19 research outputs found
Kalb-Ramond excitations in a thick-brane scenario with dilaton
We compute the full spectrum and eigenstates of the Kalb-Ramond field in a
warped non-compact Randall-Sundrum -type five-dimensional spacetime in which
the ordinary four-dimensional braneworld is represented by a sine-Gordon
soliton. This 3-brane solution is fully consistent with both the warped
gravitational field and bulk dilaton configurations. In such a background we
embed a bulk antisymmetric tensor field and obtain, after reduction, an
infinite tower of normalizable Kaluza-Klein massive components along with a
zero-mode. The low lying mass eigenstates of the Kalb-Ramond field may be
related to the axion pseudoscalar. This yields phenomenological implications on
the space of parameters, particularly on the dilaton coupling constant. Both
analytical and numerical results are given.Comment: 10 pages, 13 figures, and 2 tables. Final version to appear in The
European Physical Journal
Axion Radiation from Strings
This paper revisits the problem of the string decay contribution to the axion
cosmological energy density. We show that this contribution is proportional to
the average relative increase when axion strings decay of a certain quantity
which we define. We carry out numerical simulations of the
evolution and decay of circular and non-circular string loops, of bent strings
with ends held fixed, and of vortex-antivortex pairs in two dimensions. In the
case of string loops and of vortex-antivortex pairs, decreases by
approximately 20%. In the case of bent strings, remains constant
or increases slightly. Our results imply that the string decay contribution to
the axion energy density is of the same order of magnitude as the
well-understood contribution from vacuum realignment.Comment: 29 pages, 10 figure
Sex-ratio distorter of Drosophila simulans reduces male productivity and sperm competition ability
Synaptic distribution of the NR1, NR2A and NR2B subunits of the N-methyl-d-aspartate receptor in the rat lumbar spinal cord revealed with an antigen-unmasking technique
Missense Variants in the Histone Acetyltransferase Complex Component Gene TRRAP Cause Autism and Syndromic Intellectual Disability
Contains fulltext :
202928.pdf (publisher's version ) (Open Access)Acetylation of the lysine residues in histones and other DNA-binding proteins plays a major role in regulation of eukaryotic gene expression. This process is controlled by histone acetyltransferases (HATs/KATs) found in multiprotein complexes that are recruited to chromatin by the scaffolding subunit transformation/transcription domain-associated protein (TRRAP). TRRAP is evolutionarily conserved and is among the top five genes intolerant to missense variation. Through an international collaboration, 17 distinct de novo or apparently de novo variants were identified in TRRAP in 24 individuals. A strong genotype-phenotype correlation was observed with two distinct clinical spectra. The first is a complex, multi-systemic syndrome associated with various malformations of the brain, heart, kidneys, and genitourinary system and characterized by a wide range of intellectual functioning; a number of affected individuals have intellectual disability (ID) and markedly impaired basic life functions. Individuals with this phenotype had missense variants clustering around the c.3127G>A p.(Ala1043Thr) variant identified in five individuals. The second spectrum manifested with autism spectrum disorder (ASD) and/or ID and epilepsy. Facial dysmorphism was seen in both groups and included upslanted palpebral fissures, epicanthus, telecanthus, a wide nasal bridge and ridge, a broad and smooth philtrum, and a thin upper lip. RNA sequencing analysis of skin fibroblasts derived from affected individuals skin fibroblasts showed significant changes in the expression of several genes implicated in neuronal function and ion transport. Thus, we describe here the clinical spectrum associated with TRRAP pathogenic missense variants, and we suggest a genotype-phenotype correlation useful for clinical evaluation of the pathogenicity of the variants