Formation of Protoplanets from Massive Planetesimals in Binary Systems

More than half of stars reside in binary or multiple star systems and many planets have been found in binary systems. From theoretical point of view, however, whether or not the planetary formation proceeds in a binary system is a very complex problem, because secular perturbation from the companion star can easily stir up the eccentricity of the planetesimals and cause high-velocity, destructive collisions between planetesimals. Early stage of planetary formation process in binary systems has been studied by restricted three-body approach with gas drag and it is commonly accepted that accretion of planetesimals can proceed due to orbital phasing by gas drag. However, the gas drag becomes less effective as the planetesimals become massive. Therefore it is still uncertain whether the collision velocity remains small and planetary accretion can proceed, once the planetesimals become massive. We performed {\it N}-body simulations of planetary formation in binary systems starting from massive planetesimals whose size is about 100-500 km. We found that the eccentricity vectors of planetesimals quickly converge to the forced eccentricity due to the coupling of the perturbation of the companion and the mutual interaction of planetesimals if the initial disk model is sufficiently wide in radial distribution. This convergence decreases the collision velocity and as a result accretion can proceed much in the same way as in isolated systems. The basic processes of the planetary formation, such as runaway growth and oligarchic growth and final configuration of the protoplanets are essentially the same in binary systems and single star systems, at least in the late stage where the effect of gas drag is small.Comment: 26pages, 11 figures. ApJ accepte

The self gravity effect on the orbital stability of Twotinos

We investigate how the self gravity changes the orbital stability of Twotinos using N-body simulations in which the gravitational interaction between planetesimals are fully calculated. We show the timescale in which the half of Twotinos becomes unstable, t_{half}, obey the formula, t_{half} = 4 \times 106(Mtot0.1M\oplus)-1(mp7.6 \times 1023g)-1(hi2i1/20.002)(years), if we assume the primordial planetesimals disk have the power low surface mass density, \Sigma = \Sigma_0 \times r-2/3. Where Mtot, mp, hi2i1/2 are the total mass of large bodies of Twotinos, the maximum mass of planetesimals, and the inclination dispersion. With this formulae, we conclude the total mass of Twotinos is reduced to the order of 0.01 M\oplus by the self gravity and secular perturbation of the Planets even if there was huge mass such as several order of the earth mass in 1:2 MMR of Neptune at the early age of the solar system. These results will invoke reexamination to many previous works which tried to explain the dynamical evolution of TNOs.Comment: 22pages, 9 figur

Synthesis of ordered mesoporous ruthenium by lyotropic liquid crystals and its electrochemical conversion to mesoporous ruthenium oxide with high surface area

In ordered to prepare high capacitance pseudo-capacitive oxides, it is important to design nanostructures with appreciable mesopores. Supramolecular templating has become a popular method to synthesize ordered mesoporous metals; however, the application of the same technique to synthesis of high surface area oxides is more demanding. We present here, the synthesis of ordered mesoporous ruthenium metal by lyotropic liquid crystal templating and its electrochemical conversion to ordered mesoporous ruthenium oxide by a simple, room temperature procedure. The bulk, unsupported metallic ordered mesoporous ruthenium exhibits high surface area of 110 m(2) g(-1), which is comparable to typical supported Ru nanoparticles. The oxide analogue gives a high specific capacitance of 376 Fg(-1), owing to the porous structure. These results demonstrate a possible facile and generic process to synthesize oxides with ordered nanostructures by utilization of the various phases that can be obtained with lyotropic liquid crystalline templates such as cubic, hexagonal, lamellar, etc.ArticleJOURNAL OF POWER SOURCES. 204:244-248 (2012)journal articl

Envy-free Relaxations for Goods, Chores, and Mixed Items

In fair division problems, we are given a set $S$ of $m$ items and a set $N$ of $n$ agents with individual preferences, and the goal is to find an allocation of items among agents so that each agent finds the allocation fair. There are several established fairness concepts and envy-freeness is one of the most extensively studied ones. However envy-free allocations do not always exist when items are indivisible and this has motivated relaxations of envy-freeness: envy-freeness up to one item (EF1) and envy-freeness up to any item (EFX) are two well-studied relaxations. We consider the problem of finding EF1 and EFX allocations for utility functions that are not necessarily monotone, and propose four possible extensions of different strength to this setting. In particular, we present a polynomial-time algorithm for finding an EF1 allocation for two agents with arbitrary utility functions. An example is given showing that EFX allocations need not exist for two agents with non-monotone, non-additive, identical utility functions. However, when all agents have monotone (not necessarily additive) identical utility functions, we prove that an EFX allocation of chores always exists. As a step toward understanding the general case, we discuss two subclasses of utility functions: Boolean utilities that are $\{0,+1\}$-valued functions, and negative Boolean utilities that are $\{0,-1\}$-valued functions. For the latter, we give a polynomial time algorithm that finds an EFX allocation when the utility functions are identical.Comment: 21 pages, 1 figur

Annexin A2-STAT3-Oncostatin M receptor axis drives phenotypic and mesenchymal changes in glioblastoma

Glioblastoma (GBM) is characterized by extensive tumor cell invasion, angiogenesis, and proliferation. We previously established subclones of GBM cells with distinct invasive phenotypes and identified annexin A2 (ANXA2) as an activator of angiogenesis and perivascular invasion. Here, we further explored the role of ANXA2 in regulating phenotypic transition in GBM. We identified oncostatin M receptor (OSMR) as a key ANXA2 target gene in GBM utilizing microarray analysis and hierarchical clustering analysis of the Ivy Glioblastoma Atlas Project and The Cancer Genome Atlas datasets. Overexpression of ANXA2 in GBM cells increased the expression of OSMR and phosphorylated signal transducer and activator of transcription 3 (STAT3) and enhanced cell invasion, angiogenesis, proliferation, and mesenchymal transition. Silencing of OSMR reversed the ANXA2-induced phenotype, and STAT3 knockdown reduced OSMR protein expression. Exposure of GBM cells to hypoxic conditions activated the ANXA2-STAT3-OSMR signaling axis. Mice bearing ANXA2-overexpressing GBM exhibited shorter survival times compared with control tumor-bearing mice, whereas OSMR knockdown increased the survival time and diminished ANXA2-mediated tumor invasion, angiogenesis, and growth. Further, we uncovered a significant relationship between ANXA2 and OSMR expression in clinical GBM specimens, and demonstrated their correlation with tumor histopathology and patient prognosis. Our results indicate that the ANXA2-STAT3-OSMR axis regulates malignant phenotypic changes and mesenchymal transition in GBM, suggesting that this axis is a promising therapeutic target to treat GBM aggressiveness

Higher-order modulations in the skyrmion-lattice phase of Cu2_2OSeO3_3

Using small angle neutron scattering, we have investigated higher-order peaks in the skyrmion-lattice phase of Cu$_2$OSeO$_3$, in which two different skyrmion lattices, SkX1 and SkX2, are known to form. For each skyrmion-lattice phase, we observed two sets of symmetrically inequivalent peaks at the higher-order-reflection positions with the indices $(110)$ and $(200)$. Under the condition where the SkX1 and SkX2 coexist, we confirmed the absence of the scattering at $\mathbf{Q}$ positions combining reflections from the two phases, indicating a significantly weak double-scattering component. Detailed analysis of the peak profile, as well as the temperature and magnetic-field dependence of the peak intensity, also supports the intrinsic higher-order modulation rather than the parasitic double scattering. The two higher-order modulations show contrasting magnetic-field dependence; the former $(110)$ increases as the field is increased, whereas the latter $(200)$ decreases. This indicates that, in Cu$_2$OSeO$_3$, skyrmions are weakly distorted, and the distortion is field-dependent in a way that the dominant higher-order modulation switches from $(110)$ to $(200)$ under field. Monte Carlo simulations under sweeping external magnetic field qualitatively reproduce the observed magnetic-field dependence, and suggests that the higher-order modulations correspond to the superlattices of weak swirlings appearing in the middle of the original triangular-latticed skyrmions.Comment: 13 pages, 14 figure

タッチスクリーンを用いた新たなマウス意思決定課題の作出

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Differentiated glioblastoma cells accelerate tumor progression by shaping the tumor microenvironment via CCN1-mediated macrophage infiltration

Glioblastoma (GBM) is the most lethal primary brain tumor characterized by significant cellular heterogeneity, namely tumor cells, including GBM stem-like cells (GSCs) and differentiated GBM cells (DGCs), and non-tumor cells such as endothelial cells, vascular pericytes, macrophages, and other types of immune cells. GSCs are essential to drive tumor progression, whereas the biological roles of DGCs are largely unknown. In this study, we focused on the roles of DGCs in the tumor microenvironment. To this end, we extracted DGC-specific signature genes from transcriptomic profiles of matched pairs of in vitro GSC and DGC models. By evaluating the DGC signature using single cell data, we confirmed the presence of cell subpopulations emulated by in vitro culture models within a primary tumor. The DGC signature was correlated with the mesenchymal subtype and a poor prognosis in large GBM cohorts such as The Cancer Genome Atlas and Ivy Glioblastoma Atlas Project. In silico signaling pathway analysis suggested a role of DGCs in macrophage infiltration. Consistent with in silico findings, in vitro DGC models promoted macrophage migration. In vivo, coimplantation of DGCs and GSCs reduced the survival of tumor xenograft-bearing mice and increased macrophage infiltration into tumor tissue compared with transplantation of GSCs alone. DGCs exhibited a significant increase in YAP/TAZ/TEAD activity compared with GSCs. CCN1, a transcriptional target of YAP/TAZ, was selected from the DGC signature as a candidate secreted protein involved in macrophage recruitment. In fact, CCN1 was secreted abundantly from DGCs, but not GSCs. DGCs promoted macrophage migration in vitro and macrophage infiltration into tumor tissue in vivo through secretion of CCN1. Collectively, these results demonstrate that DGCs contribute to GSC-dependent tumor progression by shaping a mesenchymal microenvironment via CCN1-mediated macrophage infiltration. This study provides new insight into the complex GBM microenvironment consisting of heterogeneous cells