67 research outputs found

    Improving Google Flu Trends Estimates for the United States through Transformation

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    <div><p>Google Flu Trends (GFT) uses Internet search queries in an effort to provide early warning of increases in influenza-like illness (ILI). In the United States, GFT estimates the percentage of physician visits related to ILI (%ILINet) reported by the Centers for Disease Control and Prevention (CDC). However, during the 2012–13 influenza season, GFT overestimated %ILINet by an appreciable amount and estimated the peak in incidence three weeks late. Using data from 2010–14, we investigated the relationship between GFT estimates (%GFT) and %ILINet. Based on the relationship between the relative change in %GFT and the relative change in %ILINet, we transformed %GFT estimates to better correspond with %ILINet values. In 2010–13, our transformed %GFT estimates were within ±10% of %ILINet values for 17 of the 29 weeks that %ILINet was above the seasonal baseline value determined by the CDC; in contrast, the original %GFT estimates were within ±10% of %ILINet values for only two of these 29 weeks. Relative to the %ILINet peak in 2012–13, the peak in our transformed %GFT estimates was 2% lower and one week later, whereas the peak in the original %GFT estimates was 74% higher and three weeks later. The same transformation improved %GFT estimates using the recalibrated 2013 GFT model in early 2013–14. Our transformed %GFT estimates can be calculated approximately one week before %ILINet values are reported by the CDC and the transformation equation was stable over the time period investigated (2010–13). We anticipate our results will facilitate future use of GFT.</p></div

    Correction: Improving Google Flu Trends Estimates for the United States through Transformation

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    <p>Correction: Improving Google Flu Trends Estimates for the United States through Transformation</p

    Comparing estimates of the weekly percentage of physician visits related to influenza-like illness (ILI) based on Google Flu Trends (GFT) to values reported by the Centers for Disease Control and Prevention (CDC), United States, October 2010–March 2014.

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    <p>*Week 39 of 2010 and week 30 of 2013 were used to calculate transformed %GFT estimates for each of these time periods, respectively.</p><p>**During the 2010–13 seasons, 29 weeks were above baseline.</p>†<p>During the 2013–14 season, 14 weeks were above baseline.</p><p>Comparing estimates of the weekly percentage of physician visits related to influenza-like illness (ILI) based on Google Flu Trends (GFT) to values reported by the Centers for Disease Control and Prevention (CDC), United States, October 2010–March 2014.</p

    Weekly percentage of sentinel physician visits related to influenza-like illness (ILI) reported by the Centers for Disease Control and Prevention (CDC) and estimated using Google Flu Trends (GFT), United States, October 2010–March 2014.

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    <p>The final CDC value (f%ILINet; blue) is compared to the GFT estimate (%GFT; red) and the transformed GFT estimate using <i>c</i> = 0.65 (transformed %GFT; turquoise). The GFT model was recalibrated during the 2013–14 season: dashed lines show the period in which GFT estimates were retrospectively re-estimated using the 2013 GFT model.</p

    Metastasis of Primary SCC to Lymph Nodes and Lungs in <i>p19<sup> Arf</sup></i>-Deficient Mice

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    <div><p>(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).</p> <p>(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).</p> <p>(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).</p> <p>(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).</p> <p>(E) H&E stain of lymph node bearing metastatic differentiated SCC.</p> <p>(F) Immunostain with pan-keratin antibody of papilloma.</p> <p>(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.</p> <p>(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).</p> <p>(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).</p> <p>(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification.</p></div

    LOH of Wild-Type <i>p19<sup>Arf</sup></i> Allele in <i>p19<sup>Arf+/−</sup></i> Tumors

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    <div><p>(A) LOH analysis by semiquantitative PCR of the wild-type <i>p19<sup>Arf</sup></i> allele in <i>p19<sup>Arf+/−</sup></i> papillomas and carcinomas. Gradient made from kidney DNA used for quantitation of wt/mu ratio (top row). wt, wild-type allele; mu, knockout allele; asterisk, loss or reduction of <i>p19<sup>Arf</sup></i> wild-type band.</p> <p>(B) Western blot analysis of nuclear lysates from papillomas (PA) and carcinomas (CA) from <i>p19<sup>Arf+/+</sup>, p19<sup>Arf+/−</sup>,</i> and <i>p19<sup>Arf−/−</sup></i> mice.</p></div

    P-values of 308 gene sets in the data analysis: p-values of Global Test and ANCOVA Global Test after standardization vs

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    <p><b>Copyright information:</b></p><p>Taken from "Comparative evaluation of gene-set analysis methods"</p><p>http://www.biomedcentral.com/1471-2105/8/431</p><p>BMC Bioinformatics 2007;8():431-431.</p><p>Published online 7 Nov 2007</p><p>PMCID:PMC2238724.</p><p></p> SAM-GS p-values before the standardization. The line indicates equal p-values between SAM-GS and Global Tests

    Reduced p53 Expression in Skin Tumors from <i>p19<sup>Arf</sup></i>-Deficient Mice

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    <div><p>(A) Western blot analysis of nuclear lysates from skin tumors from <i>p19<sup> Arf</sup> (Arf)<sup>+/+</sup>, p19<sup> Arf+/−</sup>,</i> and <i>p19<sup> Arf−/−</sup></i> mice using p53-specific antibody. PA, papilloma; skin IR, irradiated normal skin</p> <p>(B) p53 immunostain of paraffin-embedded skin tumor sections from <i>p19<sup> Arf+/+</sup>, p19<sup> Arf+/−</sup>,</i> and <i>p19<sup> Arf−/−</sup></i> mice (arrows indicate positive stained cells) (top). p53 immunostain of irradiated papillomas (IR) from <i>p19<sup> Arf+/+</sup></i> and <i>p19<sup> Arf−/−</sup></i> mice (bottom). p53 is not detected in normal skin or tumors from <i>p19<sup> Arf−/−</sup></i> mice, but is induced by irradiation in both normal and tumor cells from <i>p19<sup> Arf−/−</sup></i> mice.</p></div

    Skin Tumor Multiplicity, Size, and Progression in <i>p19<sup> Arf</sup></i>-Deficient Mice

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    <div><p>(A) Average number of papillomas (more than 2 mm in diameter) per mouse is plotted versus the number of weeks postinitiation. Both <i>p19<sup> Arf</sup> (Arf)<sup>+/−</sup></i> and <i>p19<sup> Arf−/−</sup></i> mice show greater numbers of tumors than <i>p19<sup> Arf+/+</sup></i> mice.</p> <p>(B) Comparison of papilloma size (in mm) between <i>p19<sup> Arf+/+</sup>, p19<sup> Arf+/−</sup>,</i> and <i>p19<sup> Arf−/−</sup></i> mice through 28 wk postinitiation. An increase in the largest size class of tumors is seen in <i>p19<sup> Arf+/−</sup></i> and <i>p19<sup> Arf−/−</sup></i> mice but not <i>p19<sup> Arf+/+</sup></i> mice<i>.</i></p> <p>(C) Percentage of mice bearing at least one carcinoma is plotted versus the number of weeks postinitiation<i>. p19<sup> Arf−/−</sup></i> mice show the shortest latency and greatest incidence of carcinoma conversion, with <i>p19<sup> Arf+/−</sup></i> mice showing an incidence between the <i>p19<sup> Arf−/−</sup></i> and <i>p19<sup> Arf+/+</sup></i> mice. Time of appearance of lymph node metastasis is noted above the graph as a vertical line for each mouse analyzed. Metastasis to lymph node occurred frequently and sooner in <i>p19<sup> Arf</sup></i>-deficient mice than in wild-type mice.</p></div

    Tumor Multiplicity and Proliferative Index in <i>p19<sup> Arf</sup> /p53</i> Compound Mutant Mice

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    <div><p>(A) Average number of papillomas (more than 2 mm in diameter) per mouse is plotted against the number of weeks post-initiation.</p> <p>(B) Image of wild-type, <i>p19<sup> Arf</sup> (Arf)<sup>−/−</sup>, p53<sup>−/−</sup>,</i> and <i>p19<sup>Arf−/−</sup>p53<sup>−/−</sup></i> mice with skin tumors at time of sacrifice. Wild-type mice show large exophytic tumors, while both <i>p19<sup> Arf</sup></i>- and p53-deficient mice have endophytic tumors. Note larger tumors in <i>p19<sup>Arf</sup> /p53</i> compound mutant mice relative to <i>p53</i> single mutants.</p> <p>(C) BrdU-positive cells in papillomas from wild-type<i>, p53<sup>−/−</sup>, p19<sup> Arf−/−</sup>,</i> and <i>p19<sup> Arf−/−</sup>p53<sup>−/−</sup></i> mice at 10 wk postinitiation. (Bars represent average counts ± standard deviation from ten fields and five mice). <i>p53<sup>−/−</sup></i> tumors show significantly fewer BrdU-positive cells than either <i>p19<sup> Arf−/−</sup></i> or wild-type tumors (<i>p</i> < 0.05, Wilcoxon one-sided t-test).</p></div
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