No abstract

Using solid-to-solid couples investigation, this study characterized the reaction products evolved and quantified the diffusion kinetics when pure Mg bonded to AA6061 is subjected to thermal treatment at 300°C for 720 hours, 350°C for 360 hours, and 400°C for 240 hours. Characterization techniques include optical microscopy, scanning electron microscopy with X-ray energy dispersive spectroscopy, and transmission electron microscopy. Parabolic growth constants were determined for γ-Mg17Al12, β-Mg2Al3, and the elusive ε-phase. Similarly, the average effective interdiffusion coefficients of major constituents were calculated for Mg (ss), γ-Mg17Al12, β-Mg2Al3, and AA6061. The activation energies and pre-exponential factors for both parabolic growth constant and average effective interdiffusion coefficients were computed using the Arrhenius relationship. The activation energy for growth of γ-Mg17Al12 was significantly higher than that for β-Mg2Al3 while the activation energy for interdiffusion of γ-Mg17Al12 was only slightly higher than that for β-Mg2Al3. Comparisons are made between the results of this study and those of diffusion studies between pure Mg and pure Al [1] to examine the influence of alloying additions in AA6061.

Bone marrow transplantation (BMT) of B10.D2 mice into sublethally irradiated BALB/c mice across minor histocompatibility loci is a well-established animal model for human sclerodermatous chronic graft-versus-host disease (Scl-cGVHD) and systemic sclerosis (SSc). The p38 mitogen-activated protein kinase (MAPK) pathway is a key regulator of inflammation and of cytokine production. Furthermore, the activation of p38 MAPK plays an important role in collagen production in SSc. This study aimed to investigate the effects of p38 MAPK inhibitor on Scl-cGVHD mice. p38 MAPK inhibitor, VX702, was orally administered to Scl-cGVHD mice from day 7 to 35 after BMT. We compared skin fibrosis of Scl-cGVHD mice between the p38 MAPK inhibitor treated group and control group. Allogeneic BMT increased the phosphorylation of p38 MAPK in the skin. The administration of p38 MAPK inhibitor attenuated the skin fibrosis of Scl-cGVHD compared to the control mice. Immunohistochemical staining showed that p38 MAPK inhibitor suppressed the infiltration of CD4 + T cells, CD8 + T cells, and CD11b + cells into the dermis of Scl-cGVHD mice compared to the control mice. p38 MAPK inhibitor attenuated the mRNA expression of extracellular matrix and fibrogenic cytokines, such as IL-6 and IL-13, in the skin of Scl-cGVHD mice. In addition, p38 MAPK inhibitor directly inhibited collagen production from fibroblasts in vitro. p38 MAPK inhibitor was shown to be a promising candidate for use in treating patients with Scl-cGVHD and SSc. 305 Fli1 deficiency alters the phenotype of dermal dendritic cells, promoting the development of dermal fibrosis in bleomycin-treated mice