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Titlebook: Ocular Angiogenesis; Diseases, Mechanisms Joyce Tombrain-Tink,Colin J. Barnstable Book 2006 Humana Press 2006 eye.glaucoma.macular degenera

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书目名称Ocular Angiogenesis
副标题Diseases, Mechanisms
编辑Joyce Tombrain-Tink,Colin J. Barnstable
视频video
概述Includes supplementary material:
丛书名称Ophthalmology Research
图书封面Titlebook: Ocular Angiogenesis; Diseases, Mechanisms Joyce Tombrain-Tink,Colin J. Barnstable Book 2006 Humana Press 2006 eye.glaucoma.macular degenera
描述Leading academic and pharmaceutical researchers and clinicians from many disciplines synthesize and summarize current clinical and basic knowledge concerning abnormal growth of blood vessels in the eye, the cause of major neovascular eye diseases. The authors also identify and assess the most promising approaches with potential for commercial exploitation and discuss the challenges encountered in developing therapeutics for ocular neovascular diseases. Highlights include illuminating chapters on gene therapy and novel drug delivery systems and excellent summaries of the newest therapeutic approaches.
出版日期Book 2006
关键词eye; glaucoma; macular degeneration; retina
版次1
doihttps://doi.org/10.1007/978-1-59745-047-8
isbn_softcover978-1-4939-5667-8
isbn_ebook978-1-59745-047-8
copyrightHumana Press 2006
The information of publication is updating

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Ophthalmology Researchhttp://image.papertrans.cn/o/image/700553.jpg
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Corneal AngiogenesisCorneal neovascularization (angiogenesis) results from the formation of new vascular structures from the limbal vasculature at the corneal edge. These new blood vessels may invade the normally avascular corneal stroma at different levels within the cornea (. Fig. 1).
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Eales’ Disease retina (inflammatory stage), then sclerosis of retinal veins indicating retinal ischemia (ischemic stage), and finally retinal or optic disk neovascularization, recurrent vitreous hemorrhage with or without retinal detachment (proliferative stage) (.–.).
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Ocular Inflammation and NeovascularizationNeovascularization is an integral part of normal developmental processes and numerous pathologies, ranging from tumor growth and metastasis to inflammation and ocular disease. This process is driven by a cocktail of proangiogenic growth factors and cytokines and is tempered by an equally diverse group of inhibitors of neovascularization.
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Neovascular Glaucomay contracts to produce peripheral anterior synechiae (PAS) and progressive angle closure. The resulting increased intraocular pressure (IOP) is often difficult to control and(.) frequently causes irreversible visual loss (1).
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