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It is well known that satellite galaxies are not isotropically distributed among their host galaxies as suggested by most interpretations of the Λ cold dark matter (ΛCDM) model. One type of anisotropy recently detected in the Sloan Digital Sky Survey (and seen when examining the distribution of satellites in the Local Group and in the Centaurus group) is a tendency to be so-called lopsided. Namely, in pairs of galaxies (like Andromeda and the Milky Way) the satellites are more likely to inhabit the region in between the pair, rather than on opposing sides. Although recent studies found a similar set-up when comparing pairs of galaxies in ΛCDM simulations indicating that such a set-up is not inconsistent with ΛCDM, the origin has yet to be explained. Here we examine the origin of such lopsided set-ups by first identifying such distributions in pairs of galaxies in numerical cosmological simulations, and then tracking back the orbital trajectories of satellites (which at z = 0 display the effect). We report two main results: first, the lopsided distribution was stronger in the past and weakens towards z = 0. Secondly, the weakening of the signal is due to the interaction of satellite galaxies with the pair. Finally, we show that the z = 0 signal is driven primarily by satellites that are on first approach, who have yet to experience a ‘flyby’. This suggests that the signal seen in the observations is also dominated by dynamically young accretion events.
Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.