The boundary for quantum advantage in Gaussian boson sampling.

Identifying the boundary beyond which quantum machines provide a computational advantage over their classical counterparts is a crucial step in charting their usefulness. Gaussian boson sampling (GBS), in which photons are measured from a highly entangled Gaussian state, is a leading approach in pursuing quantum advantage. State-of-the-art GBS experiments that run in minutes would require 600 million years to simulate using the best preexisting classical algorithms. Here, we present faster classical GBS simulation methods, including speed and accuracy improvements to the calculation of loop hafnians. We test these on a ∼100,000-core supercomputer to emulate GBS experiments with up to 100 modes and up to 92 photons. This reduces the simulation time for state-of-the-art GBS experiments to several months, a nine-orders of magnitude improvement over previous estimates. Last, we introduce a distribution that is efficient to sample from classically and that passes a variety of GBS validation methods.

Evolution of late-life mortality in Drosophila melanogaster.

Aging appears to cease at late ages, when mortality rates roughly plateau in large-scale demographic studies. This anomalous plateau in late-life mortality has been explained theoretically in two ways: (1) as a strictly demographic result of heterogeneity in life-long robustness between individuals within cohorts, and (2) as an evolutionary result of the plateau in the force of natural selection after the end of reproduction. Here we test the latter theory using cohorts of Drosophila melanogaster cultured with different ages of reproduction for many generations. We show in two independent comparisons that populations that evolve with early truncation of reproduction exhibit earlier onset of mortality-rate plateaus, in conformity with evolutionary theory. In addition, we test two population genetic mechanisms that may be involved in the evolution of late-life mortality: mutation accumulation and antagonistic pleiotropy. We test mutation accumulation by crossing genetically divergent, yet demographically identical, populations, testing for hybrid vigor between the hybrid and nonhybrid parental populations. We found no difference between the hybrid and nonhybrid populations in late-life mortality rates, a result that does not support mutation accumulation as a genetic mechanism for late-life mortality, assuming mutations act recessively. Finally, we test antagonistic pleiotropy by returning replicate populations to a much earlier age of last reproduction for a short evolutionary time, testing for a rapid indirect response of late-life mortality rates. The positive results from this test support antagonistic pleiotropy as a genetic mechanism for the evolution of late-life mortality. Together these experiments comprise the first corroborations of the evolutionary theory of late-life mortality.