Influence of deflocculant on the isoelectric point of refractory powders: Considerations on the action of deflocculant

Isoelectric point changes in suspensions of refractory materials vis-a-vis the role of deflocculants used in monolithic refractories were investigated by considering the mineral compositions and adsorbed ions in four kinds of clay. Three types of curves represented the relation between the isoelectric point and the deflocculant. The surface charge of clay particles in the suspensions became negative as a result of the deflocculant, since the isoelectric point of suspensions decreased as the deflocculant was added. The isoelectric point changes of calcined alumina were also compared with those of the clays, and a similar phenomenon was observed, except that the deflocculant dispersed the calcined alumina better than it did the clays. A simple model was used to analyze the results

FK506 and Cyclosporin A Enhance IL-6 Production in Monocytes: A single-Cell Assay

The effect of FK506 and cyclosporin A (CsA) on the production of interleukin 6 (IL-6) in adherent monocytes was studied at a single-cell level by the avidinbiotin- peroxidase complex methods. The percentage of IL-6-producing monocytes increased when stimulated with lipopolysaccharide (LPS) at concentrations between 10 ng/ml and 10 μg/ml, in a dose dependent manner. Both FK506 and CsA enhanced the percentage of IL-6- producing monocytes stimulated with 100 pg/ml-1 μg/ml of LPS up to values near those obtained with 10 μg/ml of LPS. The enhancement by FK506 and CsA was not seen when monocytes were stimulated with a high concentration of LPS (10 μg/ml). When monocytes were stimulated with a low concentration of LPS (10 ng/ml), FK506 and CsA enhanced IL-6 production in a dose dependent manner, at a drug concentration of 0.12 nM–1.2 μM (0.1–1 000 ng/ml) for FK506 and 0.83 nM–8.3 μM (1–10 000 ng/ml) for CsA. The optimal effect of FK506 was achieved at a concentration 7-fold lower than that of CsA. In contrast, production of turnout necrosis factor-α (TNFα and interleukin 1β (IL-1β) was slightly suppressed by FK506 and CsA at the concentrations tested. Moreover, pretreatment of monocytes with FK506 and CsA had a significant enhancing effect on LPS-induced IL-6 production, while treatment with FK506 or CsA after LPS stimulation had no effects on IL-6 production, suggesting that the enhancing effect of each drug is exerted before LPS stimulation or at an early stage of the post-receptor pathway after LPS stimulation. These experiments demonstrate that FK506 and CsA can selectively enhance IL-6 production in monocytes under certain conditions in vitro and, possibly, also in vivo

Temporal and sequential changes of glial cells and cytokine expression during neuronal degeneration after transient global ischemia in rats

<p>Abstract</p> <p>Background</p> <p>How glial cells and cytokines are associated with the progression of delayed neuronal death induced by transient global ischemia is still unclear. To further clarify this point, we studied morphological changes in glial cells (microglial cells and astrocytes), and cytokine protein levels, during the progression of neuronal cell loss in CA1 (Cornu Ammonis 1) of the hippocampus after transient global ischemia.</p> <p>Methods</p> <p>Morphological changes in glial cells were studied immuno-histochemically. Nine cytokines (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, GM-CSF, IFN-γ and TNF-α) were simultaneously measured by a multiplexed bead-based immunoassay from 6 h to day21 after transient four vessel occlusion (4VO) in rats.</p> <p>Results</p> <p>During the process of neuronal loss, we observed four distinct phases: (1) lag phase day0-2 (no NeuN+ cell loss observed), (2) exponential phase day2-7 (NeuN+ cells reduced in number exponentially), (3) deceleration phase day7-14 (reduction rate of NeuN+ cells became low), (4) stationary phase day14 onward (NeuN+ cell loss progressed no longer). In the lag phase, activated glial cells were observed in the entire hippocampus but later were gradually restricted to CA1. Cytokine protein levels in the lag and exponential phases were lower than in the deceleration and stationary phases. IL-1α, IL-1β, IL-4, IL-6 and IFN-γ in 4VO were significantly higher in all four phases than in sham. Compared with sham level, GM-CSF was significantly high in the deceleration phase. TNF-α was significantly high in both the deceleration and stationary phases.</p> <p>Conclusion</p> <p>Ischemic stress in 4VO activated glial cells in areas beyond CA1 in the lag phase. Pyramidal neurons were injured in CA1 from the end of the lag phase and then neuronal cells reduced in CA1 in the exponential phase. After neuronal death began, the influence of dead cells on glial cells and cytokine expression gradually became stronger than the influence by ischemic stress. Therefore, from the deceleration phase, changes in glial cells and cytokine production were likely caused by dead cells. Cytokine interaction in the microenvironment may determine the functions of IL-1α, IL-1β, IL-4, IL-6 and IFN-γ in all four phases. The function of GM-CSF and TNF-α in the deceleration phase may be neurotrophic.</p

The role of calcium channels in osteocyte function

Abstract Osteocytic response to stretching, which is potentiated by PTH, is distinct from that of osteoblast to high frequency strain. A MAPK dependent signaling pathway is suggested in the osteoblast response. At least two different types of mechanotransduction pathways are present in bone cells of osteoblastic lineage