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        <title>MedWorm: Epidemiology</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest headlines from journals and sites in the Epidemiology category.</description>
        <link><![CDATA[http://www.medworm.com/rss/index.php/Epidemiology/54/]]></link>
        <lastBuildDate>Fri, 10 Oct 2008 17:58:11 +0100</lastBuildDate>
        <item>
            <title>The authors reply</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/976-a?rss=1</link>
            <description> (Source: American Journal of Epidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864840</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
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        <item>
            <title>Re: &quot;genetic susceptibility to severe infection in families with invasive pneumococcal disease&quot;</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/976?rss=1</link>
            <description> (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864839</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
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        <item>
            <title>The authors reply</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/975?rss=1</link>
            <description> (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864838</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864838</guid>        </item>
        <item>
            <title>Re: &quot;age at retirement and mortality in a general population sample: the greek epic study&quot;</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/974?rss=1</link>
            <description> (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864837</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864837</guid>        </item>
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            <title>Use of a prescribed ephedrine/caffeine combination and the risk of serious cardiovascular events: a registry-based case-crossover study</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/966?rss=1</link>
            <description>Ephedrine and herbal ephedra preparations have been shown to induce a small-to-moderate weight loss. Owing to reports on serious cardiovascular events, they were banned from the US market in 2004. There have been no large controlled studies on the possible association between prescribed ephedrine/caffeine and cardiovascular events in general. The authors linked data from four different sources within Statistics Denmark, using data on 257,364 users of prescribed ephedrine/caffeine for the period 1995&amp;ndash;2002. The data were analyzed using a case-crossover technique with a composite endpoint: death outside of a hospital, myocardial infarction, or stroke. To account for effects of chronic exposure and effects in na&amp;iuml;ve users, the authors performed a secondary case-control study nested within the cohort of ephedrine/caffeine ever users. Among 2,316 case subjects, 282 (12.2%) were current users of ephedrine/caffeine. The case-crossover analysis yielded an odds ratio of 0.84 (95% confidence interval: 0.71, 1.00); after adjustment for trends in ephedrine/caffeine use, it was 0.95 (95% confidence interval: 0.79, 1.16). Subgroup analyses revealed no strata with significantly elevated risk. In the case-control substudy, there was no increased risk among na&amp;iuml;ve users or users with large cumulative doses. Prescribed ephedrine/caffeine was not associated with a substantially increased risk of adverse cardiovascular outcomes in this study. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864836</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864836</guid>        </item>
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            <title>Linking exposure to polychlorinated biphenyls with fatty fish consumption and reduced fetal growth among danish pregnant women: a cause for concern?</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/958?rss=1</link>
            <description>In a selected group of women from the Danish National Birth Cohort, the authors investigated the association between intake of fatty fish and plasma concentrations of polychlorinated biphenyls (PCBs) on the one hand and the association between maternal PCB concentrations and fetal growth on the other. Of 70,183 women who filled in a food frequency questionnaire during 1996&amp;ndash;2002, 100 nulliparous women aged 25&amp;ndash;35 years with normal prepregnancy body mass index were selected according to their intake of fatty fish (low (0 meals/month, n = 34), medium (1&amp;ndash;3 meals/month, n = 33), or high (&amp;ge;4 meals/month, n = 33)). Women with a high intake of fatty fish had 50% (95% confidence interval (CI): 31, 72) higher plasma PCB concentrations than women with low intake. Maternal plasma PCB concentrations were inversely associated with birth weight and placental weight. The adjusted mean difference between the 75th and 25th PCB percentiles was &amp;ndash;155 g (95% CI: &amp;ndash;291, &amp;ndash;19) for birth weight and &amp;ndash;81 g (95% CI: &amp;ndash;135, &amp;ndash;26) for placental weight. These results support previous findings from this cohort, where fatty fish intake was inversely associated with fetal growth. Dietary recommendations often encourage weekly consumption of fatty fish. These results suggest that potential exposure to PCBs should be carefully considered before recommending such intakes among women of childbearing age. (Source: American Journal of Epidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864835</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864835</guid>        </item>
        <item>
            <title>Recreational physical activity and the risk of preeclampsia: a prospective cohort of norwegian women</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/952?rss=1</link>
            <description>Previous case-control studies suggest that recreational physical activity protects against preeclampsia. Using a prospective design, the authors estimated the risk of preeclampsia for pregnant women according to level of physical activity, taking other variables that influence risk into consideration. The data set comprised 59,573 pregnancies from the Norwegian Mother and Child Cohort Study (1999&amp;ndash;2006). Information on physical activity and other exposures was extracted from questionnaire responses given in pregnancy weeks 14&amp;ndash;22, whereas diagnosis of preeclampsia was retrieved from the Medical Birth Registry of Norway. Estimation and confounder control was performed with multiple logistic regression. About 24% of pregnant women reported no physical activity, and 7% reported more than 25 such activities per month. The adjusted odds ratio was 0.79 (95% confidence interval: 0.65, 0.96) for preeclampsia when comparing women who exercised 25 times or more per month with inactive women. The association appeared strongest among women whose body mass index was less than 25 kg/m2 and was absent among women whose body mass index was higher than 30 kg/m2. These results suggest that the preventive effect of recreational physical activity during pregnancy may be more limited than has been shown in case-control studies and may apply to nonobese women only. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864834</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
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            <title>Fetal growth and timing of parturition in humans</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/946?rss=1</link>
            <description>Animal studies indicate that either the fetus or the intrauterine environment, both of which set the pattern for fetal growth, may affect the timing of parturition. The authors examined the association between fetal growth and timing of spontaneous onset of labor in humans among low-risk white US women with singleton pregnancies (1987&amp;ndash;1991). They restricted the data to pregnancies which had a reliable date of the last menstrual period, normal fetal growth in the first half of pregnancy, and no history of or current pregnancy complications that might have impaired fetal growth (n = 3,360). Subjects received ultrasound examinations at 15&amp;ndash;22 and 31&amp;ndash;35 weeks&amp;rsquo; gestation. Fetal growth was adjusted for parity, fetal sex, and maternal prepregnancy weight and height. Results showed that slower or faster fetal growth in the second half of pregnancy resulted in substantially lower or higher birth weight, respectively. However, fetal growth in the second half of pregnancy, even at extremes (2 standard deviations below or above the mean), did not have a meaningful impact on the timing of parturition; neither did fetal growth acceleration or deceleration in late pregnancy. Thus, in low-risk pregnancies where fetal growth is normal in early gestation, fetal growth in the second half of pregnancy does not affect the timing of normal parturition. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864833</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864833</guid>        </item>
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            <title>Cigarette smoking and the development of premenstrual syndrome</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/938?rss=1</link>
            <description>Moderate to severe premenstrual syndrome (PMS) affects as many as 20% of premenopausal women. Although smoking may be more common in women with PMS, it is unknown whether smoking is involved in PMS etiology. In 1991&amp;ndash;2001, the authors conducted a case-control study nested within the prospective Nurses&amp;rsquo; Health Study II. Participants were US women aged 27&amp;ndash;44 years and free of PMS at baseline, including 1,057 who developed PMS over 10 years and 1,968 reporting no diagnosis of PMS and only minimal menstrual symptoms during this time. Smoking at various ages was assessed by questionnaires. After adjustment for oral contraceptives and other factors, current smokers were 2.1 times as likely as never smokers to develop PMS over the next 2&amp;ndash;4 years (95% confidence interval: 1.56, 2.83). Total pack-years and smoking during adolescence and young adulthood were also independently associated with a higher risk of PMS. For example, the relative risk for women who started smoking before age 15 years, compared with never smokers, was 2.53 (95% confidence interval: 1.70, 3.76). Results suggest that smoking, especially in adolescence and young adulthood, may increase risk of moderate to severe PMS. These findings may provide an additional incentive for young women to avoid cigarette smoking. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864832</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864832</guid>        </item>
        <item>
            <title>Risk of pancreatitis according to alcohol drinking habits: a population-based cohort study</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/932?rss=1</link>
            <description>The association between alcohol intake and pancreatitis has been examined previously in case-control studies, mostly consisting of men. The significance of beverage type and drinking pattern is unknown. The objective of this study was to assess the association between amount, type, and frequency of alcohol intake and risk of pancreatitis. For this purpose, the authors used data on 17,905 men and women who participated in the Copenhagen City Heart Study in 1976&amp;ndash;1978, 1981&amp;ndash;1983, 1991&amp;ndash;1994, and 2001&amp;ndash;2003 in Copenhagen, Denmark. Alcohol intake and covariates were assessed by questionnaire. Information on pancreatitis was obtained from national registers. A high alcohol intake was associated with a higher risk of pancreatitis. Hazard ratios associated with drinking 1&amp;ndash;6, 7&amp;ndash;13, 14&amp;ndash;20, 21&amp;ndash;34, 35&amp;ndash;48, and &amp;gt;48 drinks/week were 1.1 (95% confidence interval (CI): 0.8, 1.6), 1.2 (95% CI: 0.8, 1.8), 1.3 (95% CI: 0.8, 2.1), 1.3 (95% CI: 0.7, 2.2), 2.6 (95% CI: 1.4, 4.8), and 3.0 (95% CI: 1.6, 5.7), respectively, compared with 0 drinks/week (Ptrend &amp;lt; 0.001). Associations were similar for men and women. Drinking frequency did not seem to be independently associated with pancreatitis. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864831</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864831</guid>        </item>
        <item>
            <title>Antidiabetic medication and prostate cancer risk: a population-based case-control study</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/925?rss=1</link>
            <description>Decreased risk of prostate cancer in diabetic men has been reported. The authors evaluated the association between antidiabetic medication use and prostate cancer at the population level. All incident prostate cancer cases in Finland during 1995&amp;ndash;2002 were identified from the Finnish Cancer Registry. Matched controls were provided by the Population Register Center (24,723 case-control pairs). Information on medication use was obtained from a comprehensive prescription database. Multivariable-adjusted odds ratios were computed by using conditional logistic regression. The authors found that prostate cancer risk was decreased for antidiabetic medication users (odds ratio = 0.87, 95% confidence interval: 0.82, 0.92). The decrease was observed for most drug groups. The odds ratio decreased in a dose-dependent fashion by quantity of use. Duration of antidiabetic treatment was inversely associated with overall prostate cancer risk and risk of advanced cancer. Similar risk reduction for users of different antidiabetic drugs suggests that diabetes, instead of the medication itself, is behind the association. This finding is unlikely to be secondary because of differential uptake of the prostate-specific antigen test or different prostate-specific antigen levels between medication users and nonusers; prevalence of testing in Finland is low. Dose and time dependency of the relation probably indicates that duration of diabetes is negatively associated with risk. (Source: American Journal of Epidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864830</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864830</guid>        </item>
        <item>
            <title>Vitamin d from dietary intake and sunlight exposure and the risk of hormone-receptor-defined breast cancer</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/915?rss=1</link>
            <description>Evidence has emerged for a role of vitamin D in the development of breast cancer, and there is some suggestion that its antiproliferative effect is greater in hormone-receptor-positive cells. Few epidemiologic studies have considered the association between vitamin D and hormone-receptor-defined breast cancer, and the results are conflicting. Considering 759 cases and 1,135 controls from a case-control study (Ontario, Canada, 2003&amp;ndash;2005), the authors examined the association between vitamin D intake at specific ages and combined estrogen-receptor- (ER) and progesterone-receptor- (PR) defined breast cancer. While increased intake of vitamin D (from the sun and diet) was most consistently associated with a significantly reduced risk of ER+/PR+ tumors (e.g., odds ratio = 0.76, 95% confidence interval: 0.59, 0.97 for use of cod liver oil during adolescence), comparable nonsignificant associations were found for receptor-negative (ER&amp;ndash;/PR&amp;ndash;) (odds ratio = 0.74, 95% confidence interval: 0.53, 1.04) and mixed (ER+/PR&amp;ndash;) (odds ratio = 0.79, 95% confidence interval: 0.51, 1.22) tumors. This study suggests that vitamin D is associated with a reduced risk of breast cancer regardless of ER/PR status of the tumor. Future studies with a larger number of receptor-negative and mixed tumors are required. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864829</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864829</guid>        </item>
        <item>
            <title>Methods and software for estimating health disparities: the case of children's oral health</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/906?rss=1</link>
            <description>The National Center for Health Statistics recently issued a monograph with 11 guidelines for reporting health disparities. However, guidelines on confidence intervals (CIs) cannot be readily implemented with the complex sample surveys often used for disease surveillance. In the United States, dental caries (decay) is the most common chronic childhood disease&amp;mdash;5 times more common than asthma. Racial/ethnic minorities, immigrants, and persons of lower socioeconomic position (SEP) have a greater prevalence of caries. The authors provide methods for applying National Center for Health Statistics guidelines to complex sample surveys (health disparity indices and absolute and relative difference measures assessing associations of race/ethnicity and SEP to health outcomes with CIs); illustrate the application of those methods to children's untreated caries; provide relevant software; and report results from a simulation varying prevalence. They use data on untreated caries from the California Oral Health Needs Assessment of Children 2004&amp;ndash;2005 and school percentage of participation in free/reduced-price lunch programs to illustrate the methods. Absolute and relative measures, the Slope Index of Inequality, the Relative Index of Inequality (mean and ratio), and the Health Concentration Index were estimated. Taylor series linearization and rescaling bootstrap methods were used to estimate CIs. Oral health differed significantly between White children and all non-White children and was significantly related to SEP. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864828</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864828</guid>        </item>
        <item>
            <title>Albuminuria assessed from first-morning-void urine samples versus 24-hour urine collections as a predictor of cardiovascular morbidity and mortality</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/897?rss=1</link>
            <description>Screening for albuminuria has been advocated because it is associated with cardiovascular morbidity and all-cause mortality. The &quot;gold standard&quot; to assess albuminuria is 24-hour urinary albumin excretion (UAE). Because 24-hour urine collection is cumbersome, guidelines suggest measuring albuminuria in a first morning void, either as urinary albumin concentration (UAC) or adjusted for creatinine concentration, the albumin:creatinine ratio (ACR). To decide which albuminuria measure to use in clinical practice, it is essential to know which best predicts clinical outcome. In a sample representative of the Groningen (the Netherlands) population (n = 3,414), the authors compared UAC, ACR, and UAE as predictors of cardiovascular events and all-cause mortality. During a median follow-up of 7.5 years, which ended December 31, 2005, they observed 278 events (a major adverse cardiovascular event or mortality). The area under the receiver operating characteristic curve predicting events was 0.65 for UAE, 0.62 for UAC (P = 0.06 vs. UAE), and 0.66 for ACR (P = 0.80 vs. UAE; P = 0.01 vs. UAC). When sex-specific subgroups were considered, UAE was superior to UAC in predicting outcome (P = 0.04) for females, whereas, for males as well as females, no difference was found between ACR and UAE. To predict cardiovascular morbidity and all-cause mortality, measuring ACR in a first-morning-void urine sample is a good alternative to measuring 24-hour UAE. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864827</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864827</guid>        </item>
        <item>
            <title>Power for genetic association study of human longevity using the case-control design</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/890?rss=1</link>
            <description>The efficiency of the popular case-control design in gene-longevity association studies needs to be verified because, different from a binary trait, longevity represents only the extreme end of the continuous life span distribution without a clear cutoff for defining the phenotype. In this paper, the authors use the current Danish life tables to simulate individual life span by using a variety of scenarios and assess the empirical power for different sample sizes when cases are defined as centenarians or as nonagenarians. Results show that, although using small samples of centenarians (several hundred) provides power to detect only common alleles with large effects (a &amp;gt;20% reduction in hazard rate), large samples of centenarians (&amp;gt;1,000) achieve power to capture genes responsible for minor effects (5%&amp;ndash;10% hazard reduction depending on the mode of inheritance). Although the method provides good power for rare alleles with multiplicative or dominant effects, it performs poorly for rare recessive alleles. Power is drastically reduced when nonagenarians are considered cases, with a more than 5-fold difference in the size of the case sample required to achieve comparable power as that found with centenarians. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864826</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864826</guid>        </item>
        <item>
            <title>Estimating the single nucleotide polymorphism genotype misclassification from routine double measurements in a large epidemiologic sample</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/878?rss=1</link>
            <description>Previously, estimation of genotype misclassification of single nucleotide polymorphisms (SNPs) as encountered in epidemiologic practice and involving thousands of subjects was lacking. The authors collected representative data on approximately 14,000 subjects from 8 studies and 646,558 genotypes assessed in 2005 by means of matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Overall discordance among 57,805 double genotypes from routine quality control was 0.36%. Fitting different misclassification models by maximum likelihood assuming identical misclassification for all SNPs, the estimated misclassification probabilities ranged from 0.0000 to 0.0035. When applying the misclassification simulation and extrapolation (MC-SIMEX) method for the first time to genetic data to account for the misclassification in a reanalysis of adiponectin-encoding (APM1) gene SNP associations with plasma adiponectin in 1,770 subjects, the authors found no impact of this small error on association estimates but increased estimates for a more substantial error. This study is the first to provide large-scale epidemiologic data on SNP genotype misclassification. The estimated misclassification in this example was small and negligible for association estimates, which is reassuring and essential for detecting SNP associations. In situations with more substantial error, the presented approach using duplicate genotyping and the MC-SIMEX method is practical and helpful for quantifying the genotyping error and its impact. (Source: American Journal of Epidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864825</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864825</guid>        </item>
        <item>
            <title>Rehm et al. respond to &quot;never, or hardly ever?&quot;</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/876?rss=1</link>
            <description> (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864824</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864824</guid>        </item>
        <item>
            <title>Invited commentary: never, or hardly ever? it could make a difference</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/872?rss=1</link>
            <description>A paper showing that about one half of persons stating lifelong alcohol abstinence had previously reported drinking (Am J Epidemiol 2008;168(8):866&amp;mdash;871) reopens debate about the validity of this frequently used referent group in alcohol-health studies. Misclassification of lifelong abstainers could result in underestimation of harmful effects of heavy drinking and overestimation of benefits of lighter drinking. Imprecise and unreliable ascertainment of alcohol intake is the rule in the area of alcohol epidemiology research. However, inaccurate ascertainment of past infrequent drinking may have less effect upon outcome estimates than the consequences of other measurement errors such as underreporting of intake. Communication about alcohol-health relations would be improved if all research reports explicitly described queries and methods by which alcohol intake was categorized and if limitations were always frankly acknowledged. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864823</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864823</guid>        </item>
        <item>
            <title>Are lifetime abstainers the best control group in alcohol epidemiology? on the stability and validity of reported lifetime abstention</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/866?rss=1</link>
            <description>Lifetime abstainers have often been recommended as the comparison group in alcohol epidemiology. The objective of this study was to provide insight into the validity and stability of lifetime abstention by using data derived from the National Alcohol Survey, a national probability survey of US households conducted in 1984, and its 2 follow-up surveys conducted in 1990 and 1992. Results indicated that more than half (52.9%; all proportions were weighted to represent the US population) of those who reported never having a drink of any alcoholic beverage in the 1992 survey reported drinking in previous surveys. Depending on assumptions, this difference may result in an underestimation of alcohol-attributable mortality of 2%&amp;ndash;15% in men and 2%&amp;ndash;22% in women. Sociodemographic factors differentiated those who consistently reported lifetime abstention across surveys from the rest of the study population. Results suggest that using reported lifetime abstainers as a sole comparison group is problematic, especially if reporting is based on 1 measurement only. Establishing multiple measurement points and including irregular lifetime light drinkers with lifetime abstainers as the comparison group are recommended for future epidemiologic studies. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864822</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864822</guid>        </item>
        <item>
            <title>Evaluation of the potential excess of statistically significant findings in published genetic association studies: application to alzheimer's disease</title>
            <link>http://aje.oxfordjournals.org/cgi/content/short/168/8/855?rss=1</link>
            <description>The authors evaluated whether there is an excess of statistically significant results in studies of genetic associations with Alzheimer's disease reflecting either between-study heterogeneity or bias. Among published articles on genetic associations entered into the comprehensive AlzGene database (www.alzgene.org) through January 31, 2007, 1,348 studies included in 175 meta-analyses with 3 or more studies each were analyzed. The number of observed studies (O) with statistically significant results (P = 0.05 threshold) was compared with the expected number (E) under different assumptions for the magnitude of the effect size. In the main analysis, the plausible effect size of each association was the summary effect presented in the respective meta-analysis. Overall, 19 meta-analyses (all with eventually nonsignificant summary effects) had a documented excess of O over E: Typically single studies had significant effects pointing in opposite directions and early summary effects were dissipated over time. Across the whole domain, O was 235 (17.4%), while E was 164.8 (12.2%) (P &amp;lt; 10&amp;ndash;6). The excess showed a predilection for meta-analyses with nonsignificant summary effects and between-study heterogeneity. The excess was seen for all levels of statistical significance and also for studies with borderline P values (P = 0.05&amp;ndash;0.10). The excess of significant findings may represent significance-chasing biases in a setting of massive testing. (Source: American Journal of Epidemiology) </description>
            <author>American Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1864821</comments>
            <pubDate>Thu, 09 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1864821</guid>        </item>
        <item>
            <title>Surgery and risk of sporadic creutzfeldt-jakob disease</title>
            <link>http://content.karger.com/produktedb/produkte.asp?doi=163098</link>
            <description>Neuroepidemiology 2008;31:241-242 (DOI:10.1159/000163098) (Source: Neuroepidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>Neuroepidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1865082</comments>
            <pubDate>Wed, 08 Oct 2008 13:50:03 +0100</pubDate>
            <guid isPermaLink="false">1865082</guid>        </item>
        <item>
            <title>Surgery and risk of sporadic creutzfeldt-jakob disease in denmark and sweden: registry-based case-control studies</title>
            <link>http://content.karger.com/produktedb/produkte.asp?doi=163097</link>
            <description>Neuroepidemiology 2008;31:229-240 (DOI:10.1159/000163097) (Source: Neuroepidemiology) </description>
            <author>Neuroepidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1865083</comments>
            <pubDate>Wed, 08 Oct 2008 13:50:02 +0100</pubDate>
            <guid isPermaLink="false">1865083</guid>        </item>
        <item>
            <title>Residual oil combustion: a major source of airborne nickel in new york city</title>
            <link>http://dx.doi.org/10.1038/jes.2008.60</link>
            <description>Residual oil combustion: a major source of airborne nickel in New York City

Journal of Exposure Science and Environmental Epidemiology advance online publication, October 8, 2008. doi:10.1038/jes.2008.60

Authors: Richard E Peltier, Shao-I Hsu, Ramona Lall
&amp; Morton Lippmann (Source: Journal of Exposure Science and Environmental Epidemiology) </description>
            <author>Journal of Exposure Science and Environmental Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1862011</comments>
            <pubDate>Wed, 08 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1862011</guid>        </item>
        <item>
            <title>Evaluation of physiological measures for correcting variation in urinary output: implications for assessing environmental chemical exposure in children</title>
            <link>http://dx.doi.org/10.1038/jes.2008.48</link>
            <description>Evaluation of physiological measures for correcting variation in urinary output: Implications for assessing environmental chemical exposure in children

Journal of Exposure Science and Environmental Epidemiology advance online publication, October 8, 2008. doi:10.1038/jes.2008.48

Authors: Melanie A Pearson, Chensheng Lu, Brian J Schmotzer, Lance A Waller
&amp; Anne M Riederer (Source: Journal of Exposure Science and Environmental Epidemiology) </description>
            <author>Journal of Exposure Science and Environmental Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1862010</comments>
            <pubDate>Wed, 08 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1862010</guid>        </item>
        <item>
            <title>Acute exposure to elevated pm2.5 generated by traffic and cardiopulmonary health effects in healthy older adults</title>
            <link>http://dx.doi.org/10.1038/jes.2008.46</link>
            <description>Acute exposure to elevated PM2.5 generated by traffic and cardiopulmonary health effects in healthy older adults

Journal of Exposure Science and Environmental Epidemiology advance online publication, October 8, 2008. doi:10.1038/jes.2008.46

Authors: Zhihua (Tina) Fan, Qingyu Meng, Clifford Weisel, Robert Laumbach, Pamela Ohman-Strickland, Stuart Shalat, Marta Z Hernandez
&amp; Kathleen Black (Source: Journal of Exposure Science and Environmental Epidemiology) </description>
            <author>Journal of Exposure Science and Environmental Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1862009</comments>
            <pubDate>Wed, 08 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1862009</guid>        </item>
        <item>
            <title>More powerful haplotype sharing by accounting for the mode of inheritance</title>
            <link>http://dx.doi.org/10.1002%2Fgepi.20373</link>
            <description>The concept of haplotype sharing (HS) has received considerable attention recently, and several haplotype association methods have been proposed. Here, we extend the work of Beckmann and colleagues [2005 Hum. Hered. 59:67-78] who derived an HS statistic (BHS) as special case of Mantel's space-time clustering approach. The Mantel-type HS statistic correlates genetic similarity with phenotypic similarity across pairs of individuals. While phenotypic similarity is measured as the mean-corrected cross product of phenotypes, we propose to incorporate information of the underlying genetic model in the measurement of the genetic similarity. Specifically, for the recessive and dominant modes of inheritance we suggest the use of the minimum and maximum of shared length of haplotypes around a marker locus for pairs of individuals. If the underlying genetic model is unknown, we propose a model-free HS Mantel statistic using the max-test approach. We compare our novel HS statistics to BHS using simulated case-control data and illustrate its use by re-analyzing data from a candidate region of chromosome 18q from the Rheumatoid Arthritis (RA) Consortium. We demonstrate that our approach is point-wise valid and superior to BHS. In the re-analysis of the RA data, we identified three regions with point-wise P-values (Source: Genetic Epidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>Genetic Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1855287</comments>
            <pubDate>Tue, 07 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1855287</guid>        </item>
        <item>
            <title>Population stratification in a case-control study of brain arteriovenous malformation in latinos</title>
            <link>http://content.karger.com/produktedb/produkte.asp?doi=160215</link>
            <description>Neuroepidemiology 2008;31:224-228 (DOI:10.1159/000160215) (Source: Neuroepidemiology) </description>
            <author>Neuroepidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1859009</comments>
            <pubDate>Mon, 06 Oct 2008 15:22:44 +0100</pubDate>
            <guid isPermaLink="false">1859009</guid>        </item>
        <item>
            <title>A multiple splitting approach to linkage analysis in large pedigrees identifies a linkage to asthma on chromosome 12</title>
            <link>http://dx.doi.org/10.1002%2Fgepi.20371</link>
            <description>Large genealogies are potentially very informative for linkage analysis. However, the software available for exact non-parametric multipoint linkage analysis is limited with respect to the complexity of the families it can handle. A solution is to split the large pedigrees into sub-families meeting complexity constraints. Different methods have been proposed to &quot;best&quot; split large genealogies. Here, we propose a new procedure in which linkage is performed on several carefully chosen sub-pedigree sets from the genealogy instead of using just a single sub-pedigree set. Our multiple splitting procedure capitalizes on the sensitivity of linkage results to family structure and has been designed to control computational feasibility and global type I error. We describe and apply this procedure to the extreme case of the highly complex Hutterite pedigree and use it to perform a genome-wide linkage analysis on asthma. The detection of a genome-wide significant linkage for asthma on chromosome 12q21 illustrates the potential of this multiple splitting approach. Genet. Epidemiol. 2008. © 2008 Wiley-Liss, Inc. (Source: Genetic Epidemiology) </description>
            <author>Genetic Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1855288</comments>
            <pubDate>Mon, 06 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1855288</guid>        </item>
        <item>
            <title>Chronic particulate exposure, mortality, and coronary heart disease in the nurses' health study.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18835862&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18835862&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Chronic Particulate Exposure, Mortality, and Coronary Heart Disease in the Nurses' Health Study.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Puett RC, Schwartz J, Hart JE, Yanosky JD, Speizer FE, Suh H, Paciorek CJ, Neas LM, Laden F&lt;/p&gt;
        &lt;p&gt;Adverse health effects of exposures to acute air pollution have been well studied. Fewer studies have examined effects of chronic exposure. Previous studies used exposure estimates for narrow time periods and were limited by the geographic distribution of pollution monitors. This study examined the association of chronic particulate exposures with all-cause mortality, incident nonfatal myocardial infarction, and fatal coronary heart disease (CHD) in a prospective cohort of 66,250 women from the Nurses' Health Study in northeastern US metropolitan areas. Nonfatal outcomes were assessed through self-report and medical record review and fatalities through death certificates and medical record review. During follow-up (1992-2002), 3,785 deaths and 1,348 incident fatal CHD and nonfatal myocardial infarctions occurred. In age- and calendar-time-adjusted models, 10-mug/m(3) increases in 12-month average exposures to particulate matter &amp;lt;10 mum in diameter were associated with increased all-cause mortality (16%, 95% confidence interval: 5, 28) and fatal CHD (43%, 95% confidence interval: 10, 86). Adjustment for body mass index and physical activity weakened these associations. Body mass index and smoking modified the association between exposure to particulate matter &amp;lt;10 mum in diameter and fatal CHD. In this population, increases in such exposures were associated with increases in all-cause and CHD mortality. Never smokers with higher body mass indexes were at greatest risk of fatal CHD.&lt;/p&gt;
        &lt;p&gt;PMID: 18835862 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) </description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858811</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858811</guid>        </item>
        <item>
            <title>Childhood leukemia in relation to radio frequency electromagnetic fields in the vicinity of tv and radio broadcast transmitters.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18835863&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18835863&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Childhood Leukemia in Relation to Radio Frequency Electromagnetic Fields in the Vicinity of TV and Radio Broadcast Transmitters.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Merzenich H, Schmiedel S, Bennack S, Br&amp;#xFC;ggemeyer H, Philipp J, Blettner M, Sch&amp;#xFC;z J&lt;/p&gt;
        &lt;p&gt;A case-control study of radio frequency electromagnetic fields (RF-EMFs) and childhood leukemia was conducted in West Germany. The study region included municipalities near high-power radio and TV broadcast towers, including 16 amplitude-modulated and 8 frequency-modulated transmitters. Cases were aged 0-14 years, were diagnosed with leukemia between 1984 and 2003, and were registered at the German Childhood Cancer Registry. Three age-, gender-, and transmitter-area-matched controls per case were drawn randomly from population registries. The analysis included 1,959 cases and 5,848 controls. Individual exposure to RF-EMFs 1 year before diagnosis was estimated with a field strength prediction program. Considering total RF-EMFs, the odds ratio derived from conditional logistic regression analysis for all types of leukemia was 0.86 (95% confidence interval: 0.67, 1.11) when upper (&amp;gt;/=95%/0.701 V/m) and lower (&amp;lt;90%/0.504 V/m) quantiles of the RF-EMF distribution were compared. An analysis of amplitude-modulated and frequency-modulated transmitters separately did not show increased risks of leukemia. The odds ratio for all types of leukemia was 1.04 (95% confidence interval: 0.65, 1.67) among children living within 2 km of the nearest broadcast transmitter compared with those living at a distance of 10-&amp;lt;15 km. The data did not show any elevated risks of childhood leukemia associated with RF-EMFs.&lt;/p&gt;
        &lt;p&gt;PMID: 18835863 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) </description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858810</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858810</guid>        </item>
        <item>
            <title>Association of adiposity status and changes in early to mid-adulthood with incidence of alzheimer's disease.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18835864&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18835864&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Association of Adiposity Status and Changes in Early to Mid-Adulthood With Incidence of Alzheimer's Disease.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Beydoun MA, Lhotsky A, Wang Y, Forno GD, An Y, Metter EJ, Ferrucci L, O'Brien R, Zonderman AB&lt;/p&gt;
        &lt;p&gt;Adiposity status and change are potential risk factors for Alzheimer's disease (AD). The authors used data on 2,322 participants in the Baltimore Longitudinal Study of Aging to analyze the relation between AD incidence and adiposity in Cox proportional hazards models, with adjustment for sociodemographic factors and smoking status. Body mass index (BMI; weight (kg)/height (m)(2)) and waist circumference at specific ages were predicted by empirical Bayes estimators from mixed-effects regression models. After a median of 23.4 years of follow-up between 1958 and 2006, 187 participants developed AD. Among men, being underweight (BMI &amp;lt;/=18.5) at age 30, 40, or 45 years increased the likelihood of AD (hazard ratio (HR) = 5.76, 95% confidence interval (CI): 2.07, 16.00); among women, being obese (BMI &amp;gt;/=30) at age 30, 40, or 45 years and jointly centrally obese (waist circumference &amp;gt;/=80th percentile) at age 30, 35, or 50 years increased AD risk (HR = 6.57, 95% CI: 1.96, 22.02). Women who lost weight (BMI change &amp;lt;10th percentile) between ages 30 and 45 years were also at increased risk (HR = 2.02, 95% CI: 1.06, 3.85). Weight gain among men (BMI change &amp;gt;90th percentile) between ages 30 and 50 years increased AD risk (HR = 3.70, 95% CI: 1.43, 9.56). Future studies should identify age- and gender-specific optimal weights and weight-loss strategies for preventing AD and investigate potential mechanisms.&lt;/p&gt;
        &lt;p&gt;PMID: 18835864 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858809</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858809</guid>        </item>
        <item>
            <title>Maternal body mass index and lifestyle exposures and the risk of bilateral renal agenesis or hypoplasia: the national birth defects prevention study.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18835865&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18835865&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Maternal Body Mass Index and Lifestyle Exposures and the Risk of Bilateral Renal Agenesis or Hypoplasia: The National Birth Defects Prevention Study.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Slickers JE, Olshan AF, Siega-Riz AM, Honein MA, Aylsworth AS,  &lt;/p&gt;
        &lt;p&gt;Increased maternal body mass index, maternal smoking, and alcohol exposure during pregnancy have been inconsistently reported as potential risk factors for renal birth defects. The low incidence of the most severe renal anomaly, bilateral renal agenesis or hypoplasia (RA/H), has limited the ability to study this fatal defect. Using data from the National Birth Defects Prevention Study, a multicenter case-control study, the authors explored potential relations between RA/H and maternal body mass index, smoking, alcohol, and caffeine exposures. Data available for 75 infants with RA/H born between 1997 and 2003 and for randomly selected control infants without known birth defects (n = 868) were assessed by a model adjusted for folic acid use, all four exposures of interest, and study center. Bilateral RA/H was associated with a body mass index of greater than 30 kg/m(2) prior to pregnancy (adjusted odds ratio (aOR) = 1.92, 95% confidence interval (CI): 1.00, 3.67), smoking during the periconceptional period (aOR = 2.09, 95% CI: 1.08, 4.03), and binge drinking during the second month of pregnancy (aOR = 3.64, 95% CI: 1.19, 11.1). These results support the need for further exploration into the potential mechanisms by which such exposures could interfere with early fetal kidney formation resulting in RA/H.&lt;/p&gt;
        &lt;p&gt;PMID: 18835865 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) </description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858808</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858808</guid>        </item>
        <item>
            <title>Psychiatric epidemiology: reducing the global burden of mental illness.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18836150&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18836150&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Psychiatric Epidemiology: Reducing the Global Burden of Mental Illness.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Buka SL&lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18836150 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) </description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858807</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858807</guid>        </item>
        <item>
            <title>Combining matched and unmatched control groups in case-control studies.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18836151&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18836151&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Combining Matched and Unmatched Control Groups in Case-Control Studies.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Cessie SL, Nagelkerke N, Rosendaal FR, van Stralen KJ, Pomp ER, van Houwelingen HC&lt;/p&gt;
        &lt;p&gt;Multiple control groups in case-control studies are used to control for different sources of confounding. For example, cases can be contrasted with matched controls to adjust for multiple genetic or unknown lifestyle factors and simultaneously contrasted with an unmatched population-based control group. Inclusion of different control groups for a single exposure analysis yields several estimates of the odds ratio, all using only part of the data. Here the authors introduce an easy way to combine odds ratios from several case-control analyses with the same cases. The approach is based upon methods used for meta-analysis but takes into account the fact that the same cases are used and that the estimated odds ratios are therefore correlated. Two ways of estimating this correlation are discussed: sandwich methodology and the bootstrap. Confidence intervals for the pooled estimates and a test for checking whether the odds ratios in the separate case-control studies differ significantly are derived. The performance of the method is studied by simulation and by applying the methods to a large study on risk factors for thrombosis, the MEGA Study (1999-2004), wherein cases with first venous thrombosis were included with a matched control group of partners and an unmatched population-based control group.&lt;/p&gt;
        &lt;p&gt;PMID: 18836151 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) </description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858806</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858806</guid>        </item>
        <item>
            <title>Cognitive impairment: an increasingly important complication of type 2 diabetes: the age, gene/environment susceptibility-reykjavik study.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18836152&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18836152&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Cognitive Impairment: An Increasingly Important Complication of Type 2 Diabetes: The Age, Gene/Environment Susceptibility-Reykjavik Study.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Am J Epidemiol. 2008 Oct 3;&lt;/p&gt;
        &lt;p&gt;Authors:  Saczynski JS, J&amp;#xF3;nsd&amp;#xF3;ttir MK, Garcia ME, Jonsson PV, Peila R, Eiriksdottir G, Olafsdottir E, Harris TB, Gudnason V, Launer LJ&lt;/p&gt;
        &lt;p&gt;Persons with type 2 diabetes are at increased risk of cognitive dysfunction. Less is known about which cognitive abilities are affected and how undiagnosed diabetes and impaired fasting glucose relate to cognitive performance. The authors explored this question using data from 1,917 nondemented men and women (average age = 76 years) in the population-based Age, Gene/Environment Susceptibility-Reykjavik Study (2002-2006). Glycemic status groups included diagnosed diabetes (self-reported diabetes or diabetic medication use; n = 163 (8.5%)), undiagnosed diabetes (fasting blood glucose &amp;gt;/=7.0 mmol/L without diagnosed diabetes; n = 55 (2.9%)), and impaired fasting glucose (fasting blood glucose 5.6-6.9 mmol/L; n = 744 (38.8%)). Composites of memory, processing speed (PS), and executive function were constructed from a neuropsychological battery. Linear regression was used to investigate cross-sectional differences in cognitive performance between glycemic groups, adjusted for demographic and health factors. Persons with diagnosed diabetes had slower PS than normoglycemics (beta = -0.12; P &amp;lt; 0.05); diabetes duration of &amp;gt;/=15 years was associated with significantly poorer PS and executive function. Undiagnosed diabetics had slower PS (beta = -0.22; P &amp;lt; 0.01) and poorer memory performance (beta = -0.22; P &amp;lt; 0.05). Persons with type 2 diabetes have poorer cognitive performance than normoglycemics, particularly in PS. Those with undiagnosed diabetes have the lowest cognitive performance.&lt;/p&gt;
        &lt;p&gt;PMID: 18836152 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Am J Epidemiol) </description>
            <author>Am J Epidemiol</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858805</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858805</guid>        </item>
        <item>
            <title>Outbreak news. cholera, guinea-bissau.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18833661&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18833661&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Outbreak news. Cholera, Guinea-Bissau.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Wkly Epidemiol Rec. 2008 Oct 3;83(40):357-8&lt;/p&gt;
        &lt;p&gt;Authors: &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18833661 [PubMed - indexed for MEDLINE]&lt;/p&gt; (Source: Weekly Epidemiological Record) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>Weekly Epidemiological Record</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858690</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858690</guid>        </item>
        <item>
            <title>Outbreak news. melamine contamination, china.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18833662&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18833662&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Outbreak news. Melamine contamination, China.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Wkly Epidemiol Rec. 2008 Oct 3;83(40):358&lt;/p&gt;
        &lt;p&gt;Authors: &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18833662 [PubMed - indexed for MEDLINE]&lt;/p&gt; (Source: Weekly Epidemiological Record) </description>
            <author>Weekly Epidemiological Record</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858689</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858689</guid>        </item>
        <item>
            <title>Human cases of avian influenza a (h5n1) in north-west frontier province, pakistan, october-november 2007.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18833663&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18833663&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Human cases of avian influenza A (H5N1) in North-West Frontier Province, Pakistan, October-November 2007.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Wkly Epidemiol Rec. 2008 Oct 3;83(40):359-64&lt;/p&gt;
        &lt;p&gt;Authors: &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18833663 [PubMed - indexed for MEDLINE]&lt;/p&gt; (Source: Weekly Epidemiological Record) </description>
            <author>Weekly Epidemiological Record</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858688</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858688</guid>        </item>
        <item>
            <title>Outbreak news. yellow fever, guinea.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18837116&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18837116&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Outbreak news. Yellow fever, Guinea.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Wkly Epidemiol Rec. 2008 Oct 3;83(40):358-9&lt;/p&gt;
        &lt;p&gt;Authors: &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18837116 [PubMed - indexed for MEDLINE]&lt;/p&gt; (Source: Weekly Epidemiological Record) </description>
            <author>Weekly Epidemiological Record</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1858687</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1858687</guid>        </item>
        <item>
            <title>Surveillance for lyme disease--united states, 1992-2006.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18830214&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18830214&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Surveillance for Lyme disease--United States, 1992-2006.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;MMWR Surveill Summ. 2008 Oct 3;57(10):1-9&lt;/p&gt;
        &lt;p&gt;Authors:  Bacon RM, Kugeler KJ, Mead PS,  &lt;/p&gt;
        &lt;p&gt;PROBLEM/CONDITION: Lyme disease is a multisystem disease that occurs in North America, Europe, and Asia. In the United States, the etiologic agent is Borrelia burgdorferi sensu stricto, a spirochete transmitted to humans by infected Ixodes scapularis and I. pacificus ticks. The majority of patients with Lyme disease develop a characteristic rash, erythema migrans (EM), accompanied by symptoms of fever, malaise, fatigue, headache, myalgia, or arthralgia. Other manifestations of infection can include arthritis, carditis, and neurologic deficits. Lyme disease can be treated successfully with standard antibiotic regimens. REPORTING PERIOD: 1992--2006. DESCRIPTION OF SYSTEM: U.S. health departments report cases of Lyme disease voluntarily to CDC as part of the National Notifiable Disease Surveillance System. Variables collected include patient age, sex, race, county and state of residence, date of illness onset, and reported signs and symptoms. RESULTS: During 1992--2006, a total of 248,074 cases of Lyme disease were reported to CDC by health departments in the 50 states, the District of Columbia, and U.S. territories; the annual count increased 101%, from 9,908 cases in 1992 to 19,931 cases in 2006. During this 15-year period, 93% of cases were reported from 10 states (Connecticut, Delaware, Massachusetts, Maryland, Minnesota, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin). Incidence was highest among children aged 5--14 years, and 53% of all reported cases occurred among males. More than 65% of patients with EM had illness onset in June and July, compared with 37% of patients with arthritis. INTERPRETATION: Lyme disease is the most commonly reported vectorborne illness in the United States. The geographic distribution of cases is highly focused, with the majority of reported cases occurring in the northeastern and north-central states. During 1992--2006, the number of reported cases more than doubled. A disproportionate increasing trend was observed in children and in young males compared with other demographic groups. PUBLIC HEALTH ACTION: The results presented in this report underscore the continued emergence of Lyme disease and the need for tick avoidance and early treatment interventions. Public health practitioners can use the data presented in this report to target prevention campaigns to populations with increasing incidence (i.e., children and young males).&lt;/p&gt;
        &lt;p&gt;PMID: 18830214 [PubMed - in process]&lt;/p&gt; (Source: MMWR Surveill Summ) </description>
            <author>MMWR Surveill Summ</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1850035</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1850035</guid>        </item>
        <item>
            <title>Racial/ethnic disparities in self-rated health status among adults with and without disabilities--united states, 2004-2006.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18830209&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18830209&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Racial/Ethnic disparities in self-rated health status among adults with and without disabilities--United States, 2004-2006.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;MMWR Morb Mortal Wkly Rep. 2008 Oct 3;57(39):1069-73&lt;/p&gt;
        &lt;p&gt;Authors:   &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18830209 [PubMed - in process]&lt;/p&gt; (Source: MMWR Morb Mortal Wkl...) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>MMWR Morb Mortal Wkl...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1849606</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1849606</guid>        </item>
        <item>
            <title>Hiv prevalence estimates--united states, 2006.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18830210&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18830210&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;HIV prevalence estimates--United States, 2006.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;MMWR Morb Mortal Wkly Rep. 2008 Oct 3;57(39):1073-6&lt;/p&gt;
        &lt;p&gt;Authors:   &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18830210 [PubMed - in process]&lt;/p&gt; (Source: MMWR Morb Mortal Wkl...) </description>
            <author>MMWR Morb Mortal Wkl...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1849605</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1849605</guid>        </item>
        <item>
            <title>Rabies in a dog imported from iraq--new jersey, june 2008.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18830211&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18830211&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Rabies in a dog imported from Iraq--New Jersey, June 2008.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;MMWR Morb Mortal Wkly Rep. 2008 Oct 3;57(39):1076-8&lt;/p&gt;
        &lt;p&gt;Authors:   &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18830211 [PubMed - in process]&lt;/p&gt; (Source: MMWR Morb Mortal Wkl...) </description>
            <author>MMWR Morb Mortal Wkl...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1849604</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1849604</guid>        </item>
        <item>
            <title>Licensure of a diphtheria and tetanus toxoids and acellular pertussis adsorbed and inactivated poliovirus vaccine and guidance for use as a booster dose.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18830212&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18830212&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Licensure of a diphtheria and tetanus toxoids and acellular pertussis adsorbed and inactivated poliovirus vaccine and guidance for use as a booster dose.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;MMWR Morb Mortal Wkly Rep. 2008 Oct 3;57(39):1078-9&lt;/p&gt;
        &lt;p&gt;Authors:   &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18830212 [PubMed - in process]&lt;/p&gt; (Source: MMWR Morb Mortal Wkl...) </description>
            <author>MMWR Morb Mortal Wkl...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1849603</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1849603</guid>        </item>
        <item>
            <title>Licensure of a diphtheria and tetanus toxoids and acellular pertussis adsorbed, inactivated poliovirus, and haemophilus b conjugate vaccine and guidance for use in infants and children.</title>
            <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18830213&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18830213&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Licensure of a diphtheria and tetanus toxoids and acellular pertussis adsorbed, inactivated poliovirus, and haemophilus B conjugate vaccine and guidance for use in infants and children.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;MMWR Morb Mortal Wkly Rep. 2008 Oct 3;57(39):1079-80&lt;/p&gt;
        &lt;p&gt;Authors:   &lt;/p&gt;
        &lt;p&gt;&lt;/p&gt;
        &lt;p&gt;PMID: 18830213 [PubMed - in process]&lt;/p&gt; (Source: MMWR Morb Mortal Wkl...) </description>
            <author>MMWR Morb Mortal Wkl...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1849602</comments>
            <pubDate>Fri, 03 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1849602</guid>        </item>
        <item>
            <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.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18835524&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;&gt;&lt;a href=&quot;http://linkinghub.elsevier.com/retrieve/pii/S1047-2797(08)00169-5&quot;&gt;&lt;img src=&quot;http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif&quot; border=&quot;0&quot;/&gt;&lt;/a&gt; &lt;/td&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18835524&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;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.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Ann Epidemiol. 2008 Oct 2;&lt;/p&gt;
        &lt;p&gt;Authors:  Strasak AM, Lang S, Kneib T, Brant LJ, Klenk J, Hilbe W, Oberaigner W, Ruttmann E, Kaltenbach L, Concin H, Diem G, Pfeiffer KP, Ulmer H,  &lt;/p&gt;
        &lt;p&gt;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 (&amp;gt;/=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.&lt;/p&gt;
        &lt;p&gt;PMID: 18835524 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Annals of Epidemiology) &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;MedWorm Sponsored Message:&lt;/i&gt;&lt;/b&gt; Find out how you can &lt;a href=&quot;http://www.medworm.com/rss/medicalsponsorship.php&quot; target=&quot;_self&quot;&gt;get your message across here&lt;/a&gt; by sponsoring this MedWorm news feed.&lt;/p&gt;</description>
            <author>Annals of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1859115</comments>
            <pubDate>Thu, 02 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1859115</guid>        </item>
        <item>
            <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.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&amp;db=PubMed&amp;cmd=Retrieve&amp;list_uids=18835525&amp;dopt=Abstract</link>
            <description>&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;&gt;&lt;a href=&quot;http://linkinghub.elsevier.com/retrieve/pii/S1047-2797(08)00168-3&quot;&gt;&lt;img src=&quot;http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif&quot; border=&quot;0&quot;/&gt;&lt;/a&gt; &lt;/td&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;cmd=Display&amp;dopt=PubMed_PubMed&amp;from_uid=18835525&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Childhood Family Violence and Perpetration and Victimization of Intimate Partner Violence: Findings From a National Population-Based Study of Couples.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Ann Epidemiol. 2008 Oct 2;&lt;/p&gt;
        &lt;p&gt;Authors:  McKinney CM, Caetano R, Ramisetty-Mikler S, Nelson S&lt;/p&gt;
        &lt;p&gt;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.&lt;/p&gt;
        &lt;p&gt;PMID: 18835525 [PubMed - as supplied by publisher]&lt;/p&gt; (Source: Annals of Epidemiology) </description>
            <author>Annals of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1859114</comments>
            <pubDate>Thu, 02 Oct 2008 04:00:00 +0100</pubDate>
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        <item>
            <title>Partitioning the population attributable fraction for a sequential chain of effects</title>
            <link>http://www.epi-perspectives.com/content/5/1/5</link>
            <description>Background:
While the population attributable fraction (PAF) provides potentially valuable information regarding the community-level effect of risk factors, significant limitations exist with current strategies for estimating a PAF in multiple risk factor models.  These strategies can result in paradoxical or ambiguous measures of effect, or require unrealistic assumptions regarding variables in the model.  A method is proposed in which an overall or total PAF across multiple risk factors is partitioned into components based upon a sequential ordering of effects.  This method is applied to several hypothetical data sets in order to demonstrate its application and interpretation in diverse analytic situations.
Results:
The proposed method is demonstrated to provide clear and interpretable measures of effect, even when risk factors are related/correlated and/or when risk factors interact.  Furthermore, this strategy not only addresses, but also quantifies issues raised by other researchers who have noted the potential impact of population-shifts on population-level effects in multiple risk factor models.
Conclusions:
Combined with simple, unadjusted PAF estimates and an aggregate PAF based on all risk factors under consideration, the sequentially partitioned PAF provides valuable additional information regarding the process through which population rates of a disorder may be impacted.  In addition, the approach can also be used to statistically control for confounding by other variables, while avoiding the potential pitfalls of attempting to separately differentiate direct and indirect effects. (Source: Epidemiologic Perspectives &amp; Innovations) </description>
            <author>Epidemiologic Perspectives &amp; Innovations</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1846909</comments>
            <pubDate>Thu, 02 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1846909</guid>        </item>
        <item>
            <title>Books received</title>
            <link>http://ije.oxfordjournals.org/cgi/content/short/37/5/1197?rss=1</link>
            <description> (Source: International Journal of Epidemiology) </description>
            <author>International Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1843585</comments>
            <pubDate>Thu, 02 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1843585</guid>        </item>
        <item>
            <title>Unequal lives: health and socioeconomic inequalities. hilary graham.</title>
            <link>http://ije.oxfordjournals.org/cgi/content/short/37/5/1195?rss=1</link>
            <description> (Source: International Journal of Epidemiology) </description>
            <author>International Journal of Epidemiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1843584</comments>
            <pubDate>Thu, 02 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1843584</guid>        </item>
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