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macular degeneration/tyrosine
L'enllaç es desa al porta-retalls
Pàgina 1 des de 137 resultats
Nitration of tyrosines in complement factor H domains alters its immunological activity and mediates a pathogenic role in age related macular degeneration.
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Nitrosative stress has been implicated in the pathogenesis of age related macular degeneration (AMD). Tyrosine nitration is a unique type of post translational modification that occurs in the setting of inflammation and nitrosative stress. To date, the significance and functional implications of
Oral Tyrosine Kinase Inhibitor for Neovascular Age-Related Macular Degeneration: A Phase 1 Dose-Escalation Study.
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An oral treatment for neovascular age-related macular degeneration would be less burdensome than repeated intravitreous injections. X-82 is an oral tyrosine kinase inhibitor active against vascular endothelial growth factor (VEGF) and platelet-derived growth factor.
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Oral Tyrosine Kinase Inhibitors for Neovascular Age-Related Macular Degeneration.
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Tyrosine Kinase Inhibitors in Age-Related Macular Degeneration.
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Complement factor H, vitronectin, and opticin are tyrosine-sulfated proteins of the retinal pigment epithelium.
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Lack of tyrosine sulfation of ocular proteins results in disorganized photoreceptor structure and drastically reduced visual function, demonstrating the importance of this post-translational modification to vision. To understand the role that tyrosine sulfation plays in the function of ocular
Brivanib, a multitargeted small-molecule tyrosine kinase inhibitor, suppresses laser-induced CNV in a mouse model of neovascular AMD.
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In age-related macular degeneration (AMD), choroidal neovascularization (CNV), a major pathologic feature of neovascular AMD (nAMD), affects 10% of patients, potentially causing serious complications, including vision loss. Vascular endothelial growth factor receptor 2 (VEGFR2) and fibroblast growth
Association of complement factor H Y402H gene polymorphism with different subtypes of exudative age-related macular degeneration.
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Exudative age-related macular degeneration (AMD) is a common cause for a severe central visual loss. The complement system has been implicated in the pathogenesis of drusen. Recently, a complement factor H (CFH) polymorphism, which is characterized by a tyrosine (Y)-to-histidine (H)
Nano chitosan peptide as a potential therapeutic carrier for retinal delivery to treat age-related macular degeneration.
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We describe the synthesis and use of an efficient nano carrier molecule for retinal delivery of a nano chitosan peptide that has potential application for treating age-related macular degeneration (AMD). We chose serine-threonine-tyrosine as the peptide sequence because it is well known to
SU5416 induces premature senescence in endothelial progenitor cells from patients with age-related macular degeneration.
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We recently demonstrated increased frequency and growth potential of late outgrowth endothelial progenitor cells (OECs) in patients with neovascular age-related macular degeneration (nvAMD). This study investigated the effects of short- and long-term in vitro inhibition of vascular
VEGF-targeted therapy and beyond: pharmacotherapy and emerging treatments in agerelated macular degeneration.
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Treatment of age-related macular degeneration (AMD) has changed dramatically over the last decade. It has evolved from primarily destructive therapies (laser-based treatment strategies) to nondestructive therapies (intravitreal pharmacotherapies that target angiogenesis). Intermittent intravitreal
Molecular Mechanisms of Macular Degeneration Associated with the Complement Factor H Y402H Mutation.
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A single nucleotide polymorphism, tyrosine at position 402 to histidine (Y402H), within the gene encoding complement factor H (FH) predisposes individuals to acquiring age-related macular degeneration (AMD) after aging. This polymorphism occurs in short consensus repeat (SCR) 7 of FH and results in
Age-related macular degeneration: experimental and emerging treatments.
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This essay reviews the experimental treatments and new imaging modalities that are currently being explored by investigators to help treat patients with age-related macular degeneration (AMD).
METHODS
Interpretative essay.
METHODS
Literature review and interpretation.
RESULTS
Experimental
Anti-VEGF compounds in the treatment of neovascular age related macular degeneration.
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Age-related macular degeneration (AMD) is the leading cause of blindness among elderly patients in developed countries. Although the pathogenesis of AMD is still largely unknown, it is now well known that vascular endothelial growth factor (VEGF) plays a pivotal role in the growth of the abnormal
Current and emerging therapies for the treatment of age-related macular degeneration.
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Age-related macular degeneration (AMD) is the leading cause of vision loss in the industrialized world. In the last few decades, the mainstay of treatment for choroidal neovascularization (CNV) due to AMD has been thermal laser photocoagulation. In the last decade, photodynamic therapy with
Activated STAT 3 in choroidal neovascular membranes of patients with age-related macular degeneration.
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The Jak/STAT (Janus tyrosine kinase/signal transducers and activators of transcription) pathway is critical for growth control, developmental regulation and homeostasis. Here we studied the expression of STAT proteins in the proliferative disease of age-related macular degeneration (AMD)
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