165 research outputs found

    A Simple Near Optimal Parallel Algorithm for Recognizing Outerplanar Graphs

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    An outerplanar graph is a graph which can be embedded in the plane so that all vertices lie on the boundary of the exterior face. In this paper, we propose a simple near optimal parallel algorithm for recognizing whether a given graph G is outerplanar in ο(log n) time using ο(nα(l, n)/log n) processors on an arbitrary-CRCW PRAM in the sense that ο(log n)×ο(nα(l, n)/log n)=ο(nα(l, n)) is almost linear with respect to n, where n is the number of vertices in G, α(l, n) is the inverse Ackermann function, which grows extremely slowly with respect to l and n [9] and l=ο(n). Although a near optimal parallel algorithm for general graphs can also be obtained by combining the algorithm in [3] with the algorithm for finding biconnected components [4] [9], our algorithm uses methods completely different from the algorithm in [3]'s, e. g., the well known st-numbering, and is much simpler than [3]'s

    文章からの化学物質名を含む単語の認識法の確立と化学物質名の選択法の検討 : 特許公開公報を用いて

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    化学物質名は,多様であり,記載法も書き手に委ねられているため自動抽出が難しく化学知識の共有化を妨げている.化学物質名を自動抽出できれば,共有化に役立つ.日本語の化学物質名を抽出するために,化学物質名をタグ付けした特許公開公報のコーパスの作成を行い,文章から形態素の切り出し,切り出した形態素の連結をすることによる化学物質名の認識法を確立した.あわせて連結した単語群から化学物質名を選択する方法の基礎的な検討,及び化学物質名と間違えやすい置換基名との選択比較も行った

    Traffic jams without bottlenecks-experimental evidence for the physical mechanism of the formation of a jam

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    A traffic jam on a highway is a very familiar phenomenon. From the physical viewpoint, the system of vehicular flow is a non-equilibrium system of interacting particles (vehicles). The collective effect of the many-particle system induces the instability of a free flow state caused by the enhancement of fluctuations, and the transition to a jamming state occurs spontaneously if the average vehicle density exceeds a certain critical value. Thus, a bottleneck is only a trigger and not the essential origin of a traffic jam. In this paper, we present the first experimental evidence that the emergence of a traffic jam is a collective phenomenon like 'dynamical' phase transitions and pattern formation in a non-equilibrium system. We have performed an experiment on a circuit to show the emergence of a jam with no bottleneck. In the initial condition, all the vehicles are moving, homogeneously distributed on the circular road, with the same velocity. The average density of the vehicles is prepared for the onset of the instability. Even a tiny fluctuation grows larger and then the homogeneous movement cannot be maintained. Finally, a jam cluster appears and propagates backward like a solitary wave with the same speed as that of a jam cluster on a highway.Sugiyamal Y., Fukui M., Kikuchi M., et al. Traffic jams without bottlenecks-experimental evidence for the physical mechanism of the formation of a jam. New Journal of Physics 10, 033001 (2008); https://doi.org/10.1088/1367-2630/10/3/033001

    Phase transition in traffic jam experiment on a circuit

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    The emergence of a traffic jam is considered to be a dynamical phase transition in a physics point of view; traffic flow becomes unstable and changes phase into a traffic jam when the car density exceeds a critical value. In order to verify this view, we have been performing a series of circuit experiments. In our previous work (2008 New J. Phys. 10 033001), we demonstrated that a traffic jam emerges even in the absence of bottlenecks at a certain high density. In this study, we performed a larger indoor circuit experiment in the Nagoya Dome in which the positions of cars were observed using a high-resolution laser scanner. Over a series of sessions at various values of density, we found that jammed flow occurred at high densities, whereas free flow was conserved at low densities. We also found indications of metastability at an intermediate density. The critical density is estimated by analyzing the fluctuations in speed and the density-flow relation. The value of this critical density is consistent with that observed on real expressways. This experiment provides strong support for physical interpretations of the emergence of traffic jams as a dynamical phase transition.Tadaki S.I., Kikuchi M., Fukui M., et al. Phase transition in traffic jam experiment on a circuit. New Journal of Physics 15, 103034 (2013); https://doi.org/10.1088/1367-2630/15/10/103034

    Neutrophil Depletion Exacerbates Pregnancy Complications, Including Placental Damage, Induced by Silica Nanoparticles in Mice

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    Recent advances in nanotechnology have led to the development of nanoparticles with innovative functions in various fields. However, the biological effects of nanoparticles—particularly those on the fetus—need to be investigated in detail, because several previous studies have shown that various nanoparticles induce pregnancy complications in mice. In this regard, our previous findings in mice suggested that the increase in peripheral neutrophil count induced by treatment with silica nanoparticles with a diameter of 70 nm (nSP70) may play a role in the associated pregnancy complications. Therefore, here, we sought to define the role of neutrophils in nSP70-induced pregnancy complications. The peripheral neutrophil count in pregnant BALB/c mice at 24 h after treatment with nSP70 was significantly higher than in saline-treated mice. In addition, maternal body weight, uterine weight, and the number of fetuses in nSP70-treated mice pretreated with anti-antibodies, which deplete neutrophils, were significantly lower than those in nSP70-treated mice pretreated with phosphate-buffered saline or isotype-matched control antibodies. Histology revealed that neutrophil depletion increased nSP70-induced placental damage from the decidua through the spongiotrophoblast layer and narrowed spiral arteries in the placentae. In addition, depletion of neutrophils augmented nSP70-induced cytotoxicity to fetal vessels, which were covered with endothelium. The rate of apoptotic cell death was significantly higher in the placentae of anti-nSP70-treated mice than in those from mice pretreated with isotype-matched control antibodies. Therefore, impairment of placental vessels and apoptotic cell death due to nSP70 exposure is exacerbated in the placentae of nSP70-treated mice pretreated with anti-antibodies. Depletion of neutrophils worsens nSP70-induced pregnancy complications in mice; this exacerbation was due to enhanced impairment of placental vessels and increased apoptotic cell death in maternal placentae. Our results provide basic information regarding the mechanism underlying silica-nanoparticle-induced pregnancy complications

    Self-Contained Induction of Neurons from Human Embryonic Stem Cells

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    BACKGROUND: Neurons and glial cells can be efficiently induced from mouse embryonic stem (ES) cells in a conditioned medium collected from rat primary-cultured astrocytes (P-ACM). However, the use of rodent primary cells for clinical applications may be hampered by limited supply and risk of contamination with xeno-proteins. METHODOLOGY/PRINCIPAL FINDINGS: We have developed an alternative method for unimpeded production of human neurons under xeno-free conditions. Initially, neural stem cells in sphere-like clusters were induced from human ES (hES) cells after being cultured in P-ACM under free-floating conditions. The resultant neural stem cells could circumferentially proliferate under subsequent adhesive culture, and selectively differentiate into neurons or astrocytes by changing the medium to P-ACM or G5, respectively. These hES cell-derived neurons and astrocytes could procure functions similar to those of primary cells. Interestingly, a conditioned medium obtained from the hES cell-derived astrocytes (ES-ACM) could successfully be used to substitute P-ACM for induction of neurons. Neurons made by this method could survive in mice brain after xeno-transplantation. CONCLUSION/SIGNIFICANCE: By inducing astrocytes from hES cells in a chemically defined medium, we could produce human neurons without the use of P-ACM. This self-serving method provides an unlimited source of human neural cells and may facilitate clinical applications of hES cells for neurological diseases
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