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<title>International Journal of Epidemiology - Advance Access</title>
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<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>2009-07-02</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>2009-06-29</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>2009-06-29</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>2009-06-29</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/dyp247v1?rss=1">
<title><![CDATA[Commentary: Why diets need to change to avert harm from global warming]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp247v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Powles, J.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp247</dc:identifier>
<dc:title><![CDATA[Commentary: Why diets need to change to avert harm from global warming]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-26</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp240v1?rss=1">
<title><![CDATA[Birth cohort studies: past, present and future]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp240v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lawlor, D. A, Andersen, A.-M. N., Batty, G D.]]></dc:creator>
<dc:date>2009-06-26</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp240</dc:identifier>
<dc:title><![CDATA[Birth cohort studies: past, present and future]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-26</prism:publicationDate>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp236v1?rss=1">
<title><![CDATA[School performance and hospital admissions due to self-inflicted injury: a Swedish national cohort study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp236v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Self-inflicted injury in youth has increased in many Western countries during recent decades. Education is the most influential societal determinant of living conditions in young people after early childhood. This study tested the hypothesis that school performance predicts self-inflicted injury.</p>
<p><b>Methods</b> A national cohort of 447 929 children born during 1973&ndash;77 was followed prospectively in the National Patient Discharge Register from the end of their ninth and last year of compulsory school until 2001. Multivariate Cox analyses of proportional hazards were used to test hypotheses regarding grades in ninth grade as predictors of hospital admission due to self-inflicted injury.</p>
<p><b>Results</b> The risk of hospital admission because of self-inflicted injury increased steeply in a step-wise manner with decreasing grade point average. Hazard ratios were 6.2 (95% confidence interval 5.5&ndash;7.0) in those with the lowest level of grade point average compared with the highest. The risks were similar for women and men. Adjustment for potential socio-economic confounders in a multivariate proportional hazards regression analysis attenuated this strong gradient only marginally.</p>
<p><b>Conclusion</b> School performance is a strong factor for predicting future mental ill-health as expressed by self-inflicted injury.</p>
]]></description>
<dc:creator><![CDATA[Jablonska, B., Lindberg, L., Lindblad, F., Rasmussen, F., Ostberg, V., Hjern, A.]]></dc:creator>
<dc:date>2009-06-25</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp236</dc:identifier>
<dc:title><![CDATA[School performance and hospital admissions due to self-inflicted injury: a Swedish national cohort study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-25</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>2009-06-25</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>2009-06-25</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>2009-06-23</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/dyp162v1?rss=1">
<title><![CDATA[Obesity and cancer: Mendelian randomization approach utilizing the FTO genotype]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp162v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Obesity is a risk factor for several cancers although appears to have an inverse association with cancers strongly related to tobacco. Studying obesity is difficult due to numerous biases and confounding.</p>
<p><b>Methods</b> To avoid these biases we used a Mendelian randomization approach incorporating an analysis of variants in the <I>FTO</I> gene that are strongly associated with BMI levels among 7000 subjects from a study of lung, kidney and upper-aerodigestive cancer.</p>
<p><b>Results</b> The <I>FTO</I> A allele which is linked with increased BMI was associated with a decreased risk of lung cancer (allelic odds ratio (OR) = 0.92, 95% confidence interval (CI) 0.84&ndash;1.00). It was also associated with a weak increased risk of kidney cancer, which was more apparent before the age of 50 (OR = 1.44, CI 1.09&ndash;1.90).</p>
<p><b>Conclusion</b> Our results highlight the potential for genetic variation to act as an unconfounded marker of environmentally modifiable factors, and offer the potential to obtain estimates of the causal effect of obesity. However, far larger sample sizes than studied here will be required to undertake this with precision.</p>
]]></description>
<dc:creator><![CDATA[Brennan, P., McKay, J., Moore, L., Zaridze, D., Mukeria, A., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Mates, D., Bencko, V., Foretova, L., Janout, V., Chow, W.-H., Rothman, N., Chabrier, A., Gaborieau, V., Timpson, N., Hung, R. J, Smith, G. D.]]></dc:creator>
<dc:date>2009-06-19</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp162</dc:identifier>
<dc:title><![CDATA[Obesity and cancer: Mendelian randomization approach utilizing the FTO genotype]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-19</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp217v2?rss=1">
<title><![CDATA[Cohort Profile: The EPIC-NL study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp217v2?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Beulens, J. W J, Monninkhof, E. M, Verschuren, M. W 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, B. H B]]></dc:creator>
<dc:date>2009-06-17</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>2009-06-17</prism:publicationDate>
<prism:section>Cohort Profile</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>2009-06-15</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/dyp226v1?rss=1">
<title><![CDATA[Is education causally related to better health? A twin fixed-effect study in the USA]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp226v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> More years of schooling is generally associated with better health. However, this association may be confounded by unobserved common prior causes such as inherited ability, personality such as patience, or early family circumstances. The twin fixed-effect approach can potentially address this problem by cancelling these factors between twin pairs. The purpose of this study is to identify the causal effects of education on health and health behaviours using a twin fixed-effect approach.</p>
<p><b>Methods</b> We used twin data from the National Survey of Midlife Development in the United States, 1995&ndash;1996. The study population included 302 male [55.6% monozygotic (MZ) and 44.4% dizygotic (DZ)] and 387 female twin pairs (47.3% MZ and 52.7% DZ). A range of health outcomes [perceived global, physical and mental health, body mass index (BMI), waist circumference, waist&ndash;hip ratio, number of depressive symptoms] and health behaviours (smoking and physical activity) were examined among twin pairs who were discordant on years of schooling.</p>
<p><b>Results</b> Among MZ twins, more years of education was associated with better perceived global health. For all other health outcomes/behaviours, the point estimates of the effect of education in the fixed-effect analyses suggested a weak protective association. Among DZ male twins, each additional year of schooling lowered the prevalence of smoking by 32% [odds ratio (OR): 0.68, 95% confidence interval (CI): 0.48&ndash;0.97] in the fixed-effect analysis.</p>
<p><b>Conclusion</b> The widely reported associations between schooling and health outcomes/behaviours may not reflect causal relationships in every instance. Although low statistical power may explain some of the null associations, our twin fixed-effect analyses suggest that at least some cases of the education/health relationship reflect confounding by unobserved third variables.</p>
]]></description>
<dc:creator><![CDATA[Fujiwara, T., Kawachi, I.]]></dc:creator>
<dc:date>2009-06-15</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp226</dc:identifier>
<dc:title><![CDATA[Is education causally related to better health? A twin fixed-effect study in the USA]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-15</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp222v1?rss=1">
<title><![CDATA[Prevalence of pulmonary tuberculosis amongst the tribal population of Madhya Pradesh, central India]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp222v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This was a prevalence survey of pulmonary tuberculosis (PTB) disease in the tribal population of Madhya Pradesh state, central India.</p>
<p><b>Methods</b> A community-based cross-sectional tuberculosis (TB) disease prevalence survey was undertaken among adults aged &ge;15 years in the tribal population of Madhya Pradesh. A multistage stratified cluster sampling was adopted. A representative random sample of villages predominated by tribal populations was selected from 11 districts. All eligible individuals were questioned for chest symptoms relating to TB. Sputum samples were collected from all eligible individuals, transported to the laboratory, and examined by Ziehl&ndash;Neelsen (ZN) smear microscopy and solid media culture methods.</p>
<p><b>Results</b> Of the 23 411 individuals eligible for screening, 22 270 (95.1%) were screened for symptoms. The overall proportion of symptomatic individuals was 7.9%. Overall prevalence (culture and/or smear positive) of PTB was 387 [95% confidence interval (CI): 273&ndash;502] per 100 000 population. The prevalence increased with age and was also significantly higher among males (554/100 000; 95% CI: 415&ndash;693) as compared with females (233/100 000; 95% CI: 101&ndash;364) (<I>P</I> &lt; 0.001).</p>
<p><b>Conclusion</b> The findings suggest that the TB situation amongst the tribal population is not that different from the situation among the non-tribal population in the country. However, TB remains a major public health problem amongst the tribal population and there is a need to maintain and further strengthen TB control measures on a sustained and long-term basis.</p>
]]></description>
<dc:creator><![CDATA[Bhat, J., Rao, V. G, Gopi, P. G., Yadav, R., Selvakumar, N., Tiwari, B., Gadge, V., Bhondeley, M. K, Wares, F.]]></dc:creator>
<dc:date>2009-06-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp222</dc:identifier>
<dc:title><![CDATA[Prevalence of pulmonary tuberculosis amongst the tribal population of Madhya Pradesh, central India]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-09</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp225v1?rss=1">
<title><![CDATA[Smoking, drinking and incident tuberculosis in rural India: population-based case-control study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp225v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> To investigate the extent to which smoking and/or drinking can increase the incidence of pulmonary tuberculosis (TB), a population-based case&ndash;control study was conducted in rural south India.</p>
<p><b>Methods</b> A total of 1839 males and 870 females treated in 2000&ndash;03 by state TB clinics were interviewed at home in 2004&ndash;05 about their education, smoking and drinking habits before disease onset. As controls, 2134 men and 2119 women without TB were randomly chosen from case villages and interviewed. Incidence rate ratios (RRs) are from logistic regression, adjusted for age and education.</p>
<p><b>Results</b> No women smoked or drank. The main analyses are of men aged 35&ndash;64 years, 949 cases treated for new pulmonary TB and 1963 controls. In the study, 81.5% of the cases and 55.2% of the controls had ever smoked, yielding a standardized ever- vs never-smoker TB incidence RR of 2.7 [95% confidence interval (CI) 2.2&ndash;3.3, <I>P</I> &lt; 0.00001). Among control ever-smokers 96% still smoked, 71% used only bidis (mean 17 per day) and 28% used only cigarettes (mean 7 per day). After additional adjustment for alcohol, this RR was 2.2 (95% CI 1.7&ndash;2.7, <I>P</I> &lt; 0.00001), but even among those who had never drunk alcohol the standardized ever- vs never-smoker RR was 2.6 (95% CI 2.0&ndash;3.6, <I>P</I> &lt; 0.00001). The corresponding RRs for ever- vs never-drinking were somewhat less extreme: 2.2 (95% CI 1.8&ndash;2.6, <I>P</I> &lt; 0.00001) without adjustment for smoking, 1.5 (95% CI 1.2&ndash;1.9, <I>P</I> = 0.00004) with adjustment for smoking and 2.1 (95% CI 1.4&ndash;3.0, 2<I>P</I> = 0.0001) among those who had never smoked. Among control ever-drinkers, 96% still drank and 99% used only spirits (mean 0.3 l/week).</p>
<p><b>Conclusions</b> This study of reliably confirmed disease (by the criteria of state TB clinics) demonstrates an increased incidence of pulmonary TB among those who smoke and among those who drink. The effects of smoking after adjustment for drinking were more definite than those of drinking after adjustment for smoking.</p>
]]></description>
<dc:creator><![CDATA[Gajalakshmi, V., Peto, R.]]></dc:creator>
<dc:date>2009-06-04</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp225</dc:identifier>
<dc:title><![CDATA[Smoking, drinking and incident tuberculosis in rural India: population-based case-control study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-04</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp223v1?rss=1">
<title><![CDATA[Seasonality in maternal intake and activity influence offspring's birth size among rural Indian mothers--Pune Maternal Nutrition Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp223v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Farming populations from developing countries are exposed to seasonal energy stress due to variations in food availability and energy output related to agricultural activities. This study aims to examine the impact of seasonality in maternal intake and activity on neonatal size.</p>
<p><b>Methods</b> Maternal anthropometry, dietary intakes (24-h recall and food-frequency questionnaire) and activity pattern (questionnaire) at 18 &plusmn; 2 and 28 &plusmn; 2 weeks gestation, and neonatal anthropometry, were measured in a prospective study of 797 rural Indian women.</p>
<p><b>Results</b> Maternal energy and protein intakes were inadequate (70% of recommended dietary allowance). Both intake and activity showed seasonal variation (<I>P</I> = 0.001), with peak values in winter i.e. during harvest, at 18 weeks (median energy 1863 kcal/day, protein 47.5 g/day) and 28 weeks (median energy 1687 kcal/day, protein 43.7 g/day), coinciding with the maximum maternal activity (median score 86.1 at 18 weeks and 79.5 at 28 weeks). Mean birth weight and length (adjusted for pre-pregnant weight, parity, gestation and sex) of babies was highest in summer (peak at February 2733 g, 48.6 cm, respectively) and lowest in winter (nadir at January 2591 g, 47.1 cm, respectively). Regression analysis showed that maternal intake at 18th week had a positive association (<I>P</I> = 0.05), maternal activity at 28th week had a negative association (<I>P</I> = 0.002) and exposure (in weeks) to winter during gestation had a positive association (<I>P</I> = 0.04) with birth size. Furthermore, higher maternal intakes, coupled with lower maternal activity in late gestation were associated with higher birth weight, especially during winter.</p>
<p><b>Conclusions</b> If causal, these observations indicate that complete exposure (16 weeks) to the winter season (harvest-time) in late gestation could increase birth weight by 90 g in poor farming communities in rural India, and the benefit would increase further by lowering maternal activity. Our results underscore the importance of considering seasonality in planning targeted intervention strategies in such settings.</p>
]]></description>
<dc:creator><![CDATA[Rao, S., Kanade, A. N, Yajnik, C. S, Fall, C. H D]]></dc:creator>
<dc:date>2009-06-04</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp223</dc:identifier>
<dc:title><![CDATA[Seasonality in maternal intake and activity influence offspring's birth size among rural Indian mothers--Pune Maternal Nutrition Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-06-04</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>2009-06-03</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>2009-06-02</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>2009-06-02</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>2009-06-02</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/dyp214v1?rss=1">
<title><![CDATA[Modelling income group differences in the health and economic impacts of targeted food taxes and subsidies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp214v1?rss=1</link>
<description><![CDATA[
<p><b>Objective</b> To examine the effects, by income group, of targeted food taxes and subsidies on nutrition, health and expenditure in the UK.</p>
<p><b>Methods</b> A model based on consumption data and demand elasticity was constructed to predict the effects of four food taxation-subsidy regimens. Resulting changes in demand, expenditure, nutrition, cardiovascular disease (CVD) and cancer mortality were estimated.</p>
<p><b>Data</b> Expenditure data were taken from the Expenditure and Food Survey; estimates of price elasticities of demand for food were taken from a report based on the National Food Survey 1988&ndash;2000. Estimates of effect on CVD and cancer mortality of changing fat, salt, fruit and vegetable intake were taken from previous meta-analyses.</p>
<p><b>Results</b> (i) Taxing principal sources of dietary saturated fat is unlikely to reduce cardiovascular disease (CVD) or cancer mortality. (ii) Taxing &lsquo;less healthy&rsquo; foods (defined by the WXYfm nutrient profiling model) could increase CVD and cancer deaths by 35&ndash;1300 yearly. (iii) Taxing &lsquo;less healthy&rsquo; foods and subsidising fruits and vegetables by 17.5% could avert up to 2900 CVD and cancer deaths yearly. (iv) Taxing &lsquo;less healthy&rsquo; foods and using all tax revenue to subsidize fruits and vegetables could avert up to 6400 CVD and cancer deaths yearly. Few obesity-related CVD deaths are averted by any of the regimens. All four regimens would be economically regressive and positive health effects will not necessarily be greater in lower-income groups where the need for dietary improvement is higher.</p>
<p><b>Conclusions</b> A targeted food tax combined with the appropriate subsidy on fruits and vegetables could reduce deaths from CVD and cancer.</p>
]]></description>
<dc:creator><![CDATA[Nnoaham, K. E, Sacks, G., Rayner, M., Mytton, O., Gray, A.]]></dc:creator>
<dc:date>2009-05-29</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp214</dc:identifier>
<dc:title><![CDATA[Modelling income group differences in the health and economic impacts of targeted food taxes and subsidies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-29</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>2009-05-28</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>2009-05-18</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/dyp210v1?rss=1">
<title><![CDATA[Improving epidemiological surveys of sexual behaviour conducted by telephone]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp210v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This study assesses the impact of Telephone Audio Computer-Assisted Self-Interviewing (T-ACASI) on the reporting of sensitive (mainly heterosexual) behaviours.</p>
<p><b>Methods</b> A randomized experiment was embedded in a telephone survey that drew probability samples of the populations of the USA (<I>N</I> = 1543) and Baltimore city (<I>N</I> = 744). Respondents were randomly assigned to have questions asked either by a T-ACASI computer or by a human telephone interviewer.</p>
<p><b>Results</b> Compared with interviewer-administered telephone surveys, T-ACASI obtained more frequent reporting of a range of mainly heterosexual behaviours that were presumed to be sensitive, including recency of anal sex [adjusted odds ratio (A-OR) = 2.00, <I>P</I> &lt; 0.001), sex during menstrual period (A-OR = 1.49, <I>P</I> &lt; 0.001), giving oral sex (A-OR = 1.40, <I>P</I> = 0.001) and receiving oral sex (A-OR = 1.36, <I>P</I> = 0.002), and sexual difficulties for the respondent (A-OR = 1.45, <I>P</I> = 0.034) and their main sex partner (A-OR = 1.48, <I>P</I> = 0.0). T-ACASI also obtained less frequent reporting that respondent had a &lsquo;main sex partner&rsquo; (A-OR = 0.56, <I>P</I> = 0.011) and discussed contraception prior to first sex with that sex partner (A-OR = 0.82, <I>P</I> = 0.094). For both males and females, T-ACASI obtained more frequent reports of first vaginal sex occurring at early ages (before ages 12 through 15). &lsquo;For males only&rsquo;, T-ACASI also elicited more frequent reports that first vaginal sex had &lsquo;not&rsquo; occurred at later ages (i.e. by ages 20 through 24).</p>
<p><b>Conclusion</b> T-ACASI increases the likelihood that survey respondents will report sensitive heterosexual behaviours.</p>
]]></description>
<dc:creator><![CDATA[Turner, C. F, Al-Tayyib, A., Rogers, S. M, Eggleston, E., Villarroel, M. A, Roman, A. M, Chromy, J. R, Cooley, P. C]]></dc:creator>
<dc:date>2009-05-15</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp210</dc:identifier>
<dc:title><![CDATA[Improving epidemiological surveys of sexual behaviour conducted by telephone]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-15</prism:publicationDate>
<prism:section>Original Paper</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>2009-05-15</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>2009-05-11</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/dyp204v1?rss=1">
<title><![CDATA[Low birthweight and subsequent emotional and behavioural outcomes in 12-year-old children in Soweto, South Africa: findings from Birth to Twenty]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp204v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The fetal origins hypothesis suggests that an adverse prenatal environment, indexed by low birthweight (LBW), may increase the risk of developing later disease. Recently the hypothesis has been extended to psychological outcomes, especially depression. The aim of this analysis was to test, for the first time in a developing country setting, the association between LBW and psychological symptoms, in Soweto, South Africa.</p>
<p><b>Methods</b> A sample of 1029 children was drawn from Birth to Twenty, a longitudinal cohort followed from pregnancy to young adulthood. This sample completed the Youth Self Report at age 12 years, a validated psychological measure of behavioural and emotional adjustment. Scores were compared between LBW (&lt;2500 g) and normal birthweight children using multivariate analysis with adjustment for potential birth and life events confounding factors.</p>
<p><b>Results</b> No associations were found between LBW and total [adjusted odds ratio (OR) 1.09, 95% confidence interval (CI) 0.69&ndash;1.74], internalizing (adjusted OR 0.81, 95% CI 0.52&ndash;1.28) or externalizing profiles (adjusted OR 0.81, 95% CI 0.49&ndash;1.36). The only difference detected was for the internalizing sub-profile of Somatic Complaints (adjusted OR 2.02, 95% CI 1.21&ndash;3.38), which on subgroup analysis was greatest among females.</p>
<p><b>Conclusions</b> We found no convincing evidence of an association between LBW and emotional and behavioural outcomes in 12-year olds in this sample in urban South Africa. To our knowledge, this is the first published assessment of this association in a developing world context.</p>
]]></description>
<dc:creator><![CDATA[Sabet, F., Richter, L. M, Ramchandani, P. G, Stein, A., Quigley, M. A, Norris, S. A]]></dc:creator>
<dc:date>2009-05-11</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp204</dc:identifier>
<dc:title><![CDATA[Low birthweight and subsequent emotional and behavioural outcomes in 12-year-old children in Soweto, South Africa: findings from Birth to Twenty]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-11</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp199v1?rss=1">
<title><![CDATA[Polymorphisms of the CRP gene inhibit inflammatory response and increase susceptibility to depression: The Health in Men Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp199v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Depression has been associated with chronic changes in the serum concentration of C-reactive protein (CRP) in observational studies, but it is unclear if this association is causal or is due to confounding and bias. Genetic studies are less subject to this type of error and offer an opportunity to investigate if CRP is causally linked to depression, particularly because known polymorphisms of the <I>CRP</I> gene have been associated with high- and low-basal serum concentrations of CRP [single nucleotide polymorphisms (SNPs) rs1130864 and rs1205, respectively]. The aim of this study is to determine if polymorphisms of SNPs rs1130864 and rs1205 are associated with prevalent depression.</p>
<p><b>Methods</b> We completed a cross-sectional study of a community sample of 3700 men aged &ge;70 years, and used the 15-item Geriatric Depression Scale (GDS-15) to assess depressive symptoms. A GDS-15 score 7 or more indicates the presence of clinically significant depressive symptoms. Physical morbidity was assessed with the physical component summary score (PCS) of the SF-36 Health Survey. We collected fasting blood samples to measure high sensitivity CRP and to extract DNA for the genotyping of SNPs rs1130864 and rs1205 of the <I>CRP</I> gene.</p>
<p><b>Results</b> One hundred and eighty-two men were depressed (4.9%). The odds of depression increased by 2% (95% CI = 1&ndash;4%) for every unit (mg/l) increase of CRP and nearly doubled for men with CRP &ge; 3 mg/l vs &lt;1 mg/l [odds ratio (OR) = 1.95, 95% confidence interval (CI) = 1.27&ndash;2.98]. However, the association between high CRP (&ge;3 mg/l) and depression was no longer significant after the analyses were adjusted for smoking, age, body mass index (BMI) and PCS. Men with the CT and TT genotypes of rs1130864 had 1.36 (95% CI = 1.13&ndash;1.63) and 2.31 (95% CI = 1.65&ndash;3.24) greater odds of CRP &ge;3 mg/l than CC carriers, but there was no association between this polymorphism and the presence of prevalent depression. The G &gt; A polymorphism of SNP rs1205 was associated with 24% (95% CI = 16&ndash;32%) lower concentration of CRP compared with other genotypes. Men with the rs1205 AA genotype had 1.66 (95% CI = 1.07&ndash;2.57) and 1.67 (95% CI = 1.08&ndash;2.58) greater odds of having clinically significant depression than participants with the GA and GG genotypes, respectively.</p>
<p><b>Conclusion</b> Our study shows that clinically significant depressive symptoms in later life are unlikely to be caused by an increase in the serum concentration of CRP. Instead, we found that the risk of depression was greater amongst people who carry the rs1205 G &gt; A genetic polymorphism of the <I>CRP</I> gene, which was associated with ~20% lower serum concentration of CRP compared with other genotypes. This suggests that CRP may be a compensatory response to external insults that predispose to depression, and that an increase in the concentration of CRP might be adaptive.</p>
]]></description>
<dc:creator><![CDATA[Almeida, O. P, Norman, P. E, Allcock, R., Bockxmeer, F. v., Hankey, G. J, Jamrozik, K., Flicker, L.]]></dc:creator>
<dc:date>2009-05-11</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp199</dc:identifier>
<dc:title><![CDATA[Polymorphisms of the CRP gene inhibit inflammatory response and increase susceptibility to depression: The Health in Men Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-11</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp202v1?rss=1">
<title><![CDATA[Could mitochondrial efficiency explain the susceptibility to adiposity, metabolic syndrome, diabetes and cardiovascular diseases in South Asian populations?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp202v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> South Asians are susceptible to cardiovascular disease (CVD), especially after migration to affluent countries. Contributing factors include high prevalence of diabetes, and possibly insulin resistance. Excess adiposity centrally may underlie such metabolic disturbances. The thrifty genotype, thrifty phenotype, adipose tissue compartment and variable disease selection hypotheses are among the explanations posed.</p>
<p><b>Methods</b> Data from individual studies and review articles known to the authors were examined. A Medline bibliographic database search was also performed. Reference lists were reviewed to identify additional relevant data sources. Key references were examined by both authors. </p>
<p><b>Results</b> We propose, and evaluate, the evidence for a &lsquo;mitochondrial efficiency hypothesis&rsquo; i.e. that ancestral changes in mitochondrial coupling efficiency enhanced the successful adaptation of South Asians to environmental stressors by maximizing the conversion of energy to adenosine triphosphate (ATP) rather than heat. This adaptation may be disadvantageous when South Asians are physically inactive and consume high-caloric diets. There is evidence that common mitochondrial mutations vary geographically. Mutations, including those affecting the function of mitochondrial uncoupling proteins (UCPs), may influence the balance of energy and heat production. These may influence basal metabolic rate (BMR), energy efficiency, the tendency to gain weight and hence metabolic disease. UCP gene polymorphisms are related to differences in BMR between African-Americans and Europeans. Similar data for South Asians are lacking but the few studies comparing BMR indicate that South Asians have a lower BMR, which is explained by a lower lean body mass, and higher fat mass. Once adjusted for body composition, BMR is similar. A high fat mass, <I>per se</I>, is a strategy for reducing energy use while conserving body size. Indians in the USA had higher oxidative phosphorylation capacity than Northern European Americans.</p>
<p><b>Conclusion</b> The evidence justifies full exploration of this mitochondrial effeciency hypothesis in South Asians, which may also be relevant to other warm-climate adapted populations.</p>
]]></description>
<dc:creator><![CDATA[Bhopal, R. S, Rafnsson, S. B]]></dc:creator>
<dc:date>2009-05-07</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp202</dc:identifier>
<dc:title><![CDATA[Could mitochondrial efficiency explain the susceptibility to adiposity, metabolic syndrome, diabetes and cardiovascular diseases in South Asian populations?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-07</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>2009-05-07</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/dyp203v1?rss=1">
<title><![CDATA[Commentary: Explaining enormous variations in rates of disorder in trauma-focused psychiatric epidemiology after major emergencies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp203v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rodin, D., van Ommeren, M.]]></dc:creator>
<dc:date>2009-05-04</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp203</dc:identifier>
<dc:title><![CDATA[Commentary: Explaining enormous variations in rates of disorder in trauma-focused psychiatric epidemiology after major emergencies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-04</prism:publicationDate>
<prism:section>Commentary</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp195v1?rss=1">
<title><![CDATA[Socio-economic status and oesophageal cancer: results from a population-based case-control study in a high-risk area]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp195v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Cancer registries in the 1970s showed that parts of Golestan Province in Iran had the highest rate of oesophageal squamous cell carcinoma (OSCC) in the world. More recent studies have shown that while rates are still high, they are approximately half of what they were before, which might be attributable to improved socio-economic status (SES) and living conditions in this area. We examined a wide range of SES indicators to investigate the association between different SES components and risk of OSCC in the region.</p>
<p><b>Methods</b> Data were obtained from a population-based case&ndash;control study conducted between 2003 and 2007 with 300 histologically proven OSCC cases and 571 matched neighbourhood controls. We used conditional logistic regression to compare cases and controls for individual SES indicators, for a composite wealth score constructed using multiple correspondence analysis, and for factors obtained from factors analysis.</p>
<p><b>Results</b> We found that various dimensions of SES, such as education, wealth and being married were all inversely related to OSCC. The strongest inverse association was found with education. Compared with no education, the adjusted odds ratios (95% confidence intervals) for primary education and high school or beyond were 0.52 (0.27&ndash;0.98) and 0.20 (0.06&ndash;0.65), respectively.</p>
<p><b>Conclusions</b> The strong association of SES with OSCC after adjustment for known risk factors implies the presence of yet unidentified risk factors that are correlated with our SES measures; identification of these factors could be the target of future studies. Our results also emphasize the importance of using multiple SES measures in epidemiological studies.</p>
]]></description>
<dc:creator><![CDATA[Islami, F., Kamangar, F., Nasrollahzadeh, D., Aghcheli, K., Sotoudeh, M., Abedi-Ardekani, B., Merat, S., Nasseri-Moghaddam, S., Semnani, S., Sepehr, A., Wakefield, J., Moller, H., Abnet, C. C, Dawsey, S. M, Boffetta, P., Malekzadeh, R.]]></dc:creator>
<dc:date>2009-05-04</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp195</dc:identifier>
<dc:title><![CDATA[Socio-economic status and oesophageal cancer: results from a population-based case-control study in a high-risk area]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-05-04</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp201v1?rss=1">
<title><![CDATA[Commentary: Spatial clustering of HIV infection: providing clues for effective HIV prevention]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp201v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Karim, S. S A.]]></dc:creator>
<dc:date>2009-04-30</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp201</dc:identifier>
<dc:title><![CDATA[Commentary: Spatial clustering of HIV infection: providing clues for effective HIV prevention]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-30</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>2009-04-23</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/dyp178v2?rss=1">
<title><![CDATA[Light-at-night, circadian disruption and breast cancer: assessment of existing evidence]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp178v2?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Breast cancer incidence is increasing globally for largely unknown reasons. The possibility that a portion of the breast cancer burden might be explained by the introduction and increasing use of electricity to light the night was suggested &gt;20 years ago.</p>
<p><b>Methods</b> The theory is based on nocturnal light-induced disruption of circadian rhythms, notably reduction of melatonin synthesis. It has formed the basis for a series of predictions including that non-day shift work would increase risk, blind women would be at lower risk, long sleep duration would lower risk and community nighttime light level would co-distribute with breast cancer incidence on the population level.</p>
<p><b>Results</b> Accumulation of epidemiological evidence has accelerated in recent years, reflected in an International Agency for Research on Cancer (IARC) classification of shift work as a probable human carcinogen (2A). There is also a strong rodent model in support of the light-at-night (LAN) idea.</p>
<p><b>Conclusion</b> If a consensus eventually emerges that LAN does increase risk, then the mechanisms for the effect are important to elucidate for intervention and mitigation. The basic understanding of phototransduction for the circadian system, and of the molecular genetics of circadian rhythm generation are both advancing rapidly, and will provide for the development of lighting technologies at home and at work that minimize circadian disruption, while maintaining visual efficiency and aesthetics. In the interim, there are strategies now available to reduce the potential for circadian disruption, which include extending the daily dark period, appreciate nocturnal awakening in the dark, using dim red light for nighttime necessities, and unless recommended by a physician, not taking melatonin tablets.</p>
]]></description>
<dc:creator><![CDATA[Stevens, R. G]]></dc:creator>
<dc:date>2009-04-23</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp178</dc:identifier>
<dc:title><![CDATA[Light-at-night, circadian disruption and breast cancer: assessment of existing evidence]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism: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>2009-04-22</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>2009-04-22</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>2009-04-22</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>2009-04-22</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>2009-04-20</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>2009-04-20</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/dyp176v1?rss=1">
<title><![CDATA[Ethnic and gender differences in physical activity levels among 9-10-year-old children of white European, South Asian and African-Caribbean origin: the Child Heart Health Study in England (CHASE Study)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp176v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Ethnic differences in physical activity in children in the UK have not been accurately assessed. We made objective measurements of physical activity in 9&ndash;10-year-old British children of South Asian, black African&ndash;Caribbean and white European origin.</p>
<p><b>Methods</b> Cross-sectional study of urban primary school children (2006&ndash;07). Actigraph-GT1M activity monitors were worn by 2071 children during waking hours on at least 1 full day. Ethnic differences in mean daily activity [counts, counts per minute of registered time (CPM) and steps] were adjusted for age, gender, day of week and month. Multilevel modelling allowed for repeated days within individual and clustering within school.</p>
<p><b>Results</b> In white Europeans, mean daily counts, CPM and mean daily steps were 394 785, 498 and 10 220, respectively. South Asian and black Caribbean children recorded more registered time per day than white Europeans (34 and 36 min, respectively). Compared with white Europeans, South Asians recorded 18 789 fewer counts [95% confidence interval (CI) 6390&ndash;31 187], 41 fewer CPM 95% CI 26&ndash;57) and 905 fewer steps (95% CI 624&ndash;1187). Black African&ndash;Caribbeans recorded 25 359 more counts (95% CI 14 273&ndash;36 445), and similar CPM, but fewer steps than white Europeans. Girls recorded less activity than boys in all ethnic groups, with 74 782 fewer counts (95% CI 66 665&ndash;82 899), 84 fewer CPM (95% CI 74&ndash;95) and 1484 fewer steps (95% CI 1301&ndash;1668).</p>
<p><b>Conclusion</b> British South Asian children have lower objectively measured physical activity levels than European whites and black African&ndash;Caribbeans.</p>
]]></description>
<dc:creator><![CDATA[Owen, C. G, Nightingale, C. M, Rudnicka, A. R, Cook, D. G, Ekelund, U., Whincup, P. H]]></dc:creator>
<dc:date>2009-04-19</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp176</dc:identifier>
<dc:title><![CDATA[Ethnic and gender differences in physical activity levels among 9-10-year-old children of white European, South Asian and African-Caribbean origin: the Child Heart Health Study in England (CHASE Study)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-19</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp172v1?rss=1">
<title><![CDATA[Population adiposity and climate change]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp172v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The increasing global prevalence of overweight and obesity has serious implications for the environment, as well as for health. We estimate the impact on greenhouse gas emissions of increases in the population distribution of body mass index (BMI).</p>
<p><b>Methods</b> We estimated the food energy required to maintain basal metabolic rate in two hypothetical adult populations using the Schofield equations for males and females. Additional greenhouse gas emissions due to higher fuel energy use for transporting a heavier population were estimated.</p>
<p><b>Results</b> Compared with a normal population distribution of BMI, a population with 40% obese requires 19% more food energy for its total energy expenditure. Greenhouse gas emissions from food production and car travel due to increases in adiposity in a population of 1 billion are estimated to be between 0.4 Giga tonnes (GT) and 1.0 GT of carbon dioxide equivalents per year.</p>
<p><b>Conclusions</b> The maintenance of a healthy BMI has important environmental benefits in terms of lower greenhouse gas emissions.</p>
]]></description>
<dc:creator><![CDATA[Edwards, P., Roberts, I.]]></dc:creator>
<dc:date>2009-04-19</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp172</dc:identifier>
<dc:title><![CDATA[Population adiposity and climate change]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-19</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>2009-04-17</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>2009-04-17</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>2009-04-17</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>2009-04-08</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/dyp175v1?rss=1">
<title><![CDATA[Endometriosis risk in relation to naevi, freckles and skin sensitivity to sun exposure: the French E3N cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp175v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Endometriosis is an important women's health issue, however its aetiology remains unknown. An association between endometriosis and cutaneous melanoma was described, possibly explained through common genetic features. To further investigate this association, we assessed the link between phenotypic traits predisposing to melanoma and the risk of endometriosis.</p>
<p><b>Methods</b> Using a case&ndash;control design, we analysed data from 97 215 women of the Etude Epid&eacute;miologique aupr&egrave;s de femmes de l&rsquo;Education Nationale study, a cohort of 98 995 French women insured by a national health&nbsp;scheme&nbsp;mostly covering teachers, and aged 40&ndash;65 years at inclusion in 1990. Risk estimates were computed using unconditional logistic regression models.</p>
<p><b>Results</b> After adjustment for potential confounding factors, there was a positive dose&ndash;effect relationship between risk of endometriosis (reported as surgically ascertained, <I>n</I> = 4241) and skin sensitivity to sun exposure [moderate: odds ratio (OR) 1.09, 95% confidence interval (CI) 0.99&ndash;1.19; high: OR 1.22; 95% CI 1.10&ndash;1.36; compared with none; <I>P</I><SUB>trend</SUB> &lt; 0.0001], number of naevi (few: OR 1.19, 95% CI 1.05&ndash;1.35; many: OR 1.37, 95% CI 1.21&ndash;1.55; very many: OR 1.59, 95% CI 1.37&ndash;1.83; compared with none; <I>P</I><SUB>trend</SUB> &lt; 0.0001) and number of freckles (few: OR 1.08, 95% CI 1.00&ndash;1.17; very many/many: OR 1.11, 95% CI 1.03&ndash;1.20; compared with none; <I>P</I><SUB>trend</SUB> = 0.005).</p>
<p><b>Conclusion</b> This study is, to our knowledge, the first to report a positive dose&ndash;effect relationship between the risk of endometriosis and skin sensitivity to sun exposure, and number of naevi and freckles. These data suggest that endometriosis and melanoma may share some genetic features.</p>
]]></description>
<dc:creator><![CDATA[Kvaskoff, M., Mesrine, S., Clavel-Chapelon, F., Boutron-Ruault, M.-C.]]></dc:creator>
<dc:date>2009-04-07</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp175</dc:identifier>
<dc:title><![CDATA[Endometriosis risk in relation to naevi, freckles and skin sensitivity to sun exposure: the French E3N cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-07</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp169v1?rss=1">
<title><![CDATA[Head size at birth and long-term mortality from coronary heart disease]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp169v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Many studies have shown that low birthweight is associated with increased risk of heart disease in adulthood. It is controversial whether this association is caused by genetic or non-genetic factors, and whether life course exposures, such as adult overweight, could modify the association. We have studied the association of head circumference at birth with later deaths from coronary heart disease (CHD), and assessed whether maternal height and adult body mass could modify the association.</p>
<p><b>Methods</b> Population-based cohort study of 35 846 men and women born between 1920 and 1959 with mortality follow-up from 1961 to 2005.</p>
<p><b>Results</b> During follow-up, 630 people died from CHD and there was an inverse association of head circumference with deaths from CHD (<I>P</I><SUB>trend</SUB> = 0.010). The association was modified by maternal height (<I>P</I><SUB>interaction</SUB> = 0.01) and by adult body mass (<I>P</I><SUB>interaction</SUB> = 0.05). People in the lowest third of head circumference, who had a tall mother or a high body mass index in adulthood, were at the highest risk of death from CHD.</p>
<p><b>Conclusions</b> Head circumference at birth was inversely associated with deaths from CHD, and the combination of small head and tall mother, or small head and high adult body mass, was associated with the highest risk. These findings suggest that combined effects of genetic factors (growth potential and intrauterine growth) and non-genetic factors acting throughout the life course (intrauterine growth restriction and later weight gain) could mediate the effects of birth size on adult heart disease.</p>
]]></description>
<dc:creator><![CDATA[Risnes, K. R, Nilsen, T. I L, Romundstad, P. R, Vatten, L. J]]></dc:creator>
<dc:date>2009-04-07</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp169</dc:identifier>
<dc:title><![CDATA[Head size at birth and long-term mortality from coronary heart disease]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-07</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp171v1?rss=1">
<title><![CDATA[Unprotected sex following HIV testing among women in Uganda and Zimbabwe: short- and long-term comparisons with pre-test behaviour]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp171v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Despite widespread condom promotion for HIV prevention, prospective measurement of condom use before and after HIV testing is infrequent.</p>
<p><b>Methods</b> We analysed data from a prospective study of hormonal contraception and HIV acquisition among Zimbabwean and Ugandan women (1999&ndash;2004), in which HIV testing and counselling were performed approximately every 3 months. We used zero-inflated negative binomial (ZINB) models to examine the number and proportion of unprotected sex acts, comparing behaviour reported 2&ndash;6 months before HIV testing with behaviour reported both 2&ndash;6 months (short-term analysis) and 12&ndash;16 months (long-term analysis) after HIV testing.</p>
<p><b>Results</b> Short- and long-term analyses were similar, so we present only long-term findings from 151 HIV-infected and 650 uninfected participants. The proportion of HIV-infected women reporting any unprotected acts in a typical month declined from 74% (pre-infection behaviour) to 56% (12&ndash;16 months after HIV diagnosis). In multivariable models, HIV-infected women were twice as likely to report that all sex acts were protected by condoms after diagnosis compared with beforehand [adjusted odds ratio (aOR): 1.99, 95% confidence interval (CI): 1.12&ndash;3.53]; uninfected women were somewhat less likely to report that all acts were protected (aOR: 0.82, 95% CI: 0.64&ndash;1.04). HIV-infected women also reduced their number of unprotected acts by 38% (95% CI: &ndash;16 to &ndash;55%). However, their proportion of unprotected acts changed little (7% reduction, 95% CI: &ndash;18 to + 6%). Uninfected women reported little change in number or proportion of unprotected acts over the same time period.</p>
<p><b>Conclusions</b> HIV-infected women reduced the number, but not the proportion, of unprotected acts. HIV-negative women did not increase condom use after testing and counselling, but neither did they decrease condom use, suggesting that testing negative was not interpreted as endorsement of risky behaviour.</p>
]]></description>
<dc:creator><![CDATA[Turner, A. N., Miller, W. C, Padian, N. S, Kaufman, J. S, Behets, F. M, Chipato, T., Mmiro, F. A, Salata, R. A, Morrison, C. S]]></dc:creator>
<dc:date>2009-04-06</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp171</dc:identifier>
<dc:title><![CDATA[Unprotected sex following HIV testing among women in Uganda and Zimbabwe: short- and long-term comparisons with pre-test behaviour]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-04-06</prism:publicationDate>
<prism:section>Original Paper</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>2009-04-06</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>2009-04-06</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>2009-04-06</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>2009-04-06</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>2009-04-06</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>2009-03-31</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/dyp164v1?rss=1">
<title><![CDATA[Ethics and observational studies in medical research: various rules in a common framework]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp164v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Research ethics have become universal in their principles through international agreements. The standardization of regulations facilitates the internationalization of research concerning drugs. However, in so-called observational studies (i.e. from data collected retrospectively or prospectively, obtained without any additional therapy or monitoring procedure) the modalities used for applying the main principles vary from one country to another. This situation may entail problems for the conduct of multi-centric international studies, as well as for the publication of results if the authors and editors come from countries governed by different regulations. In particular, several French observational studies were rejected or retracted by US peer-reviewed journals, because their protocols have not been submitted to an Institutional Review Board/Independent Ethics Committee (IRB/IEC).</p>
<p><b>Methods</b> National legislation case analysis.</p>
<p><b>Results</b> In accordance with European regulation, French observational studies from data obtained without any additional therapy or monitoring procedure, do not need the approval of an IRB/IEC. Nevertheless, these studies are neither exempt from scientific opinion nor from ethical and legal authorization.</p>
<p><b>Conclusion</b> We wish to demonstrate through the study of this example that different bodies of law can provide equivalent levels of protection that respect the same ethical principles. Our purpose in writing this article was to encourage public bodies, scientific journals and researchers to gain a better understanding of the various sets of specific national regulations and to speak a common language.</p>
]]></description>
<dc:creator><![CDATA[Claudot, F., Alla, F., Fresson, J., Calvez, T., Coudane, H., Bonaiti-Pellie, C.]]></dc:creator>
<dc:date>2009-03-31</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp164</dc:identifier>
<dc:title><![CDATA[Ethics and observational studies in medical research: various rules in a common framework]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-31</prism:publicationDate>
<prism:section>Original Paper</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>2009-03-30</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>2009-03-30</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/dyp006v1?rss=1">
<title><![CDATA[Interpreting data in the face of competing explanations: assessing the hypothesis that observed spontaneous clearance of Helicobacter pylori was all measurement error]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp006v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> We previously reported frequent transient positive urea breath tests for <I>Helicobacter pylori</I> infection in a cohort study of young children, and interpreted this as evidence of frequent spontaneous clearance of this infection. In a commentary, Perry and Parsonnet suggested that all transient positive tests we observed could be false positives and thus the appearance of transient infection could be an artifact.</p>
<p><b>Methods</b> We address the logic of the implicit argument that the transient infections were an artifact and we demonstrate a simple likelihood calculation to assess the plausibility of competing explanations. We calculate the likelihood of observing our data based on a range of clearance and measurement error rates and then how this updates a set of prior beliefs.</p>
<p><b>Results</b> The likelihood calculations and resulting posterior probabilities show strong support for the hypothesis of spontaneous clearance, after allowing for measurement error, even starting with a very high prior probability of no spontaneous clearance. The scenario Perry and Parsonnet present is incompatible with our data, and thus not a plausible explanation for our observations. Attributing most observed transient infections to measurement error requires assuming a high false positive rate and a very low infection rate and/or a high false negative rate, alternatives that are not supported by evidence.</p>
<p><b>Conclusions</b> Acknowledgment of plausible levels of measurement error does not change the strong support our data provides for the hypothesis of frequent transient infection. Debate about competing explanations for observations should be accompanied by quantitative analysis that shows which is more plausible. We demonstrate one method for doing such analysis.</p>
]]></description>
<dc:creator><![CDATA[Phillips, C. V, Goodman, K. J]]></dc:creator>
<dc:date>2009-03-23</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp006</dc:identifier>
<dc:title><![CDATA[Interpreting data in the face of competing explanations: assessing the hypothesis that observed spontaneous clearance of Helicobacter pylori was all measurement error]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-23</prism:publicationDate>
<prism:section>Original Paper</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyp150v1?rss=1">
<title><![CDATA[Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp150v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In Caucasian populations, adult height is inversely associated with cardiovascular disease (CVD) risk and positively related to some cancers. However, there are few data from Asian populations and from women. We sought to determine the sex- and region-specific associations between height and cardiovascular outcomes, and deaths due to cancer, respiratory and injury in populations from the Asia-Pacific region.</p>
<p><b>Methods</b> Thirty-nine studies from the Asia Pacific Cohort Studies Collaboration database were included. We used Cox proportional hazard regression models to estimate the associations between height and pre-specified outcomes.</p>
<p><b>Results</b> A total of 510 800 participants with 21 623 deaths were included. Amongst men, inverse linear associations were observed between height and coronary heart disease (CHD), stroke, CVD, injury and total mortality. The hazard ratios [95% confidence intervals, (CI)] for a 1-SD (= 6 cm) increment in height ranged from 0.85 (0.80&ndash;0.91) for injury to 0.97 (0.95&ndash;0.98) for total mortality. Similar trends were found between height and CHD, haemorrhagic stroke and CVD in women. A positive linear association was observed between height and cancer mortality. For each standard deviation greater height, the risk of cancer was increased by 5% (2&ndash;8%) and 9% (5&ndash;14%) in men and women, respectively. No regional difference was observed between Asian and Australasian cohorts. Adjusting for markers of education did not alter the results.</p>
<p><b>Conclusions</b> The opposing relationships of height with CVD and cancer suggest that care is required in setting national policies on childhood nutrition lest they have unintended consequences on the incidence of major non-communicable diseases.</p>
]]></description>
<dc:creator><![CDATA[Lee, C. M. Y., Barzi, F., Woodward, M., Batty, G D., Giles, G. G, Wong, J. W., Jamrozik, K., Lam, T. H., Ueshima, H., Kim, H. C., Gu, D. F., Schooling, M., Huxley, R. R, for The Asia Pacific Cohort Studies Collaboration]]></dc:creator>
<dc:date>2009-03-06</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp150</dc:identifier>
<dc:title><![CDATA[Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-06</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>2009-03-05</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/dyp148v1?rss=1">
<title><![CDATA[Localized spatial clustering of HIV infections in a widely disseminated rural South African epidemic]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp148v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> South Africa contains more than one in seven of the world's HIV-positive population. Knowledge of local variation in levels of HIV infection is important for prioritization of areas for intervention. We apply two spatial analytical techniques to investigate the micro-geographical patterns and clustering of HIV infections in a high prevalence, rural population in KwaZulu-Natal, South Africa.</p>
<p><b>Methods</b> All 12 221 participants who consented to an HIV test in a population under continuous demographical surveillance were linked to their homesteads and geo-located in a geographical information system (accuracy of &lt;2 m). We then used a two-dimensional Gaussian kernel of radius 3 km to produce robust estimates of HIV prevalence that vary across continuous geographical space. We also applied a Kulldorff spatial scan statistic (Bernoulli model) to formally identify clusters of infections (<I>P</I> &lt; 0.05).</p>
<p><b>Results</b> The results reveal considerable geographical variation in local HIV prevalence (range = 6&ndash;36%) within this relatively homogenous population and provide clear empirical evidence for the localized clustering of HIV infections. Three high-risk, overlapping spatial clusters [Relative Risk (RR) = 1.34&ndash;1.62] were identified by the Kulldorff statistic along the National Road (<I>P</I> &le; 0.01), whereas three low risk clusters (RR = 0.2&ndash;0.38) were identified elsewhere in the study area (<I>P</I> &le; 0.017).</p>
<p><b>Conclusions</b> The findings show the existence of several localized HIV epidemics of varying intensity that are partly contained within geographically defined communities. Despite the overall high prevalence of HIV in many rural South African settings, the results support the need for interventions that target socio-geographic spaces (communities) at greatest risk to supplement measures aimed at the general population.</p>
]]></description>
<dc:creator><![CDATA[Tanser, F., Barnighausen, T., Cooke, G. S, Newell, M.-L.]]></dc:creator>
<dc:date>2009-03-04</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp148</dc:identifier>
<dc:title><![CDATA[Localized spatial clustering of HIV infections in a widely disseminated rural South African epidemic]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-03-04</prism:publicationDate>
<prism:section>Original Paper</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>2009-03-04</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>2009-03-02</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>2009-03-02</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>2009-03-02</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/dyp143v1?rss=1">
<title><![CDATA[Association of age, sex and seat belt use with the risk of early death in drivers of passenger cars involved in traffic crashes]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyp143v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> This study was designed to break down the association of age, sex and seat belt use with risk of death for drivers of automobiles involved in a crash into two theoretical components: intrinsic severity of the crash and occupant resilience.</p>
<p><b>Methods</b> We studied all 84 338 pairs of drivers and front-seat passengers aged &ge;18 years in passenger cars involved in traffic crashes with victims recorded in the Spanish traffic crash registry between 2000 and 2004. Relative risks (RR) for the association of age, male sex and non-seat belt use with risk of death were calculated with Poisson conditional and unconditional multiple regression models.</p>
<p><b>Results</b> For drivers, the risk of death associated with severity of the crash was slightly higher in men (RR = 1.18), and decreased with age (RR = 0.993 per year). However, resilience-dependent risk of death increased with age (RR = 1.028 per year), and especially among unbelted occupants (RR = 4.02).</p>
<p><b>Conclusions</b> We conclude that in drivers involved in traffic crashes the association of age, sex and seat belt use with risk of death depends on the component of risk considered: severity of the crash or the occupant's resilience to energy.</p>
]]></description>
<dc:creator><![CDATA[Lardelli-Claret, P., Espigares-Rodriguez, E., Amezcua-Prieto, C., Jimenez-Moleon, J. J., Luna-del-Castillo, J. d. D., Bueno-Cavanillas, A.]]></dc:creator>
<dc:date>2009-02-27</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp143</dc:identifier>
<dc:title><![CDATA[Association of age, sex and seat belt use with the risk of early death in drivers of passenger cars involved in traffic crashes]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-02-27</prism:publicationDate>
<prism:section>Original Paper</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>2009-02-25</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>2009-02-11</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/dyn375v1?rss=1">
<title><![CDATA[Post-traumatic stress reactions among Rwandan children and adolescents in the early aftermath of genocide]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn375v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Epidemiological investigations of post-traumatic stress reactions in Sub-Saharan Africa, where atrocious violence against civilians is endemic, are rare. This article is the first complete report of the key community-based findings of a 1995 psychiatric epidemiological survey of young survivors of the 1994 Rwandan Genocide.</p>
<p><b>Methods</b> The National Trauma Survey (NTS) of Rwandans aged 8&ndash;19 measured traumatic exposures using an inventory of possible war time experiences and post-traumatic stress reactions with a checklist of symptoms of Post-traumatic stress disorder (PTSD). Individuals meeting assessed PTSD diagnostic criteria are classified as cases of &lsquo;probable PTSD&rsquo;. The NTS interviewed youth residing in the community and others institutionalized in unaccompanied children's centres; the former (<I>n</I> = 1547) are the subject of the present report. Instrument change midway into the study divides respondents into two samples.</p>
<p><b>Results</b> Among respondents, over 90% witnessed killings and had their lives threatened; 35% lost immediate family members; 30% witnessed rape or sexual mutilation; 15% hid under corpses. In Sample 1, 95% of respondents reported one or more re-experiencing symptom, 95% reported three or more avoidance/blunting symptoms and 63% reported two or more arousal symptoms; in Sample 2, these figures were 96%, 95% and 56%, respectively. The overall rate of &lsquo;probable PTSD&rsquo; was 62% and 54% in Samples 1 and 2, respectively, and exhibited a dose&ndash;response relationship with exposure. Among the most heavily exposed individuals the rate was 100%. Rates of &lsquo;probable PTSD&rsquo; were higher among females than among males. Results for age were inconsistent.</p>
<p><b>Conclusion</b> In industrialized societies, most survivors of traumatizing violence experience symptoms only transiently. In the Rwanda survey, symptom levels and rates of &lsquo;probable PTSD&rsquo; were exceptionally elevated, suggesting that at the limits of catastrophic man-made violence, psychological resilience among youth is all but extinguished.</p>
]]></description>
<dc:creator><![CDATA[Neugebauer, R., Fisher, P. W, Blake Turner, J., Yamabe, S., Sarsfield, J. A, Stehling-Ariza, T.]]></dc:creator>
<dc:date>2009-02-08</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn375</dc:identifier>
<dc:title><![CDATA[Post-traumatic stress reactions among Rwandan children and adolescents in the early aftermath of genocide]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-02-08</prism:publicationDate>
<prism:section>Original Paper</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>2009-02-03</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>2009-01-30</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/dyn373v1?rss=1">
<title><![CDATA[Socioeconomic position, psychosocial work environment and cerebrovascular disease among women: the Finnish public sector study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn373v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The excess risk of fatal and non-fatal cerebrovascular disease in people from low socioeconomic positions is only partially explained by conventional cerebrovascular risk factors. This has led to the suggestion that poor psychosocial work environments provide important additional explanatory power. However, little evidence is available for women.</p>
<p><b>Methods</b> We examined whether job demands or job control contributed to the socioeconomic gradient in cerebrovascular disease among 48 361 women aged 18&ndash;65 years. Job demands, job control and behavioural risk factors were self-reported in 2000&ndash;2002; socioeconomic position (as indexed by occupational class) and all of the health measures were obtained from registers. The outcome was recorded hospitalization or death from cerebrovascular disease.</p>
<p><b>Results</b> During a mean follow-up of 3.4 years, 124 women had a new cerebrovascular disease event. The risk was 2.3 (95% CI 1.3&ndash;3.9) times higher among women in low vs high socioeconomic positions. Adjustment for conventional risk factors, such as prevalent hypertension, coronary heart disease, diabetes, smoking, heavy alcohol consumption, physical inactivity and obesity, attenuated this excess risk by 23%. In contrast, adjustment for job demands and job control actually amplified the gradient by 36% suggesting a suppression effect.</p>
<p><b>Conclusions</b> In this contemporary cohort of employed women, job demands&mdash;alone and in combination with job control&mdash;suppressed rather than explained socioeconomic differences in cerebrovascular disease.</p>
]]></description>
<dc:creator><![CDATA[Kivimaki, M., Gimeno, D., Ferrie, J. E, Batty, G D., Oksanen, T., Jokela, M., Virtanen, M., Salo, P., Akbaraly, T. N, Elovainio, M., Pentti, J., Vahtera, J.]]></dc:creator>
<dc:date>2009-01-20</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn373</dc:identifier>
<dc:title><![CDATA[Socioeconomic position, psychosocial work environment and cerebrovascular disease among women: the Finnish public sector study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2009-01-20</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>2009-01-17</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>2009-01-15</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>2009-01-08</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>2009-01-08</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>2009-01-06</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>2008-12-21</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>2008-12-11</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>2008-12-09</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>2008-12-09</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>2008-12-04</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>2008-12-04</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>2008-12-04</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>2008-12-03</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/dyn239v1?rss=1">
<title><![CDATA[Cohort Profile: NICHD International Site Development Initiative (NISDI): a prospective, observational study of HIV-exposed and HIV-infected children at clinical sites in Latin American and Caribbean countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn239v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hazra, R., Stoszek, S. K, Hance, L. F., Pinto, J., Marques, H., Peixoto, M., Alarcon, J., Mussi-Pinhata, M., Serchuck, L., for the NISDI Pediatric Study Group 2008]]></dc:creator>
<dc:date>2008-11-26</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn239</dc:identifier>
<dc:title><![CDATA[Cohort Profile: NICHD International Site Development Initiative (NISDI): a prospective, observational study of HIV-exposed and HIV-infected children at clinical sites in Latin American and Caribbean countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-11-26</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>2008-10-21</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>2008-10-21</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/dyn213v1?rss=1">
<title><![CDATA[Cohort Profile: West of Scotland Twenty-07 Study: Health in the Community]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn213v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Benzeval, M., Der, G., Ellaway, A., Hunt, K., Sweeting, H., West, P., Macintyre, S.]]></dc:creator>
<dc:date>2008-10-17</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn213</dc:identifier>
<dc:title><![CDATA[Cohort Profile: West of Scotland Twenty-07 Study: Health in the Community]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-10-17</prism:publicationDate>
<prism:section>Cohort Profile</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>2008-09-18</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/dyn192v1?rss=1">
<title><![CDATA[Cohort Profile: The Danish HIV Cohort Study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn192v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Obel, N., Engsig, F. N, Rasmussen, L. D, Larsen, M. V, Omland, L. H, Sorensen, H. T]]></dc:creator>
<dc:date>2008-09-17</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn192</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Danish HIV Cohort Study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-17</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn191v1?rss=1">
<title><![CDATA[Cohort Profile: The Danish Web-based Pregnancy Planning Study--'Snart-Gravid']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn191v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mikkelsen, E. M, Hatch, E. E, Wise, L. A, Rothman, K. J, Riis, A., Sorensen, H. T.]]></dc:creator>
<dc:date>2008-09-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn191</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Danish Web-based Pregnancy Planning Study--'Snart-Gravid']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-09</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn190v1?rss=1">
<title><![CDATA[Survival Analysis for Epidemiologic and Medical Research. Steve Selvin.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn190v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kim, L.]]></dc:creator>
<dc:date>2008-09-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn190</dc:identifier>
<dc:title><![CDATA[Survival Analysis for Epidemiologic and Medical Research. Steve Selvin.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-09</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn184v1?rss=1">
<title><![CDATA[Cohort Profile: The Newcastle Thousand Families 1947 Birth Cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn184v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pearce, M. S, Unwin, N. C, Parker, L., Craft, A. W]]></dc:creator>
<dc:date>2008-09-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn184</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The Newcastle Thousand Families 1947 Birth Cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-09</prism:publicationDate>
<prism:section>Cohort Profile</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn180v1?rss=1">
<title><![CDATA[Cohort profile: the Swiss Inflammatory Bowel Disease Cohort Study (SIBDCS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn180v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pittet, V., Juillerat, P., Mottet, C., Felley, C., Ballabeni, P., Burnand, B., Michetti, P., Vader, J.-P., the Swiss IBD Cohort Study Group]]></dc:creator>
<dc:date>2008-09-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn180</dc:identifier>
<dc:title><![CDATA[Cohort profile: the Swiss Inflammatory Bowel Disease Cohort Study (SIBDCS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-09-09</prism:publicationDate>
<prism:section>Cohort Profile</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>2008-09-04</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/dyn175v1?rss=1">
<title><![CDATA[Population and Disease: Transforming English Society, 1550-1850. Peter Razzell]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn175v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Truelsen, T.]]></dc:creator>
<dc:date>2008-08-25</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn175</dc:identifier>
<dc:title><![CDATA[Population and Disease: Transforming English Society, 1550-1850. Peter Razzell]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-08-25</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn168v1?rss=1">
<title><![CDATA[Is the incidence of psychotic disorder in decline? Epidemiological evidence from two decades of research]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn168v1?rss=1</link>
<description><![CDATA[
<p><b>Background</b> It is unclear whether the incidence of first episode psychoses is in decline. We had the opportunity to determine whether incidence had changed over a 20-year period in a single setting, and test whether this could be explained by demographic or clinical changes.</p>
<p><b>Methods</b> The entire population at-risk aged 16&ndash;54 in Nottingham over three time periods (1978&ndash;80, 1993&ndash;95 and 1997&ndash;99) were followed up. All participants presenting with an ICD-9/10 first episode psychosis were included. The remainder of the population at-risk formed the denominator. Standardized incidence rates were calculated at each time period with possible change over time assessed via Poisson regression. We studied six outcomes: substance-induced psychoses, schizophrenia, other non-affective psychoses, manic psychoses, depressive psychoses and all psychotic disorders combined.</p>
<p><b>Results</b> Three hundred and forty-seven participants with a first episode psychosis during 1.2 million person-years of follow-up over three time periods were identified. The incidence of non-affective or affective psychoses had not changed over time following standardization for age, sex and ethnicity. We observed a linear increase in the incidence of substance-induced psychosis, per annum, over time (incidence rate ratios: 1.15; 95% CI 1.05&ndash;1.25). This could not be explained by longitudinal changes in the age, sex and ethnic structure of the population at-risk.</p>
<p><b>Conclusions</b> Our findings suggest psychotic disorders are not in decline, though there has been a change in the syndromal presentation of non-affective disorders, away from schizophrenia towards other non-affective psychoses. The incidence of substance-induced psychosis has increased, consistent with increases in substance toxicity over time, rather than changes in the prevalence or vulnerability to substance misuse. Increased clinical and popular awareness of substance misuse could also not be excluded.</p>
]]></description>
<dc:creator><![CDATA[Kirkbride, J B, Croudace, T, Brewin, J, Donoghue, K, Mason, P, Glazebrook, C, Medley, I, Harrison, G, Cooper, J E, Doody, G A, Jones, P B]]></dc:creator>
<dc:date>2008-08-25</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn168</dc:identifier>
<dc:title><![CDATA[Is the incidence of psychotic disorder in decline? Epidemiological evidence from two decades of research]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-08-25</prism:publicationDate>
<prism:section>Original Paper</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>2008-07-16</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/dyn142v1?rss=1">
<title><![CDATA[Marketing Health: Smoking and the Discourse of Public Health in Britain 1945-2000.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn142v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Clancy, L.]]></dc:creator>
<dc:date>2008-07-16</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn142</dc:identifier>
<dc:title><![CDATA[Marketing Health: Smoking and the Discourse of Public Health in Britain 1945-2000.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-07-16</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn150v1?rss=1">
<title><![CDATA[Public health: ethical issues.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn150v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kar-Purkayastha, I.]]></dc:creator>
<dc:date>2008-07-15</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn150</dc:identifier>
<dc:title><![CDATA[Public health: ethical issues.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-07-15</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn123v1?rss=1">
<title><![CDATA[Comments on the study of McGeoghegan et al.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn123v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McGeoghegan, D., Binks, K., Gillies, M., Jones, S., Whalley, S.]]></dc:creator>
<dc:date>2008-07-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn123</dc:identifier>
<dc:title><![CDATA[Comments on the study of McGeoghegan et al.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-07-09</prism:publicationDate>
<prism:section>Author's Response</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn122v1?rss=1">
<title><![CDATA[Comments: The non-cancer mortality experience of male workers at British Nuclear Fuels plc, 1946-2005]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn122v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Little, M P, Tawn, E J, Tzoulaki, I, Wakeford, R, Hildebrandt, G, Tapio, S, Elliott, P]]></dc:creator>
<dc:date>2008-07-09</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn122</dc:identifier>
<dc:title><![CDATA[Comments: The non-cancer mortality experience of male workers at British Nuclear Fuels plc, 1946-2005]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-07-09</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn120v1?rss=1">
<title><![CDATA[Author's response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn120v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sinha, R., Devesa, S., Rastogi, T., Mathew, A.]]></dc:creator>
<dc:date>2008-06-20</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn120</dc:identifier>
<dc:title><![CDATA[Author's response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-06-20</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn119v1?rss=1">
<title><![CDATA[Response to 'Cancer incidence rates among South Asians in four geographic regions: India, Singapore, UK and US']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn119v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Babu, G. R]]></dc:creator>
<dc:date>2008-06-20</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn119</dc:identifier>
<dc:title><![CDATA[Response to 'Cancer incidence rates among South Asians in four geographic regions: India, Singapore, UK and US']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-06-20</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn054v1?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn054v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hanewinkel, R., Tanski, S. E, Sargent, J. D]]></dc:creator>
<dc:date>2008-03-24</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn054</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-03-24</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn053v1?rss=1">
<title><![CDATA[Exposure to alcohol use in motion pictures and teen drinking in Germany]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn053v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dinani, N., Wood, N. R, Robbe, I. J]]></dc:creator>
<dc:date>2008-03-24</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn053</dc:identifier>
<dc:title><![CDATA[Exposure to alcohol use in motion pictures and teen drinking in Germany]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-03-24</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/dyn044v1?rss=1">
<title><![CDATA[Effect on response rates of stamps vs a pre-printed business reply envelope in a mailed follow-up survey among middle-aged Danish men]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/dyn044v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Osler, M., Juhl, M., Lund, R., Andersen, A.-M. N., Kriegbaum, M., Christensen, U.]]></dc:creator>
<dc:date>2008-03-20</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn044</dc:identifier>
<dc:title><![CDATA[Effect on response rates of stamps vs a pre-printed business reply envelope in a mailed follow-up survey among middle-aged Danish men]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:publicationDate>2008-03-20</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>2008-02-22</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>2006-08-16</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>2005-06-03</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>2005-03-03</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>
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<dc:creator><![CDATA[Stoneburner, R. L., Low-Beer, D.]]></dc:creator>
<dc:date>2004-05-06</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>
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