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Seiji Saito

Publications -  27
Citations -  2678

Seiji Saito is an academic researcher. The author has contributed to research in topics: Rheumatoid arthritis & Chondrocyte. The author has an hindex of 16, co-authored 26 publications receiving 2575 citations.

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IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis

TL;DR: It is suggested that IL-17 first acts on osteoblasts, which stimulates both COX-2-dependent PGE2 synthesis and ODF gene expression, which in turn induce differentiation of osteoclast progenitors into mature osteoclasts, and that IL -17 is a crucial cytokine for osteoclastic bone resorption in RA patients.
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Activated human T cells directly induce osteoclastogenesis from human monocytes: possible role of T cells in bone destruction in rheumatoid arthritis patients.

TL;DR: The present findings suggest that excess production of RANKL by activated T cells increases the level of sRANKL in synovial fluid and may contribute to osteoclastic bone resorption in RA patients, the first to demonstrate osteoclastogenesis using human-derived T cells and monocytes.
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Tensile load and the metabolism of anterior cruciate ligament cells

TL;DR: Observations suggest that the application of cyclic tensile load on the anterior cruciate ligament cells is an important factor in the regulation of collagen synthesis in the anterior cruiser ligament.
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Is minimally invasive surgery in total knee arthroplasty really minimally invasive surgery

TL;DR: Interestingly, the midvastus approach displayed the highest RIs for creatinine phosphokinase and myoglobin between the 4 vastus-splitting approaches, whereas types of vastus -splitting approach appeared closely related to muscle damage.
Journal Article

Expression and function of the co-stimulator H4/ICOS on activated T cells of patients with rheumatoid arthritis.

TL;DR: The results suggest that local immune responses may be modulated by H4/ICOS expressed on T cells in the joints of patients with RA, and thus H4 /ICOS may be involved in the pathogenetic mechanism of RA.