Anthropometric measurements categorized by presence of food addiction by gender.

<p>Anthropometric measurements categorized by presence of food addiction by gender.</p

General characteristics of the participants categorized by presence of food addiction by gender.

<p>General characteristics of the participants categorized by presence of food addiction by gender.</p

Daily dietary energy and nutrient intakes of participants categorized by presence of food addiction.

<p>Daily dietary energy and nutrient intakes of participants categorized by presence of food addiction.</p

The correlations between YALE food addiction score and body mass index (BMI) or waist circumference (WC) of the participants with food addiction based on the gender.

<p>Scatter plot of food addiction scores and (A) BMI (kg/m²) (r = 0.464, p = 0.007) and (B) WC (cm) (r = 0.280, p = 0.114) among male participants with food addiction (n = 33). Scatter plot of food addiction scores and (C) BMI (kg/m2) (r = 0.259, p = 0.039) and (D) WC (cm) (r = 0.259, p = 0.039) among female participants with food addiction (n = 64).</p

Percentages of participants who reported having problems with certain types of food items in YFAS according to presence of food addiction.

<p>Chi-square (χ2) test was performed for nominal data analysis by gender presented as (%). FAD = ‘Food addicted’ (≥3 symptoms + satisfying clinical impairment/distress criteria), NFA = non-addicted.* = <i>p</i> < 0.05.</p

Inhibition of P2Y₁₂ receptors reduces aggregate size at high but not low shear in cone and plate(let) analyzer.

<p>Citrate-anticoagulated human blood was preincubated with vehicle, ticagrelor (20 µM) or cangrelor (10 µM) for 10 min. Blood samples were subjected to a shear rate of 500 or 5000 s⁻¹ for 2 min in a cone and plate(let) analyzer (CPA). (A) Representative images of platelet aggregates formed on the surface after 2 min (bar = 20 µm). (B) Average aggregate size in µm². Data are means ± SE (<i>n</i> = 4–6), *<i>p</i><0.05 compared to vehicle.</p

Inhibition of P2Y₁₂ receptors affects collagen-dependent thrombus formation at high but not low shear rate.

<p>Citrate-anticoagulated human blood, recalcified with CaCl₂/MgCl₂ in the presence of 2 pM tissue factor, was perfused over Horm type I collagen at a shear rate of 300 or 1000 s⁻¹. Blood samples were preincubated with vehicle, ticagrelor (20 µM) or cangrelor (10 µM), as indicated. (A) Representative phase-contrast images after 4 min of perfusion (bar = 20 µm). (B) Average size of thrombi formed in treated blood samples at different shear rates. (C) Frequency distribution of feature size on coverslips; estimated numbers of platelets per feature (aggregate) were: 9–24 (white), 24–75 (light gray), 75–400 (dark gray) and >400 (black). (D) Number of disaggregation events from individual aggregates in the 4th minute of blood perfusion at 300 or1000 s⁻¹. Data are means ± SE (<i>n</i> = 3–9), *<i>p</i><0.05 compared to vehicle.</p

Inhibition of P2Y₁₂ receptors causes unstable thrombus formation on acutely ruptured plaques in mice.

<p><i>Apoe</i>^−/− mice were infused with vehicle solution as a control. Other mice were infused with ticagrelor (210 µg/kg for 1 min, followed by 30 µg/kg/min during the experiment). In the third group of mice, cangrelor was continuously infused at 3 µg/kg/min. Infusion of ticagrelor and cangrelor started at 15 min before ultrasound treatment. (A) Brightfield image of a carotid plaque (p) with ultrasound probe (up). Further, raw fluorescence images (left) and threshold masked images (right) of CFSE-labeled platelets before and after ultrasound treatment. Dotted area indicates location of carotid artery (bars, 100 µm). Time stamps point to images at baseline (−10 s) or after plaque rupture (20 s). (B) Representative threshold masked images of thrombi on ruptured plaques of mice infused with vehicle, ticagrelor or cangrelor (bar, 100 µm). Note the microthrombi with P2Y₁₂ antagonist formed within 1 min of ultrasound treatment. (C) Time-courses of integrated CFSE fluorescence intensity above background (arbitrary units, AU) of representative thrombi formed. (D) Quantification of thrombus size at various time points after ultrasound treatment. Data are integrated fluorescence intensities from threshold masked images. (E) Number of fluorescent emboli shed during 3 min after plaque rupture. Data are means ± SE (<i>n</i> = 3–8), *<i>p</i><0.05 and ^#<i>p</i><0.1 compared to vehicle.</p

Deficiency of murine P2Y₁₂ receptors affects thrombus formation on plaque at high shear rate.

<p>Citrate-anticoagulated blood from P2Y₁₂^−/− and corresponding wild type (P2Y₁₂^+/+) mice was supplemented with OG488-fibrinogen (25 µg/ml) and co-perfused with ADP (10 µM) over homogenized murine plaque material at 1000 s⁻¹ for 4 min. (A) Representative phase-contrast and fluorescence images (bar = 20 µm). (B) Average size of thrombi after perfusion. (C) Average fluorescence intensity (arbitrary units) from fibrin(ogen)-binding platelets and thrombi. (D) Histograms of features on surface; estimated numbers of platelets per feature were 9–24 (white), 24–75 (light gray), 75–400 (dark gray) and >400 (black). (E) Disaggregation events measured per platelet aggregate per min. Data are means ± SE (<i>n</i> = 3), *<i>p</i><0.05.</p

Inhibition of murine P2Y₁₂ receptors diminishes thrombus formation and provokes platelet disaggregation under flow.

<p><i>Apoe</i>^−/− mice were infused with vehicle solution, ticagrelor or cangrelor (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0010130#pone-0010130-g001" target="_blank">Figure 1</a>). (A–C) PPACK/heparin anticoagulated blood from treated mice was perfused over native type I collagen at a shear rate of 1000 s⁻¹ for 4 min. (A) Representative phase-contrast images after 4 min perfusion (bar = 20 µm). (B) Quantitative effect of ticagrelor on surface area coverage by platelets. (C) Average number of disaggregation events measured from a preformed aggregate during flow. (D) Flow-cytometric evaluation in whole blood of platelets with active α_IIbβ₃ (JON/A mAb) by activation with ADP (20 µM), and of platelets exposing P-selectin (anti-CD62 mAb) by activation with convulxin (Cvx, 10 ng/ml). Bars give percentages of positive platelets. Data are means ± SE (<i>n</i> = 3–4), *<i>p</i><0.05.</p