63 results about "Bone lesion" patented technology

To identify molecular determinants of lytic bone disease in multiple myeloma, the expression profiles of ˜12,000 genes in CD138-enriched plasma cells from newly diagnosed multiple myeloma patients exhibiting no radiological evidence of lytic lesions (n=28) were compared to those with ≧3 lytic lesions (n=47). Two secreted WNT signaling antagonists, soluble frizzled related protein 3 (SFRP-3 / FRZB) and the human homologue of Dickkopf-1 (DKK1), were expressed in 40 of 47 with lytic bone lesions, but only 16 of 28 lacking bone lesions (P<0.05). DKK1 and FRZB were not expressed in plasma cells from 45 normal bone marrow donors or 10 Waldenstrom's macroglobulinemia, a related plasma cells malignancy that lacks bone disease. These data indicate that these factors are important mediators of multiple myeloma bone disease, and inhibitors of these proteins may be used to block bone disease.

Compounds of the present invention of formula I and formula II are disclosed in the specification and wherein the compounds are modulators of Bone Morphogenic Protein activity. Compounds are synthetic peptides having a non-growth factor heparin binding region, a linker, and sequences that bind specifically to a receptor for Bone Morphogenic Protein. Uses of compounds of the present invention in the treatment of bone lesions, degenerative joint disease and to enhance bone formation are disclosed.

The present invention relates to protein complexes or scaffold comprising cartilage oligomeric matrix protein (COMP) polypeptides bound to one or more growth factors, and methods of their use in promoting chondrogenesis and / or osteogenesis, and repair of cartilage and bone lesions.

The present invention pertains to an implant for treatment of a bone lesion site, the implant including a polymer porous film and a layer containing a biocompatible material, wherein the polymer porous film is a polymer porous membrane of a three-layer structure having a porous surface layer A, a porous surface layer B, and a macrovoid layer interposed between the surface layer A and the surface layer B; the average pore diameter of the pores in surface layer A is smaller than the average pore diameter of the pores in surface layer B; the macrovoid layer has a partition joined to the surface layers A and B and a plurality of macrovoids enclosed by the partition and the surface layers A and B; and the pores in the surface layers A and B communicate with the macrovoids.

Methods and systems for evaluating bone lesions include accessing a first dataset acquired from a patient with a first imaging modality and a second dataset acquired from the patient with a second imaging modality. A segmentation is performed on the first dataset to identify a subset of the first dataset corresponding to a skeletal structure of the patient and a patient skeletal metric representing a total bone volume of the patient is automatically calculated from the subset of the first dataset. The methods and systems further include detection of at least one lesion in the second dataset, classification of the at least one lesion as a bone or non-bone lesion, automatic calculation of a bone lesion metric based on the classification, and calculation of a lesion burden as a ratio of the bone lesion metric and the patient skeletal metric.

To identify molecular determinants of lytic bone disease in multiple myeloma, the expression profiles of ˜12,000 genes in CD138-enriched plasma cells from newly diagnosed multiple myeloma patients exhibiting no radiological evidence of lytic lesions (n=28) were compared to those with ≧3 lytic lesions (n=47). Two secreted WNT signaling antagonists, soluble frizzled related protein 3 (SFRP-3 / FRZB) and the human homologue of Dickkopf-1 (DKK1), were expressed in 40 of 47 with lytic bone lesions, but only 16 of 28 lacking bone lesions (P<0.05). DKK1 and FRZB were not expressed in plasma cells from 45 normal bone marrow donors or 10 Waldenstrom's macroglobulinemia, a related plasma cells malignancy that lacks bone disease. These data indicate that these factors are important mediators of multiple myeloma bone disease, and inhibitors of these proteins may be used to reduce tumor burden in multiple myeloma and to block bone disease.

The invention discloses a self-fluorescent bone repair magnetic slow-release microsphere and a preparation method thereof. The nano-Fe3O4 is synthesized by a solvothermal method, and the nano-Fe3O4 is uniformly dispersed in a sodium alginate solution, and the composite has the functions of promoting proliferation and promoting osteoblasts. Differentiation of traditional Chinese medicine - icariin; the mixture is passed through a microcapsule forming device and dropped into a gel bath to form primary microspheres; then the primary microspheres are immersed in chitosan solution, and chitosan and alginic acid are used to The charge complementary properties of sodium form a polyelectrolyte semipermeable membrane, and the composite microspheres are cross-linked with genipin to prepare autofluorescent magnetic sustained-release microspheres for bone repair. The present invention fully considers the requirement of cytotoxicity as an implantable bone repair material, selects chitosan and sodium alginate with excellent biocompatibility and degradability as raw materials, and can be adjusted according to the needs of bone lesions. Different voltages are used to prepare microspheres with different particle sizes.