Myosin heavy chain 11 (MYH11)-siRNA-eluting, calponin 1 (CNN1)-siRNA-eluting, leiomodin 1 (LMOD)-siRNA-eluting, smoothelin (SMTN)-siRNA-eluting, tropomyosin (TPM)-siRNA-eluting, caldesmon 1 (CALD)-siRNA-eluting, actinin (ACTN)-siRNA-eluting, actin alpha (ACTA)-siRNA-eluting, and actin beta (ACTB)-siRNA-eluting medical device capable of selective and significant inhibition of vascular smooth muscle cells (VSMC) in the same or even higher order of magnitude of sirolimus or analogs and paclitaxel or analogs that are cell antiproliferative drugs currently used in drug-eluting stents (DES), whereas said MYH11-siFRNA-eluting, CNN1-siFRNA-eluting, LMOD-siRNA-eluting, SMTN-siRNA-eluting, TPM-siRNA-eluting, CALD-siRNA-eluting, ACTN-siRNA-eluting, ACTA-siRNA-eluting, and ACTB-siRNA-eluting medical devices promote early medical device struts coverage and/or vascular re-endothelialization compared to the current DES that elute cell antiproliferative drugs such as sirolimus or analogs and, paclitaxel or analogs.

Methods and devices for the repair of articular tissue using collagen material are provided. Compositions of collagen material and related kits are also provided.

The present disclosure describes compositions and methods to promote wound healing. The compositions and methods include an interleukin-1 beta (IL-1) receptor antagonist (IL-1Ra), such as anakinra. The IL-1Ra can be administered topically to a chronic wound including a diabetic ulcer.

Methods and devices for the repair of articular tissue using collagen material are provided. Compositions of collagen material and related kits are also provided.

The present invention provides a method of promoting local bone growth by administering a therapeutic amount of a Sost antagonist to a mammalian patient in need thereof. Preferably, the Sost antagonist is an antibody or FAB fragment selectively recognizing any one of SEQ ID NOS: 1-23. The Sost antagonist may be coadministered together or sequentially with a matrix conducive to anchoring new bone growth. Orthopedic and Periodontal devices comprising an implantable portion adapted to be permanently implanted within a mammalian body and bearing an external coating of a Sost antagonist are also disclosed, as it a method of increasing bone density by administering to a mammalian patient a therapeutic amount of a Sost antagonist together with an antiresorptive drug.

Provided are methods for improving cell-based therapies by co-administration with an agent that increases the production and or levels of epoxygenated fatty acids, as well as kits, stents and patches for co-administering stem cells with an agent that increases the production and/or levels of epoxygenated fatty acids.

A method of modulating transdifferentiation of chondrocytes to osteoblast includes administering to the chondrocytes an agent that modulates GP130 receptor signaling and expression of at least one of Sox2, Oct4, or Nanog of the chondrocytes.

The present disclosure describes compositions and methods to promote wound healing. The compositions and methods include an interleukin-1 beta (IL-1B) receptor antagonist (IL-1Ra), such as anakinra.

Implantable scaffolds that treat solid tumors and escape variants and that provide effective vaccinations against cancer recurrence are described. The scaffolds include genetically-reprogrammed lymphocytes and a lymphocyte activating moiety.

Methods for inhibiting stenosis, obstruction and/or calcification of a heart valve following implantation in a vessel having a wall are disclosed. In one aspect the method includes providing a bioprosthetic heart valve mounted on an elastical stent; treating the bioprosthetic heart valve with a tissue fixative; coating the stent and the bioprosthetic valve with a coating composition including one or more therapeutic agents; implanting the bioprosthetic valve into the vessel in a diseased natural valve site; eluting the coating composition from the bioprosthetic valve; and inhibiting stenosis, obstruction and/or calcification of the bioprosthetic heart valve by preventing the attachment of stem cells to the bioprosthetic heart valve, the stem cells circulating external and proximate to the bioprosthetic heart valve by activating nitric oxide production (i) in the circulating stem cells, (ii) in an endothelial cell lining covering the bioprosthetic heart valve tissue, (iii) or both.