Provided are an anticoagulation and anticalcification biological material and a preparation method therefor. The preparation method includes the following steps: introducing, on a biological tissue, a polymerizable reactive group, and undergoing free radical copolymerization with a zwitterion. In the present disclosure, by introducing a reactive group capable of free radical polymerization to a biological tissue and undergoing free radical copolymerization with a zwitterionic monomer, collagen in the biological tissue is crosslinked at multiple sites by means of a polymer, thereby achieving sufficient crosslinking within and between collagen fibers, improving the stability of the biological tissue, and prolonging the service life of the biological tissue. Moreover, a zwitterion is introduced to the surface of the biological tissue, to improve the anticoagulation performance, promote the in-situ endothelialization of a biological valve, and prevent the calcium element deposition.

Provided is a compression resistant implant configured to fit at or near a bone defect to promote bone growth. The compression resistant implant comprises a biodegradable polymer in an amount of about 0.1 wt % to about 20 wt % of the implant and a freeze-dried oxysterol in an amount of about 5 wt % to about 90 wt % of the implant. Methods of making and use are further provided.

The invention relates to methods for disrupting cholesterol crystals and related methods for the prevention and/or treatment of disease.

The invention concerns an implantable medical device which is coated with a substance. The invention provides for rapid release of the substance.

Cell cultures for treating peripheral arterial disease, methods for producing the cell cultures and methods for treating peripheral arterial disease using the cell cultures are provided. The cell cultures may be 100 to 500 μm in size and may possess an extracellular matrix on an outer surface of the cell culture, and the like are provided.

A therapeutic agent which inhibits cytokines and/or inflammatory mediators for use in the treatment of a patient affected by inflammation associated with atherosclerosis and/or a thrombotic state, wherein the treatment includes the local administration of the therapeutic agent in a blood vessel by an intravascular medical device directly at the level of an atherosclerotic plaque, and/or a site of inflammation, and/or a site of a thrombotic phenomenon.

The invention relates to methods for disrupting cholesterol crystals and related methods for the prevention and/or treatment of disease.

A composite anti-restenosis drug for use with a coronary drug-eluting stent, and a controlled release system for the drug. The composite drug comprises arsenic trioxide and rapamycin, which may be used in combination to prevent in-stent restenosis and reduce the incidence of intravascular thrombosis. The controlled release system for the composite drug may control the release of the composite drug so as to achieve the therapeutic effect of controlling restenosis and preventing the formation of thromboses.

Methods and compositions comprising a biomaterial that are useful for treating a subject with a condition are described. More specifically, methods of treating a subject with a cardiovascular condition comprising delivering a biomaterial comprising extracellular matrix, and delivering a therapeutic cardiac device or therapeutic agents to the subject are described. In addition, methods of delivering extracellular matrix to a subject are also described.

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.