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The 24-month outcomes of intravitreal aflibercept combined with photodynamic therapy for polypoidal choroidal vasculopathy.

This study was prospectively carried out to clarify the effectiveness of visual and anatomical outcomes under combination therapy of intravitreal aflibercept (IVA) and verteporfin photodynamic therapy (vPDT) in over 24 months.

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Oleanolic Acids Inhibit Vascular Endothelial Growth Factor Receptor 2 Signaling in Endothelial Cells: Implication for Anti-Angiogenic Therapy.

Angiogenesis must be precisely controlled because uncontrolled angiogenesis is involved in aggravation of disease symptoms. Vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR-2) signaling is a key pathway leading to angiogenic responses in vascular endothelial cells (ECs). Therefore, targeting VEGF/VEGFR-2 signaling may be effective at modulating angiogenesis to alleviate various disease symptoms. Oleanolic acid was verified as a VEGFR-2 binding chemical from anticancer herbs with similar binding affinity as a reference drug in the Protein Data Bank (PDB) entry 3CJG of model A coordination. Oleanolic acid effectively inhibited VEGF-induced VEGFR-2 activation and angiogenesis in HU-VECs without cytotoxicity. We also verified that oleanolic acid inhibits angiogenesis during the development and the course of the retinopathy of prematurity (ROP) model in the mouse retina. Taken together, our results suggest a potential therapeutic benefit of oleanolic acid for inhibiting angiogenesis in proangiogenic diseases, including retinopathy.

2968 related Products with: Oleanolic Acids Inhibit Vascular Endothelial Growth Factor Receptor 2 Signaling in Endothelial Cells: Implication for Anti-Angiogenic Therapy.

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Effect of Epiretinal Membranes on Antivascular Endothelial Growth Factor Treatment for Neovascular Age-Related Macular Degeneration.

To evaluate the effect of epiretinal membranes (ERMs), detected with spectral-domain optical coherence tomography (SD-OCT), on the outcome of antivascular endothelial growth factor (VEGF) treatment for neovascular age-related macular degeneration (nAMD).

1904 related Products with: Effect of Epiretinal Membranes on Antivascular Endothelial Growth Factor Treatment for Neovascular Age-Related Macular Degeneration.

Growth Differentiation Fa Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Growth Factor (Human) Ant Mouse Vascular Endothelia Rat monoclonal anti mouse Recombinant Human Vascula Factor VIII Related Anti

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One-year outcomes of a treat-and-extend regimen of intravitreal aflibercept for polypoidal choroidal vasculopathy.

To evaluate the 1-year treatment outcomes of intravitreal aflibercept injections (IVA) using a treat-and-extend regimen for polypoidal choroidal vasculopathy (PCV).

2662 related Products with: One-year outcomes of a treat-and-extend regimen of intravitreal aflibercept for polypoidal choroidal vasculopathy.

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Optical Coherence Tomography Angiography of DME and Its Association with Anti-VEGF Treatment Response.

To investigate the structural integrity of the superficial capillary plexuses (SCPs) and deep capillary plexuses (DCPs) using optical coherence tomography (OCT) angiography (OCTA) in patients with diabetic macular edema (DME) and its association with the response to anti-vascular endothelial growth factor (VEGF) treatment.

2658 related Products with: Optical Coherence Tomography Angiography of DME and Its Association with Anti-VEGF Treatment Response.

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The Efficacy of Intravitreal Aflibercept in Submacular Hemorrhage Secondary to Wet Age-related Macular Degeneration.

To evaluate the efficacy of intravitreal aflibercept monotherapy in submacular hemorrhage (SMH) secondary to wet age-related macular degeneration (AMD).

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Prokaryotic Soluble Overexpression and Purification of Human VEGF165 by Fusion to a Maltose Binding Protein Tag.

Human vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis and plays a central role in the process of tumor growth and metastatic dissemination. Escherichia coli is one of the most common expression systems used for the production of recombinant proteins; however, expression of human VEGF in E. coli has proven difficult because the E. coli-expressed VEGF tends to be misfolded and forms inclusion bodies, resulting in poor solubility. In this study, we successfully produced semi-preparative amounts of soluble bioactive human VEGF165 (hVEGF). We created seven N-terminal fusion tag constructs with hexahistidine (His6), thioredoxin (Trx), glutathione S-transferase (GST), maltose-binding protein (MBP), N-utilization substance protein A (NusA), human protein disulfide isomerase (PDI), and the b'a' domain of PDI (PDIb'a'), and tested each construct for soluble overexpression in E. coli. We found that at 18°C, 92.8% of the MBP-tagged hVEGF to be soluble and that this tag significantly increased the protein's solubility. We successfully purified 0.8 mg of pure hVEGF per 500 mL cell culture. The purified hVEGF is stable after tag cleavage, contains very low levels of endotoxin, and is 97.6% pure. Using an Flk1+ mesodermal precursor cell (MPC) differentiation assay, we show that the purified hVEGF is not only bioactive but has similar bioactivity to hVEGF produced in mammalian cells. Previous reports on producing hVEGF in E. coli have all been based on refolding of the protein from inclusion bodies. To our knowledge, this is the first report on successfully expressing and purifying soluble hVEGF in E. coli.

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Dual blockade of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF-2) exhibits potent anti-angiogenic effects.

Both vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF or FGF-2) are potent pro-angiogenic factors and play a critical role in cancer development and progression. Clinical anti-VEGF therapy trials had a major challenge due to upregulated expression of other pro-angiogenic factor, like FGF-2. This study developed a novel chimeric decoy receptor VF-Trap fusion protein to simultaneously block activity of both VEGF and FGF pathways in order to achieve an additive or synergistic anti-tumor effect. Our in vitro data showed that VF-Trap potently blocked proliferation and migration of both VEGF- and FGF-2-induced vascular endothelial cells. In animal models, treatment of xenograft tumors with VF-Trap resulted in significant inhibition of tumor growth compared to blockage of the single molecule, like VEGF or FGF blocker. In addition, VF-Trap was also more potent in inhibition of ocular angiogenesis in a mouse oxygen-induced retinopathy (OIR) model. These data demonstrated the potent anti-angiogenic effects of this novel VF-Trap fusion protein on blockage of VEGF and FGF-2 activity in vitro and in animal models. Further study will assess its effects in clinic as a therapeutic agent for angiogenesis-related disorders, such as cancer and ocular vascular diseases.

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Response of Pigment Epithelial Detachment to Anti-Vascular Endothelial Growth Factor Treatment in Age-Related Macular Degeneration.

To evaluate the therapeutic response of pigment epithelial detachment (PED) to anti-vascular endothelial growth factor (VEGF) treatment in neovascular age-related macular degeneration (nAMD), and identify predictive factors for PED resolution after treatment.

2620 related Products with: Response of Pigment Epithelial Detachment to Anti-Vascular Endothelial Growth Factor Treatment in Age-Related Macular Degeneration.

Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Mouse Vascular Endothelia Goat Anti-Human Fibroblas Mouse Anti-Insulin-Like G Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse

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Efficacy of vitrectomy and inner limiting membrane peeling in age-related macular degeneration resistant to anti-vascular endothelial growth factor therapy, with vitreomacular traction or epiretinal membrane.

We assessed the efficacy of vitrectomy and inner limiting membrane (ILM) peeling, followed by anti-vascular endothelial growth factor (VEGF) therapy, anti-VEGF-resistant age-related macular degeneration (AMD) due to vitreomacular traction (VMT) or epiretinal membrane (ERM).

1850 related Products with: Efficacy of vitrectomy and inner limiting membrane peeling in age-related macular degeneration resistant to anti-vascular endothelial growth factor therapy, with vitreomacular traction or epiretinal membrane.

Growth Factor (Human) Ant Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Nuclear Membrane Receptor Mouse Vascular Endothelia Goat Anti-Human Fibroblas FDA Standard Frozen Tissu FDA Standard Frozen Tissu

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