Abstract: The modified polypeptides include at least one amino acid substitution that allows the polypeptide to bind better to the S surface glycoprotein of coronaviruses that use ACE2 as a cell entry receptor, either through direct increases in affinity or through improved folding and expression of ACE2. Use of the modified ACE2 polypeptides for inhibiting CoV entry, replication and/or spread, for pre-exposure and post-exposure CoV prophylaxis, and for treating a CoV infection (e.g. COVTD-19), is also described.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: A construct composed of a Kinesin-derived Angiogenesis Inhibitor peptide and one or more carrier moieties and/or stabilizing moieties is provided as are methods for inhibiting angiogenesis and treating a disease or condition characterized by excessive vascularity.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: A construct composed of a Kinesin-derived Angiogenesis Inhibitor peptide and one or more carrier moieties and/or stabilizing moieties is provided as are methods for inhibiting angiogenesis and treating a disease or condition characterized by excessive vascularity.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: This invention provides endothelial cells expressing transcription factor Er71/Etv2, and cell surface endothelial markers Flk1 and VE-cadherin prepared from induced pluripotent stem cells or embryonic stem cells, as well as methods of preparing the cells and methods of using the cells to vascularize and re-endothelialize or repair ischemic tissue in a subject.

Abstract: Disclosed are nanoparticle compositions comprising nanoparticles prepared from denatured, cross-linked albumin and a therapeutic agent for treating a neutrophil-mediated inflammation, and methods of treating neutrophil-mediated inflammation using the compositions.

Abstract: In various aspects and embodiments the invention provides methods and reagents for controlling gene expression, and for treating disorders and diseases. Embodiments provide methods and reagents specifically for the regulation of MLCK expression and for the use thereof in treating disorders and diseases. Various embodiments provide methods and reagents for specifically down regulating the expression of MLCK-L more efficiently than that of MLCK-S, and for the use thereof in treating disorders and diseases. Embodiments provide siNA for the same, particularly siRNAs. Various of the embodiments are useful for the treatment of inflammatory disorders and diseases, including, for one example in the regard, Asthma.

Abstract: In various aspects and embodiments the invention provides methods and reagents for controlling gene expression, and for treating disorders and diseases. Embodiments provide methods and reagents specifically for the regulation of MLCK expression and for the use thereof in treating disorders and diseases. Various embodiments provide methods and reagents for specifically down regulating the expression of MLCK-L more efficiently than that of MLCK-S, and for the use thereof in treating disorders and diseases. Embodiments provide siNA for the same, particularly siRNAs. Various of the embodiments are useful for the treatment of inflammatory disorders and diseases, including, for one example in this regard, Asthma.

Abstract: In various aspects and embodiments the invention provides methods and reagents for controlling gene expression, and for treating disorders and diseases. Embodiments provide methods and reagents specifically for the regulation of MLCK expression and for the use thereof in treating disorders and diseases. Various embodiments provide methods and reagents for specifically down regulating the expression of MLCK-L more efficiently than that of MLCK-S, and for the use thereof in treating disorders and diseases. Embodiments provide siNA for the same, particularly siRNAs. Various of the embodiments are useful for the treatment of inflammatory disorders and diseases, including, for one example in this regard, Asthma.

Abstract: The invention relates in embodiments to methods for identifying compounds that inhibit phosphorylation of GD-1, to compositions comprising such inhibitors, including pharmaceutical compositions, and to the use of such inhibitors and compositions to treat diseases, such as inflammatory diseases.

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 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.