Melting and metallization of silica in the cores of gas giants, ice giants and super Earths

The physical state and properties of silicates at conditions encountered in the cores of gas giants, ice giants and of Earth like exoplanets now discovered with masses up to several times the mass of the Earth remains mostly unknown. Here, we report on theoretical predictions of the properties of silica, SiO$_2$, up to 4 TPa and about 20,000K using first principle molecular dynamics simulations based on density functional theory. For conditions found in the Super-Earths and in ice giants, we show that silica remains a poor electrical conductor up to 10 Mbar due to an increase in the Si-O coordination with pressure. For Jupiter and Saturn cores, we find that MgSiO$_3$ silicate has not only dissociated into MgO and SiO$_2$, as shown in previous studies, but that these two phases have likely differentiated to lead to a core made of liquid SiO$_2$ and solid (Mg,Fe)O.Comment: 5 pages, 4 figure

Observation of step-induced magnetic domain formation in La1-xSrxMnO3 thin films by photoelectron emission microscopy

科研費報告書収録論文(課題番号:16310081/研究代表者:白井正文/ナノ磁性材料におけるスピン構造とそのダイナミクスに関する理論研究

BART Inhibits Pancreatic Cancer Cell Invasion by PKCα Inactivation through Binding to ANX7

A novel function for the binder of Arl two (BART) molecule in pancreatic cancer cells is reported. BART inhibits invasiveness of pancreatic cancer cells through binding to a Ca2+-dependent, phosphorylated, guanosine triphosphatase (GTPase) membrane fusion protein, annexin7 (ANX7). A tumor suppressor function for ANX7 was previously reported based on its prognostic role in human cancers and the cancer-prone mouse phenotype ANX7(+/−). Further investigation demonstrated that the BART–ANX7 complex is transported toward cell protrusions in migrating cells when BART supports the binding of ANX7 to the protein kinase C (PKC) isoform PKCα. Recent evidence has suggested that phosphorylation of ANX7 by PKC significantly potentiates ANX7-induced fusion of phospholipid vesicles; however, the current data suggest that the BART–ANX7 complex reduces PKCα activity. Knocking down endogenous BART and ANX7 increases activity of PKCα, and specific inhibitors of PKCα significantly abrogate invasiveness induced by BART and ANX7 knockdown. These results imply that BART contributes to regulating PKCα activity through binding to ANX7, thereby affecting the invasiveness of pancreatic cancer cells. Thus, it is possible that BART and ANX7 can distinctly regulate the downstream signaling of PKCα that is potentially relevant to cell invasion by acting as anti-invasive molecules