Publications by authors named "Ken Takebe"

Objective: Recombinant inbred mouse strains generated from an LG/J and SM/J intercross offer a unique resource to study complex genetic traits such as osteoarthritis (OA). We undertook this study to determine the susceptibility of 14 strains to various phenotypes characteristic of posttraumatic OA. We hypothesized that phenotypic variability is associated with genetic variability.

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Objective: Postoperative infections, a serious complication of orthopedic surgery, occur 2-4 times more frequently in patients with rheumatoid arthritis (RA) without adjustment for medication. Some studies have demonstrated a similar risk of postoperative infection following orthopedic surgery regardless of whether patients underwent tumor necrosis factor-α (TNF-α) inhibitor therapy; however, other studies have reported a higher risk with TNF-α inhibitor use. However, few reports have focused on the correlation between TNF-α inhibitor use and postoperative late infection.

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Periprosthetic bone loss is a well documented phenomenon after cementless total hip arthroplasty. We compared the bone mineral density (BMD) in 33 patients using the three dimension taper shape stem and 13 patients with a straight component with a distal taper. Postoperative follow-up was evaluated by dual-energy X-ray absorptiometry.

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Activation of p38 MAPK has been associated with a stress response and with apoptotic processes. However, the function of p38 MAPK in chondrocytes is not clearly understood. In this study, we analyzed the expression of p38 MAPK in chondrocytes and investigated the function of p38 MAPK in response to heat stress and mechanical stress.

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Objective: Chondrocyte apoptosis plays an important role in cartilage degeneration in osteoarthritis (OA), and mechanical injury to cartilage induces chondrocyte apoptosis. In response to DNA damage, p53 expression is up-regulated, transcription activity is increased, and apoptosis signals are initiated. The p53-regulated apoptosis-inducing protein 1 (p53AIP-1) is one of the p53-regulated genes, and is activated in response to DNA damage.

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