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<title><![CDATA[The end of the beginning for chronic disease epidemiology]]></title>
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<dc:creator><![CDATA[Smith, G. D.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyq011</dc:identifier>
<dc:title><![CDATA[The end of the beginning for chronic disease epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
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<title><![CDATA[Information for decision making: lot quality assurance sampling in the spotlight]]></title>
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<dc:creator><![CDATA[Garner, P., Smith, G. D.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyq006</dc:identifier>
<dc:title><![CDATA[Information for decision making: lot quality assurance sampling in the spotlight]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
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<title><![CDATA[Attitudes vs Actions]]></title>
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<dc:creator><![CDATA[LaPiere, R. T]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp398</dc:identifier>
<dc:title><![CDATA[Attitudes vs Actions]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
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<prism:publicationDate>2010-02-01</prism:publicationDate>
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<prism:section>Reprints and Reflections</prism:section>
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<title><![CDATA[Commentary: Ethics and the rhetorical context of human research]]></title>
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<dc:creator><![CDATA[Herrera, C.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp400</dc:identifier>
<dc:title><![CDATA[Commentary: Ethics and the rhetorical context of human research]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
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<title><![CDATA[Commentary: LaPiere and methodological opportunism]]></title>
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<dc:creator><![CDATA[Lee, R. M]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp399</dc:identifier>
<dc:title><![CDATA[Commentary: LaPiere and methodological opportunism]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
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<title><![CDATA[Commentary: The seminal contribution of Richard LaPiere's attitudes vs actions (1934) research study]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[Firmin, M. W]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp401</dc:identifier>
<dc:title><![CDATA[Commentary: The seminal contribution of Richard LaPiere's attitudes vs actions (1934) research study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
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<prism:endingPage>20</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>18</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/21?rss=1">
<title><![CDATA[Commentary: Not all attitudes are created equal]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/21?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sechrest, L.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp405</dc:identifier>
<dc:title><![CDATA[Commentary: Not all attitudes are created equal]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>24</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>21</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/25?rss=1">
<title><![CDATA[The antecedents of epidemiological methodology in Arthur Mitchell's surveillance and care of the insane]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/25?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Smith, G. D.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyq013</dc:identifier>
<dc:title><![CDATA[The antecedents of epidemiological methodology in Arthur Mitchell's surveillance and care of the insane]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>30</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>25</prism:startingPage>
<prism:section>Diversion</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/31?rss=1">
<title><![CDATA[Images of remembrance]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/31?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn030</dc:identifier>
<dc:title><![CDATA[Images of remembrance]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>31</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>31</prism:startingPage>
<prism:section>Photoessay</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/32?rss=1">
<title><![CDATA[Cochrane Column]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/32?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Young, T., Ojukwu, J. U, Okebe, J. U, Yahav, D., Paul, M., for the Cochrane Infectious Diseases Group, Stoltzfus, R.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp368</dc:identifier>
<dc:title><![CDATA[Cochrane Column]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>35</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>32</prism:startingPage>
<prism:section>Cochrane Column</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/36?rss=1">
<title><![CDATA[Cohort profile: The Hertfordshire Ageing Study (HAS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/36?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>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn275</dc:identifier>
<dc:title><![CDATA[Cohort profile: The Hertfordshire Ageing Study (HAS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>43</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>36</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/44?rss=1">
<title><![CDATA[Cohort profile: The Dynamic Analyses to Optimize Ageing (DYNOPTA) project]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/44?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Anstey, K. J, Byles, J. E, Luszcz, M. A, Mitchell, P., Steel, D., Booth, H., Browning, C., Butterworth, P., Cumming, R. G, Healy, J., Windsor, T. D, Ross, L., Bartsch, L., Burns, R. A, Kiely, K., Birrell, C. L, Broe, G. A, Shaw, J., Kendig, H.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn276</dc:identifier>
<dc:title><![CDATA[Cohort profile: The Dynamic Analyses to Optimize Ageing (DYNOPTA) project]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>51</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>44</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/52?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/39/1/52?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>Sat, 06 Feb 2010 00:02:42 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>59</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>52</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/60?rss=1">
<title><![CDATA[LQAS: User Beware]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/60?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Researchers around the world are using Lot Quality Assurance Sampling (LQAS) techniques to assess public health parameters and evaluate program outcomes. In this paper, we report that there are actually two methods being called LQAS in the world today, and that one of them is badly flawed.</p>
<p><b>Methods</b> This paper reviews fundamental LQAS design principles, and compares and contrasts the two LQAS methods. We raise four concerns with the simply-written, freely-downloadable training materials associated with the second method.</p>
<p><b>Results</b> The first method is founded on sound statistical principles and is carefully designed to protect the vulnerable populations that it studies. The language used in the training materials for the second method is simple, but not at all clear, so the second method sounds very much like the first. On close inspection, however, the second method is found to promote study designs that are biased in favor of finding programmatic or intervention success, and therefore biased against the interests of the population being studied.</p>
<p><b>Conclusion</b> We outline several recommendations, and issue a call for a new high standard of clarity and face validity for those who design, conduct, and report LQAS studies.</p>
]]></description>
<dc:creator><![CDATA[Rhoda, D. A, Fernandez, S. A, Fitch, D. J, Lemeshow, S.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn366</dc:identifier>
<dc:title><![CDATA[LQAS: User Beware]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>68</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>60</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/69?rss=1">
<title><![CDATA[Commentary: Understanding practical lot quality assurance sampling]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/69?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pagano, M., Valadez, J. J]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp406</dc:identifier>
<dc:title><![CDATA[Commentary: Understanding practical lot quality assurance sampling]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>71</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>69</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/72?rss=1">
<title><![CDATA[An assessment of Lot Quality Assurance Sampling to evaluate malaria outcome indicators: extending malaria indicator surveys]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/72?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Large investments and increased global prioritization of malaria prevention and treatment have resulted in greater emphasis on programme monitoring and evaluation (M&amp;E) in many countries. Many countries currently use large multistage cluster sample surveys to monitor malaria outcome indicators on a regional and national level. However, these surveys often mask local-level variability important to programme management. Lot Quality Assurance Sampling (LQAS) has played a valuable role for local-level programme M&amp;E. If incorporated into these larger surveys, it would provide a comprehensive M&amp;E plan at little, if any, extra cost.</p>
<p><b>Methods</b> The Mozambique Ministry of Health conducted a Malaria Indicator Survey (MIS) in June and July 2007. We applied LQAS classification rules to the 345 sampled enumeration areas to demonstrate identifying high- and low-performing areas with respect to two malaria program indicators&mdash;&lsquo;household possession of any bednet&rsquo; and &lsquo;household possession of any insecticide-treated bednet (ITN)&rsquo;<I>.</I></p>
<p><b>Results</b> As shown by the MIS, no province in Mozambique achieved the 70% coverage target for household possession of bednets or ITNs. By applying LQAS classification rules to the data, we identify 266 of the 345 enumeration areas as having bednet coverage severely below the 70% target. An additional 73 were identified with low ITN coverage.</p>
<p><b>Conclusions</b> This article demonstrates the feasibility of integrating LQAS into multistage cluster sampling surveys and using these results to support a comprehensive national, regional and local programme M&amp;E system. Furthermore, in the recommendations we outlined how to integrate the Large Country-LQAS design into macro-surveys while still obtaining results available through current sampling practices.</p>
]]></description>
<dc:creator><![CDATA[Biedron, C., Pagano, M., Hedt, B. L, Kilian, A., Ratcliffe, A., Mabunda, S., Valadez, J. J]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp363</dc:identifier>
<dc:title><![CDATA[An assessment of Lot Quality Assurance Sampling to evaluate malaria outcome indicators: extending malaria indicator surveys]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>79</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>72</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/80?rss=1">
<title><![CDATA[Bias correction of estimates of familial risk from population-based cohort studies]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/80?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In addition to guiding molecular epidemiology investigations, estimates of the increased risk of disease in relatives of affected persons are also important for screening and counselling decisions. Since precise estimation of such familial risks (FRs) requires large sample sizes, many of the estimates in common use have been obtained from historical electronic records of disease in entire populations, where the relatives of affected and unaffected persons are compared. These estimates may be biased due to failure to identify relatives as affected if they are diagnosed before the start-up date of disease registration.</p>
<p><b>Methods</b> This article presents a method for correcting the bias in FR estimates from such misclassification of family history, using a simple formula that depends on the prevalence and sensitivity of the observed family history. The sensitivity is estimated by using the R package <I>poplab</I> to create realistic populations of related individuals and then imposing the start-up effect of disease registration.</p>
<p><b>Results</b> For a range of FRs, the truncation of family history is demonstrated to result in non-differential misclassification, and sensitivity that has little or no dependence on the FR. The bias is most pronounced for high FRs and for registers with a short life span, and increases with the age of the study cohort. In all the situations studied, the bias-corrected estimates are in excellent agreement with the true values.</p>
<p><b>Conclusions</b> In summary, our method can correct the inevitable bias in FRs induced by using electronic population data, and is a feasible alternative to the use of validation samples.</p>
]]></description>
<dc:creator><![CDATA[Leu, M., Czene, K., Reilly, M.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp304</dc:identifier>
<dc:title><![CDATA[Bias correction of estimates of familial risk from population-based cohort studies]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>88</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>80</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/89?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/39/1/89?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>Sat, 06 Feb 2010 00:02:43 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>94</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>89</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/94?rss=1">
<title><![CDATA[Commentary: External validity of results of randomized trials: disentangling a complex concept]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/94?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rothwell, P. M]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp305</dc:identifier>
<dc:title><![CDATA[Commentary: External validity of results of randomized trials: disentangling a complex concept]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>96</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>94</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/97?rss=1">
<title><![CDATA[Causal thinking and complex system approaches in epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/97?rss=1</link>
<description><![CDATA[
<p> Identifying biological and behavioural causes of diseases has been one of the central concerns of epidemiology for the past half century. This has led to the development of increasingly sophisticated conceptual and analytical approaches focused on the isolation of single causes of disease states. However, the growing recognition that (i) factors at multiple levels, including biological, behavioural and group levels may influence health and disease, and (ii) that the interrelation among these factors often includes dynamic feedback and changes over time challenges this dominant epidemiological paradigm. Using obesity as an example, we discuss how the adoption of complex systems dynamic models allows us to take into account the causes of disease at multiple levels, reciprocal relations and interrelation between causes that characterize the causation of obesity. We also discuss some of the key difficulties that the discipline faces in incorporating these methods into non-infectious disease epidemiology. We conclude with a discussion of a potential way forward.</p>
]]></description>
<dc:creator><![CDATA[Galea, S., Riddle, M., Kaplan, G. A]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp296</dc:identifier>
<dc:title><![CDATA[Causal thinking and complex system approaches in epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>106</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>97</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/107?rss=1">
<title><![CDATA[Sensitivity analyses to estimate the potential impact of unmeasured confounding in causal research]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/107?rss=1</link>
<description><![CDATA[
<p><b>Background</b> The impact of unmeasured confounders on causal associations can be studied by means of sensitivity analyses. Although several sensitivity analyses are available, these are used infrequently. This article is intended as a tutorial on sensitivity analyses, in which we discuss three methods to conduct sensitivity analysis.</p>
<p><b>Methods</b> Each method is based on assumed associations between confounder and exposure, confounder and outcome and the prevalence of the confounder in the population at large. In the first method an unmeasured confounder is simulated and subsequently adjusted. The other two methods are analytical methods, in which either the (adjusted) effect estimate is multiplied with a factor based on assumed confounder characteristics, or the (adjusted) risks for the outcome among exposed and unexposed subjects are adjusted by such a factor. These methods are illustrated with a clinical example on influenza vaccine effectiveness.</p>
<p><b>Results</b> When applied to a dataset constructed to assess the effect of influenza vaccination on mortality, the three reviewed methods provided similar results. After adjustment for observed confounders, influenza vaccination reduced mortality by 42% [odds ratio (OR) 0.58, 95% confidence interval (CI) 0.46&ndash;0.73]. To arrive at a 95% CI including one requires a very common confounder (40% prevalence) with strong associations with both vaccination status and mortality, respectively OR &le;0.3 and OR &ge;3.0 (OR 0.79, 95% CI 0.62&ndash;1.00).</p>
<p><b>Conclusions</b> In every non-randomized study on causal associations the robustness of the results with respect to unmeasured confounding can, and should, be assessed using sensitivity analyses.</p>
]]></description>
<dc:creator><![CDATA[Groenwold, R. H H, Nelson, D. B, Nichol, K. L, Hoes, A. W, Hak, E.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp332</dc:identifier>
<dc:title><![CDATA[Sensitivity analyses to estimate the potential impact of unmeasured confounding in causal research]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>117</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>107</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/118?rss=1">
<title><![CDATA[Modelling relative survival in the presence of incomplete data: a tutorial]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/118?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Missing data frequently create problems in the analysis of population-based data sets, such as those collected by cancer registries. Restriction of analysis to records with complete data may yield inferences that are substantially different from those that would have been obtained had no data been missing. &lsquo;Naive&rsquo; methods for handling missing data, such as restriction of the analysis to complete records or creation of a &lsquo;missing&rsquo; category, have drawbacks that can invalidate the conclusions from the analysis. We offer a tutorial on modern methods for handling missing data in relative survival analysis.</p>
<p><b>Methods</b> We estimated relative survival for 29 563 colorectal cancer patients who were diagnosed between 1997 and 2004 and registered in the North West Cancer Intelligence Service. The method of multiple imputation (MI) was applied to account for the common example of incomplete stage at diagnosis, under the missing at random (MAR) assumption. Multivariable regression with a generalized linear model and Poisson error structure was then used to estimate the excess hazard of death of the colorectal cancer patients, over and above the background mortality, adjusting for significant predictors of mortality.</p>
<p><b>Results</b> Incomplete information on stage, morphology and grade meant that only 55% of the data could be included in the &lsquo;complete-case&rsquo; analysis. All cases could be included after indicator method (IM) or MI method. Handling missing data by MI produced a significantly lower estimate of the excess mortality for stage, morphology and grade, with the largest reductions occurring for late-stage and high-grade tumours, when compared with the results of complete-case analysis.</p>
<p><b>Conclusion</b> In complete-case analysis, almost 50% of the information could not be included, and with the IM, all records with missing values for stage were combined into a single &lsquo;missing&rsquo; category. We show that MI methods greatly improved the results by exploiting all the information in the incomplete records. This method also helped to ensure efficient inferences about survival were made from the multivariate regression analyses.</p>
]]></description>
<dc:creator><![CDATA[Nur, U., Shack, L. G, Rachet, B., Carpenter, J. R, Coleman, M. P]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp309</dc:identifier>
<dc:title><![CDATA[Modelling relative survival in the presence of incomplete data: a tutorial]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>128</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>118</prism:startingPage>
<prism:section>Theme: Methodology, Theory and Application</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/129?rss=1">
<title><![CDATA[Sibship size, Helicobacter pylori infection and chronic atrophic gastritis: a population-based study among 9444 older adults from Germany]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/129?rss=1</link>
<description><![CDATA[
<p><I><b>Background</b></I> Early-life social environment has been suggested to play an important role during the development of <I>Helicobacter pylori</I>-related gastric diseases. We aimed to assess the association of sibship size with <I>H. pylori</I> infection and chronic atrophic gastritis (CAG) in a population-based study from Germany.</p>
<p><I><b>Methods</b></I> In the baseline examination of ESTHER, a study conducted in Saarland, serological measurements of pepsinogen I and II and <I>H. pylori</I> antibodies were taken in 9444 participants aged 50&ndash;74 years. Information on potential risk factors and medical history were obtained by self-administered standardized questionnaire.</p>
<p><b>Results</b> A strong dose&ndash;response relationship between sibship size and <I>H. pylori</I> seroprevalence was observed (<I>P</I> &lt; 0.01). Adjusted odds ratios (ORs) 95% confidence interval (CI) for <I>H. pylori</I> seropositivity for subjects with 4, 5, 6 and 7 or more siblings compared with subjects without siblings were 1.45 (1.20&ndash;1.77), 1.83 (1.50&ndash;2.22) and 1.84 (1.47&ndash;2.31), respectively. A large sibship size was also associated with an increased risk of CAG with an adjusted OR of 1.42 (1.01&ndash;2.01) for 7 or more compared with less than or equal to 2 siblings. This association was attenuated but not entirely eliminated after additional adjustment for <I>H. pylori</I> infection. Notably, a significant association between large sibship size and CAG was also found among <I>H. pylori</I>-negative subjects.</p>
<p><I><b>Conclusions</b></I> Our results suggest that large sibship size is associated with increased <I>H. pylori</I> prevalence and CAG risk. The association with CAG risk may be mediated at least in part by <I>H. pylori</I> infection. However, mechanisms other than <I>H. pylori</I> infection may contribute to the &lsquo;sibling effect&rsquo; as well.</p>
]]></description>
<dc:creator><![CDATA[Gao, L., Weck, M. N, Raum, E., Stegmaier, C., Rothenbacher, D., Brenner, H.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp250</dc:identifier>
<dc:title><![CDATA[Sibship size, Helicobacter pylori infection and chronic atrophic gastritis: a population-based study among 9444 older adults from Germany]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>134</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>129</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/135?rss=1">
<title><![CDATA[Causes of death in HIV-infected women: persistent role of AIDS. The 'Mortalite 2000 & 2005' Surveys (ANRS EN19)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/135?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Little is known about the causes of death in human immunodeficiency virus (HIV)-infected women in the era of combination antiretroviral therapy (ART).</p>
<p><b>Methods</b> In the French nationwide Mortalit&eacute; 2000 and 2005 surveys, physicians reported causes of deaths in HIV-infected adults in 2000 and 2005, using a standardized questionnaire. We used multivariate logistic regression models to study the association between gender and AIDS-defining causes of death, adjusting for other characteristics.</p>
<p><b>Results</b> Of the 1013 HIV-infected adults who died in 2005, 247 (24%) were women. Half of women were infected through heterosexual contacts, compared with 25% men. In 2005, the proportion of AIDS-defining causes of death was higher in women than in men (43 vs 34%; <I>P</I> = 0.01), whereas it had been the same in 2000 (47% in women and men). In 2005, women died less frequently than men from respiratory malignancies (lung, ear/nose/throat) and cardiovascular disease (9% of all causes of death in women compared with 16% in men; <I>P</I> = 0.004), and suicides or accidents (4 vs 9%; <I>P</I> = 0.02). Socio-economic precariousness, younger age, less alcohol and tobacco consumption and lack of prior ART explained the higher proportion of deaths from AIDS in women compared with men.</p>
<p><b>Conclusions</b> The higher proportion of AIDS-related deaths in women is probably explained by two factors: (i) some HIV-infected women, especially migrants in poor socio-economic conditions, may not have access to optimal care; and (ii) a lower prevalence of risk factors for respiratory, cardiovascular and violent deaths means that the risk of dying from non-AIDS causes may be lower in women.</p>
]]></description>
<dc:creator><![CDATA[Hessamfar-Bonarek, M., Morlat, P., Salmon, D., Cacoub, P., May, T., Bonnet, F., Rosenthal, E., Costagliola, D., Lewden, C., Chene, G., the Mortalite 2000 & 2005 Study Groups]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp300</dc:identifier>
<dc:title><![CDATA[Causes of death in HIV-infected women: persistent role of AIDS. The 'Mortalite 2000 & 2005' Surveys (ANRS EN19)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>146</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>135</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/146?rss=1">
<title><![CDATA[Commentary: Treated HIV infection is a chronic disease: the case against cause of death analyses]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/146?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Justice, A. C]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp342</dc:identifier>
<dc:title><![CDATA[Commentary: Treated HIV infection is a chronic disease: the case against cause of death analyses]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>148</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>146</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/149?rss=1">
<title><![CDATA[A consistent log-linear relationship between tuberculosis incidence and body mass index]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/149?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Low weight for height is an established risk factor for tuberculosis (TB), and recent studies suggest that overweight is a protective factor. No previous systematic review has been done to explore the consistency and establish the gradient of this apparent &lsquo;dose&ndash;response&rsquo; relationship.</p>
<p><b>Methods</b> A systematic literature review was carried out to identify cohort studies that collected data on weight and height at baseline and that used a diagnosis of active TB as the study outcome. Weight-for-height measures used in the original studies were transformed into body mass index (BMI). Exponential trend lines were fitted to each data set.</p>
<p><b>Results</b> Six studies were included. In all of them, there was a log-linear inverse relationship between TB incidence and BMI, within the BMI range 18.5&ndash;30 kg/m<sup>2</sup>. The average slope gave a reduction in TB incidence of 13.8% [95% confidence interval 13.4&ndash;14.2] per unit increase in BMI. The dose&ndash;response relationship was less certain at BMI &lt;18.5 and &gt;30 kg/m<sup>2</sup>.</p>
<p><b>Conclusion</b> There is a strong and consistent log-linear relationship between TB incidence and BMI across a variety of settings with different levels of TB burden. More research is required to test the relationship at very low and very high BMI levels, to establish the biological mechanism linking BMI with risk of TB and to establish the potential impact on the global TB epidemic of changing nutritional status of populations.</p>
]]></description>
<dc:creator><![CDATA[Lonnroth, K., Williams, B. G, Cegielski, P., Dye, C.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp308</dc:identifier>
<dc:title><![CDATA[A consistent log-linear relationship between tuberculosis incidence and body mass index]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>155</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>149</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/156?rss=1">
<title><![CDATA[Does screening history explain the ethnic differences in stage at diagnosis of cervical cancer in New Zealand?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/156?rss=1</link>
<description><![CDATA[
<p><b>Background</b> There are ethnic disparities in cervical cancer survival in New Zealand. The objectives of this study were to assess the associations of screening history, ethnicity, socio-economic status (SES) and rural residence with stage at diagnosis in women diagnosed with cervical cancer in New Zealand during 1994&ndash;2005.</p>
<p><b>Methods</b> The 2323 cases were categorized as &lsquo;ever screened&rsquo; if they had had at least one smear prior to 6 months before diagnosis, and as &lsquo;regular screening&rsquo; if they had had no more than 36 months between any two smears in the period 6&ndash;114 months before diagnosis. Logistic regression was used to estimate the associations of screening history, ethnicity, SES and urban/rural residence with stage at diagnosis.</p>
<p><b>Results</b> The percentages &lsquo;ever screened&rsquo; were 43.3% overall, 24.8% in Pacific, 30.5% in Asian, 40.6% in Maori and 46.1% in &lsquo;Other&rsquo; women. The corresponding estimates for &lsquo;regular screening&rsquo; were 14.0, 5.7, 7.8, 12.5 and 15.3%. Women with &lsquo;regular screening&rsquo; had a lower risk of late stage diagnosis [odds ratio (OR) 0.16, 95% confidence interval (CI) 0.10&ndash;0.26], and the effect was greater for squamous cell carcinoma (OR 0.12, 95% CI 0.07&ndash;0.23) than for adenocarcinoma (OR 0.32, 95% CI 0.13&ndash;0.82). The increased risk of late-stage diagnosis (OR 2.72, 95% CI 1.99&ndash;3.72) in Maori (compared with &lsquo;Other&rsquo;) women decreased only slightly when adjusted for screening history (OR 2.45, 95% CI 1.77&ndash;3.39).</p>
<p><b>Conclusions</b> Over half of cases had not been &lsquo;ever screened&rsquo;. Regular screening substantially lowered the risk of being diagnosed at a late stage. However, screening history does not appear to explain the ethnic differences in stage at diagnosis.</p>
]]></description>
<dc:creator><![CDATA[Brewer, N., Pearce, N., Jeffreys, M., Borman, B., Ellison-Loschmann, L.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp303</dc:identifier>
<dc:title><![CDATA[Does screening history explain the ethnic differences in stage at diagnosis of cervical cancer in New Zealand?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>165</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>156</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/166?rss=1">
<title><![CDATA[Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/166?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Sexual contact may be the means by which head and neck cancer patients are exposed to human papillomavirus (HPV).</p>
<p><b>Methods</b> We undertook a pooled analysis of four population-based and four hospital-based case&ndash;control studies from the International Head and Neck Cancer Epidemiology (INHANCE) consortium, with participants from Argentina, Australia, Brazil, Canada, Cuba, India, Italy, Spain, Poland, Puerto Rico, Russia and the USA. The study included 5642 head and neck cancer cases and 6069 controls. We calculated odds ratios (ORs) of associations between cancer and specific sexual behaviours, including practice of oral sex, number of lifetime sexual partners and oral sex partners, age at sexual debut, a history of same-sex contact and a history of oral&ndash;anal contact. Findings were stratified by sex and disease subsite.</p>
<p><b>Results</b> Cancer of the oropharynx was associated with having a history of six or more lifetime sexual partners [OR = 1.25, 95% confidence interval (CI) 1.01, 1.54] and four or more lifetime oral sex partners (OR = 2.25, 95% CI 1.42, 3.58). Cancer of the tonsil was associated with four or more lifetime oral sex partners (OR = 3.36, 95 % CI 1.32, 8.53), and, among men, with ever having oral sex (OR = 1.59, 95% CI 1.09, 2.33) and with an earlier age at sexual debut (OR = 2.36, 95% CI 1.37, 5.05). Cancer of the base of the tongue was associated with ever having oral sex among women (OR = 4.32, 95% CI 1.06, 17.6), having two sexual partners in comparison with only one (OR = 2.02, 95% CI 1.19, 3.46) and, among men, with a history of same-sex sexual contact (OR = 8.89, 95% CI 2.14, 36.8).</p>
<p><b>Conclusions</b> Sexual behaviours are associated with cancer risk at the head and neck cancer subsites that have previously been associated with HPV infection.</p>
]]></description>
<dc:creator><![CDATA[Heck, J. E, Berthiller, J., Vaccarella, S., Winn, D. M, Smith, E. M, Shan'gina, O., Schwartz, S. M, Purdue, M. P, Pilarska, A., Eluf-Neto, J., Menezes, A., McClean, M. D, Matos, E., Koifman, S., Kelsey, K. T, Herrero, R., Hayes, R. B, Franceschi, S., Wunsch-Filho, V., Fernandez, L., Daudt, A. W, Curado, M. P., Chen, C., Castellsague, X., Ferro, G., Brennan, P., Boffetta, P., Hashibe, M.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp350</dc:identifier>
<dc:title><![CDATA[Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>181</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>166</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/182?rss=1">
<title><![CDATA[Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/182?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Quitting tobacco or alcohol use has been reported to reduce the head and neck cancer risk in previous studies. However, it is unclear how many years must pass following cessation of these habits before the risk is reduced, and whether the risk ultimately declines to the level of never smokers or never drinkers.</p>
<p><b>Methods</b> We pooled individual-level data from case&ndash;control studies in the International Head and Neck Cancer Epidemiology Consortium. Data were available from 13 studies on drinking cessation (9167 cases and 12 593 controls), and from 17 studies on smoking cessation (12 040 cases and 16 884 controls). We estimated the effect of quitting smoking and drinking on the risk of head and neck cancer and its subsites, by calculating odds ratios (ORs) using logistic regression models.</p>
<p><b>Results</b> Quitting tobacco smoking for 1&ndash;4 years resulted in a head and neck cancer risk reduction [OR 0.70, confidence interval (CI) 0.61&ndash;0.81 compared with current smoking], with the risk reduction due to smoking cessation after &ge;20 years (OR 0.23, CI 0.18&ndash;0.31), reaching the level of never smokers. For alcohol use, a beneficial effect on the risk of head and neck cancer was only observed after &ge;20 years of quitting (OR 0.60, CI 0.40&ndash;0.89 compared with current drinking), reaching the level of never drinkers.</p>
<p><b>Conclusions</b> Our results support that cessation of tobacco smoking and cessation of alcohol drinking protect against the development of head and neck cancer.</p>
]]></description>
<dc:creator><![CDATA[Marron, M., Boffetta, P., Zhang, Z.-F., Zaridze, D., Wunsch-Filho, V., Winn, D. M, Wei, Q., Talamini, R., Szeszenia-Dabrowska, N., Sturgis, E. M, Smith, E., Schwartz, S. M, Rudnai, P., Purdue, M. P, Olshan, A. F, Eluf-Neto, J., Muscat, J., Morgenstern, H., Menezes, A., McClean, M., Matos, E., Mates, I. N., Lissowska, J., Levi, F., Lazarus, P., Vecchia, C. L., Koifman, S., Kelsey, K., Herrero, R., Hayes, R. B, Franceschi, S., Fernandez, L., Fabianova, E., Daudt, A. W, Maso, L. D., Curado, M. P., Cadoni, G., Chen, C., Castellsague, X., Boccia, S., Benhamou, S., Ferro, G., Berthiller, J., Brennan, P., Moller, H., Hashibe, M.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp291</dc:identifier>
<dc:title><![CDATA[Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>196</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>182</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/197?rss=1">
<title><![CDATA[Dietary patterns and the risk of mortality: impact of cardiorespiratory fitness]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/197?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>Sat, 06 Feb 2010 00:02:43 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>209</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>197</prism:startingPage>
<prism:section>Diabetes</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/209?rss=1">
<title><![CDATA[Commentary: Relative importance of diet vs physical activity for health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/209?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ding, E. L, Hu, F. B]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp348</dc:identifier>
<dc:title><![CDATA[Commentary: Relative importance of diet vs physical activity for health]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>211</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>209</prism:startingPage>
<prism:section>Diabetes</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/211?rss=1">
<title><![CDATA[Commentary: Physical fitness: confounder or intermediary variable in the association of diet with health outcomes?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/211?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pischon, T.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp347</dc:identifier>
<dc:title><![CDATA[Commentary: Physical fitness: confounder or intermediary variable in the association of diet with health outcomes?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>213</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>211</prism:startingPage>
<prism:section>Diabetes</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/213?rss=1">
<title><![CDATA[Author's Response * Dietary patterns and the risk of mortality: impact of cardiorespiratory fitness]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/213?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Heroux, M., Janssen, I.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp349</dc:identifier>
<dc:title><![CDATA[Author's Response * Dietary patterns and the risk of mortality: impact of cardiorespiratory fitness]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>214</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>213</prism:startingPage>
<prism:section>Diabetes</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/215?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/39/1/215?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>Sat, 06 Feb 2010 00:02:43 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>222</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>215</prism:startingPage>
<prism:section>Diabetes</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/223?rss=1">
<title><![CDATA[Commentary: Heart rate and blood pressure: risk factors or risk markers?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/223?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Carnethon, M. R]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp325</dc:identifier>
<dc:title><![CDATA[Commentary: Heart rate and blood pressure: risk factors or risk markers?]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>224</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>223</prism:startingPage>
<prism:section>Diabetes</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/225?rss=1">
<title><![CDATA[Abdominal aortic aneurysms, or a relatively large diameter of non-aneurysmal aortas, increase total and cardiovascular mortality: the Tromso study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/225?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In a population-based study in Troms&oslash;, Norway, the authors assessed whether an abdominal aortic aneurysm (AAA) or the maximal infrarenal aortic diameter in a non-aneurismal aorta influence total and cardiovascular disease (CVD) mortality.</p>
<p><b>Methods</b> A total of 6640 men and women, aged 25&ndash;84 years, were included in a 10-year mortality follow-up: 345 subjects with a diagnosed AAA and 6295 subjects with a non-aneurismal aorta. Non-aneurismal aortic diameter and prevalent AAAs were categorized into seven groups.</p>
<p><b>Results</b> In subjects without an AAA, an aortic diameter &ge;30 mm increased age- and sex-adjusted total mortality [mortality rate ratio (MRR) = 3.73, 95% confidence interval (CI) 1.77&ndash;7.89] and CVD mortality (MRR = 9.24, 95% CI 4.07&ndash;20.97) compared with subjects with aortic diameter of 21&ndash;23 mm. An AAA at screening was strongly associated with deaths from aortic aneurysm and was associated with total (MRR = 1.60, 95% CI 1.31&ndash;1.96) and CVD mortality (MRR = 2.41, 95% CI 1.81&ndash;3.21). This was not explained by deaths due to an AAA. Adjustments for CVD risk factors could fully explain the increased total, but not CVD mortality in subjects with an AAA.</p>
<p><b>Conclusions</b> An AAA increases total and CVD mortality. In the large majority of subjects with a non-aneurysmal aorta, the diameter does not influence total or CVD mortality. However, in individuals with a maximal diameter &gt;26 mm (2% of the population), a positive relationship is found.</p>
]]></description>
<dc:creator><![CDATA[Forsdahl, S. H., Solberg, S., Singh, K., Jacobsen, B. K]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp320</dc:identifier>
<dc:title><![CDATA[Abdominal aortic aneurysms, or a relatively large diameter of non-aneurysmal aortas, increase total and cardiovascular mortality: the Tromso study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>232</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>225</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/233?rss=1">
<title><![CDATA[Daytime napping and mortality, with a special reference to cardiovascular disease: the JACC study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/233?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Daytime napping is associated with elevated risk of all-cause mortality in the elderly. However, the association with cardiovascular disease (CVD) risk is inconsistent.</p>
<p><b>Methods</b> From 1988 to 1990, a total of 67 129 Japanese non-workers or daytime workers (27 755 men and 39 374 women) aged 40&ndash;79 years, without a history of stroke, heart disease or cancer, completed a lifestyle questionnaire. They were followed for mortality until the end of 2003.</p>
<p><b>Results</b> During the 879 244 person-year follow-up, 9643 deaths (2852 from CVD, 3643 from cancer, 2392 from other internal causes, 738 from external causes and 18 from unspecified causes) were observed. After adjustment for possible confounders, subjects with a daytime napping habit had elevated hazard ratios (HRs) for mortality from all causes [HR 1.19, 95% confidence interval (CI) 1.14&ndash;1.24, <I>P</I> &lt; 0.001], CVD (HR 1.31, 95% CI 1.22&ndash;1.42, <I>P</I> &lt; 0.001), non-cardiovascular/non-cancer internal diseases (HR 1.26, 95% CI 1.16&ndash;1.37, <I>P</I> &lt; 0.001) and external causes (HR 1.28, 95% CI 1.10&ndash;1.50, <I>P</I> = 0.001), but not for cancer death (HR 1.03, 95% CI 0.96&ndash;1.10, <I>P</I> = 0.400). The risk of CVD mortality associated with daytime napping was diminished among overweight subjects, but pronounced in those with weight loss after age 20 years, with non-regular employment, with lower education level and with a follow-up period &lt;5 years.</p>
<p><b>Conclusions</b> Daytime napping is associated with elevated risk of CVD mortality as well as non-cardiovascular/non-cancer and external deaths. Daytime napping may elevate risk of CVD death through some biological effects but, to a larger extent, some comorbid disorders causing weight loss or associated with non-regular employment and low education level could explain this association.</p>
]]></description>
<dc:creator><![CDATA[Tanabe, N., Iso, H., Seki, N., Suzuki, H., Yatsuya, H., Toyoshima, H., Tamakoshi, A., for the JACC Study Group]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp327</dc:identifier>
<dc:title><![CDATA[Daytime napping and mortality, with a special reference to cardiovascular disease: the JACC study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>243</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>233</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/244?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/39/1/244?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>Sat, 06 Feb 2010 00:02:43 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>254</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>244</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/254?rss=1">
<title><![CDATA[Commentary: The challenge of prevention in China]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/254?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McGhee, S. M, Hedley, A. J]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp381</dc:identifier>
<dc:title><![CDATA[Commentary: The challenge of prevention in China]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>255</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>254</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/256?rss=1">
<title><![CDATA[Long-term association of routine blood count (Coulter) variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/256?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Since evidence of a long-term association between routine blood count (Coulter) variables and coronary heart disease (CHD) is inconsistent, the authors analysed white blood cell count (WBC), red blood cell count (RBC), haemoglobin (Hgb), packed cell volume (PCV) and platelet count for their long-term associations with CHD mortality in the first Northwick Park Heart Study (NPHS-I). NPHS-I has follow-up information for &gt;30 years on 2167 White men and 941 White women and holds entry and follow-up data on haematological variables and other known CHD risk factors.</p>
<p><b>Methods</b> Proportional hazards Cox models were fitted to estimate rate ratios (RRs) for the separate and joint effects of entry and follow-up Coulter variables.</p>
<p><b>Results</b> Entry RBC, PCV and Hgb were significant risk factors for CHD mortality after adjustment for gender but only PCV remained significant after adjustment for potential confounders [RR per 1 standard deviation (SD) increase = 1.17, 95% confidence interval (CI) 1.00&ndash;1.37]. This effect was partly reduced when the values of 6 years were analysed (RR per 1 SD increase = 1.10, 95% CI 0.93&ndash;1.30). No significant gender, smoking or age/time interactions were identified. PCV was the only significant predictor when all Coulter variables were studied jointly.</p>
<p><b>Conclusion</b> PCV was found to predict CHD mortality even after controlling for classical risk factors. This may give some insight into possible mechanisms, such as an influence on thrombin production.</p>
]]></description>
<dc:creator><![CDATA[Pizzi, C., De Stavola, B. L, Meade, T. W]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp245</dc:identifier>
<dc:title><![CDATA[Long-term association of routine blood count (Coulter) variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>265</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>256</prism:startingPage>
<prism:section>Cardiovascular Disease</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/266?rss=1">
<title><![CDATA[Action towards healthy living--for all]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/266?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Morris, J., Deeming, C., Wilkinson, P., Dangour, A. D]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp403</dc:identifier>
<dc:title><![CDATA[Action towards healthy living--for all]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>273</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>266</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/274?rss=1">
<title><![CDATA[Appreciation: Jerry [Jeremiah Noah] Morris, 1910-2009]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/274?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Oakley, A.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp390</dc:identifier>
<dc:title><![CDATA[Appreciation: Jerry [Jeremiah Noah] Morris, 1910-2009]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>276</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>274</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/277?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/39/1/277?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>Sat, 06 Feb 2010 00:02:43 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>284</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>277</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/285?rss=1">
<title><![CDATA[Child development in a birth cohort: effect of child stimulation is stronger in less educated mothers]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/285?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Child health has improved in many developing countries, bringing new challenges, including realization of the children's full physical and intellectual potential. This study explored child development within a birth cohort, its psychosocial determinants and interactions with maternal schooling and economic position.</p>
<p><b>Methods</b> All children born in Pelotas, Brazil, in 2004, were recruited to a birth cohort study. These children were assessed at birth and at 3, 12 and 24 months of age. In this last assessment involving 3869 children, detailed information on socio-economic and health characteristics was collected. Child development was assessed using the screening version of Battelle's Development Inventory. Five markers of cognitive stimulation and social interaction were recorded and summed to form a score ranging from 0&ndash;5. The outcomes studied were mean development score and low performance (less than 10th percentile of the sample).</p>
<p><b>Results</b> Child development was strongly associated with socio-economic position, maternal schooling and stimulation. Having been told a story and owning a book were the least frequent markers among children with score 1. These children were 8.3 times more likely to present low performance than those who scored 5. The effect of stimulation was much stronger among children from mothers with a low level of schooling&mdash;one additional point added 1.7 on the child's development for children of low-schooling mothers, whereas only 0.6 was added for children of high-schooling mothers.</p>
<p><b>Conclusions</b> Our stimulation markers cannot be directly translated into intervention strategies, but strongly suggest that suitably designed cognitive stimulation can have an important effect on children, especially those from mothers with low schooling.</p>
]]></description>
<dc:creator><![CDATA[Barros, A. J., Matijasevich, A., Santos, I. S, Halpern, R.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp272</dc:identifier>
<dc:title><![CDATA[Child development in a birth cohort: effect of child stimulation is stronger in less educated mothers]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>294</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>285</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/294?rss=1">
<title><![CDATA[Commentary: Early stimulation and child development]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/294?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Walker, S. P]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp316</dc:identifier>
<dc:title><![CDATA[Commentary: Early stimulation and child development]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>296</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>294</prism:startingPage>
<prism:section>Social Epidemiology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/297?rss=1">
<title><![CDATA[Does breastfeeding protect against childhood overweight? Hong Kong's 'Children of 1997' birth cohort]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/297?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Observational studies from mainly Western settings suggest breastfeeding may protect against childhood adiposity; however, breastfeeding and adiposity share social patterning potentially generating confounding, making evidence from other settings valuable.</p>
<p><b>Methods</b> We used multivariable linear regression to examine the prospective adjusted associations of breastfeeding with body mass index (BMI), height and weight <I>z</I>-scores at 7 years of age relative to the 2007 World Health Organization (WHO) growth reference, in a large (<I>n</I> = 8327), population-representative Hong Kong Chinese birth cohort, recruited between April and May 1997 with high follow-up (<I>n</I> = 7026).</p>
<p><b>Results</b> Low socio-economic position (SEP) was associated with never breastfeeding and with exclusive breastfeeding for &ge;3 months. We did not find any association between breastfeeding and BMI [<I>z</I>-score mean difference 0.07, 95% confidence interval (CI) &ndash;0.05 to 0.19], height (0.02, 95% CI &ndash;0.07 to 0.11) or weight (0.07, 95% CI &ndash;0.05 to 0.18), adjusted for sex, birth weight, gestational age, SEP, second-hand smoke (SHS) exposure, parity, mother's age at birth, mother's place of birth and serious infant morbidity.</p>
<p><b>Conclusions</b> In a non-European setting, breastfeeding was not associated with child adiposity, suggesting that observed protective effects may be due to socially patterned confounding by SEP, maternal adiposity and maternal smoking.</p>
]]></description>
<dc:creator><![CDATA[Kwok, M. K., Schooling, C M., Lam, T. H., Leung, G. M]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp274</dc:identifier>
<dc:title><![CDATA[Does breastfeeding protect against childhood overweight? Hong Kong's 'Children of 1997' birth cohort]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>305</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>297</prism:startingPage>
<prism:section>Pediatrics</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/306?rss=1">
<title><![CDATA[Commentary: Assessing the impact of breastfeeding on child health: where conventional methods alone fall short for reliably establishing causal inference]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/306?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Brion, M.-J.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp318</dc:identifier>
<dc:title><![CDATA[Commentary: Assessing the impact of breastfeeding on child health: where conventional methods alone fall short for reliably establishing causal inference]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>307</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>306</prism:startingPage>
<prism:section>Pediatrics</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/308?rss=1">
<title><![CDATA[Raising the bar on telomere epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/308?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ehrlenbach, S., Willeit, P., Kiechl, S., Willeit, J., Reindl, M., Schanda, K., Kronenberg, F., Brandstatter, A.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp383</dc:identifier>
<dc:title><![CDATA[Raising the bar on telomere epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>317</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>308</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/309?rss=1">
<title><![CDATA[Chronic disease prevention: the importance of calls to action]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/309?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>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn245</dc:identifier>
<dc:title><![CDATA[Chronic disease prevention: the importance of calls to action]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>310</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>309</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/310?rss=1">
<title><![CDATA[Chronic diseases and calls to action]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/310?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[De Backer, G., Kornitzer, M]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn246</dc:identifier>
<dc:title><![CDATA[Chronic diseases and calls to action]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>311</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>310</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/312?rss=1">
<title><![CDATA[Author's Response]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/312?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ebrahim, S.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn247</dc:identifier>
<dc:title><![CDATA[Author's Response]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>313</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>312</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/313?rss=1">
<title><![CDATA[Hygiene hypothesis: wanted--dead or alive]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/313?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Linneberg, A.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn269</dc:identifier>
<dc:title><![CDATA[Hygiene hypothesis: wanted--dead or alive]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>314</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>313</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/314?rss=1">
<title><![CDATA[Author's Response * Hygiene hypothesis: wanted--dead or alive]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/314?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Douwes, J., Pearce, N.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn270</dc:identifier>
<dc:title><![CDATA[Author's Response * Hygiene hypothesis: wanted--dead or alive]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>317</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>314</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/318?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/39/1/318?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dutta, S.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn349</dc:identifier>
<dc:title><![CDATA[Clinical Epidemiology: Principles, Methods and Applications for Clinical Research. D E Grobbee and A W Hoes.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>319</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>318</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/319?rss=1">
<title><![CDATA[Environmental Epidemiology--Principles and Methods. RM Merrill.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/319?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Huss, A.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</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:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>320</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>319</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/39/1/320?rss=1">
<title><![CDATA[Adverse Reactions. The Fenoterol Story. Neil Pearce.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/39/1/320?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Anderson, H. R.]]></dc:creator>
<dc:date>Sat, 06 Feb 2010 00:02:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp138</dc:identifier>
<dc:title><![CDATA[Adverse Reactions. The Fenoterol Story. Neil Pearce.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>1</prism:number>
<prism:volume>39</prism:volume>
<prism:endingPage>321</prism:endingPage>
<prism:publicationDate>2010-02-01</prism:publicationDate>
<prism:startingPage>320</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1423?rss=1">
<title><![CDATA[Don't forget to wash your hands!]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1423?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ebrahim, S.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:41 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp362</dc:identifier>
<dc:title><![CDATA[Don't forget to wash your hands!]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1424</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1423</prism:startingPage>
<prism:section>Editor's Choice</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1425?rss=1">
<title><![CDATA[Annie Darwin's death, the evolution of tuberculosis and the need for systems epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1425?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Fenner, L., Egger, M., Gagneux, S.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp367</dc:identifier>
<dc:title><![CDATA[Annie Darwin's death, the evolution of tuberculosis and the need for systems epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1428</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1425</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1429?rss=1">
<title><![CDATA[Marriages between first cousins in England and their effects]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1429?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Darwin, G. H]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp335</dc:identifier>
<dc:title><![CDATA[Marriages between first cousins in England and their effects]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1439</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1429</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1439?rss=1">
<title><![CDATA[Commentary: A Darwin family concern]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1439?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kuper, A.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp310</dc:identifier>
<dc:title><![CDATA[Commentary: A Darwin family concern]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1442</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1439</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1442?rss=1">
<title><![CDATA[Commentary: Of the same blood]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1442?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stoltenberg, C.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp312</dc:identifier>
<dc:title><![CDATA[Commentary: Of the same blood]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1447</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1442</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1448?rss=1">
<title><![CDATA[Commentary: Darwin's Origin: the Irish connection]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1448?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Evans, A.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp311</dc:identifier>
<dc:title><![CDATA[Commentary: Darwin's Origin: the Irish connection]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1452</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1448</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1453?rss=1">
<title><![CDATA[Commentary: The background and outcomes of the first-cousin marriage controversy in Great Britain]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1453?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bittles, A H]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp313</dc:identifier>
<dc:title><![CDATA[Commentary: The background and outcomes of the first-cousin marriage controversy in Great Britain]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1458</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1453</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1459?rss=1">
<title><![CDATA[Gains of stopping smoking: portraits of the dialogue between public health promotion, art and design]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1459?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Szklo, A. S, Coutinho, E. S F, Spitz, R., Gamba, N.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp251</dc:identifier>
<dc:title><![CDATA[Gains of stopping smoking: portraits of the dialogue between public health promotion, art and design]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1463</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1459</prism:startingPage>
<prism:section>Photoessay</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1464?rss=1">
<title><![CDATA[Cohort Profile: the Jerusalem longitudinal cohort study]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1464?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>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn252</dc:identifier>
<dc:title><![CDATA[Cohort Profile: the Jerusalem longitudinal cohort study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1469</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1464</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1470?rss=1">
<title><![CDATA[Cohort Profile: The biopsychosocial religion and health study (BRHS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1470?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>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn244</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The biopsychosocial religion and health study (BRHS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1478</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1470</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1479?rss=1">
<title><![CDATA[Cohort Profile: The North West Adelaide Health Study (NWAHS)]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1479?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>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn262</dc:identifier>
<dc:title><![CDATA[Cohort Profile: The North West Adelaide Health Study (NWAHS)]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1486</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1479</prism:startingPage>
<prism:section>Cohort Profiles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1487?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/38/6/1487?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>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn260</dc:identifier>
<dc:title><![CDATA[Seasonality of rotavirus disease in the tropics: a systematic review and meta-analysis]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1496</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1487</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1497?rss=1">
<title><![CDATA[Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1497?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Whereas the International Agency for Research on Cancer (IARC) Monograph concluded that the evidence for the relationship between cigarette smoking and liver cancer is sufficient, the US Surgeon General's report summarized the data as suggestive but not sufficient.</p>
<p><b>Methods</b> A meta-analysis of previous epidemiologic studies may help to clarify the potential association. We identified 38 cohort studies and 58 case&ndash;control studies in a systematic literature search for studies on liver cancer and cigarette smoking. The meta-relative risk (mRR) of liver cancer and dose&ndash;response trends were calculated. Tests for heterogeneity, publication bias assessment and influence analyses were performed.</p>
<p><b>Results</b> Compared with never smokers, the adjusted mRR was 1.51 [95% confidence interval (CI) 1.37&ndash;1.67] for current smokers and 1.12 (95% CI 0.78&ndash;1.60) for former smokers. The increased liver cancer risk among current smokers appeared to be consistent in strata of different regions, study designs, study sample sizes and publication periods.</p>
<p><b>Conclusion</b> The results of our meta-analysis show that tobacco smoking is associated with liver cancer development, which supports the conclusion by the IARC Monograph. This conclusion has an important public health message for areas with high smoking prevalence and high liver cancer incidence such as China.</p>
]]></description>
<dc:creator><![CDATA[Lee, Y.-C. A., Cohet, C., Yang, Y.-C., Stayner, L., Hashibe, M., Straif, K.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp280</dc:identifier>
<dc:title><![CDATA[Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1511</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1497</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1512?rss=1">
<title><![CDATA[Risk of cancer among hairdressers and related workers: a meta-analysis]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1512?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Hairdressers and allied occupations represent a large and fast growing group of professionals. The fact that these professionals are chronically exposed to a large number of chemicals present in their work environment, including potential carcinogens contained in hair dyes, makes it necessary to carry out a systematic evaluation of the risk of cancer in this group.</p>
<p><b>Methods</b> We retrieved studies by systematically searching Medline and other computerized databases, and by manually examining the references of the original articles and monographs retrieved. We also contacted international researchers working on this or similar topics to complete our search. We included 247 studies reporting relative risk (RR) estimates of hairdresser occupation and cancer of different sites.</p>
<p><b>Results</b> Study-specific RRs were weighted by the inverse of their variance to obtain fixed and random effects pooled estimates. The pooled RR of occupational exposure as a hairdresser was 1.27 (95% CI 1.15&ndash;1.41) for lung cancer, 1.52 [95% confidence interval (CI) 1.11&ndash;2.08] for larynx cancer, 1.30 (95% CI 1.20&ndash;1.42) for bladder cancer and 1.62 (95% CI 1.22&ndash;2.14) for multiple myeloma. Data for other anatomic sites showed increases of smaller magnitude. The results restricted to those studies carried out before the ban of two major carcinogens from hair dyes in the mid-1970s were similar to the general results.</p>
<p><b>Conclusions</b> Hairdressers have a higher risk of cancer than the general population. Improvement of the ventilation system in the hairdresser salons and implementation of hygiene measures aimed at mitigating exposure to potential carcinogens at work may reduce the risk.</p>
]]></description>
<dc:creator><![CDATA[Takkouche, B., Regueira-Mendez, C., Montes-Martinez, A.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp283</dc:identifier>
<dc:title><![CDATA[Risk of cancer among hairdressers and related workers: a meta-analysis]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1531</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1512</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1532?rss=1">
<title><![CDATA[A systematic review and meta-analysis of perinatal variables in relation to the risk of testicular cancer--experiences of the mother]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1532?rss=1</link>
<description><![CDATA[
<p><b>Background</b> We undertook a systematic review and meta-analysis of perinatal variables in relation to testicular cancer risk, with a specific focus upon characteristics of the mother.</p>
<p><b>Methods</b> EMBASE, PubMed, Scopus and Web of Science databases were searched using sensitive search strategies. Meta-analysis was undertaken using STATA 10.</p>
<p><b>Results</b> A total of 5865 references were retrieved, of which 67 met the inclusion criteria and contributed data to at least one perinatal analysis. Random effects meta-analysis found maternal bleeding during pregnancy [odds ratio (OR) 1.33, 95% confidence interval (CI) 1.02&ndash;1.73], birth order (primiparous vs not, 1.08, 95% CI 1.01&ndash;1.16; second vs first, OR 0.94, 95% CI 0.88&ndash;0.99; third vs first, OR 0.91, 95% CI 0.83&ndash;1.01; fourth vs first, OR 0.80, 95% CI 0.69&ndash;0.94) and sibship size (2 vs 1, OR 0.93, 95% CI 0.75&ndash;1.15; 3 vs 1, OR 0.89, 95% CI 0.74&ndash;1.07; 4 vs 1, OR 0.75, 95% CI 0.62&ndash;0.90) to be associated with testicular cancer risk. Meta-analyses that produced summary estimates which indicated no association included maternal age, maternal nausea, maternal hypertension, pre-eclampsia, breech delivery and caesarean section. Meta-regression provided evidence that continent of study is important in the relationship between caesarean section and testicular cancer (<I>P</I> = 0.035), and a meta-analysis restricted to the three studies from the USA was suggestive of association (OR 1.67, 95% CI 1.07&ndash;2.56).</p>
<p><b>Conclusions</b> This systematic review and meta-analysis has found evidence for associations of maternal bleeding, birth order, sibship size and possibly caesarean section with risk of testicular cancer.</p>
]]></description>
<dc:creator><![CDATA[Cook, M. B, Akre, O., Forman, D., Madigan, M P., Richiardi, L., McGlynn, K. A]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:42 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp287</dc:identifier>
<dc:title><![CDATA[A systematic review and meta-analysis of perinatal variables in relation to the risk of testicular cancer--experiences of the mother]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1542</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1532</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1543?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/38/6/1543?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>Tue, 01 Dec 2009 06:07:42 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1551</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1543</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1551?rss=1">
<title><![CDATA[Commentary: How does 'insurance' improve equity in health?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1551?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Starfield, B.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1553</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1551</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1554?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/38/6/1554?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>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1570</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1554</prism:startingPage>
<prism:section>Systematic Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1571?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/38/6/1571?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>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1579</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1571</prism:startingPage>
<prism:section>Cardiovascular Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1580?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/38/6/1580?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>Tue, 01 Dec 2009 06:07:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn258</dc:identifier>
<dc:title><![CDATA[Environmental and societal influences acting on cardiovascular risk factors and disease at a population level: a review]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1594</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1580</prism:startingPage>
<prism:section>Cardiovascular Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1595?rss=1">
<title><![CDATA[Commentary: Societal influences on cardiovascular disease: time to assess and act]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1595?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Prabhakaran, D., Roy, A.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp295</dc:identifier>
<dc:title><![CDATA[Commentary: Societal influences on cardiovascular disease: time to assess and act]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1598</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1595</prism:startingPage>
<prism:section>Cardiovascular Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1599?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/38/6/1599?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>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1611</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1599</prism:startingPage>
<prism:section>Cardiovascular Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1612?rss=1">
<title><![CDATA[Anti-retroviral therapy reduces incident tuberculosis in HIV-infected children]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1612?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>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1621</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1612</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1621?rss=1">
<title><![CDATA[Commentary: Reducing HIV-associated tuberculosis in children]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1621?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Boulle, A., Eley, B.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp301</dc:identifier>
<dc:title><![CDATA[Commentary: Reducing HIV-associated tuberculosis in children]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1623</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1621</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1624?rss=1">
<title><![CDATA[Mortality of HIV-infected patients starting potent antiretroviral therapy: comparison with the general population in nine industrialized countries]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1624?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Mortality in HIV-infected patients has declined substantially with combination antiretroviral therapy (ART), but it is unclear whether it has reached that of the general population. We compared mortality in patients starting ART in nine countries of Europe and North America with the corresponding general population, taking into account their response to ART.</p>
<p><b>Methods</b> Eligible patients were enrolled in prospective cohort studies participating in the ART Cohort Collaboration. We calculated the ratio of observed to expected deaths from all causes [standardized mortality ratio (SMR)], measuring time from 6 months after starting ART, according to risk group, clinical stage at the start of ART and CD4 cell count and viral load at 6 months. Expected numbers of deaths were obtained from age-, sex- and country-specific mortality rates.</p>
<p><b>Results</b> Among 29 935 eligible patients, 1134 deaths were recorded in 131 510 person-years of follow-up. The median age was 37 years, 8162 (27%) patients were females, 4400 (15%) were injecting drug users (IDUs) and 6738 (23%) had AIDS when starting ART. At 6 months, 23 539 patients (79%) had viral load measurements &le;500 copies/ml. The lowest SMR, 1.05 [95% confidence interval (CI) 0.82&ndash;1.35] was found for men who have sex with men (MSM) who started ART free of AIDS, reached a CD4 cell count of &ge;350 cells/&micro;L and suppressed viral replication to &le;500 copies/ml by the sixth month. In contrast, the SMR was 73.7 (95% CI 46.4&ndash;116.9) in IDUs who failed to suppress viral replication and had CD4 cell counts &lt;50 cells/&micro;L at 6 months. The percentage of patients with SMRs &lt;2 was 46% for MSM, 42% for heterosexually infected patients and 0% for patients with a history of injection drug use. Corresponding percentages for SMRs &gt;10 were 4, 14 and 47%.</p>
<p><b>Conclusions</b> In industrialized countries, the mortality experience of HIV-infected patients who start ART and survive the first 6 months continues to be higher than in the general population, but for many patients excess mortality is moderate and comparable with patients having other chronic conditions. Much of the excess mortality might be prevented by earlier diagnosis of HIV followed by timely initiation of ART.</p>
]]></description>
<dc:creator><![CDATA[The Antiretroviral Therapy Cohort Collaboration]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp306</dc:identifier>
<dc:title><![CDATA[Mortality of HIV-infected patients starting potent antiretroviral therapy: comparison with the general population in nine industrialized countries]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1633</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1624</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1634?rss=1">
<title><![CDATA[Correlates of environmental factors and human plague: an ecological study in Vietnam]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1634?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Human plague caused by <I>Yersinia pestis</I> remains a public health threat in endemic countries, because the disease is associated with increased risk of mortality and severe economic and social consequences. During the past 10 years, outbreaks of plague have occasionally occurred in Vietnam's Central Highlands region. The present study sought to describe and analyse the occurrence of plague and its association with ecological factors.</p>
<p><b>Methods</b> The study included all 510 communes of the Central Highlands region (with a total population of ~4 million) where 95% of incidence of plague cases in Vietnam had been reported from 1997 through 2002. Plague was clinically ascertained by using a standard protocol by WHO. Data on domestic fleas and rodents were obtained by using traps and periodic surveillance in accordance with the WHO guidelines. Temperature, duration of sunshine, rainfall and humidity were recorded as monthly averages by local meteorological stations. The association between these ecological factors and plague was assessed by using the Poisson regression model.</p>
<p><b>Results</b> From 1997 through 2002, 472 cases of plague were reported, of whom 24 (5.1%) died. The incidence of plague peaked during the dry season, with ~63% of cases occurring from February through April. The risk of plague occurrence was associated with an increased monthly flea index (RR and 95% CI: 1.93; 1.61&ndash;2.33 for months with the flea index &gt;1) and increased rodent density (RR 1.23; 1.15&ndash;1.32 per each 3% increase in density). Moreover, the risk of plague increased during the dry season (RR 2.07; 1.64&ndash;2.62), when rainfall fell &lt;10 mm (RR 1.44; 1.17&ndash;1.77).</p>
<p><b>Conclusions</b> These data suggest that the flea index, rodent density and rainfall could be used as ecological indicators of plague risk in Vietnam. The data also suggest that the occurrence of plague in Vietnam's Central Highlands is likely resulted from multiple causes that remain to be delineated.</p>
]]></description>
<dc:creator><![CDATA[Pham, H. V, Dang, D. T, Tran Minh, N. N, Nguyen, N. D, Nguyen, T. V]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp244</dc:identifier>
<dc:title><![CDATA[Correlates of environmental factors and human plague: an ecological study in Vietnam]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1641</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1634</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1642?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/38/6/1642?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>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1649</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1642</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1649?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/38/6/1649?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Baumgardner, D. J]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1650</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1649</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1651?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/38/6/1651?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>Tue, 01 Dec 2009 06:07:43 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1661</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1651</prism:startingPage>
<prism:section>Infectious Diseases</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1662?rss=1">
<title><![CDATA[Bayesian perspectives for epidemiologic research: III. Bias analysis via missing-data methods]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1662?rss=1</link>
<description><![CDATA[
<p> I present some extensions of Bayesian methods to situations in which biases are of concern. First, a basic misclassification problem is illustrated using data from a study of sudden infant death syndrome. Bayesian analyses are then given. These analyses can be conducted directly, or by converting actual-data records to incomplete records and prior distributions to complete-data records, then applying missing-data techniques to the augmented data set. The analyses can easily incorporate any complete (&lsquo;validation&rsquo; or second-stage) data that might be available, as well as adjustments for confounding and selection bias. The approach illustrates how conventional analyses depend on implicit certainty that bias parameters are null and how these implausible assumptions can be replaced by plausible priors for bias parameters.</p>
]]></description>
<dc:creator><![CDATA[Greenland, S.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp278</dc:identifier>
<dc:title><![CDATA[Bayesian perspectives for epidemiologic research: III. Bias analysis via missing-data methods]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1673</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1662</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1674?rss=1">
<title><![CDATA[Estimating the odds ratio when exposure has a limit of detection]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1674?rss=1</link>
<description><![CDATA[
<p><b>Background</b> In epidemiologic research, little emphasis has been placed on methods to account for left-hand censoring of &lsquo;exposures&rsquo; due to a limit of detection (LOD).</p>
<p><b>Methods</b> We calculate the odds of anti-HIV therapy naivet&eacute; in 45 HIV-infected men as a function of measured log<SUB>10</SUB> plasma HIV RNA viral load using five approaches including <I>ad hoc</I> methods as well as a maximum likelihood estimate (MLE). We also generated simulations of a binary outcome with 10% incidence and a 1.5-fold increased odds per log increase in a log-normally distributed exposure with 25, 50 and 75% of exposure data below LOD. Simulated data were analysed using the same five methods, as well as the full data.</p>
<p><b>Results</b> In the example, the estimated odds ratio (OR) varied by 1.22-fold across methods, from 1.45 to 1.77 per log<SUB>10</SUB> copies of viral load and the standard error for the log OR varied by 1.52-fold across methods, from 0.31 to 0.47. In the simulations, use of full data or the MLE was unbiased with appropriate confidence interval (CI) coverage. However, as the proportion of exposure below LOD increased, substituting LOD, LOD/2 or LOD/2 was increasingly biased with increasingly inappropriate CI coverage. Finally, exclusion of values below LOD was unbiased but imprecise.</p>
<p><b>Conclusions</b> In this example and the settings explored by simulation, and among methods readily available to investigators (i.e. sans full data), the MLE provided an unbiased and appropriately precise estimate of the exposure&ndash;outcome OR.</p>
]]></description>
<dc:creator><![CDATA[Cole, S. R, Chu, H., Nie, L., Schisterman, E. F]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp269</dc:identifier>
<dc:title><![CDATA[Estimating the odds ratio when exposure has a limit of detection]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1680</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1674</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1681?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/38/6/1681?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>Tue, 01 Dec 2009 06:07:44 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1688</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1681</prism:startingPage>
<prism:section>Methodology</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1689?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/38/6/1689?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>Tue, 01 Dec 2009 06:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn376</dc:identifier>
<dc:title><![CDATA[The effect of temperature on mortality in rural Bangladesh--a population-based time-series study]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1697</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1689</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1697?rss=1">
<title><![CDATA[Commentary: On Hashizume et al.'s 'The effect of temperature on mortality in rural Bangladesh']]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1697?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dear, K.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp271</dc:identifier>
<dc:title><![CDATA[Commentary: On Hashizume et al.'s 'The effect of temperature on mortality in rural Bangladesh']]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1699</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1697</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1700?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/38/6/1700?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>Tue, 01 Dec 2009 06:07:44 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1710</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1700</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1711?rss=1">
<title><![CDATA[Changing trends in indigenous inequalities in mortality: lessons from New Zealand]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1711?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>Tue, 01 Dec 2009 06:07:44 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1722</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1711</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1722?rss=1">
<title><![CDATA[Commentary: Trends in indigenous inequalities in mortality in New Zealand]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1722?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Harper, S.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1724</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1722</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1725?rss=1">
<title><![CDATA[Influences on the reduction of relative telomere length over 10 years in the population-based Bruneck Study: introduction of a well-controlled high-throughput assay]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1725?rss=1</link>
<description><![CDATA[
<p><b>Background</b> Telomeres play a key role in the maintenance of chromosome integrity. Short telomeres are linked to age-associated diseases and cancer. Our aim was to determine the decrease rate of relative telomere length (RTL) over 10 years and whether this rate was influenced by age, sex and smoking behaviour.</p>
<p><b>Methods</b> We compared RTL in 510 sample pairs from the longitudinal population-based Bruneck Study, which were collected in 1995 and recollected in 2005, and additionally determined RTL from 159 participants who died during follow-up. RTL were determined by a high-throughput real-time PCR assay and by applying a mathematical model.</p>
<p><b>Results</b> The telomeres shortened, on average, by 455 bp over 10 years. The RTL shortening rate was highly correlated with baseline RTL (<I>r</I> = 0.674, <I>P</I> &lt; 0.001). Participants who died within the observed period had considerably shorter telomeres than those who survived (median RTL of 0.98 vs 1.49; <I>P</I> &lt; 0.001). In contrast to previous studies, smoking behaviour had no influence on RTL and on telomere shortening.</p>
<p><b>Conclusion</b> This is the first comprehensive longitudinal study of individuals who were, on average, 60 at baseline, and who were re-evaluated 10 years later. Our methodology proved to be a reliable tool for a rapid, accurate and cost-efficient determination of RTL with a low amount of DNA.</p>
]]></description>
<dc:creator><![CDATA[Ehrlenbach, S., Willeit, P., Kiechl, S., Willeit, J., Reindl, M., Schanda, K., Kronenberg, F., Brandstatter, A.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp273</dc:identifier>
<dc:title><![CDATA[Influences on the reduction of relative telomere length over 10 years in the population-based Bruneck Study: introduction of a well-controlled high-throughput assay]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1734</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1725</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1735?rss=1">
<title><![CDATA[Commentary: Raising the bar on telomere epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1735?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Aviv, A.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp298</dc:identifier>
<dc:title><![CDATA[Commentary: Raising the bar on telomere epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1736</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1735</prism:startingPage>
<prism:section>Other Original Articles</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1737?rss=1">
<title><![CDATA[Cities, urbanization and health]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1737?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Whiting, D., Unwin, N.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1738</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1737</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1739?rss=1">
<title><![CDATA[Protection of health information in Italy: a step too far?]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1739?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cuttini, M., Marini, C., Bruzzone, S., Prati, S., Saracci, R.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1740</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1739</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1740?rss=1">
<title><![CDATA[Heterogeneous views on heterogeneity]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1740?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Patsopoulos, N. A, Evangelou, E., Ioannidis, J. P.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1742</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1740</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1743?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/38/6/1743?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Harper, S.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:45 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyn259</dc:identifier>
<dc:title><![CDATA[Rose's Strategy of Preventive Medicine. Geoffrey Rose with commentary by Kay-Tee Khaw and Michael Marmot.]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1745</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1743</prism:startingPage>
<prism:section>Essay Review</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1746?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/38/6/1746?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pearce, N.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1748</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1746</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1748?rss=1">
<title><![CDATA[Screening: Evidence and Practice. AE Raffle and JAM Gray.]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1748?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Metcalfe, C.]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</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:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1749</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1748</prism:startingPage>
<prism:section>Book Reviews</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1750?rss=1">
<title><![CDATA[Books Received]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1750?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp328</dc:identifier>
<dc:title><![CDATA[Books Received]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1750</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1750</prism:startingPage>
<prism:section>Books Received</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1751?rss=1">
<title><![CDATA[Erratum]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1751?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp344</dc:identifier>
<dc:title><![CDATA[Erratum]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1751</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1751</prism:startingPage>
<prism:section>Errata</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1752?rss=1">
<title><![CDATA[Erratum]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1752?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp338</dc:identifier>
<dc:title><![CDATA[Erratum]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1752</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1752</prism:startingPage>
<prism:section>Errata</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1753?rss=1">
<title><![CDATA[Corrigendum]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1753?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp346</dc:identifier>
<dc:title><![CDATA[Corrigendum]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1753</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1753</prism:startingPage>
<prism:section>Corrigendum</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/6/1754?rss=1">
<title><![CDATA[Reviewers]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/6/1754?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 01 Dec 2009 06:07:46 PST</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp355</dc:identifier>
<dc:title><![CDATA[Reviewers]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1756</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1754</prism:startingPage>
<prism:section>Reviewers</prism:section>
</item>

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

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1172?rss=1">
<title><![CDATA[Hidden in plain sight]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1172?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bresnahan, M., Li, G., Susser, E.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp293</dc:identifier>
<dc:title><![CDATA[Hidden in plain sight]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1174</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1172</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

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

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1192?rss=1">
<title><![CDATA[Commentary: Smoking and lung cancer: reflections on a pioneering paper]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1192?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cox, D. R]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp290</dc:identifier>
<dc:title><![CDATA[Commentary: Smoking and lung cancer: reflections on a pioneering paper]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1193</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1192</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1193?rss=1">
<title><![CDATA[Commentary: 'Smoking and lung cancer'--the embryogenesis of modern epidemiology]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1193?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Vandenbroucke, J. P]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp292</dc:identifier>
<dc:title><![CDATA[Commentary: 'Smoking and lung cancer'--the embryogenesis of modern epidemiology]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1196</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1193</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1197?rss=1">
<title><![CDATA[Commentary: Cornfield on cigarette smoking and lung cancer and how to assess causality]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1197?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Zwahlen, M.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp294</dc:identifier>
<dc:title><![CDATA[Commentary: Cornfield on cigarette smoking and lung cancer and how to assess causality]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1198</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1197</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

<item rdf:about="http://ije.oxfordjournals.org/cgi/content/short/38/5/1199?rss=1">
<title><![CDATA[Commentary: Cornfield, Epidemiology and Causality]]></title>
<link>http://ije.oxfordjournals.org/cgi/content/short/38/5/1199?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Greenhouse, J. B]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 03:14:24 PDT</dc:date>
<dc:identifier>info:doi/10.1093/ije/dyp299</dc:identifier>
<dc:title><![CDATA[Commentary: Cornfield, Epidemiology and Causality]]></dc:title>
<dc:publisher>International Epidemiological Association</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>38</prism:volume>
<prism:endingPage>1201</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1199</prism:startingPage>
<prism:section>Reprints and Reflections</prism:section>
</item>

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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