1,860 research outputs found

    Geometry and Topology of Escape II: Homotopic Lobe Dynamics

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    We continue our study of the fractal structure of escape-time plots for chaotic maps. In the preceding paper, we showed that the escape-time plot contains regular sequences of successive escape segments, called epistrophes, which converge geometrically upon each endpoint of every escape segment. In the present paper, we use topological techniques to: (1) show that there exists a minimal required set of escape segments within the escape-time plot; (2) develop an algorithm which computes this minimal set; (3) show that the minimal set eventually displays a recursive structure governed by an ``Epistrophe Start Rule'': a new epistrophe is spawned Delta = D+1 iterates after the segment to which it converges, where D is the minimum delay time of the complex.Comment: 13 pages, 8 figures, to appear in Chaos, second of two paper

    Geometry and Topology of Escape I: Epistrophes

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    We consider a dynamical system given by an area-preserving map on a two-dimensional phase plane and consider a one-dimensional line of initial conditions within this plane. We record the number of iterates it takes a trajectory to escape from a bounded region of the plane as a function along the line of initial conditions, forming an ``escape-time plot''. For a chaotic system, this plot is in general not a smooth function, but rather has many singularities at which the escape time is infinite; these singularities form a complicated fractal set. In this article we prove the existence of regular repeated sequences, called ``epistrophes'', which occur at all levels of resolution within the escape-time plot. (The word ``epistrophe'' comes from rhetoric and means ``a repeated ending following a variable beginning''.) The epistrophes give the escape-time plot a certain self-similarity, called ``epistrophic'' self-similarity, which need not imply either strict or asymptotic self-similarity.Comment: 15 pages, 9 figures, to appear in Chaos, first of two paper

    Analytically Derived Switching-Functions For Exact H-2(+) Eigenstates

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    Electron translation factors (ETF\u27s) appropriate for slow atomic collisions may be constructed using switching functions. In this paper we derive a set of switching functions for the H2+ system by an analytical two-center decomposition of the exact molecular eigenstates. These switching functions are closely approximated by the simple form f=bη, where η is the angle variable of prolate spheroidal coordinates. For given united atom angular momentum quantum numbers (l,m), the characteristic parameter blm depends only on the quantity c2=-∊R22, where ∊ is the electronic binding energy and R the internuclear distance in a.u. The resulting parameters are in excellent agreement with those found in our earlier work by a heuristic optimization scheme based on a study of coupling matrix-element behavior for a number of H2+ states. An approximate extension to asymmetric cases (HeH2+) has also been made. Nonadiabatic couplings based on these switching functions have been used in recent close-coupling calculations for H+-H(1s) collisions and He2+-H(1s) collisions at energies 1.0-20 keV

    Accumulation of driver and passenger mutations during tumor progression

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    Major efforts to sequence cancer genomes are now occurring throughout the world. Though the emerging data from these studies are illuminating, their reconciliation with epidemiologic and clinical observations poses a major challenge. In the current study, we provide a novel mathematical model that begins to address this challenge. We model tumors as a discrete time branching process that starts with a single driver mutation and proceeds as each new driver mutation leads to a slightly increased rate of clonal expansion. Using the model, we observe tremendous variation in the rate of tumor development - providing an understanding of the heterogeneity in tumor sizes and development times that have been observed by epidemiologists and clinicians. Furthermore, the model provides a simple formula for the number of driver mutations as a function of the total number of mutations in the tumor. Finally, when applied to recent experimental data, the model allows us to calculate, for the first time, the actual selective advantage provided by typical somatic mutations in human tumors in situ. This selective advantage is surprisingly small, 0.005 +- 0.0005, and has major implications for experimental cancer research

    Differential cross sections for pion charge exchange on the proton at 27.5 MeV

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    We have measured pion single charge exchange differential cross sections on the proton at 27.5 MeV incident π−\pi^- kinetic energy in the center of momentum angular range between 0∘0^\circ and 55∘55^\circ. The extracted cross sections are compared with predictions of the standard pion-nucleon partial wave analysis and found to be in excellent agreement.Comment: ReVTeX v3.0 with aps.sty, 23 pages in e-print format, 7 PostScript Figures and 4 Tables, also available via anonymous ftp at ftp://helena.phys.virginia.edu/pub/preprints/scx.p

    The Negative Feedback-Loop between the Oncomir Mir-24-1 and Menin Modulates the Men1 Tumorigenesis by Mimicking the “Knudson’s Second Hit”

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    Multiple endocrine neoplasia type 1 (MEN1) syndrome is a rare hereditary cancer disorder characterized by tumors of the parathyroids, of the neuroendocrine cells, of the gastro-entero-pancreatic tract, of the anterior pituitary, and by non-endocrine neoplasms and lesions. MEN1 gene, a tumor suppressor gene, encodes menin protein. Loss of heterozygosity at 11q13 is typical of MEN1 tumors, in agreement with the Knudson’s two-hit hypothesis. In silico analysis with Target Scan, Miranda and Pictar-Vert softwares for the prediction of miRNA targets indicated miR-24-1 as capable to bind to the 3â€ČUTR of MEN1 mRNA. We investigated this possibility by analysis of miR-24-1 expression profiles in parathyroid adenomatous tissues from MEN1 gene mutation carriers, in their sporadic non-MEN1 counterparts, and in normal parathyroid tissue. Interestingly, the MEN1 tumorigenesis seems to be under the control of a “negative feedback loop” between miR-24-1 and menin protein, that mimics the second hit of Knudson’s hypothesis and that could buffer the effect of the stochastic factors that contribute to the onset and progression of this disease. Our data show an alternative way to MEN1 tumorigenesis and, probably, to the “two-hit dogma”. The functional significance of this regulatory mechanism in MEN1 tumorigenesis is also the basis for opening future developments of RNA antagomir(s)-based strategies in the in vivo control of tumorigenesis in MEN1 carriers
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