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1.  Macrophage migration inhibitory factor enhances osteoclastogenesis through upregulation of RANKL expression from fibroblast-like synoviocytes in patients with rheumatoid arthritis 
Macrophage migration inhibitory factor (MIF) is one of key regulators in acute and chronic immune-inflammatory conditions including rheumatoid arthritis (RA). We examined the effect of MIF on osteoclastogenesis, which is known to play a crucial role in bone destruction in RA.
The concentration of MIF and receptor activator of nuclear factor-κB ligand (RANKL) in the synovial fluid was measured by ELISA. MIF-induced RANKL expression of RA synovial fibroblasts was determined by real-time PCR and western blot. Osteoclastogenesis was analyzed in culture of human peripheral blood mononuclear cells (PBMC) with MIF. Osteoclastogenesis was also determined after co-cultures of rhMIF-stimulated RA synovial fibroblasts with human PBMC.
Synovial fluid MIF concentration in RA patients was significantly higher than in osteoarthritis (OA) patients. The concentration of RANKL correlated with that of MIF in RA synovial fluids (r = 0.6, P < 0.001). MIF stimulated the expression of RANKL mRNA and protein in RA synovial fibroblasts, which was partially reduced by blocking of interleukin (IL)-1β. Osteoclasts were differentiated from PBMC cultures with MIF and M-CSF, even without RANKL. Osteoclastogenesis was increased after co-culture of MIF-stimulated RA synovial fibroblasts with PBMC and this effect was diminished by RANKL neutralization. Blocking of PI3 kinase, p38 MAP kinase, JAK-2, NF-κB, and AP-1 also led to a marked reduction in RANKL expression and osteoclastogenesis.
The interactions among MIF, synovial fibroblasts, osteoclasts, RANKL, and IL-1β have a close connection in osteoclastogenesis and they could be a potential gateway leading to new therapeutic approaches in treating bone destruction in RA.
PMCID: PMC3132025  PMID: 21401926
2.  The Primary Patency and Fracture Rates of Self-Expandable Nitinol Stents Placed in the Popliteal Arteries, Especially in the P2 and P3 Segments, in Korean Patients 
Korean Journal of Radiology  2011;12(2):203-209.
We wanted to evaluate the status of self-expandable nitinol stents implanted in the P2 and P3 segments of the popliteal artery in Korean patients.
Materials and Methods
We retrospectively analyzed 189 consecutive patients who underwent endovascular treatment for stenoocclusive lesions in the femoropopliteal artery from July 2003 to March 2009, and 18 patients who underwent stent placement in popliteal arterial P2 and P3 segments were finally enrolled. Lesion patency was evaluated by ultrasound or CT angiography, and stent fracture was assessed by plain X-rays at 1, 3, 6 and 12 months and annually thereafter.
At the 1-month follow-up, stent fracture (Type 2) was seen in one limb (up to P3, 1 of 18, 6%) and it was identified in seven limbs at the 3-month follow-up (Type 2, Type 3, Type 4) (n = 1: up to P2; n = 6: P3). At the 6-month follow-up, one more fracture (Type 1) (up to P3) was noted. At the 1-year follow-up, there were no additional stent fractures. Just four limbs (up to P2) at the 2-year follow-up did not have stent fracture. The primary patency was 94%, 61% and 44% at 1, 3 and 6 months, respectively, and the group with stent implantation up to P3 had a higher fracture rate than that of the group that underwent stenting up to P2 (p < 0.05).
We suggest that stent placement up to the popliteal arterial P3 segment and over P2 in an Asian population can worsen the stent patency owing to stent fracture. It may be necessary to develop a stent design and structure for the Asian population that can resist the bending force in the knee joint.
PMCID: PMC3052611  PMID: 21430937
Artery; Stent; Intervention; Fluoroscopy; Fracture; Angioplasty

Results 1-2 (2)