Real and virtual photons in an external constant electromagnetic field of most general form

The photon behavior in an arbitrary superposition of constant magnetic and electric fields is considered on most general grounds basing on the first principles like Lorentz- gauge- charge- and parity-invariance. We make model- and approximation-independent, but still rather informative, statements about the behavior that the requirement of causal propagation prescribes to massive and massless branches of dispersion curves, and describe the way the eigenmodes are polarized. We find, as a consequence of Hermiticity in the transparency domain, that adding a smaller electric field to a strong magnetic field in parallel to the latter causes enhancement of birefringence. We find the magnetic field produced by a point electric charge far from it (a manifestation of magneto-electric phenomenon). We establish degeneracies of the polarization tensor that (under special kinematic conditions) occur due to space-time symmetries of the vacuum left after the external field is imposed.Comment: 30 pages, 1 figure, 57 equations, reference list of 38 item

Convergent Pathways in Idiopathic Autism Revealed by Time Course Transcriptomic Analysis of Patient-Derived Neurons

Potentially pathogenic alterations have been identified in individuals with autism spectrum disorders (ASDs) within a variety of key neurodevelopment genes. While this hints at a common ASD molecular etiology, gaps persist in our understanding of the neurodevelopmental mechanisms impacted by genetic variants enriched in ASD patients. Induced pluripotent stem cells (iPSCs) can model neurodevelopment in vitro, permitting the characterization of pathogenic mechanisms that manifest during corticogenesis. Taking this approach, we examined the transcriptional differences between iPSC-derived cortical neurons from patients with idiopathic ASD and unaffected controls over a 135-day course of neuronal differentiation. Our data show ASD-specific misregulation of genes involved in neuronal differentiation, axon guidance, cell migration, DNA and RNA metabolism, and neural region patterning. Furthermore, functional analysis revealed defects in neuronal migration and electrophysiological activity, providing compelling support for the transcriptome analysis data. This study reveals important and functionally validated insights into common processes altered in early neuronal development and corticogenesis and may contribute to ASD pathogenesis