Abstract: The present invention relates to peptides for inhibiting angiogenesis. The present invention also relates to methods of inhibiting angiogenesis and methods of treating disorders associated with VEGF-induced vascular permeability using the peptides of the invention.

Abstract: The present invention relates to peptides for inhibiting angiogenesis. The present invention also relates to methods of inhibiting angiogenesis and methods of treating disorders associated with VEGF-induced vascular permeability using the peptides of the invention.

Abstract: The present invention relates to peptides for inhibiting angiogenesis. The present invention also relates to methods of inhibiting angiogenesis and methods of treating disorders associated with VEGF-induced vascular permeability using the peptides of the invention.

Abstract: The present invention relates to peptides for inhibiting angiogenesis. The present invention also relates to methods of inhibiting angiogenesis and methods of treating disorders associated with VEGF-induced vascular permeability using the peptides of the invention.

Abstract: Provided herein are peptide inhibitors of the interaction between End Binding Protein 3 (EB3) and Inositol 1,4,5-Trisphosphate Receptor Type 3 (IP3R3). Also provided are methods and materials for treating lung injury, including acute lung injury, which may include hyperpermeability of lung vessels, vascular leakage, the development of edema, asthma, anaphylaxis, angioedema, systemic vascular permeability syndromes, and nasal congestion.

Abstract: Provided herein are peptide inhibitors of the interaction between End Binding Protein 3 (EB3) and Inositol 1,4,5-Trisphosphate Receptor Type 3 (IP3R3). Also provided are methods and materials for treating lung injury, including acute lung injury, which may include hyperpermeability of lung vessels, vascular leakage, the development of edema, asthma, anaphylaxis, angioedema, systemic vascular permeability syndromes, and nasal congestion.

Abstract: Provided herein are peptide inhibitors of the interaction between End Binding Protein 3 (EB3) and Inositol 1,4,5-Trisphosphate Receptor Type 3 (IP3R3). Also provided are methods and materials for treating lung injury, including acute lung injury, which may include hyperpermeability of lung vessels, vascular leakage, the development of edema, asthma, anaphylaxis, angioedema, systemic vascular permeability syndromes, and nasal congestion.

Abstract: Provided herein are peptide inhibitors of the interaction between End Binding Protein 3 (EB3) and Inositol 1,4,5-Trisphosphate Receptor Type 3 (IP3R3). Also provided are methods and materials for treating lung injury, including acute lung injury, which may include hyperpermeability of lung vessels, vascular leakage, the development of edema, asthma, anaphylaxis, angioedema, systemic vascular permeability syndromes, and nasal congestion.

Abstract: Methods of treating endotoxin-mediated disorders are provided.

Abstract: The present invention is a method for preparing a substantially pure population of endothelial progenitor cells wherein said cells express Flk-1, CD34, ?5?1 integrin fibronectin, and vWF and exhibit an adherent phenotype and methods for using the same to decrease the severity of lung injury, prevent pulmonary edema, restore endothelial barrier function, induce productive wound healing and angiogenesis, and increase survival rate in acute lung injury (ALI).

Abstract: The present application is directed to siRNA-based silencing of the type II receptor of TGF?. siRNAs that target this receptor abrogate the receptor protein and transcript, TGF?-mediated processes such as fibronectin assembly and cell migration also are inhibited and the molecules of the invention are efficacious in reducing the inflammatory response and matrix deposition. These findings show that siRNAs can be successfully delivered both in vitro and in vivo to regulate the TGF? type II receptor level and modulate wound response. Methods and compositions exploiting the findings of the present invention have a wide-ranging application, extending from treatment of disorders of the eye to other organs and tissues throughout the body.

Abstract: Provided herein are methods and materials for treating pulmonary hypertension (PH) in a subject. Also provided herein is a method of diagnosing whether a has PH by detecting a PH marker. A PKG pulmonary hypertension marker has been identified and may be useful in predicting PH disease progression and assessing a subject's response to PH therapy.

Abstract: Methods of treating endotoxin-mediated disorders are provided.

Abstract: The present application is directed to siRNA-based silencing of the type II receptor of TGF?. siRNAs that target this receptor abrogate the receptor protein and transcript, TGF?-mediated processes such as fibronectin assembly and cell migration also are inhibited and the molecules of the invention are efficacious in reducing the inflammatory response and matrix deposition. These findings show that siRNAs can be successfully delivered both in vitro and in vivo to regulate the TGF? type II receptor level and modulate wound response. Methods and compositions exploiting the findings of the present invention have a wide-ranging application, extending from treatment of disorders of the eye to other organs and tissues throughout the body.

Abstract: The present invention is directed to compositions based on myeloperoxidase amino acid sequence which may be used as therapeutic agents or as delivery vehicles for the delivery of other therapeutic agents.

Abstract: The present invention is a method for preparing a substantially pure population of endothelial progenitor cells wherein said cells express Flk-1, CD34, ?5?1 integrin fibronectin, and vWF and exhibit an adherent phenotype and methods for using the same to decrease the severity of lung injury, prevent pulmonary edema, restore endothelial barrier function, induce productive wound healing and angiogenesis, and increase survival rate in acute lung injury (ALI).