Relativistic Coulomb Sum Rules for (e,e′)(e,e^\prime)

A Coulomb sum rule is derived for the response of nuclei to $(e,e^\prime)$ scattering with large three-momentum transfers. Unlike the nonrelativistic formulation, the relativistic Coulomb sum is restricted to spacelike four-momenta for the most direct connection with experiments; an immediate consequence is that excitations involving antinucleons, e.g., $N{\bar N}$ pair production, are approximately eliminated from the sum rule. Relativistic recoil and Fermi motion of target nucleons are correctly incorporated. The sum rule decomposes into one- and two-body parts, with correlation information in the second. The one-body part requires information on the nucleon momentum distribution function, which is incorporated by a moment expansion method. The sum rule given through the second moment (RCSR-II) is tested in the Fermi gas model, and is shown to be sufficiently accurate for applications to data.Comment: 32 pages (LaTeX), 4 postscript figures available from the author

Inelastic nucleon contributions in (e,e′)(e,e^\prime) nuclear response functions

We estimate the contribution of inelastic nucleon excitations to the $(e,e^\prime)$ inclusive cross section in the CEBAF kinematic range. Calculations are based upon parameterizations of the nucleon structure functions measured at SLAC. Nuclear binding effects are included in a vector-scalar field theory, and are assumed have a minimal effect on the nucleon excitation spectrum. We find that for q\lsim 1 GeV the elastic and inelastic nucleon contributions to the nuclear response functions are comparable, and can be separated, but with roughly a factor of two uncertainty in the latter from the extrapolation from data. In contrast, for q\rsim 2 GeV this uncertainty is greatly reduced but the elastic nucleon contribution is heavily dominated by the inelastic nucleon background.Comment: 20 pages, 7 figures available from the authors at Department of Physics and Astronomy, University of Rochester, Rochester NY 1462

Wolbachia-Mediated Male Killing Is Associated with Defective Chromatin Remodeling

Male killing, induced by different bacterial taxa of maternally inherited microorganisms, resulting in highly distorted female-biased sex-ratios, is a common phenomenon among arthropods. Some strains of the endosymbiont bacteria Wolbachia have been shown to induce this phenotype in particular insect hosts. High altitude populations of Drosophila bifasciata infected with Wolbachia show selective male killing during embryonic development. However, since this was first reported, circa 60 years ago, the interaction between Wolbachia and its host has remained unclear. Herein we show that D. bifasciata male embryos display defective chromatin remodeling, improper chromatid segregation and chromosome bridging, as well as abnormal mitotic spindles and gradual loss of their centrosomes. These defects occur at different times in the early development of male embryos leading to death during early nuclear division cycles or large defective areas of the cellular blastoderm, culminating in abnormal embryos that die before eclosion. We propose that Wolbachia affects the development of male embryos by specifically targeting male chromatin remodeling and thus disturbing mitotic spindle assembly and chromosome behavior. These are the first observations that demonstrate fundamental aspects of the cytological mechanism of male killing and represent a solid base for further molecular studies of this phenomenon

Journal of Computational Neuroscience 6, 263–277 (1999) c ○ 1999 Kluwer Academic Publishers. Manufactured in The Netherlands. Computational Rules for Chemotaxis in the Nematode C. elegans

Abstract. We derive a linear neural network model of the chemotaxis control circuit in the nematode Caenorhabditis elegans and demonstrate that this model is capable of producing nematodelike chemotaxis. By expanding the analytic solution for the network output in time-derivatives of the network input, we extract simple computational rules that reveal how the model network controls chemotaxis. Based on these rules we find that optimized linear networks typically control chemotaxis by computing the first time-derivative of the chemical concentration and modulating the body turning rate in response to this derivative. We argue that this is consistent with behavioral studies and a plausible mechanism for at least one component of chemotaxis in real nematodes