>
]]></description>
<dc:creator><![CDATA[Barrozo, L. V, Mendes, R. P, Marques, S. A, Benard, G., Silva, M. E S., Bagagli, E.]]></dc:creator>
<dc:date>Mon, 11 May 2009 09:24:56 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp207</dc:identifier>
<dc:title><![CDATA[Climate and acute/subacute paracoccidioidomycosis in a hyper-endemic area in Brazil]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-11</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp200v1?rss=1">
<title><![CDATA[Elevated maternal cortisol levels during pregnancy are associated with reduced childhood IQ]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp200v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In animal models, there is evidence to suggest a causal link between maternal cortisol levels during pregnancy and offspring outcomes; however, evidence for this relationship in humans is inconclusive. We address important confounders of this association by estimating the relationship between maternal cortisol levels in late pregnancy and childhood IQ in a birth cohort and in a subsample of siblings.</p>
<p><b>Methods</b> This study included 832 children who were members of the Collaborative Perinatal Project. Maternal serum collected between 1959 and 1966 during the third trimester of pregnancy was analysed for free cortisol. We investigated the relationship between maternal cortisol in quintiles and full, verbal and performance scale scores on the Wechsler Intelligence Scale for Children at age 7 years, adjusting for prenatal and family characteristics. We repeated this analysis among 74 discordant sibling pairs using a fixed effects approach, which adjusts for shared family characteristics.</p>
<p><b>Results</b> Maternal cortisol levels were negatively related to full-scale IQ, an effect driven by verbal IQ scores. Compared with those in the lowest quintile of cortisol exposure, the verbal IQ of children in the highest quintile of exposure was 3.83 points lower [95% confidence interval (CI): &ndash;6.44 to &ndash;1.22]. Within sibling pairs, being in the highest quintile of exposure was associated with verbal IQ scores 5.5 points lower (95% CI: &ndash;11.24 to 0.31) compared with the other quintiles.</p>
<p><b>Conclusion</b> These findings are consistent with prior human and animal studies, and suggest that exposure to high levels of maternal cortisol during pregnancy may be negatively related to offspring cognitive skills independently of family attributes that characterize the postnatal environment.</p>
]]></description>
<dc:creator><![CDATA[LeWinn, K. Z, Stroud, L. R, Molnar, B. E, Ware, J. H, Koenen, K. C, Buka, S. L]]></dc:creator>
<dc:date>Thu, 07 May 2009 07:44:23 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp200</dc:identifier>
<dc:title><![CDATA[Elevated maternal cortisol levels during pregnancy are associated with reduced childhood IQ]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-07</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp192v1?rss=1">
<title><![CDATA[Intervening on risk factors for coronary heart disease: an application of the parametric g-formula]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp192v1?rss=1</link>
<description><![CDATA[
<p>Estimating the population risk of disease under hypothetical interventions&mdash;such as the population risk of coronary heart disease (CHD) were everyone to quit smoking and start exercising or to start exercising if diagnosed with diabetes&mdash;may not be possible using standard analytic techniques. The parametric g-formula, which appropriately adjusts for time-varying confounders affected by prior exposures, is especially well suited to estimating effects when the intervention involves multiple factors (joint interventions) or when the intervention involves decisions that depend on the value of evolving time-dependent factors (dynamic interventions). We describe the parametric g-formula, and use it to estimate the effect of various hypothetical lifestyle interventions on the risk of CHD using data from the Nurses&rsquo; Health Study. Over the period 1982&ndash;2002, the 20-year risk of CHD in this cohort was 3.50%. Under a joint intervention of no smoking, increased exercise, improved diet, moderate alcohol consumption and reduced body mass index, the estimated risk was 1.89% (95% confidence interval: 1.46&ndash;2.41). We discuss whether the assumptions required for the validity of the parametric g-formula hold in the Nurses&rsquo; Health Study data. This work represents the first large-scale application of the parametric g-formula in an epidemiologic cohort study.</p>
]]></description>
<dc:creator><![CDATA[Taubman, S. L, Robins, J. M, Mittleman, M. A, Hernan, M. A]]></dc:creator>
<dc:date>Thu, 23 Apr 2009 09:35:39 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp192</dc:identifier>
<dc:title><![CDATA[Intervening on risk factors for coronary heart disease: an application of the parametric g-formula]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-23</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp198v1?rss=1">
<title><![CDATA[Author's Response: Response to commentary: Meningioma and mobile phone use--a collaborative case-control study in five North European countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp198v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Auvinen, A., Lahkola, A., Feychting, M., Swerdlow, A. J, Johansen, C., Tynes, T., on behalf of the authors]]></dc:creator>
<dc:date>Wed, 22 Apr 2009 10:07:15 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp198</dc:identifier>
<dc:title><![CDATA[Author's Response: Response to commentary: Meningioma and mobile phone use--a collaborative case-control study in five North European countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-22</prism:publicationDate>
<prism:section>Author's Response</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp197v1?rss=1">
<title><![CDATA[Reader's Response: Meningioma and mobile phone use--a collaborative case-control study in five North European countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp197v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Morgan, L L.]]></dc:creator>
<dc:date>Wed, 22 Apr 2009 10:07:14 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp197</dc:identifier>
<dc:title><![CDATA[Reader's Response: Meningioma and mobile phone use--a collaborative case-control study in five North European countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-22</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp196v1?rss=1">
<title><![CDATA[Meningioma and mobile phone use]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp196v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Milham, S.]]></dc:creator>
<dc:date>Wed, 22 Apr 2009 10:07:14 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp196</dc:identifier>
<dc:title><![CDATA[Meningioma and mobile phone use]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-22</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp193v1?rss=1">
<title><![CDATA[Breast cancer survival in Canada and the USA: meta-analytic evidence of a Canadian advantage in low-income areas]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp193v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This study tested the hypothesis that relatively poor Canadian women with breast cancer have a survival advantage over their counterparts in the USA.</p>
<p><b>Methods</b> Seventy-eight independent retrospective cohort (incidence between 1984 and 2000, followed until 2006) outcomes were synthesized. Fixed effects meta-regression models compared women with breast cancer in low-income areas of Canada and the USA.</p>
<p><b>Results</b> Low-income Canadian women were advantaged on survival [rate ratio (RR) = 1.14; 95% confidence interval (CI) 1.13&ndash;1.15] and their advantage was even larger among women &lt;65 years of age who are not yet eligible for Medicare coverage in the USA (RR = 1.21, 95% CI 1.18&ndash;1.24). Canadian advantages were also larger for node positive breast cancer, which may present with greater clinical and managerial discretion (RR = 1.40, 95% CI 1.30&ndash;1.50), and smaller when Hawaii, the state providing the most Canadian-like access, was the US comparator (RR = 1.12, 95% CI 1.01&ndash;1.20).</p>
<p><b>Conclusions</b> More inclusive health care insurance coverage in Canada vs the USA, particularly among each country's relatively poor people, seems the most plausible explanation for such Canadian advantages. Provision of health care for all Americans would likely prevent countless early deaths, particularly among the relatively poor.</p>
]]></description>
<dc:creator><![CDATA[Gorey, K. M]]></dc:creator>
<dc:date>Wed, 22 Apr 2009 10:07:13 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp193</dc:identifier>
<dc:title><![CDATA[Breast cancer survival in Canada and the USA: meta-analytic evidence of a Canadian advantage in low-income areas]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-22</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp191v1?rss=1">
<title><![CDATA[Dietary patterns and the risk of mortality: impact of cardiorespiratory fitness]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp191v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> While dietary patterns that are both predictive of chronic disease and mortality have been identified, the confounding effects of cardiorespiratory fitness have not been properly addressed. The primary objective was to assess the relation between dietary patterns with all-cause mortality, while controlling for the potentially confounding effects of fitness.</p>
<p><b>Methods</b> This was a prospective cohort study. Participants consisted of 13 621 men and women from the Aerobics Center Longitudinal Study (ACLS). Participants completed a clinical exam and 3-day diet record between 1987 and 1999. Participants were followed for mortality until 2003. Reduced rank regression (RRR) was used to identify dietary patterns that predicted unfavourable total and high-density lipoprotein-cholesterol, triglyceride, glucose, blood pressure, uric acid, white blood cell and body mass index values.</p>
<p><b>Results</b> One primary dietary pattern emerged and was labelled the Unhealthy Eating Index. This pattern was characterized by elevated consumption of processed and red meat, white potato products, non-whole grains, added fat and reduced consumption of non-citrus fruits. The hazard ratio for all-cause mortality in the fifth vs the first quintile of the Unhealthy Eating Index was 1.40 (1.02&ndash;1.91). This risk estimate was reduced by 13.5 and 55.0% after controlling for self-reported physical activity and fitness, respectively.</p>
<p><b>Conclusion</b> In this study the association between diet and overall mortality was, in large part, confounded by fitness.</p>
]]></description>
<dc:creator><![CDATA[Heroux, M., Janssen, I., Lam, M., Lee, D.-c., Hebert, J. R, Sui, X., Blair, S. N]]></dc:creator>
<dc:date>Mon, 20 Apr 2009 02:06:46 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp191</dc:identifier>
<dc:title><![CDATA[Dietary patterns and the risk of mortality: impact of cardiorespiratory fitness]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-20</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp186v1?rss=1">
<title><![CDATA[Cohort Profile: The Metabolic syndrome and Cancer project (Me-Can)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp186v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stocks, T., Borena, W., Strohmaier, S., Bjorge, T., Manjer, J., Engeland, A., Johansen, D., Selmer, R., Hallmans, G., Rapp, K., Concin, H., Jonsson, H., Ulmer, H., Stattin, P.]]></dc:creator>
<dc:date>Mon, 20 Apr 2009 02:06:45 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp186</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Metabolic syndrome and Cancer project (Me-Can)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-20</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp189v1?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp189v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Vandenbroucke, J. P]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 08:28:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp189</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-17</prism:publicationDate>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp188v1?rss=1">
<title><![CDATA[Acknowledge and fix the multiple testing problem]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp188v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Young, F. S S]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 08:28:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp188</dc:identifier>
<dc:title><![CDATA[Acknowledge and fix the multiple testing problem]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-17</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp174v1?rss=1">
<title><![CDATA[How to assess the external validity of therapeutic trials: a conceptual approach]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp174v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> External validity of study results is an important issue from a clinical point of view. From a methodological point of view, however, the concept of external validity is more complex than it seems to be at first glance.</p>
<p><b>Methods</b> Methodological review to address the concept of external validity.</p>
<p><b>Results</b> External validity refers to the question whether results are generalizable to persons other than the population in the original study. The only formal way to establish the external validity would be to repeat the study for that specific target population. We propose a three-way approach for assessing the external validity for specified target populations. (i) The study population might not be representative for the eligibility criteria that were intended. It should be addressed whether the study population differs from the intended source population with respect to characteristics that influence outcome. (ii) The target population will, by definition, differ from the study population with respect to geographical, temporal and ethnical conditions. Pondering external validity means asking the question whether these differences may influence study results. (iii) It should be assessed whether the study's conclusions can be generalized to target populations that do not meet all the eligibility criteria.</p>
<p><b>Conclusion</b> Judging the external validity of study results cannot be done by applying given eligibility criteria to a single target population. Rather, it is a complex reflection in which prior knowledge, statistical considerations, biological plausibility and eligibility criteria all have place.</p>
]]></description>
<dc:creator><![CDATA[Dekkers, O M, Elm, E v., Algra, A, Romijn, J A, Vandenbroucke, J P]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 08:28:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp174</dc:identifier>
<dc:title><![CDATA[How to assess the external validity of therapeutic trials: a conceptual approach]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-17</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp173v1?rss=1">
<title><![CDATA[Cohort Profile: Risk patterns and processes for psychopathology emerging during adolescence: the ROOTS project]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp173v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Goodyer, I. M, Croudace, T., Dunn, V., Herbert, J., Jones, P. B]]></dc:creator>
<dc:date>Wed, 08 Apr 2009 23:28:34 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp173</dc:identifier>
<dc:title><![CDATA[Cohort Profile: Risk patterns and processes for psychopathology emerging during adolescence: the ROOTS project]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-08</prism:publicationDate>
<prism:section>COHORT PROFILE</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp158v1?rss=1">
<title><![CDATA[Author's: Response Heterogeneity metrics: not perfect, but would not abandon]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp158v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Patsopoulos, N. A, Ioannidis, J. P A]]></dc:creator>
<dc:date>Mon, 06 Apr 2009 10:47:17 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp158</dc:identifier>
<dc:title><![CDATA[Author's: Response Heterogeneity metrics: not perfect, but would not abandon]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-06</prism:publicationDate>
<prism:section>Author's Response</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp157v1?rss=1">
<title><![CDATA[Comment on: heterogeneity in meta-analysis should be expected and appropriately quantified]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp157v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Coory, M. D]]></dc:creator>
<dc:date>Mon, 06 Apr 2009 10:47:16 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp157</dc:identifier>
<dc:title><![CDATA[Comment on: heterogeneity in meta-analysis should be expected and appropriately quantified]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-06</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp155v1?rss=1">
<title><![CDATA[Cohort Profile: The Scottish Health Surveys Cohort: linkage of study participants to routinely collected records for mortality, hospital discharge, cancer and offspring birth characteristics in three nationwide studies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp155v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Gray, L., Batty, G D., Craig, P., Stewart, C., Whyte, B., Finlayson, A., Leyland, A. H]]></dc:creator>
<dc:date>Mon, 06 Apr 2009 10:47:16 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp155</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Scottish Health Surveys Cohort: linkage of study participants to routinely collected records for mortality, hospital discharge, cancer and offspring birth characteristics in three nationwide studies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-06</prism:publicationDate>
<prism:section>COHORT PROFILE</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp147v1?rss=1">
<title><![CDATA[A systematic review of chronic fatigue, its syndromes and ethnicity: prevalence, severity, co-morbidity and coping]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp147v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Chronic Fatigue Syndrome (CFS) is characterized by unexplained fatigue that lasts for at least 6 months alongside a constellation of other symptoms. CFS was historically thought to be most common among White women of higher socio-economic status. However, some recent studies in the USA suggest that the prevalence is actually higher in some minority ethnic groups. If there are convincing differences in prevalence and risk factors across all or some ethnic groups, investigating the causes of these can help unravel the pathophysiology of CFS.</p>
<p><b>Methods</b> A systematic review was conducted to explore the relationship between fatigue, chronic fatigue (CF&mdash;fatigue lasting for 6 months), CFS and ethnicity. Studies were population-based and health service-based. Meta-analysis was also conducted to examine the population prevalence of CF and CFS across ethnic groups.</p>
<p><b>Results</b> Meta-analysis showed that compared with the White American majority, African Americans and Native Americans have a higher risk of CFS [Odds Ratio (OR) 2.95, 95% confidence interval (CI): 0.69&ndash;10.4; OR = 11.5, CI: 1.1&ndash;56.4, respectively] and CF (OR = 1.56, CI: 1.03&ndash;2.24; OR = 3.28, CI: 1.63&ndash;5.88, respectively). Minority ethnic groups with CF and CFS experience more severe symptoms and may be more likely to use religion, denial and behavioural disengagement to cope with their condition compared with the White majority.</p>
<p><b>Conclusions</b> Although available studies and data are limited, it does appear that some ethnic minority groups are more likely to suffer from CF and CFS compared with White people. Ethnic minority status alone is insufficient to explain ethnic variation of prevalence. Psychosocial risk factors found in high-risk groups and ethnicity warrant further investigation to improve our understanding of aetiology and the management of this complex condition.</p>
]]></description>
<dc:creator><![CDATA[Dinos, S., Khoshaba, B., Ashby, D., White, P. D, Nazroo, J., Wessely, S., Bhui, K. S]]></dc:creator>
<dc:date>Mon, 06 Apr 2009 10:47:15 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp147</dc:identifier>
<dc:title><![CDATA[A systematic review of chronic fatigue, its syndromes and ethnicity: prevalence, severity, co-morbidity and coping]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-06</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp005v1?rss=1">
<title><![CDATA[Environmental Epidemiology--Principles and Methods. RM Merrill.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp005v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Huss, A.]]></dc:creator>
<dc:date>Mon, 06 Apr 2009 10:47:13 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp005</dc:identifier>
<dc:title><![CDATA[Environmental Epidemiology--Principles and Methods. RM Merrill.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-06</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp165v1?rss=1">
<title><![CDATA[Cohort Profile: Mamanengane or the Africa Centre Vertical Transmission Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp165v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bland, R., Coovadia, H., Coutsoudis, A, Rollins, N., Newell, M.]]></dc:creator>
<dc:date>Tue, 31 Mar 2009 00:11:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp165</dc:identifier>
<dc:title><![CDATA[Cohort Profile: Mamanengane or the Africa Centre Vertical Transmission Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-31</prism:publicationDate>
<prism:section>COHORT PROFILE</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp161v1?rss=1">
<title><![CDATA[Cohort Profile: The Golestan Cohort Study--a prospective study of oesophageal cancer in northern Iran]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp161v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pourshams, A., Khademi, H., Malekshah, A. F., Islami, F., Nouraei, M., Sadjadi, A. R., Jafari, E., Rakhshani, N., Salahi, R., Semnani, S., Kamangar, F., Abnet, C. C, Ponder, B., Day, N., Dawsey, S. M, Boffetta, P., Malekzadeh, R.]]></dc:creator>
<dc:date>Mon, 30 Mar 2009 07:18:39 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp161</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Golestan Cohort Study--a prospective study of oesophageal cancer in northern Iran]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-30</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp156v1?rss=1">
<title><![CDATA[Changing trends in indigenous inequalities in mortality: lessons from New Zealand]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp156v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> We describe trends from 1951 to 2006 in inequalities in mortality between the indigenous (Maori) and non-indigenous (non-Maori, mainly European-descended) populations of New Zealand. We relate these trends to the historical context in which they occurred, including major structural adjustment of the economy from the mid 1980s to the mid 1990s, followed by a retreat from neoliberal social and economic policies from the late 1990s onwards. This was accompanied by economic recovery and the introduction of health reforms, including a reorientation of the health system towards primary health care.</p>
<p><b>Methods</b> Abridged period lifetables for Maori and non-Maori from 1951 to 2006 were constructed using standard demographic methods. Absolute [standardized rate difference (SRD)] and relative [standardized rate ratio (SRR)] mortality inequalities for Maori compared with European/Other ethnic groups (aged 1&ndash;74 years) were measured using the New Zealand Census-Mortality Study (an ongoing data linkage study that links mortality to census records) from 1981&ndash;84 to 2001&ndash;04. The SRDs were decomposed into their contributions from major causes of death. Poisson regression modelling was used to estimate the extent of socio-economic mediation of the ethnic mortality inequality over time.</p>
<p><b>Results</b> Life expectancy gaps and relative inequalities in mortality rates (aged 1&ndash;74 years) widened and then narrowed again, in tandem with the trends in social inequalities (allowing for a short lag). Among females, the contribution of cardiovascular disease to absolute mortality inequalities steadily decreased, but was partly offset by an increasing contribution from cancer. Among males, the contribution of CVD increased from the early 1980s to the 1990s, then decreased again. The extent of socio-economic mediation of the ethnic mortality inequality peaked in 1991&ndash;94, again more notably among males.</p>
<p><b>Conclusion</b> Our results are consistent with a causal association between changing economic inequalities and changing health inequalities between ethnic groups. However, causality cannot be established from a historical analysis alone. Three lessons nevertheless emerge from the New Zealand experience: the lag between changes in ethnic social inequality and ethnic health inequality may be short (&lt;5 years); both changes in the distribution of the social determinants of health and an appropriate health system response may be required to address ethnic health inequalities; and timely monitoring of ethnic health inequalities, based on high-quality ethnicity data, may help to sustain political commitment to pro-equity health and social policies.</p>
]]></description>
<dc:creator><![CDATA[Tobias, M., Blakely, T., Matheson, D., Rasanathan, K., Atkinson, J.]]></dc:creator>
<dc:date>Mon, 30 Mar 2009 07:18:38 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp156</dc:identifier>
<dc:title><![CDATA[Changing trends in indigenous inequalities in mortality: lessons from New Zealand]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-30</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp152v1?rss=1">
<title><![CDATA[Are republicans healthier than democrats?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp152v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Subramanian, S V, Perkins, J. M]]></dc:creator>
<dc:date>Thu, 05 Mar 2009 06:30:51 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp152</dc:identifier>
<dc:title><![CDATA[Are republicans healthier than democrats?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-05</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn258v1?rss=1">
<title><![CDATA[Environmental and societal influences acting on cardiovascular risk factors and disease at a population level: a review]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn258v1?rss=1</link>
<description><![CDATA[
<p>It has long been known that cardiovascular disease (CVD) rates vary considerably among populations, across space and through time. It is now apparent that most of the attributable risk for myocardial infarction &lsquo;within&rsquo; populations from across the world can be ascribed to the varying levels of a limited number of risk factors among individuals in a population. Individual risk factors (e.g. blood pressure) can be modified with resulting health gains. Yet, the persistence of large international variations in cardiovascular risk factors and resulting CVD incidence and mortality indicates that there are additional factors that apply to &lsquo;populations&rsquo; that are important to understand as part of a comprehensive approach to CVD control. This article reviews the evidence on why certain populations are more at risk than others.</p>
]]></description>
<dc:creator><![CDATA[Chow, C. K., Lock, K., Teo, K., Subramanian, S., McKee, M., Yusuf, S.]]></dc:creator>
<dc:date>Wed, 04 Mar 2009 01:52:57 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn258</dc:identifier>
<dc:title><![CDATA[Environmental and societal influences acting on cardiovascular risk factors and disease at a population level: a review]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-04</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn247v1?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn247v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ebrahim, S.]]></dc:creator>
<dc:date>Mon, 02 Mar 2009 02:31:56 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn247</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-02</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn246v1?rss=1">
<title><![CDATA[Chronic diseases and calls to action]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn246v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[De Backer, G., Kornitzer, M]]></dc:creator>
<dc:date>Mon, 02 Mar 2009 02:31:56 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn246</dc:identifier>
<dc:title><![CDATA[Chronic diseases and calls to action]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-02</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn245v1?rss=1">
<title><![CDATA[Chronic disease prevention: the importance of calls to action]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn245v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Asaria, P., Beaglehole, R., Chisholm, D., Gaziano, T. A, Horton, R., Leeder, S., Lim, S. S., Mathers, C., Reddy, S., Strong, K., Voute, J.]]></dc:creator>
<dc:date>Mon, 02 Mar 2009 02:31:55 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn245</dc:identifier>
<dc:title><![CDATA[Chronic disease prevention: the importance of calls to action]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-02</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp149v1?rss=1">
<title><![CDATA[Bad Science. Ben Goldacre.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp149v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lefanu, J.]]></dc:creator>
<dc:date>Wed, 25 Feb 2009 05:00:15 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp149</dc:identifier>
<dc:title><![CDATA[Bad Science. Ben Goldacre.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-02-25</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp138v1?rss=1">
<title><![CDATA[Adverse Reactions. The Fenoterol Story. Neil Pearce.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp138v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Anderson, H. R.]]></dc:creator>
<dc:date>Wed, 11 Feb 2009 05:18:16 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp138</dc:identifier>
<dc:title><![CDATA[Adverse Reactions. The Fenoterol Story. Neil Pearce.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-02-11</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp003v1?rss=1">
<title><![CDATA[Are children born to light drinkers not at high risk of developing clinically relevant cognitive-behavioural problems? A response to Kelly et al.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp003v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kodituwakku, P. W, Ceccanti, M.]]></dc:creator>
<dc:date>Tue, 03 Feb 2009 03:59:02 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp003</dc:identifier>
<dc:title><![CDATA[Are children born to light drinkers not at high risk of developing clinically relevant cognitive-behavioural problems? A response to Kelly et al.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-02-03</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn376v1?rss=1">
<title><![CDATA[The effect of temperature on mortality in rural Bangladesh--a population-based time-series study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn376v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Studies in urban cities have consistently shown evidence of increased mortality in association with hot and cold weather. However, few studies have examined temperature&ndash;mortality relationship in the rural areas of developing countries. In this study we therefore aimed to characterize the daily temperature&ndash;mortality relationships in rural Bangladesh.</p>
<p><b>Methods</b> A generalized linear Poisson regression model was used to regress a time-series of daily mortality for all-cause and selected causes against temperature, controlling for seasonal and interannual variations, day of week and public holidays. A total of 13 270 all-cause deaths excluding external causes for residents under demographic surveillance in Matlab, Bangladesh were available between January 1994 and December 2002.</p>
<p><b>Results</b> There was a marked increase in all-cause deaths and deaths due to cardiovascular, respiratory and perinatal causes at low temperatures over a lag of 0&ndash;13 days. Every 1&deg;C decrease in mean temperature was associated with a 3.2% (95% CI 0.9&ndash;5.5) increase in all-cause mortality. However, there was no clear heat effect on all-cause mortality for any of the lags examined.</p>
<p><b>Conclusions</b> This study found that daily mortality increased with low temperatures in the preceding weeks, while there was no association found between high temperatures and daily mortality in rural Bangladesh. Preventive measures during low temperatures should be considered especially for young infants.</p>
]]></description>
<dc:creator><![CDATA[Hashizume, M., Wagatsuma, Y., Hayashi, T., Saha, S. K, Streatfield, K., Yunus, M.]]></dc:creator>
<dc:date>Fri, 30 Jan 2009 06:18:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn376</dc:identifier>
<dc:title><![CDATA[The effect of temperature on mortality in rural Bangladesh--a population-based time-series study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-30</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn276v1?rss=1">
<title><![CDATA[Cohort profile: The Dynamic Analyses to Optimize Ageing (DYNOPTA) project]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn276v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Anstey, K. J, Byles, J. E, Luszcz, M. A, Mitchell, P., Steel, D., Booth, H., Browning, C., Butterworth, P., Cumming, R. G, Healy, J., Windsor, T. D, Ross, L., Bartsch, L., Burns, R. A, Kiely, K., Birrell, C. L, Broe, G. A, Shaw, J., Kendig, H.]]></dc:creator>
<dc:date>Sat, 17 Jan 2009 00:29:49 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn276</dc:identifier>
<dc:title><![CDATA[Cohort profile: The Dynamic Analyses to Optimize Ageing (DYNOPTA) project]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-17</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn365v1?rss=1">
<title><![CDATA[Recommendations like 'should always' should arouse us]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn365v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stang, A., Kuss, O.]]></dc:creator>
<dc:date>Thu, 15 Jan 2009 07:49:41 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn365</dc:identifier>
<dc:title><![CDATA[Recommendations like 'should always' should arouse us]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-15</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn350v1?rss=1">
<title><![CDATA[Answer to the commentary: Politics and public health--some conceptual considerations concerning welfare state characteristics and public health outcomes]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn350v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Espelt, A, Borrell, C, Rodriguez-Sanz, M, Muntaner, C, Pasarin, M., Benach, J, Schaap, M, Kunst, A., Navarro, V]]></dc:creator>
<dc:date>Thu, 08 Jan 2009 22:39:31 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn350</dc:identifier>
<dc:title><![CDATA[Answer to the commentary: Politics and public health--some conceptual considerations concerning welfare state characteristics and public health outcomes]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-08</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn275v1?rss=1">
<title><![CDATA[Cohort profile: The Hertfordshire Ageing Study (HAS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn275v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Syddall, H E, Simmonds, S J, Martin, H J, Watson, C., Dennison, E M, Cooper, C, Sayer, A A., for the Hertfordshire Cohort Study Group]]></dc:creator>
<dc:date>Thu, 08 Jan 2009 04:35:49 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn275</dc:identifier>
<dc:title><![CDATA[Cohort profile: The Hertfordshire Ageing Study (HAS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-08</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn351v1?rss=1">
<title><![CDATA[Politics and public health--some conceptual considerations concerning welfare state characteristics and public health outcomes]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn351v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lundberg, O]]></dc:creator>
<dc:date>Tue, 06 Jan 2009 02:38:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn351</dc:identifier>
<dc:title><![CDATA[Politics and public health--some conceptual considerations concerning welfare state characteristics and public health outcomes]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-06</prism:publicationDate>
<prism:section>Authors' Response</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn349v1?rss=1">
<title><![CDATA[Clinical Epidemiology: Principles, Methods and Applications for Clinical Research. D E Grobbee and A W Hoes.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn349v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dutta, S.]]></dc:creator>
<dc:date>Sun, 21 Dec 2008 23:16:18 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn349</dc:identifier>
<dc:title><![CDATA[Clinical Epidemiology: Principles, Methods and Applications for Clinical Research. D E Grobbee and A W Hoes.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-21</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn262v1?rss=1">
<title><![CDATA[Cohort Profile: The North West Adelaide Health Study (NWAHS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn262v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Grant, J. F, Taylor, A. W, Ruffin, R. E, Wilson, D. H, Phillips, P. J, Adams, R. J., Price, K., the North West Adelaide Health Study Team]]></dc:creator>
<dc:date>Thu, 11 Dec 2008 04:28:29 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn262</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The North West Adelaide Health Study (NWAHS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-11</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn270v1?rss=1">
<title><![CDATA[Hygiene hypothesis: wanted--dead or alive]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn270v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Douwes, J., Pearce, N.]]></dc:creator>
<dc:date>Tue, 09 Dec 2008 04:33:59 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn270</dc:identifier>
<dc:title><![CDATA[Hygiene hypothesis: wanted--dead or alive]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-09</prism:publicationDate>
<prism:section>Authors' Response</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn269v1?rss=1">
<title><![CDATA[Hygiene hypothesis: wanted--dead or alive]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn269v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Linneberg, A.]]></dc:creator>
<dc:date>Tue, 09 Dec 2008 04:33:59 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn269</dc:identifier>
<dc:title><![CDATA[Hygiene hypothesis: wanted--dead or alive]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-09</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn260v1?rss=1">
<title><![CDATA[Seasonality of rotavirus disease in the tropics: a systematic review and meta-analysis]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn260v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> To date little conclusive evidence exists on the seasonality of rotavirus incidence in the tropics. We present a systematic review and meta-analysis on the seasonal epidemiology of rotavirus in the tropics, including 26 studies reporting continuous monthly rotavirus incidence for which corresponding climatological data was available.</p>
<p><b>Methods</b> Using linear regression models that account for serial correlation between months, monthly rotavirus incidence was significantly negatively correlated with temperature, rainfall and relative humidity in 65%, 55% and 60% of studies, respectively. We carried out pooled analyses using a generalized estimating equation (GEE) that accounts for correlation from between-study variation and serial correlation between months within a given study.</p>
<p><b>Results</b> For every 1&deg;C (1.8&deg;F) increase in mean temperature, 1 cm (0.39 in.) increase in mean monthly rainfall, and 1% increase in relative humidity (22%) this analysis showed reductions in rotavirus incidence of 10% (95% CI: 6&ndash;13%), 1% (95% CI: 0&ndash;1%), and 3% (95% CI:0&ndash;5%), respectively.</p>
<p><b>Conclusions</b> On the basis of the evidence, we conclude that rotavirus responds to changes in climate in the tropics, with the highest number of infections found at the colder and drier times of the year.</p>
]]></description>
<dc:creator><![CDATA[Levy, K., Hubbard, A. E, Eisenberg, J. N.]]></dc:creator>
<dc:date>Thu, 04 Dec 2008 04:35:09 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn260</dc:identifier>
<dc:title><![CDATA[Seasonality of rotavirus disease in the tropics: a systematic review and meta-analysis]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-04</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn259v1?rss=1">
<title><![CDATA[Rose's Strategy of Preventive Medicine. Geoffrey Rose with commentary by Kay-Tee Khaw and Michael Marmot.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn259v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Harper, S.]]></dc:creator>
<dc:date>Thu, 04 Dec 2008 04:35:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn259</dc:identifier>
<dc:title><![CDATA[Rose's Strategy of Preventive Medicine. Geoffrey Rose with commentary by Kay-Tee Khaw and Michael Marmot.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-04</prism:publicationDate>
<prism:section>Essay Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn252v1?rss=1">
<title><![CDATA[Cohort Profile: the Jerusalem longitudinal cohort study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn252v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jacobs, J. M, Cohen, A., Bursztyn, M., Azoulay, D., Ein-Mor, E., Stessman, J.]]></dc:creator>
<dc:date>Thu, 04 Dec 2008 04:35:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn252</dc:identifier>
<dc:title><![CDATA[Cohort Profile: the Jerusalem longitudinal cohort study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-04</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn244v1?rss=1">
<title><![CDATA[Cohort Profile: The biopsychosocial religion and health study (BRHS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn244v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lee, J. W, Morton, K. R, Walters, J., Bellinger, D. L, Butler, T. L, Wilson, C., Walsh, E., Ellison, C. G, McKenzie, M. M, Fraser, G. E]]></dc:creator>
<dc:date>Wed, 03 Dec 2008 06:23:04 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn244</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The biopsychosocial religion and health study (BRHS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-12-03</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn235v1?rss=1">
<title><![CDATA[Heterogeneous views on heterogeneity]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn235v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Patsopoulos, N. A, Evangelou, E., Ioannidis, J. P.]]></dc:creator>
<dc:date>Tue, 21 Oct 2008 03:13:04 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn235</dc:identifier>
<dc:title><![CDATA[Heterogeneous views on heterogeneity]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-10-21</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn233v1?rss=1">
<title><![CDATA[Screening: Evidence and Practice. AE Raffle and JAM Gray.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn233v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Metcalfe, C.]]></dc:creator>
<dc:date>Tue, 21 Oct 2008 03:13:04 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn233</dc:identifier>
<dc:title><![CDATA[Screening: Evidence and Practice. AE Raffle and JAM Gray.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-10-21</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn198v1?rss=1">
<title><![CDATA[Hyping Health Risks: Environmental Hazards in Daily Life and the Science of Epidemiology. Kabat GC.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn198v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pearce, N.]]></dc:creator>
<dc:date>Thu, 18 Sep 2008 05:25:37 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn198</dc:identifier>
<dc:title><![CDATA[Hyping Health Risks: Environmental Hazards in Daily Life and the Science of Epidemiology. Kabat GC.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-18</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn185v1?rss=1">
<title><![CDATA[Protection of health information in Italy: a step too far?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn185v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cuttini, M., Marini, C., Bruzzone, S., Prati, S., Saracci, R.]]></dc:creator>
<dc:date>Thu, 04 Sep 2008 20:23:11 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn185</dc:identifier>
<dc:title><![CDATA[Protection of health information in Italy: a step too far?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-04</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn152v1?rss=1">
<title><![CDATA[Cities, urbanization and health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn152v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Whiting, D., Unwin, N.]]></dc:creator>
<dc:date>Wed, 16 Jul 2008 03:13:20 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn152</dc:identifier>
<dc:title><![CDATA[Cities, urbanization and health]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-07-16</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn030v1?rss=1">
<title><![CDATA[Images of remembrance]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn030v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Fri, 22 Feb 2008 04:27:50 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn030</dc:identifier>
<dc:title><![CDATA[Images of remembrance]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-02-22</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyl124v1?rss=1">
<title><![CDATA[The Cholera's Coming]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyl124v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Anon,  ]]></dc:creator>
<dc:date>Wed, 16 Aug 2006 03:40:56 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyl124</dc:identifier>
<dc:title><![CDATA[The Cholera's Coming]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2006-08-16</prism:publicationDate>
<prism:section>Diversion</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyi118v1?rss=1">
<title><![CDATA[A response to Dr Michael Oakes: advancing research into SES mechanisms that affect health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyi118v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Smith, P., Frank, J.]]></dc:creator>
<dc:date>Fri, 03 Jun 2005 06:50:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyi118</dc:identifier>
<dc:title><![CDATA[A response to Dr Michael Oakes: advancing research into SES mechanisms that affect health]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2005-06-03</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyi045v1?rss=1">
<title><![CDATA[One Thousand Pages of Research]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyi045v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yezierska, A.]]></dc:creator>
<dc:date>Thu, 03 Mar 2005 07:02:41 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyi045</dc:identifier>
<dc:title><![CDATA[One Thousand Pages of Research]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2005-03-03</prism:publicationDate>
<prism:section>Diversion</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyh094v1?rss=1">
<title><![CDATA[Sexual partner reductions explain human immunodeficiency virus declines in Uganda: comparative analyses of HIV and behavioural data in Uganda, Kenya, Malawi, and Zambia]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyh094v1?rss=1</link>
<description><![CDATA[
<p><P><B>Background</B> A better understanding of behavioural factors associated with the interruption of human immunodeficiency virus (HIV) dynamics in Uganda are fundamental for guiding HIV prevention strategies. A comparative analysis of population level HIV surveillance and behavioural data in Uganda and countries with similar epidemic dynamics offers a framework to identify distinctive elements of the Ugandan success.</P>
<P><B>Methods</B> We analysed HIV prevalence among pregnant women attending antenatal surveillance sites between 1990-1998 in Uganda, Kenya, Zambia, and Malawi, and AIDS behavioural data collected in Uganda (1989, 1995), Kenya (1998), Zambia, and Malawi (1996).</P>
<P><B>Results</B> In Uganda between 1991 and 1998, HIV prevalence rates fell 54% overall, with 75% and 57% declines among 15-19 and 20-24 age groups in urban areas, respectively. HIV declines were associated with a 60% reduction in multiple sexual partners between 1989 and 1995, as well as increased condom use and sexual abstinence. The lack of comparable HIV declines in comparison countries with similar rates of abstinence and condom use, but with multiple sexual partnership rates similar to Uganda in 1989, suggests that partner reduction is paramount in interrupting sexual HIV dynamics. Comparatively, Ugandans were more likely to acknowledge people with AIDS and communicate about HIV through personal networks. Modelling suggests an 80% reduction in incidence among youth early in the 1990s, suggesting a preceding behavioural process during the late 1980s, which reduced HIV risk.</P>
<P><B>Conclusion</B> The distinctive element explaining declines in HIV prevalence in Uganda is sexual partner reduction. The Ugandan response to AIDS involved a primary HIV intervention whose key outcome was risk avoidance through partner reduction. This focus for HIV prevention could prove more effective than other widely advocated strategies in sub-Saharan Africa.</P>
]]></description>
<dc:creator><![CDATA[Stoneburner, R. L., Low-Beer, D.]]></dc:creator>
<dc:date>Thu, 06 May 2004 07:34:15 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyh094</dc:identifier>
<dc:title><![CDATA[Sexual partner reductions explain human immunodeficiency virus declines in Uganda: comparative analyses of HIV and behavioural data in Uganda, Kenya, Malawi, and Zambia]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2004-05-06</prism:publicationDate>
<prism:section>Original paper</prism:section>
</item>

</rdf:RDF>