Study of the plasma near the plasma electrode by probes and photodetachment in ECR-driven negative ion source

Contributions to the conference will be published, following peer review, in the American Institute of Physics conference proceedings.International audienceThe effect of the plasma electrode bias on the plasma characteristics near the extraction aperture in a large volume hybrid multicusp negative ion source, driven by 2.45 GHz microwaves, is reported. Spatially resolved negative ion and electron density measurements were performed under various pressures (1-4 mTorr) by means of electrostatic probe and photodetachment technique

Can distributed delays perfectly stabilize dynamical networks?

Signal transmission delays tend to destabilize dynamical networks leading to oscillation, but their dispersion contributes oppositely toward stabilization. We analyze an integro-differential equation that describes the collective dynamics of a neural network with distributed signal delays. With the gamma distributed delays less dispersed than exponential distribution, the system exhibits reentrant phenomena, in which the stability is once lost but then recovered as the mean delay is increased. With delays dispersed more highly than exponential, the system never destabilizes.Comment: 4pages 5figure

Inhibition of Tendon Cell Proliferation and Matrix Glycosaminoglycan Synthesis by Non-Steroidal Anti-Inflammatory Drugs in vitro

The purpose of this study was to investigate the effects of some commonly used non-steroidal anti-inflammatory drugs (NSAIDs) on human tendon. Explants of human digital flexor and patella tendons were cultured in medium containing pharmacological concentrations of NSAIDs. Cell proliferation was measured by incorporation of 3H-thymidine and glycosaminoglycan synthesis was measured by incorporation of 35S-Sulphate. Diclofenac and aceclofenac had no significant effect either on tendon cell proliferation or glycosaminoglycan synthesis. Indomethacin and naproxen inhibited cell proliferation in patella tendons and inhibited glycosaminoglycan synthesis in both digital flexor and patella tendons. If applicable to the in vivo situation, these NSAIDs should be used with caution in the treatment of pain after tendon injury and surgery

Nimesulide reduces interleukin-1β-induced cyclooxygenase-2 gene expression in human synovial fibroblasts

AbstractObjective To characterize the effects of nimesulide (NIM) on basal and induced cyclo-oxygenase-2 (COX-2) gene expression in human synovial fibroblasts (HSF) and to define the intracellular mechanisms that mediate the changes in COX-2 expression and synthesis in response to the drug.Design HSF were incubated with NIM and NS-398 (0, 0.03, 0.3, 3μg/ml) in the absence or presence of the COX-2 inducers interleukin-1β (IL-1β) or endotoxin (LPS). Treated cells were analysed for COX-2 mRNA and protein by Northern and Western blotting analysis, respectively. Putative transcriptional, post-transcriptional, and signaling effects of NIM on basal and induced-COX-2 expression were investigated by human COX-2 promoter studies, calcium studies, reactive oxygen species (ROS) evaluations, electrophoretic mobility shift analysis (EMSA) and half-life studies of COX-2 mRNA.Results NIM inhibited IL-1β-induced COX-2 expression and protein at sub and therapeutic concentrations (0.03–0.3μg/ml) while the non-specific NSAID, naproxen, did not. Both drugs suppressed PGE2 release by about 95%. NIM had no effect on (1) IL-1β-induced increases in NF-κB or c/EBP signaling, or (2) human COX-2 promoter activity. Stability of induced COX-2 mRNA was unaffected by NIM treatments. Pre-treatment of cells with O2radical scavengers (e.g. PDTC) or with Ca++channel blockers (e.g. verapamil) had a modest effect on IL-1β-induced COX-2 expression. NIM blocked ionomycin+thapsigargin and H2O2-induced increases in COX-2 protein synthesis.Conclusion NIM inhibits cytokine-induced COX-2 expression and protein at sub and therapeutic concentrations. At least part of this activity may be the result of NIM inhibition of calcium and/or free radical generation induced by cytokines