Reaction between CaO‐SiO2‐Al2O3 Slags and H2 + HCl + H2O Gas Mixtures

To better understand the thermodynamic behaviour of chlorine in blast furnaces, CaO‐SiO₂‐Al₂O₃ slags were brought into equilibrium with Ar + H₂ + HCl + H₂O gas mixtures at temperatures between 1673 K and 1798 K. The dissolution of chlorine into molten slags could be well interpreted through a reaction: (1/2) {CaO}_slag + (HCl) = {Ca_1/2Cl}_slag + (1/2) (H₂O). Conforming to this formula, a linear relation was observed between log (%CI) and log with an anticipated slope of 1/2.     

氢电弧等离子体法制备纳米金粒子

在H2 Ar气氛中，采用氢电弧等离子体法制备纳米金粒子。电弧等离子的高温使得金块熔化、蒸发，金原子在上升过程中与Ar原子碰撞、成核并最终形成纳米金粒子。通过SEM观察，纳米金粒子形状规则，平均尺寸在30nm左右。XRD结果表明纳米金纯度高，DSC实验表明其熔点是483℃。     

Glutathione is a cofactor for H2O2-mediated stimulation of Ca2+-induced Ca2+ release in cardiac myocytes

Reactive oxygen species are known to cause attenuation of cardiac muscle contraction. This attenuation is usually preceded by transient augmentation of twitch amplitude as well as cytosolic Ca2+. The present study examines the role of an endogenous antioxidant, glutathione in the mechanism of H2O2-mediated augmentation of Ca2+ release from the sarcoplasmic reticulum. Whole-cell patch-clamped single rat ventricular myocytes were dialyzed with the Cs+-rich internal solution containing 200 microM fura-2 and 2 mM glutathione (reduced form). After equilibration of the myocyte with intracellular dialyzing solution, Ca2+ current-induced Ca2+ release from the sarcoplasmic reticulum was monitored. Rapid perfusion with H2O2 (100 microM or 1 mM) for 20 s inhibited Ca2+ current, but enhanced the intracellular Ca2+ transients for 3-4 min. Thus, the efficacy of Ca2+-induced Ca2+ release mechanism was augmented in 71% of myocytes (n = 7). This enhancement ranged between 1.5- to threefold as the concentrations of H2O2 were raised from 100 microM to 1 mM. If glutathione were excluded from the patch pipette or replaced with glutathione disulfide, the enhancement of Ca2+-induced Ca2+ release was seen in only a minority (20%) of the myocytes. H2O2 exposure did not increase the basal intracellular Ca2+ levels, suggesting that the mechanism of H2O2 action was not mediated by inhibition of the sarcoplasmic reticulum Ca2+ uptake or activation of passive Ca2+ leak pathway. H2O2-mediated stimulation of Ca2+-induced Ca2+ release was also observed in myocytes dialyzed with dithiothreitol (0.5 mM). Therefore, reduced thiols support the action of H2O2 to enhance the efficacy of Ca2+-induced Ca2+ release, suggesting that redox reactions might regulate Ca2+ channel-gated Ca2+ release by the ryanodine receptor.