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  • Book
    edited by Hua Yan.
    Summary: This book covers sports-related eye injuries, presenting standard processes to enable clinical practitioners to make appropriate decisions on the management of these patients. Sports-related activities are responsible for a large percentage of ocular injuries, particularly among young people, and can even lead to blindness. Given the increasing trend in these injuries and the potential functional loss they entail, it is important to understand how to prevent and to accurately diagnose and treat them. This book discusses the definition, etiology, clinical presentations and signs, treatment, and prevention of sports-related eye injuries, and includes typical clinical cases, together with a wealth of images and illustrative figures. Offering a systematic and symptom-based guide to clinical practice, it will help clinical practitioners to fully prepare for the various challenges posed by sports-related eye injuries.

    Contents:
    1. Introduction
    2. Epidemics of Sports-related Eye Injuries
    3. Risk Classification of Sports Events
    4. Classification and Mechanism of Sports related eye injury
    5. Sports-related injuries of the anterior segment
    6. Posterior Segment of Sports-related Eye Injuries
    7. Ocular Adnexal of Sports-Related Eye Injuries
    8. Burns and Radiation Exposure
    9. Prevention of Sports-related Eye Injuries
    10. The application of protective devices in sports-related eye injuries
    11. Guideliness of Return To Play
    12. Sideline evaluation of the injured player
    13. Screening of Sports-related Eye Injuries
    14. Controversial Issue.
    Digital Access Springer 2020
  • Article
    Dusting GJ, Moncada S, Vane JR.
    Eur J Pharmacol. 1978 May 01;49(1):65-72.
    The effects of arachidonate and its major metabolites were examined in vascular beds perfused via the femoral and mesenteric arteries of chloralose-anaesthetised dogs. Close intra-arterial injection of prostacyclin (PGI2, 0.02--2 microgram), PGE2 (0.05--1 microgram) and their precursors, the endoperoxide PGH2 (0.5--2 microgram) and sodium arachidonate (100--550 microgram), all induced vasodilatation. Sodium linoleate (500 microgram) was inactive. Prostacyclin was equally active in both vascular beds, but PGE2 was more potent in the femoral and less so in the mesenteric bed. PGH2 was of similar potency to prostacyclin in both beds, but 6-oxo-PGF 1 alpha (10--100 microgram) was inactive. Thromboxane A2 (TXA2, 1--2 microgram) was a potent vasoconstrictor of the mesenteric bed, but not the femoral bed, although the endoperoxide analogue U46619 was vasocontrictor in both vasculatures. Fatty acid hydroperoxides did not specifically modify the vasodilator effects of PGH2 or arachidonate, presumably because these inhibitors are rapidly reduced in vivo. Indomethacin and meclofenamate potentiated vasodilatation induced by prostacyclin or endoperoxide, but reduced or abolished that caused by arachidonate. The rise in perfusion pressure induced by TXA2 was potentiated and prolonged by indomethacin. Inhibition of synthesis of endogenous prostacyclin, by exacerbating the vasoconstrictor action of TXA2, may have contributed to this effect.
    Digital Access Access Options