15 research outputs found

    The Influence of performance parameters on market value

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    Research question: We uncover the influence of performance parameters on market value of football players in German Bundesliga. Hereby, the analyses should in some places reach beyond the current state of research by, for example, using relative operating times or running kilometres in the analysis. Research methods: To this end, we analysed all players in the season 2015/16 who had at least one significant participation in a game. Because of the unclear functional form of the links of the market value of players to the influencing variables, we carried out the analysis using Boosted Regression Trees in order to be able to map and interpret both different scale levels and nonlinearities. Results and Findings: We found the highest relative influence in the ranking of TV money from the preseason (>50%) and goals and high pass rate (each >10%). Partial-dependence plots recover the nonlinear influence of variable on the market value of players. Implications: It seems that the market value depends significantly less on sports performance than assumed. On the one hand, the preselection of the players in the respective clubs causes a clear difference in the market values of the individual players. In addition, the often-assumed linearity for some variables is just as little as the quadratic correlation, which is often assumed for old age, which is why classical OLS estimates cannot be sufficiently argued

    Preharvest Applications of Oxalic Acid and Salicylic Acid Increase Fruit Firmness and Polyphenolic Content in Blueberry (<i>Vaccinium corymbosum</i> L.)

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    Blueberry exports that imply transport times of more than 25 d deteriorate their quality. The use of elicitors in preharvest has shown positive effects on the quality of berries such as grapes. The objective of this study was to evaluate preharvest applications (21, 14, and 7 d before harvest) of oxalic acid (OA) and salicylic acid (SA) on fruit firmness and phenolic compounds in blueberry. The treatments of 0, 2, and 4 mM OA in ‘Kirra’ and 0, 2, and 4 mM SA are in ‘Stella blue’. With the earlier preharvest application, ‘Kirra’ presented better firmness than ‘Stella blue’; however, 2 mM OA and SA in both cultivars increased fruit firmness, maintaining its weight and diameter with respect to the control. It should be noted that the treatment with 2 mM SA generated a 100% increase in polyphenolic content and antioxidant capacity (p −1 and 80 mg 100 g−1 fresh weight (FW), respectively. In Kirra, OA treatments did not have a significant impact on the polyphenol content, but 4 mM OA increased by 100% and 20%, total anthocyanin and antioxidant capacity of blueberry fruit, respectively. Based on our results, three pre-harvest applications of OA and SA during the fruit development until the beginning of ripening improve fruit firmness by up to 20% at different times of harvest

    Genomic and phenotypic characterization of myxoma virus from Great Britain reveals multiple evolutionary pathways distinct from those in Australia

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    <div><p>The co-evolution of myxoma virus (MYXV) and the European rabbit occurred independently in Australia and Europe from different progenitor viruses. Although this is the canonical study of the evolution of virulence, whether the genomic and phenotypic outcomes of MYXV evolution in Europe mirror those observed in Australia is unknown. We addressed this question using viruses isolated in the United Kingdom early in the MYXV epizootic (1954–1955) and between 2008–2013. The later UK viruses fell into three distinct lineages indicative of a long period of separation and independent evolution. Although rates of evolutionary change were almost identical to those previously described for MYXV in Australia and strongly clock-like, genome evolution in the UK and Australia showed little convergence. The phenotypes of eight UK viruses from three lineages were characterized in laboratory rabbits and compared to the progenitor (release) Lausanne strain. Inferred virulence ranged from highly virulent (grade 1) to highly attenuated (grade 5). Two broad disease types were seen: cutaneous nodular myxomatosis characterized by multiple raised secondary cutaneous lesions, or an amyxomatous phenotype with few or no secondary lesions. A novel clinical outcome was acute death with pulmonary oedema and haemorrhage, often associated with bacteria in many tissues but an absence of inflammatory cells. Notably, reading frame disruptions in genes defined as essential for virulence in the progenitor Lausanne strain were compatible with the acquisition of high virulence. Combined, these data support a model of ongoing host-pathogen co-evolution in which multiple genetic pathways can produce successful outcomes in the field that involve both different virulence grades and disease phenotypes, with alterations in tissue tropism and disease mechanisms.</p></div

    Kaplan-Meier survival plots.

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    <p>(A) Perthshire lineage 1. There is a statistically significant difference between Perthshire 1792 and Perthshire 1527 (p = 0.0035; log rank test), but not between Perthshire 1527 and Perthshire 1537 (p = 0.11) nor between Perthshire 1792 and Perthshire 1537 (p = 0.79). (B) Perthshire lineage 2. There is no significant difference between the two viruses studied (p = 0.25). (C) Yorkshire lineage. There is a significant difference between Yorkshire 135 and Yorkshire Col (p = 0.0015) and Yorkshire 135 and Yorkshire 127 (p = 0.019), but not between Yorkshire col and Yorkshire 127 (p = 0.53). (D) Lausanne. There is a significant difference in survival time between Yorkshire 135 and Lu (p = 0.013).</p

    Nodular and amyxomatous phenotypes.

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    <p>(A) Lu day 10: grossly swollen almost granulomatous eyelids and swollen drooping ears; note the large swelling at the base of the ears. (B) Perthshire 1527 day 10; secondary lesions on ears but otherwise mild clinical signs with this grade 5 virus. (C) Perthshire 1537 day 10: moderately swollen ears, eyelids and head. Despite the alert appearance and mild clinical signs, the rabbit died with acute collapse less than 24 hours later. (D) Lu day 10: domed primary lesion oozing at top. (E) Lu day 12: section through primary lesion. (F) Perthshire 1792 day 10: amyxomatous phenotype showing very limited reaction at inoculation site. (G) Lu: histology of upper part of primary lesion day 12. Destruction of epidermis and dermis with scab formation and hemorrhage (arrowed); H: remnant hair follicle. (H) Lu primary lesion–deeper within the same lesion; short arrow indicates blue-grey staining mucinous material; long arrow indicates muscle necrosis and inflammatory cells (neutrophils). (I) Perthshire 2282 day 14: histopathology of primary lesion; note relatively normal architecture with some hyperplasia of epidermis and disruption of collagen fibres in dermis. E: epidermis; D: dermis; H: hair follicle. Scale bars = 100 μm.</p

    Evolutionary history of MXYV.

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    <p>(A) Maximum clade credibility (MCC) tree of 57 isolates of MYXV from the Australian and European epizootics including a sequence from Spain [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1006252#ppat.1006252.ref023" target="_blank">23</a>], four from Germany and one from Poland [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1006252#ppat.1006252.ref024" target="_blank">24</a>]. Sequence labels are color-coded to reflect virulence grade: grade 1, 2 = red, grade 3 = green, grade 4–5 = blue, non-quantified grade = black. The Lausanne and SLS progenitor strains are shown in bold italic. Tip times reflect the year of sampling. Estimated times to common ancestry are shown for key nodes and posterior probability values greater than 0.95 are marked by the * symbol. The different lineages of UK lineages are marked. (B) Regression of root-to-tip MYXV genetic distances against the year of sampling. Australian viruses are shaded blue and those from Europe in yellow. (C) Bayesian estimates of substitution rate utilizing different evolutionary models: A = Australian viruses, HKY+Γ nucleotide substitution model, relaxed clock, constant population size; B = Australian viruses, HKY+Γ, strict clock, constant population size; C = European viruses, HKY+Γ, relaxed clock, constant population size; D = European viruses, HKY+Γ, strict clock, constant population size; E = All viruses, GTR+Γ, relaxed clock, Bayesian skyride; F = All viruses, HKY+Γ, relaxed clock, constant population size; G = All viruses, HKY+Γ, relaxed clock, Bayesian skyride; H = All viruses, HKY+Γ, strict clock, constant population size (shown in red as this was used to infer the MCC tree); I = All viruses, HKY+Γ, strict clock, Bayesian skyride.</p
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