retinal vein occlusion/tyrosine

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Activation of protein tyrosine phosphorylation after retinal branch vein occlusion in cats.

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OBJECTIVE The authors examine the effect of retinal branch vein occlusion (BVO), a common retinal vascular disorder, on protein tyrosine phosphorylation, production of angiogenic growth factors, and activation of signal proteins in the tyrosine kinase pathways in the retina. METHODS Retinal branch

Alterations in protein tyrosine kinase pathways following retinal vein occlusion in the rat.

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OBJECTIVE To determine whether an experimental retinal vein occlusion in the rat activates protein tyrosine kinase pathways and increases angiogenic growth factors in the retina. METHODS Retinal vein occlusion (RVO) was induced in the rat retina with argon laser photocoagulation. Retinas were

An Unusual Case of Central Retinal Vein Occlusion and Review of the Toxicity Profile of Regorafenib in GIST Patients.

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Gastrointestinal stromal tumor (GIST) is the most common sarcoma of the gastrointestinal tract with around 5000 new cases per year. Outcomes for patients with GIST dramatically improved after the development of tyrosine kinase inhibitors targeted against the aberrant signaling pathways that drive

In retinal vein occlusion platelet response to thrombin is increased.

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BACKGROUND Retinal vein occlusion is a major cause of ocular morbidity. The precise mechanism leading to thrombosis in retinal vein occlusion has not yet been clearly elucidated. Several risk factors have been identified, including hypertension diabetes, history of cardiovascular disease,

Inhibition of inflammatory cells delays retinal degeneration in experimental retinal vein occlusion in mice.

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The role of microglia in retinal inflammation is still ambiguous. Branch retinal vein occlusion initiates an inflammatory response whereby resident microglia cells are activated. They trigger infiltration of neutrophils that exacerbate blood-retina barrier damage, regulate postischemic inflammation

Topical administration of a multi-targeted kinase inhibitor suppresses choroidal neovascularization and retinal edema.

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Age-related macular degeneration, diabetic retinopathy, and retinal vein occlusions are complicated by neovascularization and macular edema. Multi-targeted kinase inhibitors that inhibit select growth factor receptor tyrosine kinases and/or components of their down-stream signaling cascades (such as

Aflibercept (VEGF-TRAP): the next anti-VEGF drug.

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The inflammatory cytokine, vascular endothelial growth factor (VEGF), plays a central role in human growth and development, and vascular maintenance. VEGF mediated angiogenesis is essential for tumor growth, as well as exudative age-related macular degeneration, proliferative diabetic retinopathy

Metastatic renal cell carcinoma: the first report of unilateral fundus hemorrhage induced by sorafenib.

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BACKGROUND Renal cell carcinoma (RCC) is the most common type of kidney tumor with increasing incidence. Tyrosine Kinase Inhibitors (TKIs) are considered important treatment in the management of metastatic RCC. Some previous studies demonstrated that sorafenib treatment is associated with a

Molecular pathogenesis of retinal and choroidal vascular diseases.

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There are two major types of ocular neovascularization that affect the retina, retinal neovascularization (NV) and subretinal or choroidal NV. Retinal NV occurs in a group of diseases referred to as ischemic retinopathies in which damage to retinal vessels results in retinal ischemia. Most prevalent

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