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Journal Article
Journal Article
Arthritis & Rheumatology, ISSN 2326-5191, 11/2014, Volume 66, Issue 11, pp. 2989 - 3000
Objective. Colony-stimulating factor 1 receptor (CSF-1R) essentially modulates monocyte proliferation, migration, and activation, which are considered... 
RHEUMATOID-ARTHRITIS | COLLAGEN-INDUCED ARTHRITIS | HUMAN SYNOVIAL FIBROBLASTS | TUMOR-NECROSIS-FACTOR | M-CSF | TRANSGENIC EXPRESSION | DENDRITIC CELLS | C-FMS | AUTOIMMUNE ARTHRITIS | INFLAMMATORY ARTHRITIS | RHEUMATOLOGY | Bone and Bones - pathology | Receptor, Macrophage Colony-Stimulating Factor - antagonists & inhibitors | Arthritis, Experimental - drug therapy | Cartilage - pathology | Humans | Middle Aged | Dendritic Cells - pathology | Synovial Membrane - pathology | Antibodies, Monoclonal - therapeutic use | Male | Monocytes - metabolism | Cartilage - drug effects | Synovial Membrane - drug effects | Case-Control Studies | Receptor, Macrophage Colony-Stimulating Factor - metabolism | Arthritis, Experimental - metabolism | Bone and Bones - drug effects | Arthritis, Experimental - pathology | Arthritis, Rheumatoid - metabolism | Bone and Bones - metabolism | Monocytes - pathology | Female | Mice, Inbred DBA | Osteoarthritis - pathology | Antibodies, Monoclonal - immunology | Dendritic Cells - metabolism | Disease Models, Animal | Osteoclasts - pathology | Macrophages - pathology | Antibodies, Monoclonal - pharmacology | Osteoarthritis - metabolism | Cartilage - metabolism | Osteoclasts - metabolism | Synovial Membrane - metabolism | Arthritis, Rheumatoid - pathology | Macrophages - metabolism | Animals | Mice | Receptor, Macrophage Colony-Stimulating Factor - drug effects | Rheumatism | Rodents | Arthritis
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2015, Volume 10, Issue 8, p. e0133917
Journal Article
Nature, ISSN 0028-0836, 06/2015, Volume 522, Issue 7554, pp. 106 - 110
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2016, Volume 11, Issue 5, p. e0154680
The receptor-activator of nuclear kappaB ligand (RANKL) signaling pathway plays an important role in the regulation of bone growth and mediates the formation... 
GIANT-CELL TUMOR | DENOSUMAB | MULTIDISCIPLINARY SCIENCES | Osteosarcoma - drug therapy | RANK Ligand - metabolism | Humans | Male | Antineoplastic Agents - therapeutic use | Fibrous Dysplasia of Bone - drug therapy | RNA, Messenger - metabolism | Bone Neoplasms - pathology | Giant Cell Tumor of Bone - pathology | Chondrosarcoma - genetics | Chondrosarcoma - pathology | Bone Cysts, Aneurysmal - metabolism | Bone Neoplasms - genetics | Fibrous Dysplasia of Bone - genetics | Chondroma - drug therapy | Osteoclasts - pathology | Bone Cysts, Aneurysmal - pathology | Multiple Myeloma - genetics | Osteosarcoma - pathology | Bone Cysts, Aneurysmal - drug therapy | Chondroma - genetics | Gene Expression Regulation, Neoplastic | Chondroma - metabolism | Chondroma - pathology | Bone Neoplasms - metabolism | Denosumab - therapeutic use | Multiple Myeloma - drug therapy | Giant Cell Tumor of Bone - drug therapy | RNA, Messenger - antagonists & inhibitors | Female | Bone Neoplasms - drug therapy | Giant Cell Tumor of Bone - genetics | Osteosarcoma - metabolism | Fibrous Dysplasia of Bone - pathology | RNA, Messenger - genetics | Multiple Myeloma - metabolism | Organ Specificity | Chondrosarcoma - drug therapy | Fibrous Dysplasia of Bone - metabolism | Osteoclasts - metabolism | Bone Resorption - prevention & control | RANK Ligand - genetics | Multiple Myeloma - pathology | Giant Cell Tumor of Bone - metabolism | RANK Ligand - antagonists & inhibitors | Chondrosarcoma - metabolism | Osteosarcoma - genetics | Osteoclasts - drug effects | Bone Cysts, Aneurysmal - genetics | Bone resorption | Bones | Dosage and administration | Denosumab | Growth | Analysis | Immunohistochemistry | Chondrosarcoma | Multiple myeloma | Aneurysm | Bone tumors | Metastasis | Bone surgery | Metastases | Osteoprotegerin | Signal transduction | Bone growth | Biomedical materials | Osteosarcoma | Fibrous dysplasia | Bone dysplasia | Biocompatibility | Lesions | TRANCE protein | University graduates | Dysplasia | Statistical analysis | Bone lesions | Gene expression | Osteoclastogenesis | Signaling | Bone cancer | Hospitals | Biopsy | Stromal cells | Orthopedics | Monoclonal antibodies | Ligands | Osteoclasts | Bone | Prostate cancer | Tumors
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2014, Volume 184, Issue 2, pp. 472 - 482
Journal Article
Journal of Dental Research, ISSN 0022-0345, 7/2014, Volume 93, Issue 7, pp. 663 - 670
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2014, Volume 9, Issue 10, p. e109524
Introduction: Osteoclasts are responsible for the bone loss associated with rheumatoid arthritis (RA). The secreted adipokine angiopoietin-like 4 (ANGPTL4)... 
TARGET | HYPOXIA-INDUCIBLE FACTOR | ACTIVATION | SYNOVIUM | CHONDROCLASTS | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | OSTEOCLAST DIFFERENTIATION FACTOR | EROSION | JOINT | Arthritis, Rheumatoid - blood | Stromal Cells - pathology | Humans | Middle Aged | Synovial Fluid - metabolism | Male | Synovial Fluid - chemistry | Case-Control Studies | Plasma Cells - pathology | Angiopoietin-like 4 Protein | RANK Ligand - blood | Bone Resorption - genetics | Female | Plasma Cells - metabolism | Osteoarthritis - pathology | Arthritis, Rheumatoid - diagnosis | Bone Resorption - diagnosis | Diagnosis, Differential | Osteoclasts - pathology | Bone Resorption - blood | Macrophages - pathology | Signal Transduction | Endothelial Cells - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Stromal Cells - metabolism | Gene Expression Regulation | Osteoarthritis - blood | Biomarkers - blood | Angiopoietins - blood | Osteoarthritis - diagnosis | Osteoclasts - metabolism | Osteoarthritis - genetics | Arthritis, Rheumatoid - pathology | RANK Ligand - genetics | Arthritis, Rheumatoid - genetics | Macrophages - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - blood | Bone Resorption - pathology | Aged | Angiopoietins - genetics | Endothelial Cells - pathology | Bone resorption | Rheumatoid factor | B cells | Comparative analysis | Osteoarthritis | Hypoxia-inducible factor 1 | Angiopoietin | Arthritis | Macrophages | Rheumatoid synovium | Ethics | Angiogenesis | Synovial fluid | Hypoxia-inducible factor 1a | Biomedical materials | Biocompatibility | TRANCE protein | Bone loss | Age | Hypoxia-inducible factors | Cloning | Rheumatology | Gene expression | Patients | Endothelial cells | Overexpression | Rheumatoid synovitis | Rheumatoid arthritis | Stromal cells | Plasma cells | Hypoxia | Osteoclasts | Bone
Journal Article