Gravitational Phase Operator and Cosmic Strings

A quantum equivalence principle is formulated by means of a gravitational phase operator which is an element of the Poincare group. This is applied to the spinning cosmic string which suggests that it may (but not necessarily) contain gravitational torsion. A new exact solution of the Einstein- Cartan-Sciama-Kibble equations for the gravitational field with torsion is obtained everywhere for a cosmic string with uniform energy density, spin density and flux. A novel effect due to the quantized gravitational field of the cosmic string on the wave function of a particle outside the string is used to argue that spacetime points are not meaningful in quantum gravity.Comment: 22 pages, to be published Phys. Rev. D. Some minor changes have been made and a reference has been added to the paper of D.V. Gal'tsov and P.S. Letelier, Phys. Rev. D 47 (1993) 4273, which first contained the metric (2.2) external to the cosmic string. The present paper extends this solution to a regular solution inside the string as wel

Cosmic optical activity in the spacetime of a scalar-tensor screwed cosmic string

Measurements of radio emission from distant galaxies and quasars verify that the polarization vectors of these radiations are not randomly oriented as naturally expected. This peculiar phenomenon suggests that the spacetime intervening between the source and observer may be exhibiting some sort of optical activity, the origin of which is not known. In the present paper we provide a plausible explanation to this phenomenon by investigating the r\^ole played by a Chern-Simons-like term in the background of an ordinary or superconducting screwed cosmic string in a scalar-tensor gravity. We discuss the possibility that the excess in polarization of the light from radio-galaxies and quasars can be understood as if the electromagnetic waves emitted by these cosmic objects interact with a scalar-tensor screwed cosmic string through a Chern-Simons coupling. We use current astronomical data to constrain possible values for the coupling constant of this theory, and show that it turns out to be: $\lambda \sim 10^{-26}$ eV, which is two orders of magnitude larger than in string-inspired theories.Comment: Revised version, to appear in Phys. Rev.

High-Throughput Sequencing of mGluR Signaling Pathway Genes Reveals Enrichment of Rare Variants in Autism

Identification of common molecular pathways affected by genetic variation in autism is important for understanding disease pathogenesis and devising effective therapies. Here, we test the hypothesis that rare genetic variation in the metabotropic glutamate-receptor (mGluR) signaling pathway contributes to autism susceptibility. Single-nucleotide variants in genes encoding components of the mGluR signaling pathway were identified by high-throughput multiplex sequencing of pooled samples from 290 non-syndromic autism cases and 300 ethnically matched controls on two independent next-generation platforms. This analysis revealed significant enrichment of rare functional variants in the mGluR pathway in autism cases. Higher burdens of rare, potentially deleterious variants were identified in autism cases for three pathway genes previously implicated in syndromic autism spectrum disorder, TSC1, TSC2, and SHANK3, suggesting that genetic variation in these genes also contributes to risk for non-syndromic autism. In addition, our analysis identified HOMER1, which encodes a postsynaptic density-localized scaffolding protein that interacts with Shank3 to regulate mGluR activity, as a novel autism-risk gene. Rare, potentially deleterious HOMER1 variants identified uniquely in the autism population affected functionally important protein regions or regulatory sequences and co-segregated closely with autism among children of affected families. We also identified rare ASD-associated coding variants predicted to have damaging effects on components of the Ras/MAPK cascade. Collectively, these findings suggest that altered signaling downstream of mGluRs contributes to the pathogenesis of non-syndromic autism