In Vivo Degradation Behavior of Magnesium Alloy for Bone Implants with Improving Biological Activity, Mechanical Properties, and Corrosion Resistance.

This study aimed to establish a surface modification technology for ZK60 magnesium alloy implants that can degrade uniformly over time and promote bone healing. It proposes a special micro-arc oxidation (MAO) treatment on ZK60 alloy that enables the composite electrolytes to create a coating with better corrosion resistance and solve the problems of uneven and excessive degradation. A magnesium alloy bone screw made in this way was able to promote the bone healing reaction after implantation in rabbits. Additionally, it was found that the MAO-treated samples could be sustained in simulated body-fluid solution, exhibiting excellent corrosion resistance and electrochemical stability. The Ca ions deposited in the MAO coating were not cytotoxic and were beneficial in enhancing bone healing after implantation.

Plasmacytoid dendritic cells suppress Th2 responses induced by epicutaneous sensitization.

Epicutaneous (EC) sensitization with protein allergens is the most important sensitization route for atopic dermatitis. Plasmacytoid dendritic cells (pDCs) are characterized by massive secretion of interferon-α (IFNα). B6 mice are T helper type 1 (Th1)-prone and are representative of non-atopic humans, whereas BALB/c mice are Th2-prone and are representative of atopic humans. Here, we show that naïve BALB/c mice contain a greater number of nonactivated pDCs in peripheral lymph nodes (LNs) than do naïve B6 mice. Naïve BALB/c mice also have more of the CD8α- subset in LNs than naïve B6 mice. Moreover, in vivo depletion of pDCs during EC sensitization results in enhanced Th2 responses in BALB/c mice, but not in B6 mice. Mechanistically, when BALB/c mice undergo EC sensitization, there is an increase in pDCs entering draining LNs. These cells exhibit modest activation including comparable costimulation expression but increased cytokine expression compared with those of naïve mice. In vivo depletion of pDCs during EC sensitization significantly increases the activation of dermal dendritic cells (dDCs) suggesting a regulatory effect on these cells. To this end, a suppressive effect of pDCs on conventional dendritic cells was also demonstrated in vitro. Further, in vivo blockade of IFNα by an anti-IFNAR antibody (Ab) or in vivo reduction of IFNα production of pDCs by anti-siglec-H Ab both resulted in enhanced activation of dDCs. Collectively, our results demonstrate that pDCs suppress Th2 responses induced by EC sensitization via IFNα-mediated regulation of dDCs.

Reactions of cumene hydroperoxide mixed with sodium hydroxide.

Decomposition of cumene hydroperoxide (CHP) was undertaken in a free radical chain reaction. The peroxyl group is very active and unstable, while the remainder of the molecule is inert. CHP reacted with various concentrations of dilute sodium hydroxide as a catalyst to cleave at ambient and decomposition temperature. The products were verified by GC/MS, and were quantitatively analyzed by chromatography. CHP cleaved heterolytic with NaOH at 250 degrees C, whose major product was dimethylphenyl carbinol (DMPC); however, the main products become acetophenone and alpha-methylstyrene by cleaved homolytic pathway. The catalytic concentrations of NaOH significantly affected the branch ratios of DMPC under decomposition. Based on the experimental results, a radical cleavage mechanism was proposed. To sum up, the reaction parameters, such as temperature, Lewis base, etc., could affect the incompatibilities and decomposition pathways for proper CHP cleavage process. In addition, exothermic onset temperatures (T0) and heat of decomposition (Delta Hd) of incompatible mixtures and CHP itself were studied by differential scanning calorimetry (DSC). Comparisons of T0, Delta Hd and peak power were assessed to corroborate the severity of thermal hazards. From the decay rate of CHP concentration, the reaction order was determined to be 0.5, and the Arrhenius parameters were measured as Ea=92.1 kJ/mol and frequency factor A=2.42 x 10(10)min(-1).