9 research outputs found
Multivariate prediction of diabetes according to CDP and biomarker risk score.
<p>WC, waist circumference; FG, fasting glucose; HT, hypertension; TNF-α R2: tumor neurosis factor-alpha receptor 2.</p
Comparisons of AUCs of different diabetes prediction models.
<p>AUC, Area under the curve; All biomarker levels were sex-specific except for hsCRP;</p><p>CDP: Sex, Age, Waist circumference, fasting glucose, hypertension, dyslipidaemia, family history of diabetes, physical activity and smoking status.</p><p>TNF-α R2: tumor neurosis factor-alpha receptor 2; hsCRP, high sensitivity C-reactive protein; IL-6, Interleukin-6; A-FABP, adipocyte-fatty acid-binding protein.</p
Baseline clinical and biochemical characteristics of subjects with and without incident type 2 DM in 5.3 years.
<p>Mean ± SD, median (interquartile-range), or percentage as appropriate.</p>a<p>Physical activity: active if having moderate intensity exercise for at least 30 minutes in one month. <sup>b</sup>Sex-adjusted; <sup>c</sup>Adjusted for hypertensive treatment; <sup>d</sup>Log transformed before analysis. <sup>e</sup>Excluded subjects on lipid treatment;</p><p>Central obesity: waist circumference ≥90 cm (M)/80 cm (F).</p><p>Hypertension: systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or on hypertensive treatment.</p><p>Dyslipidaemia: triglycerides ≥1.7 mmol/L, HDL cholesterol <1.0 mmol/L (M)/1.3 mmol/L (F), LDL cholesterol ≥3.4 mmol/L, or on lipid treatment.</p
Log-likelihood ratio tests comparing the change before and after addition of biomarkers.
<p>-2LL, -2log-likelihood; p-value (χ<sup>2</sup>, df = 1);</p><p>All biomarker levels were sex specific (except for hsCRP).</p><p>CDP: Sex, Age, Waist circumference, fasting glucose, hypertension, dyslipidaemia, family history of diabetes, physical activity and smoking status.</p><p>TNF-α R2: tumor neurosis factor-alpha receptor 2; hsCRP, high sensitivity C-reactive protein; IL-6, Interleukin-6; A-FABP, adipocyte-fatty acid-binding protein.</p
Prepandemic seroprevalence and the epidemic curve of pdmH1N1 in Hong Kong.
<p><b>A</b> Age-stratified pre-pandemic MN titer distributions which were estimated from serum samples collected in June and early-July 2009. For samples collected after July 2009, we only tested whether they were MN<sub>1∶20</sub> and MN<sub>1:40</sub> seropositive because of logistical constraints. <b>B</b> Epidemic curves of pdmH1N1 in Hong Kong and Shenzhen. Estimated weekly numbers of lab-confirmed cases in Shenzhen were extracted from <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004054#ppat.1004054-Xie1" target="_blank">[38]</a>.</p
Posterior distributions of parameter estimates.
<p>Different colors correspond to different POLYMOD contact matrices. <b>A</b> Age-dependent parameters including IARs (first column), <i>ISP</i><sub>40</sub> (second), and age-specific susceptibility (third). <b>B</b> Other parameters including <i>R</i>(0), <i>T<sub>g</sub></i>, <i>ISP</i><sub>20</sub>, reduction in within-age-group mixing due to school closure (<i>π</i><sub>0</sub>, <i>π</i><sub>1</sub>, <i>π</i><sub>2</sub>), seed size, and scaling factor for FOI from Shenzhen (<i>ε<sub>SZ</sub></i>).</p
Comparison of the data and the fitted model.
<p>The hospitalization and serial cross-sectional seroprevalence data are shown in blue (vertical bars indicate 95% confidence intervals). Posterior intervals of hospitalizations and seroprevalence in the fitted model are shown as heat shades in which darker colors represent higher probability densities (i.e. highest density in red and zero density in white).</p
Model parameters and their posterior statistics.
<p>Model parameters and their posterior statistics.</p
Age-specific Δ<i>S</i><sub>40</sub>/Δ<i>S</i><sub>20</sub> during the first wave of pdmH1N1 in Hong Kong.
<p>Δ<i>S</i><sub>40</sub> and Δ<i>S</i><sub>20</sub> at each cross-section were estimated using the method described in our previous work <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004054#ppat.1004054-Wu1" target="_blank">[11]</a>. If ISP<sub>20</sub> and ISP<sub>40</sub> (among all pdmH1N1 infections) were the same as the proportions of clinical cases that became MN<sub>1:20</sub> and MN<sub>1∶40</sub> seropositive (i.e. around 100% and 90%, respectively <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004054#ppat.1004054-Hung1" target="_blank">[23]</a>, <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004054#ppat.1004054-Veguilla1" target="_blank">[24]</a>), Δ<i>S</i><sub>40</sub>/Δ<i>S</i><sub>20</sub> should have remained close to 0.9–1 (the horizontal dashed line) throughout the first wave, which was not the case in reality as shown here.</p