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1  type II collagen by collagenase, as well as synovial hyperplasia.
2 that a defect in apoptosis may contribute to synovial hyperplasia.
3                  The arthritic joints showed synovial hyperplasia and erosions, but there was a pauci
4 osteophyte formation, meniscal ossification, synovial hyperplasia and fibrosis, and cruciate ligament
5       Histological analyses indicated marked synovial hyperplasia and inflammatory cell infiltration
6  articular joints, characterized by invasive synovial hyperplasia and pathological neovascularization
7 , such as increased epiphyseal growth plate, synovial hyperplasia, and increased cellularity in the j
8  severe cellular infiltration in the joints, synovial hyperplasia, and joint erosion, this pathology
9 g minimal to no cartilage and bone erosions, synovial hyperplasia, and pannus formation, and reduced
10 inical inflammation, formation of pannus and synovial hyperplasia, and the erosion of cartilage and b
11  rats with PIA, while DA rats had pronounced synovial hyperplasia, angiogenesis, inflammatory infiltr
12 egradation, glycosaminoglycan depletion, and synovial hyperplasia as compared with the WT mice.
13 lowing immunization that is characterized by synovial hyperplasia, cellular infiltration, and cartila
14 filtration of inflammatory cells, edema, and synovial hyperplasia in the joint were significantly att
15  Specifically, OSM + TNFalpha induced marked synovial hyperplasia, inflammation, and cartilage and bo
16 hronic inflammatory disease characterized by synovial hyperplasia, inflammatory cell infiltration, ir
17 rthritis; decreased macrophage infiltration, synovial hyperplasia, osteoclast formation, joint destru
18 itic joints from OPN-deficient mice revealed synovial hyperplasia, pannus formation, mononuclear cell
19  with DA, including significant reduction in synovial hyperplasia, pannus, angiogenesis, inflammatory
20 mation, immune reactivity, angiogenesis, and synovial hyperplasia persisted in RA-SCID grafts for 12
21 artilage injury, Gdf5-lineage cells underpin synovial hyperplasia through proliferation, are recruite
22 days before the onset of arthritis) revealed synovial hyperplasia without leukocytic infiltration.

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