Sedation is necessary for MRI examinations in children who have difficulty restraining their body movements. We prepared a sedative protocol using triclofos, which is widely used in Japan, and evaluated its efficacy and safety. We retrospectively reviewed the planned MRI examinations in children aged from 1 month to 7 years old between October 2014 and March 2017. Patients considered to be at high risk for sedation were excluded. Triclofos 60 to 80 mg/kg was orally administered, and midazolam, hydroxyzine or pentazocine was added intravenously when sedation was insufficient. With this regimen, the planned MRI examinations were completed in 223 of 225 patients, and the median dose of triclofos was 68.2 mg/kg. One hundred fifty-two patients (68.2%) were sedated with triclofos alone, and 71 (31.8%) required multiple drugs. The median age, median dose of triclofos, average sedation time, and number of adverse events were significantly higher in the multiple drug group. The cut-off age of patients who could be sedated with triclofos alone was 16 months. The multiple drug group tended to be older, leading to prolonged sedation time and an increase in adverse events.
Abnormal synovial proliferation is one of the major characteristics of rheumatoid arthritis (RA). However, the molecular mechanisms behind this process are still unclear. In this study, analysis of gene expression by quantitative real time-PCR was performed to identify cell cycle regulators whose expression is induced by pro-inflammatory cytokines in RA and osteoarthritis synovial fibroblasts. Stimulation with tumor necrosis factor (TNF) α or interleukin (IL) 1β, but not IL-6, induced gene expression of the cell cycle regulator, cyclin-dependent kinase (CDK) 6 in RA and osteoarthritis synovial fibroblasts. TNFα mediated CDK6 gene expression through both the NFκB and AP1 pathways. Furthermore, TNFα-stimulated proliferation of cultured RA synovial fibroblasts was inhibited by siRNA for CDK6 or CDK4, both of which are D-type cyclin partners. The expression of CDK6 is induced by TNFα through both the NFκB and AP1 pathways in RA synovial fibroblasts, suggesting that anti-CDK6 drugs might offer therapeutic benefits in RA.