480 research outputs found
Constraints on Automorphic Forms of Higher Derivative Terms from Compactification
By dimensionally reducing the higher derivative corrections of
ten-dimensional IIB theory on a torus we deduce constraints on the E_{n+1}
automorphic forms that occur in d=10-n dimensions. In particular we argue that
these automorphic forms involve the representation of E_{n+1} with fundamental
weight \lambda^{n+1}, which is also the representation to which the string
charges in d dimensions belong. We also consider a similar calculation for the
reduction of higher derivative terms in eleven-dimensional M-theory.Comment: Minor corrections, to appear in JHE
Higher derivative type II string effective actions, automorphic forms and E11
By dimensionally reducing the ten-dimensional higher derivative type IIA
string theory effective action we place constraints on the automorphic forms
that appear in the effective action in lower dimensions. We propose a number of
properties of such automorphic forms and consider the prospects that E11 can
play a role in the formulation of the higher derivative string theory effective
action.Comment: 34 page
A Dynamic Model of Interactions of Ca^(2+), Calmodulin, and Catalytic Subunits of Ca^(2+)/Calmodulin-Dependent Protein Kinase II
During the acquisition of memories, influx of Ca^(2+) into the postsynaptic spine through the pores of activated N-methyl-D-aspartate-type glutamate receptors triggers processes that change the strength of excitatory synapses. The pattern of Ca^(2+) influx during the first few seconds of activity is interpreted within the Ca^(2+)-dependent signaling network such that synaptic strength is eventually either potentiated or depressed. Many of the critical signaling enzymes that control synaptic plasticity, including Ca^(2+)/calmodulin-dependent protein kinase II (CaMKII), are regulated by calmodulin, a small protein that can bind up to 4 Ca^(2+) ions. As a first step toward clarifying how the Ca^(2+)-signaling network decides between potentiation or depression, we have created a kinetic model of the interactions of Ca^(2+), calmodulin, and CaMKII that represents our best understanding of the dynamics of these interactions under conditions that resemble those in a postsynaptic spine. We constrained parameters of the model from data in the literature, or from our own measurements, and then predicted time courses of activation and autophosphorylation of CaMKII under a variety of conditions. Simulations showed that species of calmodulin with fewer than four bound Ca^(2+) play a significant role in activation of CaMKII in the physiological regime, supporting the notion that processing ofCa^(2+) signals in a spine involves competition among target enzymes for binding to unsaturated species of CaM in an environment in which the concentration of Ca^(2+) is fluctuating rapidly. Indeed, we showed that dependence of activation on the frequency of Ca^(2+) transients arises from the kinetics of interaction of fluctuating Ca^(2+) with calmodulin/CaMKII complexes. We used parameter sensitivity analysis to identify which parameters will be most beneficial to measure more carefully to improve the accuracy of predictions. This model provides a quantitative base from which to build more complex dynamic models of postsynaptic signal transduction during learning
Liquid-gas phase transition in nuclear multifragmentation
The equation of state of nuclear matter suggests that at suitable beam
energies the disassembling hot system formed in heavy ion collisions will pass
through a liquid-gas coexistence region. Searching for the signatures of the
phase transition has been a very important focal point of experimental
endeavours in heavy ion collisions, in the last fifteen years. Simultaneously
theoretical models have been developed to provide information about the
equation of state and reaction mechanisms consistent with the experimental
observables. This article is a review of this endeavour.Comment: 63 pages, 27 figures, submitted to Adv. Nucl. Phys. Some typos
corrected, minor text change
New Measurement of Parity Violation in Elastic Electron-Proton Scattering and Implications for Strange Form Factors
We have measured the parity-violating electroweak asymmetry in the elastic
scattering of polarized electrons from the proton. The result is A = -15.05 +-
0.98(stat) +- 0.56(syst) ppm at the kinematic point theta_lab = 12.3 degrees
and Q^2 = 0.477 (GeV/c)^2. The measurement implies that the value for the
strange form factor (G_E^s + 0.392 G_M^s) = 0.025 +- 0.020 +- 0.014, where the
first error is experimental and the second arises from the uncertainties in
electromagnetic form factors. This measurement is the first fixed-target parity
violation experiment that used either a `strained' GaAs photocathode to produce
highly polarized electrons or a Compton polarimeter to continuously monitor the
electron beam polarization.Comment: 8 pages, 4 figures, Tex, elsart.cls; revised version as accepted for
Phys. Lett.
Display of probability densities for data from a continuous distribution
Based on cumulative distribution functions, Fourier series expansion and
Kolmogorov tests, we present a simple method to display probability densities
for data drawn from a continuous distribution. It is often more efficient than
using histograms.Comment: 5 pages, 4 figures, presented at Computer Simulation Studies XXIV,
Athens, GA, 201
The Etiology of Multiple Sclerosis: Genetic Evidence for the Involvement of the Human Endogenous Retrovirus HERV-Fc1
We have investigated the role of human endogenous retroviruses in multiple sclerosis by analyzing the DNA of patients and controls in 4 cohorts for associations between multiple sclerosis and polymorphisms near viral restriction genes or near endogenous retroviral loci with one or more intact or almost-intact genes. We found that SNPs in the gene TRIM5 were inversely correlated with disease. Conversely, SNPs around one retroviral locus, HERV-Fc1, showed a highly significant association with disease. The latter association was limited to a narrow region that contains no other known genes. We conclude that HERV-Fc1 and TRIM5 play a role in the etiology of multiple sclerosis. If these results are confirmed, they point to new modes of treatment for multiple sclerosis
- …