19 research outputs found

    ASSESSING DEER DAMAGE IN YOUNG FRUIT ORCHARDS

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    Evaluations of systematic damage assessments of 5, 10 and 20 percent of all apple trees in 12 orchards were compared. The 10% assessment technique was selected as the most accurate and efficient in estimating summer and fall damage. Analysis of several parameters of tree vigor found significant differences between browsed and unbrowsed trees for tree basal diameter and central leader diameter over 2 successive years. These subtle yet important differences in tree development were felt to severely limit the possibilities of relating browsing to growth and. later, yields. Methods and considerations for making control decisions on a per acre basis are discussed

    Jesus Silva Merit Scholarship Recipients Recital

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    The students performing tonight are recipients of the Jesus Silva Merit Scholarship for the 2016-2017 academic year. The Jesus Silva Merit Scholarship Fund was established in 1991 to assist talented guitarists in Virginia Commonwealth University\u27s Department of Music

    Accelerating functional gene discovery in osteoarthritis.

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    Osteoarthritis causes debilitating pain and disability, resulting in a considerable socioeconomic burden, yet no drugs are available that prevent disease onset or progression. Here, we develop, validate and use rapid-throughput imaging techniques to identify abnormal joint phenotypes in randomly selected mutant mice generated by the International Knockout Mouse Consortium. We identify 14 genes with functional involvement in osteoarthritis pathogenesis, including the homeobox gene Pitx1, and functionally characterize 6 candidate human osteoarthritis genes in mouse models. We demonstrate sensitivity of the methods by identifying age-related degenerative joint damage in wild-type mice. Finally, we phenotype previously generated mutant mice with an osteoarthritis-associated polymorphism in the Dio2 gene by CRISPR/Cas9 genome editing and demonstrate a protective role in disease onset with public health implications. We hope this expanding resource of mutant mice will accelerate functional gene discovery in osteoarthritis and offer drug discovery opportunities for this common, incapacitating chronic disease

    Accelerating functional gene discovery in osteoarthritis.

    Get PDF
    Osteoarthritis causes debilitating pain and disability, resulting in a considerable socioeconomic burden, yet no drugs are available that prevent disease onset or progression. Here, we develop, validate and use rapid-throughput imaging techniques to identify abnormal joint phenotypes in randomly selected mutant mice generated by the International Knockout Mouse Consortium. We identify 14 genes with functional involvement in osteoarthritis pathogenesis, including the homeobox gene Pitx1, and functionally characterize 6 candidate human osteoarthritis genes in mouse models. We demonstrate sensitivity of the methods by identifying age-related degenerative joint damage in wild-type mice. Finally, we phenotype previously generated mutant mice with an osteoarthritis-associated polymorphism in the Dio2 gene by CRISPR/Cas9 genome editing and demonstrate a protective role in disease onset with public health implications. We hope this expanding resource of mutant mice will accelerate functional gene discovery in osteoarthritis and offer drug discovery opportunities for this common, incapacitating chronic disease

    ā€˜Browningā€™ the cardiac and peri-vascular adipose tissues to modulate cardiovascular risk

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    Excess visceral adiposity, in particular that located adjacent to the heart and coronary arteries is associated with increased cardiovascular risk. In the pathophysiological state, dysfunctional adipose tissue secretes an array of factors modulating vascular function and driving atherogenesis. Conversely, brown and beige adipose tissues utilise glucose and lipids to generate heat and are associated with improved cardiometabolic health. The cardiac and thoracic perivascular adipose tissues are now understood to be composed of brown adipose tissue in the healthy state and undergo a brown-to-white transition i.e. during obesity which may be a driving factor of cardiovascular disease. In this review we discuss the risks of excess cardiac and vascular adiposity and potential mechanisms by which restoring the brown phenotype i.e. ā€œre-browningā€ could potentially be achieved in clinically relevant populations
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