A spin-1 ferromagnetic Bose-Einstein condensate subject to a certain magnetic field exhibits a broken-axisymmetry phase in which the magnetization tilts against the applied magnetic field due to the competition between ferromagnetism and linear and quadratic Zeeman effects. The Bogoliubov analysis shows that in this phase two Goldstone modes associated with U(1) and SO(2) symmetry breakings exist, in which phonons and magnons are coupled to restore the two broken symmetries. PACS numbers: 03.75.Mn, 67.40.Db, 67.57.Jj −ζ−1Θ0(νp−νm)+ζ0Θ−1νp J ζ−1Θ1(νp−νm)−ζ1Θ−1(νp+νm) J ζ1Θ0(νp+νm)−ζ0Θ1νp J ζ−1Θ0(µp−µm)−ζ0Θ−1µp J −ζ−1Θ1(µp−µm)+ζ1Θ−1(µp+µm) J −ζ1Θ0(µp+µm)+ζ0Θ1µp J
In view of a cytoprotective effect of elastase inhibitor on chemokine-mediated tissue injury, we examined the neuroprotective effect of ONO-5046, a speci®c inhibitor of neutrophil elastase, in rats with spinal cord injury. Standardized spinal cord compression markedly increased cytokine-induced neutrophil chemo-attractant (CINC)-1 mRNA and protein.Their increases correlated with neurologic severity of injured rats. Immunohistochemically, CINC-1 protein was detected sequentially in vascular endothelial cells at 4 h, in perivascular neutrophils at 8 h, and in neutrophils in®ltrating into cord substance at 12 h. Pretreatment with ONO-5046 (50 mg/kg) markedly ameliorated motor disturbance in injured rats, and reduced CINC-1 protein and mRNA expression. ONO-5046 also signi®cantly reduced the increase of neutrophil accumulation or in®ltration estimated by myeloperoxidase activity, and the extent of vascular permeability by Evans blue extravasation in the injured cord segment in comparison to control animals receiving vehicle. These results suggest that CINC-1 contributed to in¯ammation in rat spinal cord injury and ONO-5046 attenuated neurologic damage partly by blocking CINC-1 production of the chemoattractant, preventing neutrophil activation and vascular endothelial cell injury.
We have reported that N-(p-coumaroyl) serotonin (CS) and its derivatives with antioxidative activity are present in safflower seeds. As reactive oxygen species (ROS) are implicated in the signaling of lipopolysaccharide (LPS), we examined whether CS has a suppressive effect on inflammatory cytokine generation from human monocytes in vitro. CS at 50-200 microM reduced tumor necrosis factor (TNF), interleukin-1 (IL-1), and IL-6 activities in the culture supernatants from LPS-stimulated human blood monocytes without cytotoxicity. ELISA assay revealed that the production of TNF-alpha, IL-1alpha, IL-1beta, and IL-6 was inhibited by CS. Northern blot analysis showed that LPS-induced expression of these cytokine mRNA in monocytes was suppressed by CS. NF-kappaB activation was also inhibited by CS. These findings indicate that CS has a suppressive effect on proinflammatory cytokine production from monocytes, and this effect is based in part on the suppression of cytokine mRNA expression through inhibition of NF-kappaB activation.
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