Dynamical friction on satellite galaxies

For a rigid model satellite, Chandrasekhar's dynamical friction formula describes the orbital evolution quite accurately, when the Coulomb logarithm is chosen appropriately. However, it is not known if the orbital evolution of a real satellite with the internal degree of freedom can be described by the dynamical friction formula. We performed N-body simulation of the orbital evolution of a self-consistent satellite galaxy within a self-consistent parent galaxy. We found that the orbital decay of the simulated satellite is significantly faster than the estimate from the dynamical friction formula. The main cause of this discrepancy is that the stars stripped out of the satellite are still close to the satellite, and increase the drag force on the satellite through two mechanisms. One is the direct drag force from particles in the trailing tidal arm, a non-axisymmetric force that slows the satellite down. The other is the indirect effect that is caused by the particles remaining close to the satellite after escape. The force from them enhances the wake caused in the parent galaxy by dynamical friction, and this larger wake in turn slows the satellite down more than expected from the contribution of its bound mass. We found these two have comparable effects, and the combined effect can be as large as 20% of the total drag force on the satellite.Comment: 15 pages, 10 figures, submitted to PASJ; v2: 14 pages, 13 figures, accepted by PAS

Particle-Particle Particle-Tree: A Direct-Tree Hybrid Scheme for Collisional N-Body Simulations

In this paper, we present a new hybrid algorithm for the time integration of collisional N-body systems. In this algorithm, gravitational force between two particles is divided into short-range and long-range terms, using a distance-dependent cutoff function. The long-range interaction is calculated using the tree algorithm and integrated with the constant-timestep leapfrog integrator. The short-range term is calculated directly and integrated with the high-order Hermite scheme. We can reduce the calculation cost per orbital period from O(N^2) to O(N log N), without significantly increasing the long-term integration error. The results of our test simulations show that close encounters are integrated accurately. Long-term errors of the total energy shows random-walk behaviour, because it is dominated by the error caused by tree approximation.Comment: 22 pages, 15 figure

Missing Dwarf Problem in Galaxy Clusters

We investigated the formation and evolution of CDM subhalos in galaxy-sized and cluster-sized halos by means of N-body simulations. Our aim is to make clear what the ``dwarf galaxy problem'' is. It has been argued that the number of subhalos in simulated galaxy-sized halos is too large compared to the observed number of dwarfs in the local group, while that in cluster-sized halos is consistent with observed number of galaxies in clusters such as the Virgo cluster. We simulated nine halos with several different mass resolutions and physical scales. We found that the dependence of the cumulative number of subhalos N_c on their maximum circular velocity V_c is given by N_c \propto V_c^-3, down to the reliability limit, independent of the mass of the main halo. This implies that simulations for cluster-sized halos give too many halos with V_c ~ 140km/s or less. Previous comparisons of cluster-sized halos gave much smaller number of subhalos in this regime simply because of their limited resolution. Our result implies that any theory which attempts to resolve the missing dwarf problem should also explain the discrepancy of the simulation and observation in cluster-sized halos.Comment: 10 pages, 20 figures, submitted to PAS

Evolution of Massive Black Hole Binaries

We present the result of large-scale N-body simulations of the stellar-dynamical evolution of a massive black-hole binary at the center of a spherical galaxy. We focus on the dependence of the hardening rate on the relaxation timescale of the parent galaxy. A simple theoretical argument predicts that a binary black hole creates the ``loss cone'' around it. Once the loss cone is formed, the hardening rate is determined by the rate at which field stars diffuse into the loss cone. Therefore the hardening timescale becomes proportional to the relaxation timescale. Recent N-body simulations, however, have failed to confirm this theory and various explanations have been proposed. By performing simulations with sufficiently large N (up to $10^6$) for sufficiently long time, we found that the hardening rate does depend on N. Our result is consistent with the simple theoretical prediction that the hardening timescale is proportional to the relaxation timescale. This dependence implies that most massive black hole binaries are unlikely to merge within the Hubble time through interaction with field stars and gravitational wave radiation alone.Comment: Reviced version accepted for publication in ApJ. Scheduled to appear in the February 10, 2004 issu

Evolution of Massive Blackhole Triples I -- Equal-mass binary-single systems

We present the result of $N$-body simulations of dynamical evolution of triple massive blackhole (BH) systems in galactic nuclei. We found that in most cases two of the three BHs merge through gravitational wave (GW) radiation in the timescale much shorter than the Hubble time, before ejecting one BH through a slingshot. In order for a binary BH to merge before ejecting out the third one, it has to become highly eccentric since the gravitational wave timescale would be much longer than the Hubble time unless the eccentricity is very high. We found that two mechanisms drive the increase of the eccentricity of the binary. One is the strong binary-single BH interaction resulting in the thermalization of the eccentricity. The second is the Kozai mechanism which drives the cyclic change of the inclination and eccentricity of the inner binary of a stable hierarchical triple system. Our result implies that many of supermassive blackholes are binaries.Comment: 20 pages, 12 figure

Reconstruction of Insulin Signal Flow from Phosphoproteome and Metabolome Data

SummaryCellular homeostasis is regulated by signals through multiple molecular networks that include protein phosphorylation and metabolites. However, where and when the signal flows through a network and regulates homeostasis has not been explored. We have developed a reconstruction method for the signal flow based on time-course phosphoproteome and metabolome data, using multiple databases, and have applied it to acute action of insulin, an important hormone for metabolic homeostasis. An insulin signal flows through a network, through signaling pathways that involve 13 protein kinases, 26 phosphorylated metabolic enzymes, and 35 allosteric effectors, resulting in quantitative changes in 44 metabolites. Analysis of the network reveals that insulin induces phosphorylation and activation of liver-type phosphofructokinase 1, thereby controlling a key reaction in glycolysis. We thus provide a versatile method of reconstruction of signal flow through the network using phosphoproteome and metabolome data

Reconstruction of Insulin Signal Flow from Phosphoproteome and Metabolome Data

Cellular homeostasis is regulated by signals through multiple molecular networks that include protein phosphorylation and metabolites. However, where and when the signal flows through a network and regulates homeostasis has not been explored. We have developed a reconstruction method for the signal flow based on time-course phosphoproteome and metabolome data, using multiple databases, and have applied it to acute action of insulin, an important hormone for metabolic homeostasis. An insulin signal flows through a network, through signaling pathways that involve 13 protein kinases, 26 phosphorylated metabolic enzymes, and 35 allosteric effectors, resulting in quantitative changes in 44 metabolites. Analysis of the network reveals that insulin induces phosphorylation and activation of liver-type phosphofructokinase 1, thereby controlling a key reaction in glycolysis. We thus provide a versatile method of reconstruction of signal flow through the network using phosphoproteome and metabolome data.UTokyo Research掲載「細胞内のビッグデータから大規模ネットワークの再構築に成功」URI: http://www.u-tokyo.ac.jp/ja/utokyo-research/research-news/reconstruction-of-molecular-network-from-cellular-big-data/UTokyo Research "Reconstruction of molecular network from cellular big data" URI: http://www.u-tokyo.ac.jp/en/utokyo-research/research-news/reconstruction-of-molecular-network-from-cellular-big-data