472 research outputs found

    Site-Specific Risk Factors for Ray Blight in Tasmanian Pyrethrum Fields

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    Ray blight of pyrethrum (Tanacetum cinerariifolium), caused by Phoma ligulicola var. inoxydablis, can cause defoliation and reductions of crop growth and pyrethrin yield. Logistic regression was used to model relationships among edaphic factors and interpolated weather variables associated with severe disease outbreaks (i.e., defoliation severity ≥40%). A model for September defoliation severity included a variable for the product of number of days with rain of at least 0.1 mm and a moving average of maximum temperatures in the last 14 days, which correctly classified (accuracy) the disease severity class for 64.8% of data sets. The percentage of data sets where disease severity was correctly classified as at least 40% defoliation severity (sensitivity) or below 40% defoliation severity (specificity) were 55.8 and 71%, respectively. A model for October defoliation severity included the number of days with at least 1 mm of rain in the past 14 days, stem height in September, and the product of the number of days with at least 10 mm of rain in the last 30 days and September defoliation severity. Accuracy, sensitivity, and specificity were 72.6, 73.6, and 71.4%, respectively. Youden\u27s index identified predictive thresholds of 0.25 and 0.57 for the September and October models, respectively. When economic considerations of the costs of false positive and false negative decisions and disease prevalence were integrated into receiver operating characteristic (ROC) curves for the October model, the optimal predictive threshold to minimize average management costs was 0 for values of disease prevalence greater than 0.2 due to the high cost of false negative predictions. ROC curve analysis indicated that management of the disease should be routine when disease prevalence is greater than 0.2. The models developed in this research are the first steps toward identifying and weighting site and weather disease risk variables to develop a decision-support aid for the management of ray blight of pyrethrum

    Psychophysical responses to a speech stressor: Correlation of plasma beta-endorphin levels at rest and after psychological stress with thermally measured pain threshold in patients with coronary artery disease

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    OBJECTIVES: We tested the hypothesis that psychological stress alters plasma levels of opioid peptides and that these plasma levels are related to pain perception in patients with coronary artery disease. BACKGROUND: Public speaking psychological stress has previously been shown to be associated with silent ischemia. METHODS: After instrumentation and a 30-min rest period, venous blood samples for beta-endorphin were obtained before and immediately after psychological stress in 20 patients with coronary artery disease. Pain threshold was then assessed using a thermal probe technique at baseline and immediately after stress. Patients gave three brief speeches lasting a total of 15 min about real-life hassle situations. RESULTS: Psychological stress significantly increases plasma beta-endorphin levels (4.3 +/- 0.9 pmol/liter [mean +/- SE] at rest to 8.3 +/- 2 pmol/liter after stress, p < 0.05). There was a significant positive correlation between pain threshold and beta-endorphin levels after stress (r = 0.577, p = 0.008). This significant positive correlation was still present while rest blood pressure and change in blood pressure during stress were controlled for by analysis of covariance techniques. CONCLUSIONS: In patients with coronary artery disease and exercise-induced ischemia, public speaking produces psychological stress manifested by increased cardiovascular reactivity and causes an increase in plasma beta-endorphin levels that is significantly correlated with pain thresholds. These findings may explain the predominance of silent ischemia during psychological stress in patients with coronary artery disease

    Social determinants of health and cardiovascular outcomes in patients with heart failure

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    BackgroundWe examined the associations between family income and educational attainment with incident atrial fibrillation (AF), myocardial infarction (MI), stroke and cardiovascular (CV) death among patients with newly-diagnosed heart failure (HF).MethodsIn a nationwide Danish registry of HF patients diagnosed between 2008 and 2018, we established a cohort for each outcome. When examining AF, MI and stroke, respectively, patients with a history of these outcomes at diagnosis of HF were excluded. We used cause-specific proportional hazard models to estimate hazard ratios for tertile groups of family income and three levels of educational attainment.ResultsAmong 27,947 AF-free patients, we found no association between income or education and incident AF. Among 27,309 MI-free patients, we found that lower income (hazard ratio 1.28 [95% CI 1.11-1.48] and 1.11 [0.96-1.28] for lower and medium vs. higher income) and education (1.23 [1.04-1.45] and 1.15 [0.97-1.36] for lower and medium vs. higher education) were associated with MI. Among 36,801 stroke-free patients, lower income was associated with stroke (1.38 [1.23-1.56] and 1.27 [1.12-1.44] for lower and medium vs. higher income) but not education. Lower income (1.56 [1.46-1.67] and 1.32 [1.23-1.42] for lower and medium vs. higher income) and education (1.20 [1.11-1.29] and 1.07 [0.99-1.15] for lower and medium vs. higher education) were associated with CV death.ConclusionsIn patients with newly-diagnosed HF, lower family income was associated with higher rates of acute MI, stroke and cardiovascular death. Lower educational attainment was associated with higher rates of acute MI and cardiovascular death. There was no evidence of associations between income and education with incident AF
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