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<title>Epidemiology RSS : Gourt</title>
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<dc:rights>Copyright 2007, Gourt.com</dc:rights>
<dc:date>2009-11-06T20:04+31:00
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<title>Table of contents</title>
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<title>Subscriptions</title>
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<title>Editorial Board</title>
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<title>Cover</title>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1195?rss=1">
<title>Towards Reducing Disparities in Disparities Research</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1195?rss=1</link>
<description><![CDATA[ ]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1197?rss=1">
<title>Discovery Properties of Genome-wide Association Signals From Cumulatively Combined Data Sets</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1197?rss=1</link>
<description><![CDATA[
Genetic effects for common variants affecting complex disease risk are subtle. Single genome-wide association (GWA) studies are typically underpowered to detect these effects, and combination of several GWA data sets is needed to enhance discovery. The authors investigated the properties of the discovery process in simulated cumulative meta-analyses of GWA study-derived signals allowing for potential genetic model misspecification and between-study heterogeneity. Variants with null effects on average (but also between-data set heterogeneity) could yield false-positive associations with seemingly homogeneous effects. Random effects had higher than appropriate false-positive rates when there were few data sets. The log-additive model had the lowest false-positive rate. Under heterogeneity, random-effects meta-analyses of 2&ndash;10 data sets averaging 1,000 cases/1,000 controls each did not increase power, or the meta-analysis was even less powerful than a single study (power desert). Upward bias in effect estimates and underestimation of between-study heterogeneity were common. Fixed-effects calculations avoided power deserts and maximized discovery of association signals at the expense of much higher false-positive rates. Therefore, random- and fixed-effects models are preferable for different purposes (fixed effects for initial screenings, random effects for generalizability applications). These results may have broader implications for the design and interpretation of large-scale multiteam collaborative studies discovering common gene variants.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1207?rss=1">
<title>Meta- and Pooled Analyses of the Methylenetetrahydrofolate Reductase (MTHFR) C677T Polymorphism and Colorectal Cancer: A HuGE-GSEC Review</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1207?rss=1</link>
<description><![CDATA[
Worldwide, over 1 million cases of colorectal cancer (CRC) were reported in 2002, with a 50% mortality rate, making CRC the second most common cancer in adults. Certain racial/ethnic populations continue to experience a disproportionate burden of CRC. A common polymorphism in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene has been associated with a lower risk of CRC. The authors performed both a meta-analysis (29 studies; 11,936 cases, 18,714 controls) and a pooled analysis (14 studies; 5,068 cases, 7,876 controls) of the C677T MTHFR polymorphism and CRC, with stratification by racial/ethnic population and behavioral risk factors. There were few studies on different racial/ethnic populations. The overall meta-analysis odds ratio for CRC for persons with the TT genotype was 0.83 (95% confidence interval (CI): 0.77, 0.90). An inverse association was observed in whites (odds ratio = 0.83, 95% CI: 0.74, 0.94) and Asians (odds ratio = 0.80, 95% CI: 0.67, 0.96) but not in Latinos or blacks. Similar results were observed for Asians, Latinos, and blacks in the pooled analysis. The inverse association between the MTHFR 677TT polymorphism and CRC was not significantly modified by smoking status or body mass index; however, it was present in regular alcohol users only. The MTHFR 677TT polymorphism seems to be associated with a reduced risk of CRC, but this may not hold true for all populations.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1222?rss=1">
<title>Genetic Variations in Xenobiotic Metabolic Pathway Genes, Personal Hair Dye Use, and Risk of Non-Hodgkin Lymphoma</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1222?rss=1</link>
<description><![CDATA[
From 1996 to 2000, the authors conducted a population-based case-control study among Connecticut women to test the hypothesis that genetic variation in xenobiotic metabolic pathway genes modifies the relation between hair dye use and risk of non-Hodgkin lymphoma. No effect modifications were found for women who started using hair dyes in 1980 or afterward. For women who started using hair dye before 1980 as compared with never users, a statistically significantly increased risk of non-Hodgkin lymphoma was found for carriers of CYP2C9 Ex3-52C&gt;T TT/CT genotypes (odds ratio (OR) = 2.9, 95% confidence interval (CI): 1.4, 6.1), CYP2E1 -332T&gt;A AT/AA genotypes (OR = 2.0, 95% CI: 1.2, 3.4), a homozygous or heterozygous 3-base-pair deletion in intron 6 of GSTM3 (OR = 2.3, 95% CI: 1.3, 4.1), GSTP1 Ex5-24A&gt;G AA genotypes (OR = 1.8, 95% CI: 1.1, 2.9), or NAT2 genotypes conferring intermediate/rapid acetylator status (OR = 1.6, 95% CI: 1.0, 2.7). The observed associations were mainly seen for follicular lymphoma. In contrast, no significantly increased risk was observed for starting hair dye use before 1980 (relative to never use) among women who were homozygous wild-type for the CYP2C9, CYP2E1, or GSTM3 polymorphisms, women carrying 1 or 2 copies of the variant GSTP1 allele, or women who were slow NAT2 acetylators. A possible role of genetic variation in xenobiotic metabolism in the carcinogenicity of hair dye use needs to be confirmed in larger studies.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1231?rss=1">
<title>Body Size, Recreational Physical Activity, and B-Cell Non-Hodgkin Lymphoma Risk Among Women in the California Teachers Study</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1231?rss=1</link>
<description><![CDATA[
Nutritional status and physical activity are known to alter immune function, which may be relevant to lymphomagenesis. The authors examined body size measurements and recreational physical activity in relation to risk of B-cell non-Hodgkin lymphoma (NHL) in the prospective California Teachers Study. Between 1995 and 2007, 574 women were diagnosed with incident B-cell NHL among 121,216 eligible women aged 22&ndash;84 years at cohort entry. Multivariable-adjusted relative risks and 95% confidence intervals were estimated by fitting Cox proportional hazards models for all B-cell NHL combined and for the 3 most common subtypes: diffuse large B-cell lymphoma, follicular lymphoma, and B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma. Height was positively associated with risk of all B-cell NHLs (for &gt;1.70 vs. 1.61&ndash;1.65 m, relative risk = 1.50, 95% confidence interval: 1.16, 1.96) and chronic lymphocytic leukemia/small lymphocytic lymphoma (relative risk = 1.93, 95% confidence interval: 1.09, 3.41). Weight and body mass index at age 18 years were positive predictors of B-cell NHL risk overall. These findings indicate that greater height, which may reflect genetics, early life immune function, infectious exposures, nutrition, or growth hormone levels, may play a role in NHL etiology. Adiposity at age 18 years may be more relevant to NHL etiology than that in later life.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1241?rss=1">
<title>Genetic Variation in the Progesterone Receptor and Metabolism Pathways and Hormone Therapy in Relation to Breast Cancer Risk</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1241?rss=1</link>
<description><![CDATA[
The relevance of progesterone to breast carcinogenesis is highlighted by evidence indicating that use of combined estrogen-progesterone therapy (EPT) is more strongly related to breast cancer risk than is use of unopposed estrogen therapy. However, few investigators have assessed how genetic variation in progesterone-related genes modifies the effect of EPT on risk. In an analysis combining data from 2 population-based case-control studies of postmenopausal breast cancer (1,296 cases and 1,055 controls) conducted in Washington State in 1997&ndash;1999 and 2000&ndash;2004, the authors evaluated how 51 single nucleotide polymorphisms in 7 progesterone-related genes (AKR1C1, AKR1C2, AKR1C3, CYP3A4, SRD5A1, SRD5A2, and PGR) influenced breast cancer risk. There was no appreciable association with breast cancer risk overall for any single nucleotide polymorphism. For rs2854482 in AKR1C2, carrying 1 or 2 A alleles was associated with a 2.0-fold increased breast cancer risk in EPT users (95% confidence interval: 1.0, 4.0) but not in never users (Pheterogeneity = 0.03). For rs12387 in AKR1C3, the presence of 1 or 2 G alleles was associated with a 1.5-fold increased risk among EPT users (95% confidence interval: 1.1, 2.2) but not in never users (Pheterogeneity = 0.02). Interpretation of these subgroup associations must await the results of similar studies conducted in other populations.
]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1250?rss=1">
<title>Physical Activity&#x27;s Impact on the Association of Fat and Fiber Intake With Survival After Breast Cancer</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1250?rss=1</link>
<description><![CDATA[
This study examined whether, after a breast cancer diagnosis, high intake of animal fat was associated with increased breast cancer mortality and high intake of fiber was associated with decreased breast cancer mortality. Participants were 3,846 US female nurses diagnosed with stages I&ndash;III breast cancer between 1976 and 2001 and followed until death or May 2006. Breast cancer mortality was calculated according to dietary intake quintiles first assessed at least 12 months after diagnosis and was cumulatively averaged and updated. There were 446 breast cancer deaths. In simple models adjusted for time since diagnosis, age, and energy intake, animal fat intake was associated with increased breast cancer death, and cereal fiber intake was associated with reduced breast cancer death. However, no associations were found in fully adjusted models: for animal fat, the relative risks for increasing quintiles were 1.00, 0.89, 0.86, 0.85, and 0.89 (95% confidence interval: 0.61, 1.28), P = 0.68; for cereal fiber, they were 1.00, 0.95, 0.76, 0.81, and 1.00 (95% confidence interval: 0.71, 1.40), P = 0.59. Results of simple models adjusted additionally for physical activity were similar to those for full multivariate models. Results show that physical activity strongly confounds the association between diet and survival.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1257?rss=1">
<title>Postmenopausal Breast Cancer Risk and Dietary Patterns in the E3N-EPIC Prospective Cohort Study</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1257?rss=1</link>
<description><![CDATA[
Since evidence relating diet to breast cancer risk is not sufficiently consistent to elaborate preventive proposals, the authors examined the association between dietary patterns and breast cancer risk in a large French cohort study. The analyses included 2,381 postmenopausal invasive breast cancer cases diagnosed during a median 9.7-year follow-up period (1993&ndash;2005) among 65,374 women from the E3N-EPIC cohort. Scores for dietary patterns were obtained by factor analysis, and breast cancer hazard ratios were estimated by Cox proportional hazards regression for the highest quartile of dietary pattern score versus the lowest. Two dietary patterns were identified: "alcohol/Western" (essentially meat products, French fries, appetizers, rice/pasta, potatoes, pulses, pizza/pies, canned fish, eggs, alcoholic beverages, cakes, mayonnaise, and butter/cream) and "healthy/Mediterranean" (essentially vegetables, fruits, seafood, olive oil, and sunflower oil). The first pattern was positively associated with breast cancer risk (hazard ratio = 1.20, 95% confidence interval (CI): 1.03, 1.38; P = 0.007 for linear trend), especially when tumors were estrogen receptor-positive/progesterone receptor-positive. The "healthy/Mediterranean" pattern was negatively associated with breast cancer risk (hazard ratio = 0.85, 95% CI: 0.75, 0.95; P = 0.003 for linear trend), especially when tumors were estrogen receptor-positive/progesterone receptor-negative. Adherence to a diet comprising mostly fruits, vegetables, fish, and olive/sunflower oil, along with avoidance of Western-type foods, may contribute to a substantial reduction in postmenopausal breast cancer risk.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1268?rss=1">
<title>Association of Perfluorooctanoic Acid and Perfluorooctane Sulfonate With Serum Lipids Among Adults Living Near a Chemical Plant</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1268?rss=1</link>
<description><![CDATA[
Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are compounds that do not occur in nature but have been widely used since World War II and persist indefinitely in the environment. They are present in the serum of Americans with median levels of 4 ng/mL and 21 ng/mL, respectively. PFOA has been positively associated with cholesterol in several studies of workers. A cross-sectional study of lipids and PFOA and PFOS was conducted among 46,294 community residents aged 18 years or above, who drank water contaminated with PFOA from a chemical plant in West Virginia. The mean levels of serum PFOA and PFOS in 2005&ndash;2006 were 80 ng/mL (median, 27 ng/mL) and 22 ng/mL (median, 20 ng/mL), respectively. All lipid outcomes except high density lipoprotein cholesterol showed significant increasing trends by increasing decile of either compound; high density lipoprotein cholesterol showed no association. The predicted increase in cholesterol from lowest to highest decile for either compound was 11&ndash;12 mg/dL. The odds ratios for high cholesterol (&ge;240 mg/dL), by increasing quartile of PFOA, were 1.00, 1.21 (95% confidence interval (CI): 1.12, 1.31), 1.33 (95% CI: 1.23, 1.43), and 1.40 (95% CI: 1.29, 1.51) and were similar for PFOS quartiles. Because these data are cross-sectional, causal inference is limited. Nonetheless, the associations between these compounds and lipids raise concerns, given their common presence in the general population.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1279?rss=1">
<title>Correlates of Multiple Chronic Disease Behavioral Risk Factors in Canadian Children and Adolescents</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1279?rss=1</link>
<description><![CDATA[
The authors assessed individual, social, and school correlates of multiple chronic disease behavioral risk factors (physical inactivity, sedentary behavior, tobacco smoking, alcohol drinking, and high body mass index) in a representative sample of Canadian youth aged 10&ndash;15 years (mean = 12.5 years) attending public schools. Cross-sectional data (n = 1,747) from cycle 4 (2000&ndash;2001) of the National Longitudinal Survey of Children and Youth were used. Ordinal regression models were constructed to investigate associations between selected covariates and multiple behavioral risk-factor levels (0/1, 2, 3, or 4/5 risk factors). Older age (odds ratio (OR) = 1.95, 95% confidence interval (CI): 1.21, 3.13), caregiver smoking (OR = 1.49, 95% CI: 1.09, 2.03), reporting that most/all of one's peers smoked (OR = 7.31, 95% CI: 4.00, 13.35) or drank alcohol (OR = 3.77, 95% CI: 2.18, 6.53), and living in a lone-parent family (OR = 1.94, 95% CI: 1.31, 2.88) increased the likelihood of having multiple behavioral risk factors. Youth with high self-esteem (OR = 0.92, 95% CI: 0.85, 0.99) and youth from families with postsecondary education (OR = 0.58, 95% CI: 0.41, 0.82) were less likely to have a higher number of risk factors. Although several individual and social characteristics were associated with multiple behavioral risk factors, no school-related correlates emerged. These variables should be considered when planning prevention programs.
]]></description>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1290?rss=1">
<title>The Aftermath of Hip Fracture: Discharge Placement, Functional Status Change, and Mortality</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1290?rss=1</link>
<description><![CDATA[
The authors prospectively explored the consequences of hip fracture with regard to discharge placement, functional status, and mortality using the Survey on Assets and Health Dynamics Among the Oldest Old (AHEAD). Data from baseline (1993) AHEAD interviews and biennial follow-up interviews were linked to Medicare claims data from 1993&ndash;2005. There were 495 postbaseline hip fractures among 5,511 respondents aged &ge;69 years. Mean age at hip fracture was 85 years; 73% of fracture patients were white women, 45% had pertrochanteric fractures, and 55% underwent surgical pinning. Most patients (58%) were discharged to a nursing facility, with 14% being discharged to their homes. In-hospital, 6-month, and 1-year mortality were 2.7%, 19%, and 26%, respectively. Declines in functional-status-scale scores ranged from 29% on the fine motor skills scale to 56% on the mobility index. Mean scale score declines were 1.9 for activities of daily living, 1.7 for instrumental activities of daily living, and 2.2 for depressive symptoms; scores on mobility, large muscle, gross motor, and cognitive status scales worsened by 2.3, 1.6, 2.2, and 2.5 points, respectively. Hip fracture characteristics, socioeconomic status, and year of fracture were significantly associated with discharge placement. Sex, age, dementia, and frailty were significantly associated with mortality. This is one of the few studies to prospectively capture these declines in functional status after hip fracture.
]]></description>
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<title>Optimizing Influenza Sentinel Surveillance at the State Level</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1300?rss=1</link>
<description><![CDATA[
Influenza-like illness data are collected via an Influenza Sentinel Provider Surveillance Network at the state level. Because participation is voluntary, locations of the sentinel providers may not reflect optimal geographic placement. The purpose of this study was to determine the "best" locations for sentinel providers in Iowa by using a maximal coverage model (MCM) and to compare the population coverage obtained with that of the current sentinel network. The authors used an MCM to maximize the Iowa population located within 20 miles (32.2 km) of 1&ndash;143 candidate sites and calculated the coverage provided by each additional site. The first MCM location covered 15% of the population; adding a second increased coverage to 25%. Additional locations provided more coverage but with diminishing marginal returns. In contrast, the existing 22 Iowa sentinel locations covered 56% of the population, the same coverage achieved with just 10 MCM sites. Using 22 MCM sites covered more than 75% of the population, an improvement over the current site placement, adding nearly 600,000 Iowa residents. Given scarce public health resources, MCMs can help surveillance efforts by prioritizing recruitment of sentinel locations.
]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1307?rss=1">
<title>Analyses of Injury Count Data: Some Do&#x27;s and Don&#x27;ts</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1307?rss=1</link>
<description><![CDATA[
The analysis of injury data requires different considerations from the analysis of other types of outcomes because an individual can experience the outcome many times. When describing injury patterns using numerator-only data (e.g., proportion of upper-extremity injuries vs. lower-extremity injuries), simple comparisons of proportions are inappropriate because 1) individuals are compared with themselves and 2) multiple testing increases the potential for incorrect inference. Bootstrapping (resampling) techniques can be used to determine confidence intervals and whether the frequencies significantly differ across categories. When describing injury rates, the authors suggest plotting the observed injury rate against the number of exposures to obtain a visual representation of the heterogeneity of risk across individuals. Because the distribution of injury rates is often skewed, some research questions may be best addressed by comparing the weighted median injury rates instead of the weighted mean injury rates (which are given by standard formulae). Again, resampling techniques can be used to obtain a null distribution for injury rates in order to determine whether there are subjects who have unexpectedly high injury rates. More advanced analyses are required to account for multiplicity.
]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1316?rss=1">
<title>Applying Quantitative Bias Analysis to Epidemiologic Data: By Timothy L. Lash, Matthew P. Fox, and Aliza K. Fink</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1316?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1317?rss=1">
<title>Statistical Modeling for Biomedical Researchers: A Simple Introduction to the Analysis of Complex Data, 2nd Edition: By William D. Dupont</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1317?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1319?rss=1">
<title>Re: &#x22;Determinants of Quality of Interview and Impact on Risk Estimates in a Case-Control Study of Bladder Cancer&#x22;</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1319?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1319-a?rss=1">
<title>Three Authors Reply</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1319-a?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1320?rss=1">
<title>Re: &#x22;Methods of Covariate Selection: Directed Acyclic Graphs and the Change-in-Estimate Procedure&#x22;</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1320?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/170/10/1320-a?rss=1">
<title>Three of the Authors Reply</title>
<link>http://aje.oxfordjournals.org/cgi/content/short/170/10/1320-a?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/1?rss=1">
<title>The Burden of Mental Disorders</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/1?rss=1</link>
<description><![CDATA[
In the last decade, there has been an increase in interest in the burden of chronic and disabling health conditions that are not necessarily fatal, such as the mental disorders. This review systematically summarizes data on the burden associated with 11 major mental disorders of adults. The measures of burden include estimates of prevalence, mortality associated with the disorders, disabilities and impairments related to the disorders, and costs. This review expands the range of mental disorders considered in a report on the global burden of disease, updates the literature, presents information on the range and depth of sources of information on burden, and adds estimates of costs. The purpose is to provide an accessible guide to the burden of mental disorders, especially for researchers and policy makers who may not be familiar with this subfield of epidemiology.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/15?rss=1">
<title>Dementia of the Alzheimer Type</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/15?rss=1</link>
<description><![CDATA[
Dementia of the Alzheimer type is a progressive, fatal neurodegenerative condition characterized by deterioration in cognition and memory, progressive impairment in the ability to carry out activities of daily living, and a number of neuropsychiatric symptoms. This narrative review summarizes the literature regarding descriptive epidemiology, clinical course, and characteristic neuropathological changes of dementia of the Alzheimer type. Although there are no definitive imaging or laboratory tests, except for brain biopsy, for diagnosis, brief screening instruments and neuropsychiatric test batteries used to assess the disease are discussed. Insufficient evidence exists for the use of biomarkers in clinical practice for diagnosis or disease management, but promising discoveries are summarized. Optimal treatment requires both nonpharmacological and pharmacological interventions, yet none have been shown to modify the disease's clinical course. This review describes the current available options and summarizes promising new avenues for treatment. Issues related to the care of persons with dementia of the Alzheimer type, including caregiver burden, long-term care, and the proliferation of dementia special care units, are discussed. Although advances have been made, more research is needed to address the gaps in our understanding of the disease.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/35?rss=1">
<title>Dementia Prevention: Methodological Explanations for Inconsistent Results</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/35?rss=1</link>
<description><![CDATA[
The prevention of neurodegenerative dementias, such as Alzheimer disease, is a growing public health concern, because of a lack of effective curative treatment options and a rising global prevalence. Various potential risk or preventive factors have been suggested by epidemiologic research, including modifiable lifestyle factors, such as social contacts, leisure activities, physical exercise, and diet, as well as some preventive pharmacologic strategies, such as hormone replacement therapy, nonsteroidal antiinflammatory drugs, and Ginkgo biloba. Some factors have been targeted by interventions tested in randomized controlled trials, but many of the results are in conflict with observational evidence. The aim of this paper is to review the epidemiologic data linking potential protective factors to dementia or cognitive decline and to discuss the methodological limitations that could explain conflicting results. A thorough review of the literature suggests that, even if there are consistent findings from large observational studies regarding preventive or risk factors for dementia, few randomized controlled trials have been designed specifically to prove the protective effects of interventions based on such factors on dementia incidence. Because of the multifactorial origin of dementia, it appears that multidomain interventions could be a suitable candidate for preventive interventions, but designing such trials remains very challenging for researchers.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/67?rss=1">
<title>Schizophrenia: A Concise Overview of Incidence, Prevalence, and Mortality</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/67?rss=1</link>
<description><![CDATA[
Recent systematic reviews have encouraged the psychiatric research community to reevaluate the contours of schizophrenia epidemiology. This paper provides a concise overview of three related systematic reviews on the incidence, prevalence, and mortality associated with schizophrenia. The reviews shared key methodological features regarding search strategies, analysis of the distribution of the frequency estimates, and exploration of the influence of key variables (sex, migrant status, urbanicity, secular trend, economic status, and latitude). Contrary to previous interpretations, the incidence of schizophrenia shows prominent variation between sites. The median incidence of schizophrenia was 15.2/100,000 persons, and the central 80% of estimates varied over a fivefold range (7.7&ndash;43.0/100,000). The rate ratio for males:females was 1.4:1. Prevalence estimates also show prominent variation. The median lifetime morbid risk for schizophrenia was 7.2/1,000 persons. On the basis of the standardized mortality ratio, people with schizophrenia have a two- to threefold increased risk of dying (median standardized mortality ratio = 2.6 for all-cause mortality), and this differential gap in mortality has increased over recent decades. Compared with native-born individuals, migrants have an increased incidence and prevalence of schizophrenia. Exposures related to urbanicity, economic status, and latitude are also associated with various frequency measures. In conclusion, the epidemiology of schizophrenia is characterized by prominent variability and gradients that can help guide future research.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/77?rss=1">
<title>Population-based Cohort Studies on Premorbid Cognitive Function in Schizophrenia</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/77?rss=1</link>
<description><![CDATA[
Many previous studies have found associations between poor cognitive function and schizophrenia. However, the majority of these studies used retrospective data, leading to the possibility of selection and recall biases. Retrospective studies are also unable to distinguish whether cognitive deficits exist prior to the onset of schizophrenia, suggesting that they are important in etiology, or following onset, suggesting that they are secondary to the disorder or its treatment. The current review used a systematic search strategy to identify and summarize the results of all studies that have used population-based cohorts to examine associations between prospectively collected data on premorbid cognitive functioning in childhood or adolescence and subsequent risk for schizophrenia. Three broad categories of study have addressed these questions: birth cohort designs with cognitive testing during childhood, army conscript designs with cognitive performance measured at conscription, and studies using school grades. Birth cohort and conscript studies are consistent in reporting strong associations between poor performance on cognitive batteries and increased risk of schizophrenia. Studies on school performance have been less consistent, although the largest such study showed strong associations across all school subjects. In conclusion, children and adolescents with poor cognitive abilities in childhood are at increased risk of schizophrenia. This suggests that poor cognitive function is either directly causal or associated with causal factors that are involved in etiology.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/84?rss=1">
<title>Psychosis and Place</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/84?rss=1</link>
<description><![CDATA[
One important line of epidemiologic inquiry implicating social context in the etiology of psychosis is the examination of spatial variation in the distribution of psychotic illness. The authors conducted a systematic review of evidence from urbanicity and neighborhood studies regarding spatial variation in the incidence of psychosis in developed countries since 1950. A total of 44 studies (20 of urbanicity and 24 of neighborhood) were culled from three databases with similar time frames: Medline (1950&ndash;2007), PsychInfo (1950&ndash;2007), and Sociological Abstracts (1952&ndash;2007). With a special emphasis on social factors potentially relevant to etiology, the authors elucidated contributions, limitations, and issues related to study design, measurement, and theory. Evidence from both arenas supports a possible etiologic role for social context. Studies of urbanicity indicate that early-life exposure may be important; dose-response relations, spatial patterning of schizophrenia, and interactions with other factors may exist. Neighborhood studies indicate heterogeneity in rates, hint at spatial patterning of schizophrenia, and offer intriguing evidence implying more proximal social (as opposed to physical) exposures. The authors encourage the exploration of social pathways engaging theory, methodological advances, and the life-course perspective. They also propose a conceptual shift from studies of spatial variation in outcomes to research addressing the etiologic effect of exposures shaped by place as a reservoir of risk or resilience.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/101?rss=1">
<title>Blues from the Neighborhood? Neighborhood Characteristics and Depression</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/101?rss=1</link>
<description><![CDATA[
Unipolar major depression ranks among the leading contributors to the global burden of disease. Although established risk factors for depression include a variety of individual-level characteristics, neighborhood etiologic factors have been relatively understudied, with several such attributes (neighborhood socioeconomic status, physical conditions, services/amenities, social capital, social disorder) possessing plausible linkages to depression. Using the PubMed database (1966&ndash;2008) and the Social Sciences Citation Index database (1956&ndash;2008), the author undertook a systematic review of the published literature on the associations between these characteristics and depression in adults. Across studies, the evidence generally supports harmful effects of social disorder and, to a lesser extent, suggests protective effects for neighborhood socioeconomic status. Few investigations have explored the relations for neighborhood physical conditions, services/amenities, and social capital, and less consistently point to salutary effects. The unsupportive findings may be attributed to the lack of representative studies within and across societies or to methodological gaps, including lack of control for other neighborhood/non-neighborhood exposures and lack of implementation of more rigorous methodological approaches. Establishing mediating pathways and effect-modifying factors will vitally advance understanding of neighborhood effects on depression. Overall, addressing these gaps will help to identify what specific neighborhood features matter for depression, how, and for whom, and will contribute to curtailing the burden of disease associated with this major disorder.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/118?rss=1">
<title>The Relation between Work-related Psychosocial Factors and the Development of Depression</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/118?rss=1</link>
<description><![CDATA[
This review is based on a literature search made in January 2007 on request by the Danish National Board of Industrial Injuries. The search in PubMed, EMBASE, and PsycINFO resulted in more than 1,000 publications. This was reduced to 14 after the titles, abstracts, and papers were evaluated by using the following criteria: 1) a longitudinal study, 2) exposure to work-related psychosocial factors, 3) the outcome a measure of depression, 4) relevant statistical estimates, and 5) nonduplicated publication. Of the 14 studies, seven used standardized diagnostic instruments as measures of depression, whereas the other seven studies used self-administered questionnaires. The authors found moderate evidence for a relation between the psychological demands of the job and the development of depression, with relative risks of approximately 2.0. However, indication of publication bias weakens the evidence. Social support at work was associated with a decrease in risk for future depression, as all four studies dealing with this exposure showed associations with relative risks of about 0.6. Even if this literature study has identified work-related psychosocial factors that in high-quality epidemiologic studies predict depression, studies are still needed that assess in more detail the duration and intensity of exposure necessary for developing depression.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/133?rss=1">
<title>Suicide and Suicidal Behavior</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/133?rss=1</link>
<description><![CDATA[
Suicidal behavior is a leading cause of injury and death worldwide. Information about the epidemiology of such behavior is important for policy-making and prevention. The authors reviewed government data on suicide and suicidal behavior and conducted a systematic review of studies on the epidemiology of suicide published from 1997 to 2007. The authors' aims were to examine the prevalence of, trends in, and risk and protective factors for suicidal behavior in the United States and cross-nationally. The data revealed significant cross-national variability in the prevalence of suicidal behavior but consistency in age of onset, transition probabilities, and key risk factors. Suicide is more prevalent among men, whereas nonfatal suicidal behaviors are more prevalent among women and persons who are young, are unmarried, or have a psychiatric disorder. Despite an increase in the treatment of suicidal persons over the past decade, incidence rates of suicidal behavior have remained largely unchanged. Most epidemiologic research on suicidal behavior has focused on patterns and correlates of prevalence. The next generation of studies must examine synergistic effects among modifiable risk and protective factors. New studies must incorporate recent advances in survey methods and clinical assessment. Results should be used in ongoing efforts to decrease the significant loss of life caused by suicidal behavior.
]]></description>
</item>

<item rdf:about="http://epirev.oxfordjournals.org/cgi/content/short/30/1/155?rss=1">
<title>Comorbid Forms of Psychopathology: Key Patterns and Future Research Directions</title>
<link>http://epirev.oxfordjournals.org/cgi/content/short/30/1/155?rss=1</link>
<description><![CDATA[
The purpose of this review is to systematically appraise the peer-reviewed literature about clustered forms of psychopathology and to present a framework that can be useful for studying comorbid psychiatric disorders. The review focuses on four of the most prevalent types of mental health problems: anxiety, depression, conduct disorder, and substance abuse. The authors summarize existing empirical research on the distribution of concurrent and sequential comorbidity in children and adolescents and in adults, and they review existing knowledge about exogenous risk factors that influence comorbidity. The authors include articles that used a longitudinal study design and used psychiatric definitions of the disorders. A total of 58 articles met the inclusion criteria and were assessed. Current evidence demonstrates a reciprocal, sequential relation between most comorbid pairs, although the mechanisms that mediate such links remain to be explained. Methodological concerns include the inconsistency of measurement of the disorders across studies, small sample sizes, and restricted follow-up times. Given the significant mental health burden placed by comorbid disorders, and their high prevalence across populations, research on the key risk factors for clustering of psychopathology is needed.
]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayIssue?jid=HYG&#x26;volumeId=137&#x26;issueId=12">
<title>Volume 137 Issue 12</title>
<link>http://journals.cambridge.org/action/displayIssue?jid=HYG&#x26;volumeId=137&#x26;issueId=12</link>
<description><![CDATA[Epidemiology and Infection, Volume 137 Issue 12 Increased frequency in 2007 - now 8 issues per year!  
 Epidemiology and Infection  publishes original reports and reviews on all aspects of infection in humans and animals. Particular emphasis is given to the epidemiology, prevention and control of infectious diseases. The field covered is broad and includes the zoonoses, tropical infections, food hygiene, vaccine studies, statistics and the clinical, social and public-health aspects of infectious disease. Papers covering microbiology and immunology which have an epidemiological relevance are part of this broad field. Papers come from medical and veterinary scientists worldwide.  It has become the key periodical in which to find the latest reports on recently discovered infections and new technology. For those concerned with policy and planning for the control of infections, the papers on mathematical modelling of epidemics caused by historical, current and emergent infections, will be of particular value.  To celebrate 100 years of the journal, a series of important papers has been selected and each, together with a modern commentary on the paper by an expert, will be published on-line.  This journal has now moved over to electronic submission, using the Scholar One system. Click  here  to go to the submission website. Guidance on how to upload your manuscript is available on the site by clicking &quot;User Tutorials&quot;.
 

Online manuscript submission (now) available, please go to http://mc.manuscriptcentral.com/cup/hyg
 ]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418356">
<title>HYG volume 137 issue 12 Cover and Front matter</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418356</link>
<description><![CDATA[Miscellaneous Epidemiology and Infection, Volume 137 Issue 12 , pp f1-f2Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418364">
<title>HYG volume 137 issue 12 Cover and Back matter</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418364</link>
<description><![CDATA[Miscellaneous Epidemiology and Infection, Volume 137 Issue 12 , pp b1-b2Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418260">
<title>Surveillance for antimicrobial resistant organisms: potential sources and magnitude of bias</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418260</link>
<description><![CDATA[Review ArticlesO. R. REMPEL, K. B. LAUPLAND,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1665-1673Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418092">
<title>Surveillance for severe community-associated methicillin-resistant   Staphylococcus aureus  infection</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418092</link>
<description><![CDATA[Research ArticlesP. WIERSMA, M. TOBIN D'ANGELO, W. R. DALEY, J. TUTTLE, K. E. ARNOLD, S. M. RAY, J. L. LADSON, S. N. BULENS, C. L. DRENZEK,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1674-1678Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418224">
<title>Rates of   Stenotrophomonas maltophilia  colonization and infection in relation to antibiotic cycling protocols</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418224</link>
<description><![CDATA[Brief ReportA. L. PAKYZ, B. M. FARR,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1679-1683Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418104">
<title>Humoral immunity to respiratory syncytial virus in young and elderly adults</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418104</link>
<description><![CDATA[Brief ReportC. TERROSI, G. Di GENOVA, B. MARTORELLI, M. VALENTINI, M. G. CUSI,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1684-1686Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418344">
<title>The lack of protective immunity against RSV in the elderly</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418344</link>
<description><![CDATA[Article CommentaryO. SCHILDGEN,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1687-1690Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418188">
<title>Estimation of incidence of tuberculosis infection in health-care workers using repeated interferon-&#x3B3; assays</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418188</link>
<description><![CDATA[Research ArticlesT. YOSHIYAMA, N. HARADA, K. HIGUCHI, Y. NAKAJIMA, H. OGATA,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1691-1698Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418200">
<title>Data mining of tuberculosis patient data using multiple correspondence analysis</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418200</link>
<description><![CDATA[Research ArticlesT. W. RENNIE, W. ROBERTS,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1699-1704Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418272">
<title>Household clustering of gastroenteritis</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418272</link>
<description><![CDATA[Research ArticlesK. LEDER, M. SINCLAIR, A. FORBES, D. WAIN,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1705-1712Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418284">
<title>Massive outbreak of viral gastroenteritis associated with consumption of municipal drinking water in a European capital city</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418284</link>
<description><![CDATA[Research ArticlesD. WERBER, D. LAUŠEVIĆ, B. MUGOŠA, Z. VRATNICA, L. IVANOVIĆ-NIKOLIĆ, L. ŽIŽIĆ, A. ALEXANDRE-BIRD, L. FIORE, F. M. RUGGERI, I. DI BARTOLO, A. BATTISTONE, B. GASSILLOUD, S. PERELLE, D. NITZAN KALUSKI, M. KIVI, R. ANDRAGHETTI, K. G. J. POLLOCK,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1713-1720Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418176">
<title>Norovirus outbreaks in nursing homes: the evaluation of infection control measures</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418176</link>
<description><![CDATA[Research ArticlesI. H. M. FRIESEMA, H. VENNEMA, J. C. M. HEIJNE, C. M. de JAGER, G. MORROY, J. H. T. C. van den KERKHOF, E. J. M. de COSTER, B. A. WOLTERS, H. L. G. ter WAARBEEK, E. B. FANOY, P. F. M. TEUNIS, R. van der LINDE, Y. T. H. P. van DUYNHOVEN,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1722-1733Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418140">
<title>Estimation of sample sizes for pooled faecal sampling for detection of   Salmonella  in pigs</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418140</link>
<description><![CDATA[Research ArticlesM. E. ARNOLD, A. J. C. COOK,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1734-1741Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418128">
<title>Danish strategies to control   Campylobacter  in broilers and broiler meat: facts and effects</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418128</link>
<description><![CDATA[Research ArticlesH. ROSENQUIST, L. BOYSEN, C. GALLIANO, S. NORDENTOFT, S. ETHELBERG, B. BORCK,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1742-1750Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418296">
<title>Higher rate of culture-confirmed   Campylobacter  infections in Australia than in the USA: is this due to differences in healthcare-seeking behaviour or stool culture frequency?</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418296</link>
<description><![CDATA[Research ArticlesH. VALLY, G. HALL, E. SCALLAN, M. D. KIRK, F. J. ANGULO,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1751-1758Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418152">
<title>A measles outbreak in the Irish traveller ethnic group after attending a funeral in England, March&#x2013;June 2007</title>
<link>http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418152</link>
<description><![CDATA[Research ArticlesS. COHUET, A. BUKASA, R. HEATHCOCK, J. WHITE, K. BROWN, M. RAMSAY, G. FRASER,  Epidemiology and Infection, Volume 137 Issue 12 , pp 1759-1765Abstract]]></description>
</item>

<item rdf:about="http://journals.cambridge.org/action/displayAbstract?fromPage=online&#x26;aid=6418116">
<title>GIS-based spatial, temporal, and space&#x2013;time analysis of haemorrhagic fever with renal syndrome</title>
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