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These observations suggest that the degree of vessel normalization in terms of improved perfusion may be used as a tool to distinguish responders to anti-angiogenic therapy from non-responding patients [312, 313]

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Several mechanisms have been proposed to explain chronic hyperglycemia-induced nerve damage, such as intracellular accumulation of sorbitol, glycation reactions, and oxidative and nitrosative stress (reviewed in 69)

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J., Palacios, G., Daz-Martnez,

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