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<title>American Journal of Epidemiology - current issue</title>
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<prism:coverDisplayDate>15 February 2010</prism:coverDisplayDate>
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<title><![CDATA[Cover]]></title>
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<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwq033</dc:identifier>
<dc:title><![CDATA[Cover]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
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<prism:publicationDate>2010-02-15</prism:publicationDate>
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<title><![CDATA[Editorial Board]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwq034</dc:identifier>
<dc:title><![CDATA[Editorial Board]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
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<title><![CDATA[Subscriptions]]></title>
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<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwq035</dc:identifier>
<dc:title><![CDATA[Subscriptions]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
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<prism:publicationDate>2010-02-15</prism:publicationDate>
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<title><![CDATA[Table of contents]]></title>
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<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwq036</dc:identifier>
<dc:title><![CDATA[Table of contents]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
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<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/391?rss=1">
<title><![CDATA[Neighborhood Poverty and Injection Cessation in a Sample of Injection Drug Users]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/391?rss=1</link>
<description><![CDATA[
<p>Neighborhood socioeconomic environment may be a determinant of injection drug use cessation. The authors used data from a prospective cohort study of Baltimore City, Maryland, injection drug users assessed between 1990 and 2006. The study examined the relation between living in a poorer neighborhood and the probability of injection cessation among active injectors, independent of individual characteristics and while respecting the temporality of potential confounders, exposure, and outcome. Participants&rsquo; residences were geocoded, and the crude, adjusted, and inverse probability of exposure weighted associations between neighborhood poverty and injection drug use cessation were estimated. Weighted models showed a strong association between neighborhood poverty and injection drug use cessation; living in a neighborhood with fewer than 10%, compared with more than 30%, of residents in poverty was associated with a 44% increased odds of not injecting in the prior 6 months (odds ratio = 1.44, 95% confidence interval: 1.14, 1.82). Results show that neighborhood environment may be an important determinant of drug injection behavior independent of individual-level characteristics.</p>
]]></description>
<dc:creator><![CDATA[Nandi, A., Glass, T. A., Cole, S. R., Chu, H., Galea, S., Celentano, D. D., Kirk, G. D., Vlahov, D., Latimer, W. W., Mehta, S. H.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp416</dc:identifier>
<dc:title><![CDATA[Neighborhood Poverty and Injection Cessation in a Sample of Injection Drug Users]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>398</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>391</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/399?rss=1">
<title><![CDATA[Variation in Child Cognitive Ability by Week of Gestation Among Healthy Term Births]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/399?rss=1</link>
<description><![CDATA[
<p>The authors investigated variations in cognitive ability by gestational age among 13,824 children at age 6.5 years who were born at term with normal weight, using data from a prospective cohort recruited in 1996&ndash;1997 in Belarus. The mean differences in the Wechsler Abbreviated Scales of Intelligence were examined by gestational age in completed weeks and by fetal growth after controlling for maternal and family characteristics. Compared with the score for those born at 39&ndash;41 weeks, the full-scale intelligence quotient (IQ) score was 1.7 points (95% confidence interval (CI): &ndash;2.7, &ndash;0.7) lower in children born at 37 weeks and 0.4 points (95% CI: &ndash;1.1, 0.02) lower at 38 weeks after controlling for confounders. There was also a graded relation in postterm children: a 0.5-points (95% CI: &ndash;2.6, 1.6) lower score at 42 weeks and 6.0 points (95% CI: &ndash;15.1, 3.1) lower at 43 weeks. Compared with children born large for gestational age (&gt;90th percentile), children born small for gestational age (&lt;10th percentile) had the lowest IQ, followed by those at the 10th&ndash;50th percentile and those at the &gt;50th&ndash;90th percentile. These findings suggest that, even among healthy children born at term, cognitive ability at age 6.5 years is lower in those born at 37 or 38 weeks and those with suboptimal fetal growth.</p>
]]></description>
<dc:creator><![CDATA[Yang, S., Platt, R. W., Kramer, M. S.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp413</dc:identifier>
<dc:title><![CDATA[Variation in Child Cognitive Ability by Week of Gestation Among Healthy Term Births]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>406</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>399</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/407?rss=1">
<title><![CDATA[Maternal Dietary Glycemic Intake and the Risk of Neural Tube Defects]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/407?rss=1</link>
<description><![CDATA[
<p>Both maternal diabetes and obesity have been associated with an increased risk of neural tube defects (NTD), possibly due to a sustained state of hyperglycemia and/or hyperinsulinemia. Data were collected in the Boston University Slone Birth Defects Study (a case-control study) from 1988 to 1998. The authors examined whether high dietary glycemic index (DGI) and high dietary glycemic load (DGL) increased the risk of NTDs in nondiabetic women. Mothers of NTD cases and nonmalformed controls were interviewed in person within 6 months after delivery about diet and other exposures. Odds ratios and 95% confidence intervals were estimated from logistic regression for high DGI (&ge;60) and high DGL (&ge;205), with cutpoints determined by cubic spline. Of 698 case mothers, 25% had high DGI and 4% had high DGL. Of 696 control mothers, 15% had high DGI and 2% had high DGL. After adjustment for sociodemographic factors and other dietary factors, the odds ratio for high DGI was 1.5 (95% confidence interval: 1.1, 2.0); for high DGL, it was 1.8 (95% confidence interval: 0.8, 4.0). Diets with proportionally high DGI or DGL may put the developing fetus at risk of an NTD, adding further evidence that hyperglycemia lies within the pathogenic pathway.</p>
]]></description>
<dc:creator><![CDATA[Yazdy, M. M., Liu, S., Mitchell, A. A., Werler, M. M.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp395</dc:identifier>
<dc:title><![CDATA[Maternal Dietary Glycemic Intake and the Risk of Neural Tube Defects]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>414</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>407</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/415?rss=1">
<title><![CDATA[Menopausal Hormone Therapy Use and Risk of Invasive Colon Cancer: The California Teachers Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/415?rss=1</link>
<description><![CDATA[
<p>Results from epidemiologic studies of hormone therapy use and colon cancer risk are inconsistent. This question was investigated in the California Teachers Study (1995&ndash;2006) among 56,864 perimenopausal or postmenopausal participants under 80 years of age with no prior colorectal cancer by using Cox proportional hazards regression. Incident invasive colon cancer was diagnosed among 442 participants. Baseline-recent hormone therapy users were at 36% lower risk for colon cancer versus baseline-never users (baseline-recent users: relative risk (RR) = 0.64, 95% confidence interval (CI): 0.51, 0.80). Results did not differ by formulation. Estimated risk was lower among baseline-recent hormone therapy users with increasing duration between 5 and 15 years of use (RR = 0.49, 95% CI: 0.35, 0.68), but the trend did not persist in the longest duration group, more than 15 years of use (RR = 0.69, 95% CI: 0.52, 0.92; <I>P</I><SUB>trend</SUB> = 0.60). Long-term recreational physical activity, obesity, regular use of nonsteroidal antiinflammatory medications, and daily alcohol intake did not modify these effects; baseline-recent use was more strongly associated with colon cancer risk among women with a family history of colorectal cancer (<I>P</I><SUB>heterogeneity</SUB> = 0.04). Baseline-recent hormone therapy use was inversely associated with invasive colon cancer risk among perimenopausal and postmenopausal women in the California Teachers Study.</p>
]]></description>
<dc:creator><![CDATA[DeLellis Henderson, K., Duan, L., Sullivan-Halley, J., Ma, H., Clarke, C. A., Neuhausen, S. L., Templeman, C., Bernstein, L.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp434</dc:identifier>
<dc:title><![CDATA[Menopausal Hormone Therapy Use and Risk of Invasive Colon Cancer: The California Teachers Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>425</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>415</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/426?rss=1">
<title><![CDATA[Cardiorespiratory Fitness Levels Among US Adults 20-49 Years of Age: Findings From the 1999-2004 National Health and Nutrition Examination Survey]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/426?rss=1</link>
<description><![CDATA[
<p>Data from the 1999&ndash;2004 National Health and Nutrition Examination Survey were used to describe the distribution of cardiorespiratory fitness and its association with obesity and leisure-time physical activity (LTPA) for adults 20&ndash;49 years of age without physical limitations or indications of cardiovascular disease. A sample of 7,437 adults aged 20&ndash;49 years were examined at a mobile examination center. Of 4,860 eligible for a submaximal treadmill test, 3,250 completed the test and were included in the analysis. The mean maximal oxygen uptake (<f><inline-fig>
<link locator="amjepidkwp412fx1_ht"></inline-fig></f>max) was estimated as 44.5, 42.8, and 42.2 mL/kg/minute for men 20&ndash;29, 30&ndash;39, and 40&ndash;49 years of age, respectively. For women, it was 36.5, 35.4, and 34.4 mL/kg/minute for the corresponding age groups. Non-Hispanic black women had lower fitness levels than did non-Hispanic white and Mexican-American women. Regardless of gender or race/ethnicity, people who were obese had a significantly lower estimated maximal oxygen uptake than did nonobese adults. Furthermore, a positive association between fitness level and LTPA participation was observed for both men and women. These results can be used to track future population assessments and to evaluate interventions. The differences in fitness status among population subgroups and by obesity status or LTPA can also be used to develop health policies and targeted educational campaigns.</p>
]]></description>
<dc:creator><![CDATA[Wang, C.-Y., Haskell, W. L., Farrell, S. W., LaMonte, M. J., Blair, S. N., Curtin, L. R., Hughes, J. P., Burt, V. L.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp412</dc:identifier>
<dc:title><![CDATA[Cardiorespiratory Fitness Levels Among US Adults 20-49 Years of Age: Findings From the 1999-2004 National Health and Nutrition Examination Survey]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>435</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>426</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/436?rss=1">
<title><![CDATA[Dairy Intake and the Risk of Bladder Cancer in the Netherlands Cohort Study on Diet and Cancer]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/436?rss=1</link>
<description><![CDATA[
<p>The authors examined the association between the intake of different dairy products and the risk of bladder cancer in 120,852 men and women aged 55&ndash;69 years participating in the Netherlands Cohort Study on Diet and Cancer. Dairy product intake was assessed in 1986 by using a 150-item food frequency questionnaire. The cohort was followed for 16.3 years, and 1,549 incident cases of bladder cancer were analyzed. Cox proportional hazards analysis was applied with a case-cohort approach by using the follow-up data of a random subcohort (<I>n</I> = 5,000). Multivariate hazard ratio estimates comparing the highest with the lowest quintile of total dairy intake were 1.01 (95% confidence interval (CI): 0.81, 1.27; <I>P</I><SUB>trend</SUB> = 0.68). A statistically significant association for fermented milk products was found only for the second quintile (median, 12 g/day) (hazard ratio = 0.71, 95% CI: 0.56, 0.91). Compared with nonconsumers, women with 25&ndash;75 g/day of butter consumption had a hazard ratio of 1.61 (95% CI: 1.03, 2.50; <I>P</I><SUB>trend</SUB> &lt; 0.01). No association was found with cheese, calcium, lactose, or nonfermented dairy intake. These results provide weak evidence that bladder cancer risk is inversely associated with low intake of fermented dairy products and suggest a positive association with butter intake in women.</p>
]]></description>
<dc:creator><![CDATA[Keszei, A. P., Schouten, L. J., Goldbohm, R. A., van den Brandt, P. A.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp399</dc:identifier>
<dc:title><![CDATA[Dairy Intake and the Risk of Bladder Cancer in the Netherlands Cohort Study on Diet and Cancer]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>446</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>436</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/447?rss=1">
<title><![CDATA[Presence of Gallstones or Kidney Stones and Risk of Type 2 Diabetes]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/447?rss=1</link>
<description><![CDATA[
<p>Recent evidence suggests that gallstones and kidney stones are associated with insulin resistance, but the relation between stone diseases and the risk of developing type 2 diabetes mellitus is not clear. Participants in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study (Potsdam, Germany) provided information about the presence of gallstones and kidney stones at recruitment between 1994 and 1998. On biennial questionnaires, participants reported newly diagnosed type 2 diabetes mellitus, and confirmation was obtained from treating physicians. During a mean follow-up period of 7.0 years between 1994 and 2005, 849 incident cases of type 2 diabetes were identified among 25,166 participants. After adjustment for sex, age, waist circumference, and lifestyle risk factors, persons with reported gallstones (<I>n</I> = 3,293) had an increased risk of type 2 diabetes (relative risk = 1.42, 95% confidence interval: 1.21, 1.68). Among the 23,817 participants with information on reported kidney stones (784 cases of incident diabetes), those who developed kidney stones (<I>n</I> = 2,468) were not at increased risk of diabetes in multivariable-adjusted models (relative risk = 1.05, 95% confidence interval: 0.86, 1.27). These findings suggest that gallstones, but not kidney stones, may predict the risk of developing type 2 diabetes, providing physicians with an interventional opportunity to implement adequate prevention measures.</p>
]]></description>
<dc:creator><![CDATA[Weikert, C., Weikert, S., Schulze, M. B., Pischon, T., Fritsche, A., Bergmann, M. M., Willich, S. N., Boeing, H.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp411</dc:identifier>
<dc:title><![CDATA[Presence of Gallstones or Kidney Stones and Risk of Type 2 Diabetes]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>454</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>447</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/455?rss=1">
<title><![CDATA[Pesticide Use and Thyroid Disease Among Women in the Agricultural Health Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/455?rss=1</link>
<description><![CDATA[
<p>Thyroid disease is common, and evidence of an association between organochlorine exposure and thyroid disease is increasing. The authors examined the cross-sectional association between ever use of organochlorines and risk of hypothyroidism and hyperthyroidism among female spouses (<I>n</I> = 16,529) in Iowa and North Carolina enrolled in the Agricultural Health Study in 1993&ndash;1997. They also assessed risk of thyroid disease in relation to ever use of herbicides, insecticides, fungicides, and fumigants. Prevalence of self-reported clinically diagnosed thyroid disease was 12.5%, and prevalence of hypothyroidism and hyperthyroidism was 6.9% and 2.1%, respectively. There was an increased odds of hypothyroidism with ever use of organochlorine insecticides (adjusted odds ratio (OR<SUB>adj</SUB>) = 1.2 (95% confidence interval (CI): 1.0, 1.6) and fungicides (OR<SUB>adj</SUB> = 1.4 (95% CI: 1.1, 1.8) but no association with ever use of herbicides, fumigants, organophosphates, pyrethroids, or carbamates. Specifically, ever use of the organochlorine chlordane (OR<SUB>adj</SUB> = 1.3 (95% CI: 0.99, 1.7), the fungicides benomyl (OR<SUB>adj</SUB> = 3.1 (95% CI: 1.9, 5.1) and maneb/mancozeb (OR<SUB>adj</SUB> = 2.2 (95% CI: 1.5, 3.3), and the herbicide paraquat (OR<SUB>adj</SUB> = 1.8 (95% CI: 1.1, 2.8) was significantly associated with hypothyroidism. Maneb/mancozeb was the only pesticide associated with both hyperthyroidism (OR<SUB>adj</SUB> = 2.3 (95% CI: 1.2, 4.4) and hypothyroidism. These data support a role of organochlorines, in addition to fungicides, in the etiology of thyroid disease among female spouses enrolled in the Agricultural Health Study.</p>
]]></description>
<dc:creator><![CDATA[Goldner, W. S., Sandler, D. P., Yu, F., Hoppin, J. A., Kamel, F., LeVan, T. D.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp404</dc:identifier>
<dc:title><![CDATA[Pesticide Use and Thyroid Disease Among Women in the Agricultural Health Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>464</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>455</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/465?rss=1">
<title><![CDATA[Estimates of the Transmissibility of the 1968 (Hong Kong) Influenza Pandemic: Evidence of Increased Transmissibility Between Successive Waves]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/465?rss=1</link>
<description><![CDATA[
<p>The transmissibility of the strain of influenza virus which caused the 1968 influenza pandemic is poorly understood. Increases in outbreak size between the first and second waves suggest that it may even have increased between successive waves. The authors estimated basic and effective reproduction numbers for both waves of the 1968 influenza pandemic. Epidemic curves and overall attack rates for the 1968 pandemic, based on clinical and serologic data, were retrieved from published literature. The basic and effective reproduction numbers were estimated from 46 and 17 data sets for the first and second waves, respectively, based on the growth rate and/or final size of the epidemic. Estimates of the basic reproduction number (<I>R</I><SUB>0</SUB>) were in the range of 1.06&ndash;2.06 for the first wave and, assuming cross-protection, 1.21&ndash;3.58 in the second. Within each wave, there was little geographic variation in transmissibility. In the 10 settings for which data were available for both waves, <I>R</I><SUB>0</SUB> was estimated to be higher during the second wave than during the first. This might partly explain the larger outbreaks in the second wave as compared with the first. This potential for change in viral behavior may have consequences for future pandemic mitigation strategies.</p>
]]></description>
<dc:creator><![CDATA[Jackson, C., Vynnycky, E., Mangtani, P.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp394</dc:identifier>
<dc:title><![CDATA[Estimates of the Transmissibility of the 1968 (Hong Kong) Influenza Pandemic: Evidence of Increased Transmissibility Between Successive Waves]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>478</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>465</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/479?rss=1">
<title><![CDATA[Comparing 3 Dietary Pattern Methods--Cluster Analysis, Factor Analysis, and Index Analysis--With Colorectal Cancer Risk: The NIH-AARP Diet and Health Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/479?rss=1</link>
<description><![CDATA[
<p>The authors compared dietary pattern methods&mdash;cluster analysis, factor analysis, and index analysis&mdash;with colorectal cancer risk in the National Institutes of Health (NIH)&ndash;AARP Diet and Health Study (<I>n</I> = 492,306). Data from a 124-item food frequency questionnaire (1995&ndash;1996) were used to identify 4 clusters for men (3 clusters for women), 3 factors, and 4 indexes. Comparisons were made with adjusted relative risks and 95% confidence intervals, distributions of individuals in clusters by quintile of factor and index scores, and health behavior characteristics. During 5 years of follow-up through 2000, 3,110 colorectal cancer cases were ascertained. In men, the vegetables and fruits cluster, the fruits and vegetables factor, the fat-reduced/diet foods factor, and all indexes were associated with reduced risk; the meat and potatoes factor was associated with increased risk. In women, reduced risk was found with the Healthy Eating Index-2005 and increased risk with the meat and potatoes factor. For men, beneficial health characteristics were seen with all fruit/vegetable patterns, diet foods patterns, and indexes, while poorer health characteristics were found with meat patterns. For women, findings were similar except that poorer health characteristics were seen with diet foods patterns. Similarities were found across methods, suggesting basic qualities of healthy diets. Nonetheless, findings vary because each method answers a different question.</p>
]]></description>
<dc:creator><![CDATA[Reedy, J., Wirfalt, E., Flood, A., Mitrou, P. N., Krebs-Smith, S. M., Kipnis, V., Midthune, D., Leitzmann, M., Hollenbeck, A., Schatzkin, A., Subar, A. F.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp393</dc:identifier>
<dc:title><![CDATA[Comparing 3 Dietary Pattern Methods--Cluster Analysis, Factor Analysis, and Index Analysis--With Colorectal Cancer Risk: The NIH-AARP Diet and Health Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>487</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>479</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/488?rss=1">
<title><![CDATA[Biochemical Validation of Food Frequency Questionnaire-Estimated Carotenoid, {alpha}-Tocopherol, and Folate Intakes Among African Americans and Non-Hispanic Whites in the Southern Community Cohort Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/488?rss=1</link>
<description><![CDATA[
<p>Few food frequency questionnaires (FFQs) have been developed specifically for use among African Americans, and reports of FFQ performance among African Americans or low-income groups assessed using biochemical indicators are scarce. The authors conducted a validation study within the Southern Community Cohort Study to evaluate FFQ-estimated intakes of -carotene, &beta;-carotene, &beta;-cryptoxanthin, lutein/zeaxanthin, lycopene, folate, and -tocopherol in relation to blood levels of these nutrients. Included were 255 nonsmoking participants (125 African Americans, 130 non-Hispanic whites) who provided a blood sample at the time of study enrollment and FFQ administration in 2002&ndash;2004. Levels of biochemical indicators of each micronutrient (-tocopherol among women only) significantly increased with increasing FFQ-estimated intake (adjusted correlation coefficients: -carotene, 0.35; &beta;-carotene, 0.28; &beta;-cryptoxanthin, 0.35; lutein/zeaxanthin, 0.28; lycopene, 0.15; folate, 0.26; -tocopherol, 0.26 among women; all <I>P</I>'s &lt; 0.05). Subjects in the top decile of FFQ intake had blood levels that were 27% (lycopene) to 178% (&beta;-cryptoxanthin) higher than those of subjects in the lowest decile. Satisfactory FFQ performance was noted even for participants with less than a high school education. Some variation was noted in the FFQ's ability to predict blood levels for subgroups defined by race, sex, and other characteristics, but overall the Southern Community Cohort Study FFQ appears to generate useful dietary exposure rankings in the cohort.</p>
]]></description>
<dc:creator><![CDATA[Signorello, L. B., Buchowski, M. S., Cai, Q., Munro, H. M., Hargreaves, M. K., Blot, W. J.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp402</dc:identifier>
<dc:title><![CDATA[Biochemical Validation of Food Frequency Questionnaire-Estimated Carotenoid, {alpha}-Tocopherol, and Folate Intakes Among African Americans and Non-Hispanic Whites in the Southern Community Cohort Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>497</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>488</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/498?rss=1">
<title><![CDATA[A Comparison of Sample Size and Power in Case-Only Association Studies of Gene-Environment Interaction]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/498?rss=1</link>
<description><![CDATA[
<p>Assuming continuous, normally distributed environmental and categorical genotype variables, the authors compare 6 case-only designs for tests of association in gene-environment interaction. Novel tests modeling the environmental variable as either the response or the predictor and allowing a genetic variable with multiallelic variants are included. The authors show that tests imposing the same genotypic pattern of inheritance perform similarly regardless of whether genotype is the response variable or the predictor variable. The novel tests using the genetic variable as the response variable are advantageous because they are robust to non-normally distributed environmental exposures. Dominance deviance&mdash;deviation from additivity in the main or interaction effects&mdash;is key to test performance: When it is zero or modest, tests searching for a trend with increasing risk alleles are optimal; when it is large, tests for genotypic effects are optimal. However, the authors show that dominance deviance is attenuated when it is observed at a proxy locus, which is common in genome-wide association studies, so large dominance deviance is likely to be rare. The authors conclude that the trend test is the appropriate tool for large-scale association scans where the true gene-environment interaction model is unknown. The common practice of assuming a dominant pattern of inheritance can cause serious losses of power in the presence of any recessive, or modest dominant, effects.</p>
]]></description>
<dc:creator><![CDATA[Clarke, G. M., Morris, A. P.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp398</dc:identifier>
<dc:title><![CDATA[A Comparison of Sample Size and Power in Case-Only Association Studies of Gene-Environment Interaction]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>505</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>498</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/171/4/506?rss=1">
<title><![CDATA[Marginal Structural Models for Sufficient Cause Interactions]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/171/4/506?rss=1</link>
<description><![CDATA[
<p>Sufficient cause interactions concern cases in which there is a particular causal mechanism for some outcome that requires the presence of 2 or more specific causes to operate. Empirical conditions have been derived to test for sufficient cause interactions. However, when regression outcome models are used to control for confounding variables in tests for sufficient cause interactions, the outcome models impose restrictions on the relation between the confounding variables and certain unidentified background causes within the sufficient cause framework; often, these assumptions are implausible. By using marginal structural models, rather than outcome regression models, to test for sufficient cause interactions, modeling assumptions are instead made on the relation between the causes of interest and the confounding variables; these assumptions will often be more plausible. The use of marginal structural models also allows for testing for sufficient cause interactions in the presence of time-dependent confounding. Such time-dependent confounding may arise in cases in which one factor of interest affects both the second factor of interest and the outcome. It is furthermore shown that marginal structural models can be used not only to test for sufficient cause interactions but also to give lower bounds on the prevalence of such sufficient cause interactions.</p>
]]></description>
<dc:creator><![CDATA[VanderWeele, T. J., Vansteelandt, S., Robins, J. M.]]></dc:creator>
<dc:date>Thu, 04 Feb 2010 17:09:30 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp396</dc:identifier>
<dc:title><![CDATA[Marginal Structural Models for Sufficient Cause Interactions]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>171</prism:volume>
<prism:endingPage>514</prism:endingPage>
<prism:publicationDate>2010-02-15</prism:publicationDate>
<prism:startingPage>506</prism:startingPage>
<prism:section>RESEARCH-ARTICLE</prism:section>
</item>

</rdf:RDF>