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In order to understand the corrosion behavior of high-velocity oxygen-fuel (HVOF) TiAlNb coatings in molten Zn-0.2 wt.% Al, the different kinds of TiAlNb coating were deposited on 316L stainless steel substrate and the corrosion tests in molten zinc were carried out. The coating morphologies, phase composition, and characteristics of HVOF TiAlNb coatings at different stages of immersion time were studied by means of scanning electron microscopy (SEM), X-ray diffraction (XRD), and energy-dispersive X-ray spectrometry (EDX). The results indicated that the HVOF sprayed TiAlNb intermetallic compound coatings have excellent corrosion resistance to molten zinc. The corrosion type of the HVOF TiAlNb coatings in molten Zn-0.2 wt.% Al is pitting corrosion and crack corrosion. In the whole corrosion stage of molten Zn-0.2 wt.% Al, the corrosion time has no effect on the phase compositions of the HVOF TiAlNb coatings.

The L1 cell adhesion molecule (L1CAM) has been implicated in tumor progression of many types of cancers, but its role in prostate cancer and its application in targeted gene therapy have not been investigated. Herein, we demonstrated that the L1CAM was expressed in androgen-insensitive and highly metastatic human prostate cancer cell lines. The correlation between L1CAM expression and prostate cancer metastasis was also validated in serum samples of prostate cancer patients. Knockdown of L1CAM expression in prostate cancer cells by RNA interference significantly decreased their aggressive behaviors, including colony formation, migration and invasion in vitro, and tumor formation in a metastatic murine model. These anti-malignant phenotypes of L1CAM-knockdown cancer cells were accompanied by G0/G1 cell cycle arrest and suppression of matrix metalloproteinase (MMP)-2 and MMP-9 expression and nuclear factor NF-κB activation. In vivo targeting of L1CAM expression using liposome-encapsulated L1CAM siRNAs effectively inhibited prostate cancer growth in mouse bone, which was associated with decreased L1CAM expression and cell proliferation by tumor cells. These results provide the first evidence for L1CAM being a major contributor to prostate cancer metastasis and translational application of siRNA-based L1CAM-targeted therapy.

High Nb containing TiAl based alloys exhibit excellent corrosion resistance to molten zinc. They are expected to serve as the potential coating materials of corrosion resistance to molten zinc. Four TiAl-Nb alloys of good oxidation resistance and their powders were prepared by arc-melting and ball milling, respectively. The Microstructure, Hardness, Coefficient of thermal expansion, and grain size distribution of four as-cast TiAl-Nb alloys and their powders were investigated. In addition, EPMA analysis was employed to further examine the existential state of element Y in as-cast TiAl-Nb alloys. It was found that element Y existed in the form of YAl2 phase in the grain boundaries and triple junctions. Higher content of Al in TiAl-Nb alloy results in bigger Coefficient of thermal expansion. Lamellar microstructures and fine grains exert a positive influence on hardness. Powders prepared by ball milling displayed angular and irregular morphology. © (2012) Trans Tech Publications.

The DOC-2/DAB2 interactive protein (DAB2IP) is a new member of the Ras GTPase-activating protein family. Recent studies have shown that, in addition to its tumor suppressive role in various tumors, DAB2IP also plays an important role in regulating neuronal migration and positioning during brain development. In this study, we determined the roles of DAB2IP in the neuronal differentiation of human mesenchymal stem cells (hMSCs). We found that lentiviral short hairpin RNA (shRNA)-mediated knockdown of DAB2IP promoted the mesenchymal-to-neuroepithelial stem cell transition (MtNeST) and neuronal differentiation, which were accompanied by a reduction of cell proliferation but not apoptosis or cellular senescence. This suggests that DAB2IP plays an important role in the neuronal induction of hMSCs. Moreover, our finding that reduction of glycogen synthase kinase 3 beta (GSK3β) activity upon LiCl pretreatment inhibited both the MtNeST and production of MAP2-positive cells upon DAB2IP knockdown suggests that this transition is most likely mediated by regulation of the GSK3β signaling pathway. Our study demonstrates that DAB2IP participates in the first step of neuron induction of hMSCs, which implies a potentially important role for DAB2IP in the MtNeST during neurogenesis.

Enhancer of zeste homolog 2 (EZH2) regulates stem cells renewal, maintenance, and differentiation into different cell lineages including neuron. Changes in intracellular Ca(2+) concentration play a critical role in the differentiation of neurons. However, whether EZH2 modulates intracellular Ca(2+) signaling in regulating neuronal differentiation from human mesenchymal stem cells (hMSCs) still remains unclear. When hMSCs were treated with a Ca(2+) chelator or a PLC inhibitor to block IP(3)-mediated Ca(2+) signaling, neuronal differentiation was disrupted. EZH2 bound to the promoter region of PIP5K1C to suppress its transcription in proliferating hMSCs. Interestingly, knockdown of EZH2 enhanced the expression of PIP5K1C, which in turn increased the amount of PI(4,5)P(2), a precursor of IP(3), and resulted in increasing the intracellular Ca(2+) level, suggesting that EZH2 negatively regulates intracellular Ca(2+) through suppression of PIP5K1C. Knockdown of EZH2 also enhanced hMSCs differentiation into functional neuron both in vitro and in vivo. In contrast, knockdown of PIP5K1C significantly reduced PI(4,5)P(2) contents and intracellular Ca(2+) release in EZH2-silenced cells and resulted in the disruption of neuronal differentiation from hMSCs. Here, we provide the first evidence to demonstrate that after induction to neuronal differentiation, decreased EZH2 activates the expression of PIP5K1C to evoke intracellular Ca(2+) signaling, which leads hMSCs to differentiate into functional neuron lineage. Activation of intracellular Ca(2+) signaling by repressing or knocking down EZH2 might be a potential strategy to promote neuronal differentiation from hMSCs for application to neurological dysfunction diseases.