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        <title>Emerging Themes in Epidemiology - Most accessed articles</title>
        <link>http://www.ete-online.com</link>
        <description>The most accessed research articles published by Emerging Themes in Epidemiology</description>
        <dc:date>2009-12-09T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.ete-online.com/content/3/1/16" />
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                    It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit
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        <item rdf:about="http://www.ete-online.com/content/3/1/16">
        <title>Ethical issues in epidemiologic research and public health practice</title>
        <description>A rich and growing body of literature has emerged on ethics in epidemiologic research and public health practice. Recent articles have included conceptual frameworks of public health ethics and overviews of historical developments in the field. Several important topics in public health ethics have also been highlighted. Attention to ethical issues can facilitate the effective planning, implementation, and growth of a variety of public health programs and research activities. Public health ethics is consistent with the prevention orientation of public health. Ethical concerns can be anticipated or identified early and effectively addressed through careful analysis and consultation.</description>
        <link>http://www.ete-online.com/content/3/1/16</link>
                <dc:creator>Steven Coughlin</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2006, 3:16</dc:source>
        <dc:date>2006-10-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-3-16</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>3</prism:volume>
        <prism:startingPage>16</prism:startingPage>
        <prism:publicationDate>2006-10-03T00:00:00Z</prism:publicationDate>
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        <title>Dengue fever: new paradigms for a changing epidemiology</title>
        <description>Dengue is the most important arthropod-borne viral disease of public health significance. Compared with nine reporting countries in the 1950s, today the geographic distribution includes more than 100 countries worldwide. Many of these had not reported dengue for 20 or more years and several have no known history of the disease. The World Health Organization estimates that more than 2.5 billion people are at risk of dengue infection. First recognised in the 1950s, it has become a leading cause of child mortality in several Asian and South American countries.This paper reviews the changing epidemiology of the disease, focusing on host and societal factors and drawing on national and regional journals as well as international publications. It does not include vaccine and vector issues. We have selected areas where the literature raises challenges to prevailing views and those that are key for improved service delivery in poor countries.Shifts in modal age, rural spread, and social and biological determinants of race- and sex-related susceptibility have major implications for health services. Behavioural risk factors, individual determinants of outcome and leading indicators of severe illness are poorly understood, compromising effectiveness of control programmes. Early detection and case management practices were noted as a critical factor for survival. Inadequacy of sound statistical methods compromised conclusions on case fatality or disease-specific mortality rates, especially since the data were often based on hospitalised patients who actively sought care in tertiary centres.Well-targeted operational research, such as population-based epidemiological studies with clear operational objectives, is urgently needed to make progress in control and prevention.</description>
        <link>http://www.ete-online.com/content/2/1/1</link>
                <dc:creator>Debarati Guha-Sapir</dc:creator>
                <dc:creator>Barbara Schimmer</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2005, 2:1</dc:source>
        <dc:date>2005-03-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-2-1</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2005-03-02T00:00:00Z</prism:publicationDate>
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        <title>Seven mistakes and potential solutions in epidemiology, including a call for a World Council of Epidemiology and Causality</title>
        <description>All sciences make mistakes, and epidemiology is no exception. I have chosen 7 illustrative mistakes and derived 7 solutions to avoid them. The mistakes (Roman numerals denoting solutions) are:1. Failing to provide the context and definitions of study populations. (I Describe the study population in detail)2. Insufficient attention to evaluation of error. (II Don&apos;t pretend error does not exist.)3. Not demonstrating comparisons are like-for-like. (III Start with detailed comparisons of groups.)4. Either overstatement or understatement of the case for causality. (IV Never say this design cannot contribute to causality or imply causality is ensured by your design.)5. Not providing both absolute and relative summary measures. (V Give numbers, rates and comparative measures, and adjust summary measures such as odds ratios appropriately.)6. In intervention studies not demonstrating general health benefits. (VI Ensure general benefits (mortality/morbidity) before recommending application of cause-specific findings.)7. Failure to utilise study data to benefit populations. (VII Establish a World Council on Epidemiology to help infer causality from associations and apply the work internationally.)Analysis of these and other common mistakes is needed to benefit from the increasing discovery of associations that will be multiplying as data mining, linkage, and large-scale scale epidemiology become commonplace.</description>
        <link>http://www.ete-online.com/content/6/1/6</link>
                <dc:creator>Raj Bhopal</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2009, 6:6</dc:source>
        <dc:date>2009-12-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-6-6</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2009-12-09T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ete-online.com/content/2/1/7">
        <title>Assessing influenza-related mortality: Comment on Zucs et al.</title>
        <description>None</description>
        <link>http://www.ete-online.com/content/2/1/7</link>
                <dc:creator>Jonathan Dushoff</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2005, 2:7</dc:source>
        <dc:date>2005-07-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-2-7</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2005-07-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ete-online.com/content/2/1/11">
        <title>The Bradford Hill considerations on causality: a counterfactual perspective</title>
        <description>Bradford Hill&apos;s considerations published in 1965 had an enormous influence on attempts to separate causal from non-causal explanations of observed associations. These considerations were often applied as a checklist of criteria, although they were by no means intended to be used in this way by Hill himself. Hill, however, avoided defining explicitly what he meant by &quot;causal effect&quot;.This paper provides a fresh point of view on Hill&apos;s considerations from the perspective of counterfactual causality. I argue that counterfactual arguments strongly contribute to the question of when to apply the Hill considerations. Some of the considerations, however, involve many counterfactuals in a broader causal system, and their heuristic value decreases as the complexity of a system increases; the danger of misapplying them can be high. The impacts of these insights for study design and data analysis are discussed. The key analysis tool to assess the applicability of Hill&apos;s considerations is multiple bias modelling (Bayesian methods and Monte Carlo sensitivity analysis); these methods should be used much more frequently.</description>
        <link>http://www.ete-online.com/content/2/1/11</link>
                <dc:creator>Michael Hofler</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2005, 2:11</dc:source>
        <dc:date>2005-11-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-2-11</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2005-11-03T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ete-online.com/content/6/1/3">
        <title>Can we apply the Mendelian randomization methodology without considering epigenetic effects?
</title>
        <description>IntroductionInstrumental variable (IV) methods have been used in econometrics for several decades now, but have only recently been introduced into the epidemiologic research frameworks. Similarly, Mendelian randomization studies, which use the IV methodology for analysis and inference in epidemiology, were introduced into the epidemiologist&apos;s toolbox only in the last decade.AnalysisMendelian randomization studies using instrumental variables (IVs) have the potential to avoid some of the limitations of observational epidemiology (confounding, reverse causality, regression dilution bias) for making causal inferences. Certain limitations of randomized controlled trials, such as problems with generalizability, feasibility and ethics for some exposures, and high costs, also make the use of Mendelian randomization in observational studies attractive. Unlike conventional randomized controlled trials (RCTs), Mendelian randomization studies can be conducted in a representative sample without imposing any exclusion criteria or requiring volunteers to be amenable to random treatment allocation.Within the last decade, epigenetics has gained recognition as an independent field of study, and appears to be the new direction for future research into the genetics of complex diseases. Although previous articles have addressed some of the limitations of Mendelian randomization (such as the lack of suitable genetic variants, unreliable associations, population stratification, linkage disequilibrium (LD), pleiotropy, developmental canalization, the need for large sample sizes and some potential problems with binary outcomes), none has directly characterized the impact of epigenetics on Mendelian randomization. The possibility of epigenetic effects (non-Mendelian, heritable changes in gene expression not accompanied by alterations in DNA sequence) could alter the core instrumental variable assumptions of Mendelian randomization.This paper applies conceptual considerations, algebraic derivations and data simulations to question the appropriateness of Mendelian randomization methods when epigenetic modifications are present.
Conclusion:
Given an inheritance of gene expression from parents, Mendelian randomization studies not only need to assume a random distribution of alleles in the offspring, but also a random distribution of epigenetic changes (e.g. gene expression) at conception, in order for the core assumptions of the Mendelian randomization methodology to remain valid. As an increasing number of epidemiologists employ Mendelian randomization methods in their research, caution is therefore needed in drawing conclusions from these studies if these assumptions are not met.</description>
        <link>http://www.ete-online.com/content/6/1/3</link>
                <dc:creator>Ikechukwu Ogbuanu</dc:creator>
                <dc:creator>Hongmei Zhang</dc:creator>
                <dc:creator>Wilfried Karmaus</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2009, 6:3</dc:source>
        <dc:date>2009-05-11T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-6-3</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2009-05-11T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ete-online.com/content/6/1/5">
        <title>Efficacy dilution in randomized placebo-controlled vaginal microbicide trials</title>
        <description>Background:
To date different vaginal gel microbicides have been evaluated in phase 2b/3 trials, but none have demonstrated effectiveness for preventing HIV infection. Failure to demonstrate effectiveness however does not necessarily indicate that a product is truly inefficacious, as several sources of efficacy dilution may compromise our ability to identify products that may have been truly efficacious.
Methods:
For four individual sources of dilution, we describe the dilution mechanisms and quantify the expected effectiveness. An overall expected effectiveness that combines all sources of dilution in a trial is derived as well.
Results:
Under conditions that have been observed in recent microbicide trials, the overall expected effectiveness assuming an active gel with true efficacy of 50% and 75% are in the range of [16%; 33%] and [28%; 50%], respectively, when considering the four major sources of dilution. In contrast the diluting effect due to adherence alone (assuming an adherence of 80%) leads to higher expected effectiveness, 40% and 60% assuming an active gel with true efficacy of 50% and 75%, respectively. Individual sources of dilution may demonstrate a small effect when evaluated independently, but the overall dilution effect in a trial with several sources of dilution can be quite substantial.
Conclusion:
Currently planned phase 2b/3 microbicide trials of new candidate vaginal microbicides are not immune from these shortcomings. A good understanding of dilution effects is necessary to properly interpret microbicide trial results and to identify products worthy of further development and evaluation. Greater attention should be devoted to reducing and assessing the impact of efficacy dilution and to carefully selecting the effect size in the design of future trials.</description>
        <link>http://www.ete-online.com/content/6/1/5</link>
                <dc:creator>Benoit Masse</dc:creator>
                <dc:creator>Marie-Claude Boily</dc:creator>
                <dc:creator>Dobromir Dimitrov</dc:creator>
                <dc:creator>Kamal Desai</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2009, 6:5</dc:source>
        <dc:date>2009-10-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-6-5</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2009-10-09T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ete-online.com/content/6/1/2">
        <title>Methodological issues in estimating survival in patients with multiple primary cancers: an application to women with breast cancer as a first tumour.</title>
        <description>Background:
Comparing survival of patients with a single tumour and patients with multiple primaries poses different methodological problems. In population based studies, where we cannot rely on detailed clinical information, the issue is disentangling the share of survival probability from the first and second cancer, and their compounded effect. We examined three hypotheses: A) the survival probability since the first tumour does not change with the occurrence of a second tumour; B) the probability of surviving a tumour does not change with the presence of a previous primary; C) the probabilities of surviving two subsequent primary tumours are independent (additivity hypothesis on mortality rates).
Methods:
We studied the survival probabilities modelling mortality rates according to hypotheses A), B) and C). Mortality rates were calculated using Aalen-Johansen estimators which allowed to discount for the lag-time survival before developing a second tumour. We applied this approach to a cohort of 436 women with breast cancer (BC) and a subsequent tumour in the resident population of Turin, Italy, between 1985 and 2002.
Results:
We presented our results in term of a Standardised Mortality Ratio calculated (SMRAJ) after 10 years of follow-up. For hypothesis A we observed a significant excess mortality of 2.21 (95% C.I. 1.94 &#8211; 2.45). Concerning hypothesis B we found a not significant SMRAJ of 0.98 (95% C.I. 0.87 &#8211; 1.10). The additivity hypothesis (C) was not confirmed as it overestimated the risk of death, in fact SMRsAJ were all below 1: 0.75 (95% C.I. 0.66 &#8211; 0.84) for BC and all subsequent cancers, 0.72 (95% C.I. 0.55 &#8211; 0.94) for BC and colon-rectum cancer, 0.76 (95% C.I. 0.48 &#8211; 1.14) for BC and corpus uteri cancer (not significant).
Conclusion:
This method proved to be useful in disentangling the effect of different subsequent cancers on mortality. In our application it shows a worse long-term mortality for women with two cancers than that with BC only. However, the increase in mortality was lower than expected under the additivity assumption.</description>
        <link>http://www.ete-online.com/content/6/1/2</link>
                <dc:creator>Stefano Rosso</dc:creator>
                <dc:creator>Fulvio Ricceri</dc:creator>
                <dc:creator>Lea Terracini</dc:creator>
                <dc:creator>Roberto Zanetti</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2009, 6:2</dc:source>
        <dc:date>2009-02-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-6-2</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2009-02-27T00:00:00Z</prism:publicationDate>
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        <title>Assessment of methods for prediction of human West Nile virus (WNV) disease from WNV-infected dead birds</title>
        <description>Background:
West Nile virus (WNV) is currently the leading cause of arboviral-associated encephalitis in the U.S., and can lead to long-term neurologic sequelae. Improvements in dead bird specimen processing time, including the availability of rapid field laboratory tests, allows reassessment of the effectiveness of using WNV-positive birds in forecasting human WNV disease.
Methods:
Using New York State integrated WNV surveillance data from transmissions seasons in 2001&#8211;2003, this study determined which factors associated with WNV-positive dead birds are most closely associated with human disease. The study also addressed the &apos;delay&apos; period between the distribution of the dead bird variable and the distribution of the human cases. In the last step, the study assessed the relative risk of contracting WNV disease for people who lived in counties with a &apos;signal&apos; value of the predictor variable versus people who lived in counties with no &apos;signal&apos; value of the predictor variable.
Results:
The variable based on WNV-positive dead birds [(Positive/Tested)*(Population/Area)] was identified as the optimum variable for predicting WNV human disease at a county level. The delay period between distribution of the variable and human cases was determined to be approximately two weeks. For all 3 years combined, the risk of becoming a WNV case for people who lived in &apos;exposed&apos; counties (those with levels of the positive dead bird variable above the signal value) was about 2 times higher than the risk for people who lived in &apos;unexposed&apos; counties, but risk varied by year.
Conclusion:
This analysis develops a new variable based on WNV-positive dead birds, [(Positive/Tested)*(Population/Area)] to be assessed in future real-time studies for forecasting the number of human cases in a county. A delay period of approximately two weeks between increases in this variable and the human case onset was identified. Several threshold &apos;signal&apos; values were assessed and found effective at indicating human case risk, although specific thresholds are likely to vary by region and surveillance system differences.</description>
        <link>http://www.ete-online.com/content/6/1/4</link>
                <dc:creator>Anna Veksler</dc:creator>
                <dc:creator>Millicent Eidson</dc:creator>
                <dc:creator>Igor Zurbenko</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2009, 6:4</dc:source>
        <dc:date>2009-06-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-6-4</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2009-06-05T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ete-online.com/content/1/1/6">
        <title>Conflict and HIV: A framework for risk assessment to prevent HIV in conflict-affected settings in Africa</title>
        <description>In sub-Saharan Africa, HIV/AIDS and violent conflict interact to shape population health and development in dramatic ways. HIV/AIDS can create conditions conducive to conflict. Conflict can affect the epidemiology of HIV/AIDS. Conflict is generally understood to accelerate HIV transmission, but this view is simplistic and disregards complex interrelationships between factors that can inhibit and accelerate the spread of HIV in conflict and post conflict settings, respectively. This paper provides a framework for understanding these factors and discusses their implications for policy formulation and program planning in conflict-affected settings.</description>
        <link>http://www.ete-online.com/content/1/1/6</link>
                <dc:creator>Nancy Mock</dc:creator>
                <dc:creator>Sambe Duale</dc:creator>
                <dc:creator>Lisanne Brown</dc:creator>
                <dc:creator>Ellen Mathys</dc:creator>
                <dc:creator>Heather O'Maonaigh</dc:creator>
                <dc:creator>Nina Abul-Husn</dc:creator>
                <dc:creator>Sterling Elliott</dc:creator>
                <dc:source>Emerging Themes in Epidemiology 2004, 1:6</dc:source>
        <dc:date>2004-10-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1742-7622-1-6</dc:identifier>
        <prism:publicationName>Emerging Themes in Epidemiology</prism:publicationName>
        <prism:issn>1742-7622</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2004-10-29T00:00:00Z</prism:publicationDate>
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