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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.annalsofepidemiology.org/?rss=yes"><title>Annals of Epidemiology</title><description>Annals of Epidemiology RSS feed: Current Issue.   Annals of Epidemiology  is a peer reviewed, international journal devoted to epidemiologic research and methodological development. The journal emphasizes the application of epidemiologic methods to issues that affect the distribution and determinants of human illness in diverse contexts. Its primary focus is on chronic and acute conditions of diverse etiologies and of major importance to clinical medicine, public health, and health care delivery.  Annals  encourages the use of epidemiology in a multidisciplinary approach to understanding disease etiology. Review articles, reports from U.S. Federal and International sources, Editorials, Commentaries, Brief Communications, Letters to the Editor, Book Reviews, and selected papers from major symposia are also published.  For more information concerning The American College of Epidemiology (ACE), please contact them at: The American College of Epidemiology 1500 Sunday Drive Suite 201 Raleigh, NC 27607 Tel: (919)787-5181 Fax: (919)787-4916 E-mail:  info@acepidemiology.org   or visit their home page at  http://acepidemiology.org/ . </description><link>http://www.annalsofepidemiology.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2008 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:issn>1047-2797</prism:issn><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:publicationDate>January 2009</prism:publicationDate><prism:copyright> © 2008 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003293/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708002846/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708001701/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708001695/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708001683/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003177/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003165/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003189/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003207/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003219/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003220/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS104727970800330X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalsofepidemiology.org/article/PIIS1047279708003311/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003293/abstract?rss=yes"><title>Editorial Board</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003293/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1047-2797(08)00329-3</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708002846/abstract?rss=yes"><title>Endometrial Hyperplasia Risk in Relation to Recent Use of Oral Contraceptives and Hormone Therapy</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708002846/abstract?rss=yes</link><description>Purpose: We sought to examine the relationship between recent use of oral contraceptives and hormone therapy and endometrial hyperplasia (EH) risk.Methods: Cases comprised women diagnosed with complex EH (n = 289) or atypical EH (n = 173) between 1985 and 2003. One age-matched control was selected for each case; excluded were women with a prior hysterectomy or diagnosis of EH or endometrial cancer. Hormone use in the 6 months prior to the date of the case's first symptoms was ascertained using a pharmacy database and medical records. Odds ratios (OR) and 95% confidence intervals (CI) were calculated.Results: Three (1.1%) cases had used oral contraceptives, compared to 16 (6.0%) controls (OR = 0.2, 95% CI: 0.0–0.6). Fifty-one (16.8%) cases had taken estrogen-only hormone therapy, in contrast to two (0.7%) controls (OR = 37.6, 95% CI: 8.8–160.0). The risk of EH among estrogen plus progestin hormone users did not differ from that of non-users (OR = 0.7, 95% CI: 0.4–1.1).Conclusions: This study suggests that previous findings of the association of estrogen-only hormone therapy with increased risk of EH and the lack of an association between estrogen plus progestin hormone therapy and EH risk are likely to apply to both complex EH and atypical EH. Further examination of the association between oral contraceptives and EH, with greater numbers of OC users, is warranted.</description><dc:title>Endometrial Hyperplasia Risk in Relation to Recent Use of Oral Contraceptives and Hormone Therapy</dc:title><dc:creator>Meira Epplein, Susan D. Reed, Lynda F. Voigt, Katherine M. Newton, Victoria L. Holt, Noel S. Weiss</dc:creator><dc:identifier>10.1016/j.annepidem.2008.08.099</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>7</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708001701/abstract?rss=yes"><title>The Effect of Age at Migration on Cardiovascular Mortality Among Elderly Mexican Immigrants</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708001701/abstract?rss=yes</link><description>Purpose: In this study, we evaluated the influence of age at migration on cardiovascular mortality among older Mexican Americans immigrants.Methods: A population-based cohort of Mexican-origin (N=907) participants ages 60+ was followed up to 8 years. The association between migration before age 20 compared with after age 20 and mortality was analyzed with the use of multivariate Cox proportional models.Results: Compared with those who migrated later, those who migrated before the age of 20 years had higher income and education, were more likely to speak English, were culturally more Anglo, and more likely to be men. Immigration before 20 years of age was associated with greater rates of cardiovascular mortality (hazard ratio, 2.39; 95% confidence interval, 1.16–4.94) compared with those migrating at older ages, even after adjustment for age, sex, education, income, and baseline cardiovascular health. No age at migration differences were observed for noncardiovascular deaths.Conclusions: Mexican Americans who migrated in early life experienced greater cardiovascular disease death rates than later migrants. Early experiences related to migration may have consequences for late-life disease that are not mitigated by the higher socioeconomic status achieved by early migrants. Health or economic selection related to migration may play a role although accounting for health and socioeconomic status actually increased differences between early and later migrants.</description><dc:title>The Effect of Age at Migration on Cardiovascular Mortality Among Elderly Mexican Immigrants</dc:title><dc:creator>Vivian Colón-López, Mary N. Haan, Allison E. Aiello, Debashis Ghosh</dc:creator><dc:identifier>10.1016/j.annepidem.2008.08.010</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>8</prism:startingPage><prism:endingPage>14</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708001695/abstract?rss=yes"><title>Use of Penalized Splines in Extended Cox-Type Additive Hazard Regression to Flexibly Estimate the Effect of Time-varying Serum Uric Acid on Risk of Cancer Incidence: A Prospective, Population-Based Study in 78,850 Men</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708001695/abstract?rss=yes</link><description>Purpose: We sough to investigate the effect of serum uric acid (SUA) levels on risk of cancer incidence in men and to flexibly determine the shape of this association by using a novel analytical approach.Methods: A population-based cohort of 78,850 Austrian men who received 264,347 serial SUA measurements was prospectively followed-up for a median of 12.4 years. Data were collected between 1985 and 2003. Penalized splines (P-splines) in extended Cox-type additive hazard regression were used to flexibly model the association between SUA, as a time-dependent covariate, and risk of overall and site-specific cancer incidence and to calculate adjusted hazard ratios with their 95% confidence intervals.Results: During follow-up 5189 incident cancers were observed. Restricted maximum-likelihood optimizing P-spline models revealed a moderately J-shaped effect of SUA on risk of overall cancer incidence, with statistically significantly increased hazard ratios in the upper third of the SUA distribution. Increased SUA (≥8.00mg/dL) further significantly increased risk for several site-specific malignancies, with P-spline analyses providing detailed insight about the shape of the association with these outcomes.Conclusions: Our study is the first to demonstrate a dose–response association between SUA and cancer incidence in men, simultaneously reporting on the usefulness of a novel methodological framework in epidemiologic research.</description><dc:title>Use of Penalized Splines in Extended Cox-Type Additive Hazard Regression to Flexibly Estimate the Effect of Time-varying Serum Uric Acid on Risk of Cancer Incidence: A Prospective, Population-Based Study in 78,850 Men</dc:title><dc:creator>Alexander M. Strasak, Stefan Lang, Thomas Kneib, Larry J. Brant, Jochen Klenk, Wolfgang Hilbe, Willi Oberaigner, Elfriede Ruttmann, Lalit Kaltenbach, Hans Concin, Günter Diem, Karl P. Pfeiffer, Hanno Ulmer, The VHM&amp;PP Study Group</dc:creator><dc:identifier>10.1016/j.annepidem.2008.08.009</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>15</prism:startingPage><prism:endingPage>24</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708001683/abstract?rss=yes"><title>Childhood Family Violence and Perpetration and Victimization of Intimate Partner Violence: Findings From a National Population-Based Study of Couples</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708001683/abstract?rss=yes</link><description>Purpose: We sought to examine the relation between childhood family violence and intimate partner violence (IPV).Methods: We surveyed 1615 couples from the U.S. household population by using multistage cluster sampling. Childhood family violence measures included moderate and severe child physical abuse and witnessing interparental threats or physical violence. IPV was categorized as nonreciprocal male-to-female partner violence (MFPV), nonreciprocal female-to-male partner violence (FMPV), reciprocal IPV (MFPV and FMPV), and no IPV. We used multinomial logistic regression to estimate unadjusted and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) between childhood family violence and IPV.Results: Men who experienced moderate (adjusted OR [AOR] 3.9, 95% CI, 1.3–11.8) or severe (AOR 4.5, 95% CI: 1.1–19.3) child physical abuse were at increased risk of nonreciprocal MFPV; a male history of severe childhood physical abuse or witnessing interparental violence was associated with a twofold increased risk of reciprocal IPV. Women who witnessed interparental threats of violence (AOR 1.9, 95% CI, 0.8–4.6) or interparental physical violence (AOR 3.4, 95% CI, 1.5–7.9) in childhood were at increased risk of nonreciprocal FMPV. Women exposed to any type of childhood family violence were more than 1.5 times as likely to engage in reciprocal IPV. Many strong positive ORs had CIs compatible with no association.Conclusion: We provide new evidence that childhood family violence is associated with an increased risk of nonreciprocal and reciprocal IPV. Treatment providers and policy makers should consider childhood family violence history in both men and women in the context of IPV.</description><dc:title>Childhood Family Violence and Perpetration and Victimization of Intimate Partner Violence: Findings From a National Population-Based Study of Couples</dc:title><dc:creator>Christy M. McKinney, Raul Caetano, Suhasini Ramisetty-Mikler, Scott Nelson</dc:creator><dc:identifier>10.1016/j.annepidem.2008.08.008</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>25</prism:startingPage><prism:endingPage>32</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003177/abstract?rss=yes"><title>Quantifying the Impact of Selection Bias Caused by Nonparticipation in a Case–Control Study of Mobile Phone Use</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003177/abstract?rss=yes</link><description>Purpose: To quantitatively assess the impact of selection bias caused by nonparticipation in a multinational case–control study of mobile phone use and brain tumor.Methods: Non-response questionnaires (NRQ) were completed by a sub-set of nonparticipants. Selection bias factors were calculated based on the prevalence of mobile phone use reported by nonparticipants with NRQ data, and on scenarios of hypothetical exposure prevalence for other nonparticipants.Results: Regular mobile phone use was reported less frequently by controls and cases who completed the NRQ (controls, 56%; cases, 50%) than by those who completed the full interview (controls, 69%; cases, 66%). This relationship was consistent across study centers, sex, and age groups. Lower education and more recent start of mobile phone use were associated with refusal to participate. Bias factors varied between 0.87 and 0.92 in the most plausible scenarios.Conclusions: Refusal to participate in brain tumor case–control studies seems to be related to less prevalent use of mobile phones, and this could result in a downward bias of around 10% in odds ratios for regular mobile phone use. The use of simple selection bias estimation methods in case–control studies can give important insights into the extent of any bias, even when nonparticipant information is incomplete.</description><dc:title>Quantifying the Impact of Selection Bias Caused by Nonparticipation in a Case–Control Study of Mobile Phone Use</dc:title><dc:creator>Martine Vrijheid, Lesley Richardson, Bruce K. Armstrong, Anssi Auvinen, Gabriele Berg, Matthew Carroll, Angela Chetrit, Isabelle Deltour, Maria Feychting, Graham g. Giles, Martine Hours, Ivano Iavarone, Susanna Lagorio, Stefan Lönn, Mary Mcbride, Marie-Elise Parent, Siegal Sadetzki, Tina Salminen, Marie Sanchez, Birgitte Schlehofer, Joachim Schüz, Jack Siemiatycki, Tore Tynes, Alistair Woodward, Naohito Yamaguchi, Elisabeth Cardis</dc:creator><dc:identifier>10.1016/j.annepidem.2008.10.006</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>33</prism:startingPage><prism:endingPage>41.e1</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003165/abstract?rss=yes"><title>A Population-Based Cohort Study of Occupational Exposure to Magnetic Fields and Cardiovascular Disease Mortality</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003165/abstract?rss=yes</link><description>Purpose: This cohort study aims to examine cardiovascular disease (CVD) mortality risks among workers in occupations potentially exposed to magnetic fields (MF).Methods: Risks for major CVD mortality by potential job-related MF exposure were examined in a sample of U.S. workers from the National Longitudinal Mortality Study using multivariate proportional hazards models.Results: After adjustment for demographic factors, there were no significant excess risks between individuals with medium (0.15 to &lt;0.20 μT), high (0.20 to &lt;0.30 μT), or very high (≥0.30 μT) exposure levels as compared with individuals with background exposure levels of MF (&lt;0.15 μT) for the CVD mortality outcomes. Indirect adjustment for potential confounding by current smoking prevalence did not change the pattern of these results.Conclusion: Our study does not provide evidence for an association between occupational MF exposure and CVD mortality risk.</description><dc:title>A Population-Based Cohort Study of Occupational Exposure to Magnetic Fields and Cardiovascular Disease Mortality</dc:title><dc:creator>Anna R. Cooper, Edwin Van Wijngaarden, Susan G. Fisher, M. Jacob Adams, Michael G. Yost, Joseph D. Bowman</dc:creator><dc:identifier>10.1016/j.annepidem.2008.10.001</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>42</prism:startingPage><prism:endingPage>48</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003189/abstract?rss=yes"><title>Cross-Sectional and Longitudinal Associations of Neighborhood Cohesion and Stressors with Depressive Symptoms in the Multiethnic Study of Atherosclerosis</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003189/abstract?rss=yes</link><description>Purpose: This study examined associations of neighborhood social cohesion, violence, and aesthetic quality with depressive symptoms among 2,619 healthy adults aged 45–84 years enrolled in the Multiethnic Study of Atherosclerosis.Methods: Neighborhood characteristics were estimated by surveying a separate sample of area residents. Measures of aesthetic environment, social cohesion, and violence were combined into a summary score with increasing scores indicating more favorable environments. Depressive symptoms were measured using the Center for Epidemiologic Studies-Depression (CES-D) scale. Marginal maximum likelihood estimation was used to assess associations of neighborhood characteristics with CES-D score at baseline and with the odds of developing incident depression (CES-D score ≥16 or use of antidepressants) over a 4–5 year follow-up among persons with CES-D less than 16 at baseline. Models were adjusted for age, income, education, and race/ethnicity.Results: Lower levels of social cohesion and aesthetic quality and higher levels of violence were associated with higher mean CES-D scores in men and women (P for trend &lt;0.01, adjusted mean difference in CES-D per 1 SD increase in summary score −1.01 [95% confidence interval = −1.85, −0.17] and −1.08 [95% confidence interval = −1.88, −0.28] in men and women, respectively). Associations of neighborhood characteristics with incident depression were in the expected direction for women but confidence intervals were wide (odds ratio of incident depression = 0.89 [0.63, 1.26]). No association was seen for men (odds ratio = 0.96 [0.74, 1.25]).Conclusion: Neighborhood social cohesion, aesthetic quality, and violence are associated with the presence of depressive symptoms in residents.</description><dc:title>Cross-Sectional and Longitudinal Associations of Neighborhood Cohesion and Stressors with Depressive Symptoms in the Multiethnic Study of Atherosclerosis</dc:title><dc:creator>Christina Mair, Ana V. Diez Roux, Mingwu Shen, Steven Shea, Theresa Seeman, Sandra Echeverria, Ellen S. O'meara</dc:creator><dc:identifier>10.1016/j.annepidem.2008.10.002</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>49</prism:startingPage><prism:endingPage>57</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003207/abstract?rss=yes"><title>The Epidemiology and Pathogenesis of Neoplasia in the Small Intestine</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003207/abstract?rss=yes</link><description>Purpose: The mucosa of the small intestine encompasses about 90% of the luminal surface area of the digestive system, but only 2% of the total annual gastrointestinal cancer incidence in the United States.Methods: The remarkable contrast in age-standardized cancer incidence between the small and large intestine has been reviewed with respect to the cell type patterns, demographic features, and molecular characteristics of neoplasms.Results: Particularly noteworthy is the predominance of adenocarcinoma in the colon, which exceeds 98% of the total incidence by cell type, in contrast to that of 30% to 40% in the small intestine, resulting in an age-standardized ratio of rates exceeding 50-fold. The prevalence of adenomas and carcinomas is most prominent in the duodenum and proximal jejunum. The positive correlation in global incidence rates of small and large intestinal neoplasms and the reciprocal increases in risk of second primary adenocarcinomas suggest that there are common environmental risk factors. The pathophysiology of Crohn inflammatory bowel disease and the elevated risk of adenocarcinoma demonstrate the significance of the impaired integrity of the mucosal barrier and of aberrant immune responses to luminal indigenous and potentially pathogenic microorganisms.Conclusion: In advancing a putative mechanism for the contrasting mucosal susceptibilities of the small and large intestine, substantial differences are underscored in the diverse taxonomy, concentration and metabolic activity of anaerobic organisms, rate of intestinal transit, changing pH, and the enterohepatic recycling and metabolism of bile acids. Experimental and epidemiologic studies are cited that suggest that the changing microecology, particularly in the colon, is associated with enhanced metabolic activation of ingested and endogenously formed procarcinogenic substrates.</description><dc:title>The Epidemiology and Pathogenesis of Neoplasia in the Small Intestine</dc:title><dc:creator>David Schottenfeld, Jennifer L. Beebe-Dimmer, Fawn D. Vigneau</dc:creator><dc:identifier>10.1016/j.annepidem.2008.10.004</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>58</prism:startingPage><prism:endingPage>69</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003219/abstract?rss=yes"><title>Prior Abortions Elevate Risk of Extremely Preterm Births</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003219/abstract?rss=yes</link><description>To the Editor:   Preterm newborns have elevated risk of mental retardation, cerebral palsy (CP), blindness, deafness, respiratory distress, and others . In 2006 an article by Raatikainen  has a title that assures readers that: “Induced Abortion: Not an Independent Risk Factor for Pregnancy Outcome…”. The best evidence points strongly toward higher risk of preterm birth . In 2006, eminent scientist Greg Alexander, ScD, on behalf of the Institute of Medicine, identified “Prior first trimester induced abortion” as an “Immutable Medical Risk Factor Associated with Preterm Birth” (along with 13 other preterm birth risk factors .</description><dc:title>Prior Abortions Elevate Risk of Extremely Preterm Births</dc:title><dc:creator>Brent Rooney</dc:creator><dc:identifier>10.1016/j.annepidem.2008.10.007</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>70</prism:startingPage><prism:endingPage>71</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003220/abstract?rss=yes"><title>Letter</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003220/abstract?rss=yes</link><description>To the Editor:   We thank Brent Rooney, MSc, Research Director, from Reduce Preterm Risk Coalition for the criticism he has presented on our scientific article (Raatikainen K, Heiskanen N, Heinonen S. Induced Abortion: Not an Independent Risk Factor for Pregnancy Outcome, But a Challenge for Health Counseling. Ann Epidemiol 2006;16:587–592). Mr. Rooney says that “No single study (that is, not a valid very extensive review or valid meta-analysis) can settle a medical issue” and he goes on: “Raatikainen et al. cannot objectively declare that prior induced abortion is or is not a risk factor for pregnancy outcomes.” We agree with Mr. Rooney in the classical scientific assessment of meta-analyses upon single research articles. However, writing review articles might be challenged by avoiding bias toward positive results and even more so, when the study subject is ethically, religiously and politically interesting, as the subject of induced abortion is.</description><dc:title>Letter</dc:title><dc:creator>Kaisa Raatikainen, Nonna Heiskanen, Seppo Heinonen</dc:creator><dc:identifier>10.1016/j.annepidem.2008.10.005</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>72</prism:startingPage><prism:endingPage>72</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS104727970800330X/abstract?rss=yes"><title>Table of Contents</title><link>http://www.annalsofepidemiology.org/article/PIIS104727970800330X/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1047-2797(08)00330-X</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A1</prism:endingPage></item><item rdf:about="http://www.annalsofepidemiology.org/article/PIIS1047279708003311/abstract?rss=yes"><title>Masthead</title><link>http://www.annalsofepidemiology.org/article/PIIS1047279708003311/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1047-2797(08)00331-1</dc:identifier><dc:source>Annals of Epidemiology 19, 1 (2009)</dc:source><dc:date>2009-01-01</dc:date><prism:publicationName>Annals of Epidemiology</prism:publicationName><prism:publicationDate>2009-01-01</prism:publicationDate><prism:volume>19</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1047-2797(08)X0012-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A2</prism:endingPage></item></rdf:RDF>