162 research outputs found
The geometry of recursion operators
We study the fields of endomorphisms intertwining pairs of symplectic
structures. Using these endomorphisms we prove an analogue of Moser's theorem
for simultaneous isotopies of two families of symplectic forms. We also
consider the geometric structures defined by pairs and triples of symplectic
forms for which the squares of the intertwining endomorphisms are plus or minus
the identity. For pairs of forms we recover the notions of symplectic pairs and
of holomorphic symplectic structures. For triples we recover the notion of a
hypersymplectic structure, and we also find three new structures that have not
been considered before. One of these is the symplectic formulation of
hyper-Kaehler geometry, which turns out to be a strict generalization of the
usual definition in terms of differential or Kaehler geometry.Comment: cosmetic changes only; to appear in Comm. Math. Phy
Holomorphic Factorization for a Quantum Tetrahedron
We provide a holomorphic description of the Hilbert space H(j_1,..,j_n) of
SU(2)-invariant tensors (intertwiners) and establish a holomorphically
factorized formula for the decomposition of identity in H(j_1,..,j_n).
Interestingly, the integration kernel that appears in the decomposition formula
turns out to be the n-point function of bulk/boundary dualities of string
theory. Our results provide a new interpretation for this quantity as being, in
the limit of large conformal dimensions, the exponential of the Kahler
potential of the symplectic manifold whose quantization gives H(j_1,..,j_n).
For the case n=4, the symplectic manifold in question has the interpretation of
the space of "shapes" of a geometric tetrahedron with fixed face areas, and our
results provide a description for the quantum tetrahedron in terms of
holomorphic coherent states. We describe how the holomorphic intertwiners are
related to the usual real ones by computing their overlap. The semi-classical
analysis of these overlap coefficients in the case of large spins allows us to
obtain an explicit relation between the real and holomorphic description of the
space of shapes of the tetrahedron. Our results are of direct relevance for the
subjects of loop quantum gravity and spin foams, but also add an interesting
new twist to the story of the bulk/boundary correspondence.Comment: 45 pages; published versio
Fermions in three-dimensional spinfoam quantum gravity
We study the coupling of massive fermions to the quantum mechanical dynamics
of spacetime emerging from the spinfoam approach in three dimensions. We first
recall the classical theory before constructing a spinfoam model of quantum
gravity coupled to spinors. The technique used is based on a finite expansion
in inverse fermion masses leading to the computation of the vacuum to vacuum
transition amplitude of the theory. The path integral is derived as a sum over
closed fermionic loops wrapping around the spinfoam. The effects of quantum
torsion are realised as a modification of the intertwining operators assigned
to the edges of the two-complex, in accordance with loop quantum gravity. The
creation of non-trivial curvature is modelled by a modification of the pure
gravity vertex amplitudes. The appendix contains a review of the geometrical
and algebraic structures underlying the classical coupling of fermions to three
dimensional gravity.Comment: 40 pages, 3 figures, version accepted for publication in GER
Error estimates for a mixed finite element discretization of some degenerate parabolic equations
Search for the standard model Higgs boson decaying into two photons in pp collisions at sqrt(s)=7 TeV
A search for a Higgs boson decaying into two photons is described. The
analysis is performed using a dataset recorded by the CMS experiment at the LHC
from pp collisions at a centre-of-mass energy of 7 TeV, which corresponds to an
integrated luminosity of 4.8 inverse femtobarns. Limits are set on the cross
section of the standard model Higgs boson decaying to two photons. The expected
exclusion limit at 95% confidence level is between 1.4 and 2.4 times the
standard model cross section in the mass range between 110 and 150 GeV. The
analysis of the data excludes, at 95% confidence level, the standard model
Higgs boson decaying into two photons in the mass range 128 to 132 GeV. The
largest excess of events above the expected standard model background is
observed for a Higgs boson mass hypothesis of 124 GeV with a local significance
of 3.1 sigma. The global significance of observing an excess with a local
significance greater than 3.1 sigma anywhere in the search range 110-150 GeV is
estimated to be 1.8 sigma. More data are required to ascertain the origin of
this excess.Comment: Submitted to Physics Letters
Measurement of isolated photon production in pp and PbPb collisions at sqrt(sNN) = 2.76 TeV
Isolated photon production is measured in proton-proton and lead-lead
collisions at nucleon-nucleon centre-of-mass energies of 2.76 TeV in the
pseudorapidity range |eta|<1.44 and transverse energies ET between 20 and 80
GeV with the CMS detector at the LHC. The measured ET spectra are found to be
in good agreement with next-to-leading-order perturbative QCD predictions. The
ratio of PbPb to pp isolated photon ET-differential yields, scaled by the
number of incoherent nucleon-nucleon collisions, is consistent with unity for
all PbPb reaction centralities.Comment: Submitted to Physics Letters
Testing microscopically derived descriptions of nuclear collectivity : Coulomb excitation of 22Mg
Many-body nuclear theory utilizing microscopic or chiral potentials has developed to the point that collectivity might be studied within a microscopic or ab initio framework without the use of effective charges; for example with the proper evolution of the E2 operator, or alternatively, through the use of an appropriate and manageable subset of particle–hole excitations. We present a precise determination of E2 strength in 22Mg and its mirror 22Ne by Coulomb excitation, allowing for rigorous comparisons with theory. No-core symplectic shell-model calculations were performed and agree with the new B(E2) values while in-medium similarity-renormalization-group calculations consistently underpredict the absolute strength, with the missing strength found to have both isoscalar and isovector components. The discrepancy between two microscopic models demonstrates the sensitivity of E2 strength to the choice of many-body approximation employed
Loss-of-Function Mutations in the Cell-Cycle Control Gene CDKN2A Impact on Glucose Homeostasis in Humans.
At the CDKN2A/B locus, three independent signals for type 2 diabetes risk are located in a non-coding region near CDKN2A. The disease-associated alleles have been implicated in reduced β-cell function, but the underlying mechanism remains elusive. In mice, β-cell specific loss of Cdkn2a causes hyperplasia whilst overexpression leads to diabetes, highlighting CDKN2A as a candidate effector transcript. Rare CDKN2A loss-of-function mutations are a cause of familial melanoma and offer the opportunity to determine the impact of CDKN2A haploinsufficiency on glucose homeostasis in humans. To test the hypothesis that such individuals have improved β-cell function, we performed oral and intravenous glucose tolerance tests on mutation carriers and matched controls. Compared with controls, carriers displayed increased insulin secretion, impaired insulin sensitivity and reduced hepatic insulin clearance. These results are consistent with a model whereby CDKN2A-loss affects a range of different tissues, including pancreatic β-cells and liver. To test for direct effects of CDKN2A-loss on β-cell function, we performed knockdown in a human β-cell line, EndoC-bH1. This revealed increased insulin secretion independent of proliferation. Overall, we demonstrate that CDKN2A is an important regulator of glucose homeostasis in humans, thus supporting its candidacy as an effector transcript for type 2 diabetes-associated alleles in the region
Loss-of-Function Mutations in the Cell-Cycle Control Gene CDKN2A Impact on Glucose Homeostasis in Humans.
At the CDKN2A/B locus, three independent signals for type 2 diabetes risk are located in a non-coding region near CDKN2A. The disease-associated alleles have been implicated in reduced β-cell function, but the underlying mechanism remains elusive. In mice, β-cell specific loss of Cdkn2a causes hyperplasia whilst overexpression leads to diabetes, highlighting CDKN2A as a candidate effector transcript. Rare CDKN2A loss-of-function mutations are a cause of familial melanoma and offer the opportunity to determine the impact of CDKN2A haploinsufficiency on glucose homeostasis in humans. To test the hypothesis that such individuals have improved β-cell function, we performed oral and intravenous glucose tolerance tests on mutation carriers and matched controls. Compared with controls, carriers displayed increased insulin secretion, impaired insulin sensitivity and reduced hepatic insulin clearance. These results are consistent with a model whereby CDKN2A-loss affects a range of different tissues, including pancreatic β-cells and liver. To test for direct effects of CDKN2A-loss on β-cell function, we performed knockdown in a human β-cell line, EndoC-bH1. This revealed increased insulin secretion independent of proliferation. Overall, we demonstrate that CDKN2A is an important regulator of glucose homeostasis in humans, thus supporting its candidacy as an effector transcript for type 2 diabetes-associated alleles in the region
- …