Spheroidization of Nickel Powder and Coating with Carbon Layer through Laser Heating.

We developed a simple and efficient process, laser heating of nickel powder in ethanol, to produce carbon-encapsulated nickel microspheres. Long-pulse-width laser heated nickel powder suspended in pure ethanol into liquid droplets. In turn, the latter droplets became sphere-like, pyrolyzed surrounding ethanol and dissolved the produced carbon atoms. Because of their lower solubility in solid nickel, excess carbon atoms were then expelled from the metal core after solidification, thus forming graphite-like shells on the laser-modified Ni spheres. Hence, after pyrolysis the transformation of carbon was found to follow the dissolution-precipitation mechanism. The produced carbon-encapsulated nickel microspheres exhibited higher oxidation resistance compared with the initial nickel powder, while keeping their magnetic properties essentially unchanged.

Decreased Sp1 Expression Mediates Downregulation of SHIP2 in Gastric Cancer Cells.

Past studies have shown that the Src homology 2-containing inositol 5-phosphatase 2 (SHIP2) is commonly downregulated in gastric cancer, which contributes to elevated activation of PI3K/Akt signaling, proliferation and tumorigenesis of gastric cancer cells. However, the mechanisms underlying the reduced expression of SHIP2 in gastric cancer remain unclear. While gene copy number variation analysis and exon sequencing indicated the absence of genomic alterations of SHIP2, bisulfite genomic sequencing (BGS) showed promoter hypomethylation of SHIP2 in gastric cancer cells. Analysis of transcriptional activity of SHIP2 promoter revealed Specificity protein 1 (Sp1) was responsible for the regulation of SHIP2 expression in gastric cancer cells. Furthermore, Sp1 expression, but not Sp3, was frequently downregulated in gastric cancer compared with normal gastric mucosa, which was associated with a paralleled reduction in SHIP2 levels in gastric cancer. Moreover, overexpression of Sp1 inhibited cell proliferation, induced apoptosis, suppressed cell motility and invasion in gastric cancer cells in vitro, which was, at least in part, due to transcriptional activation of SHIP2 mediated by Sp1, thereby inactivating Akt. Collectively, these results indicate that decreased expression of transcription factor Sp1 contributes to suppression of SHIP2 in gastric cancer cells.