RESUMEN
For dark matter to be detectable with gravitational waves from binary black holes, it must reach higher than average densities in their vicinity. In the case of light (wavelike) dark matter, the density of dark matter between the binary can be significantly enhanced by accretion from the surrounding environment. Here we show that the resulting dephasing effect on the last ten orbits of an equal mass binary is maximized when the Compton wavelength of the scalar particle is comparable to the orbital separation, 2π/µâ¼d. The phenomenology of the effect is different from the channels that are usually discussed, where dynamical friction (along the orbital path) and radiation of energy and angular momentum drive the dephasing, and is rather dominated by the radial force (the spacetime curvature in the radial direction) towards the overdensity between the black holes. While our numerical studies limit us to scales of the same order, this effect may persist at larger separations and/or particle masses, playing a significant role in the merger history of binaries.
RESUMEN
For the first time we analyze gravitational-wave strain data using waveforms constructed from strong gravity simulations of cosmic string loops collapsing to Schwarzschild black holes; a previously unconsidered source. Since the expected signal is dominated by a black-hole ringdown, it can mimic the observed gravitational waves from high-mass binary black hole mergers. To illustrate this, we consider GW190521, a short duration gravitational-wave event observed in the third LIGO-Virgo-KAGRA observing run. We show that describing this event as a collapsing cosmic string loop is favored over previous cosmic string analyses by an approximate log Bayes factor of 22. The binary black hole hypothesis is still preferred, mostly because the cosmic string remnant is nonspinning. It remains an open question whether a spinning remnant could form from loops with angular momentum, but if possible, it would likely bring into contention the binary black hole preference. Finally, we suggest that searches for ringdown-only waveforms would be a viable approach for identifying collapsing cosmic string events and estimating their event rate. This Letter opens up an important new direction for the cosmic-string and gravitational-wave communities.
RESUMEN
NR5A1/SF-1 (Steroidogenic factor-1) variants may cause mild to severe differences of sex development (DSD) or may be found in healthy carriers. The NR5A1/SF-1 c.437G>C/p.Gly146Ala variant is common in individuals with a DSD and has been suggested to act as a susceptibility factor for adrenal disease or cryptorchidism. Since the allele frequency is high in the general population, and the functional testing of the p.Gly146Ala variant revealed inconclusive results, the disease-causing effect of this variant has been questioned. However, a role as a disease modifier is still possible given that oligogenic inheritance has been described in patients with NR5A1/SF-1 variants. Therefore, we performed next generation sequencing (NGS) in 13 DSD individuals harboring the NR5A1/SF-1 p.Gly146Ala variant to search for other DSD-causing variants and clarify the function of this variant for the phenotype of the carriers. Panel and whole-exome sequencing was performed, and data were analyzed with a filtering algorithm for detecting variants in NR5A1- and DSD-related genes. The phenotype of the studied individuals ranged from scrotal hypospadias and ambiguous genitalia in 46,XY DSD to opposite sex in both 46,XY and 46,XX. In nine subjects we identified either a clearly pathogenic DSD gene variant (e.g. in AR) or one to four potentially deleterious variants that likely explain the observed phenotype alone (e.g. in FGFR3, CHD7). Our study shows that most individuals carrying the NR5A1/SF-1 p.Gly146Ala variant, harbor at least one other deleterious gene variant which can explain the DSD phenotype. This finding confirms that the NR5A1/SF-1 p.Gly146Ala variant may not contribute to the pathogenesis of DSD and qualifies as a benign polymorphism. Thus, individuals, in whom the NR5A1/SF-1 p.Gly146Ala gene variant has been identified as the underlying genetic cause for their DSD in the past, should be re-evaluated with a NGS method to reveal the real genetic diagnosis.
