Taken together, caspase activation and Fas/FasL interaction was found to be involved in tanghinigenin-induced HL-60 cell apoptosis. (C) 2010 Elsevier B.V. All rights reserved.”
“Objective. Our prospective study aimed to demonstrate that the cumulative synovial power Doppler (PD) ultrasound scores correlate with radiographic progression better than conventional measures in patients with rheumatoid arthritis (RA). We also investigated the difference between antirheumatic agents.\n\nMethods. Sixty-nine
patients with RA who had recently received either methotrexate (MTX; n = 23), tumor necrosis factor selleckchem (TNF) antagonists (n = 28), or tocilizumab (TCZ; n = 18) were enrolled. Patients underwent clinical, laboratory, and ultrasonographic assessment at baseline, 12 weeks, and 24 weeks. Radiographic damage was evaluated using van der Heijde modified total Sharp score (TSS) at baseline and 24 weeks.\n\nResults. Fifty-seven patients continued the same treatment regimen for 24 weeks and completed the study, and 21 patients (36.8%) showed radiographic progression during the study period. In all patients, Delta Lonafarnib solubility dmso TSS significantly
correlated both with cumulative 28-joint Disease Activity Score C-reactive protein (DAS28-CRP; rho = 0.342, p = 0.009) and cumulative total PD scores (rho = 0.357, p = 0.006). In MTX-treated patients, cumulative total PD scores significantly correlated with ATSS (rho = 0.679, p = 0.004), whereas cumulative DAS28-CRP did not (rho = 0.487, p = 0.056). However, cumulative total PD scores did not correlate selleck chemicals with Delta TSS in TNF antagonist treated or TCZ-treated patients.\n\nConclusion. Our data confirm the evidence that synovial PD activity more accurately reflects active synovial inflammation (which actually causes joint destruction) than do conventional measures in patients treated with MTX. Our data also indicate that TNF antagonists can inhibit short-term radiographic progression in the presence of active synovitis.”
“The association
between vitamin D and thyroid cancer is unclear. It is unknown if CYP27A1 or CYP2R1 are present in normal thyroid or cancer cells and there is limited information regarding response to treatment with vitamin D. SV40 immortalized follicular cells (N-thy) and six thyroid cancer cell lines were treated with 10 mu M vitamin D-3, 0.1 mu M 1,25(OH)(2)D-3 or vehicle x 24 h. CYP27A1, CYP2R1, CYP27B1 and CYP24A1 mRNA were measured using quantitative real-time-PCR before and after treatment. Cell proliferation was also evaluated in TPC1 and C643 cells after treatment with D-3, 25(OH)D-3 and 1,25(OH)(2)D-3. Baseline CYP27A1 and CYP27B1 mRNA were present in all cells, CYP2R1 was higher and CYP24A1 mRNA was lower in cancer cell lines versus N-thy. TPC1 cells had increased CYP24A1 mRNA levels when treated with both D-3 (3.49, p < 0.001) and 1,25(OH)(2)D-3 (5.