The Peak of the Fallback Rate from Tidal Disruption Events: Dependence on Stellar Type

A star completely destroyed in a tidal disruption event (TDE) ignites a luminous flare that is powered by the fallback of tidally stripped debris to a supermassive black hole (SMBH) of mass $M_{\bullet}$. We analyze two estimates for the peak fallback rate in a TDE, one being the "frozen-in" model, which predicts a strong dependence of the time to peak fallback rate, $t_{\rm peak}$, on both stellar mass and age, with $15\textrm{ days} \lesssim t_{\rm peak} \lesssim 10$ yr for main sequence stars with masses $0.2\le M_{\star}/M_{\odot} \le 5$ and $M_{\bullet} = 10^6M_{\odot}$. The second estimate, which postulates that the star is completely destroyed when tides dominate the maximum stellar self-gravity, predicts that $t_{\rm peak}$ is very weakly dependent on stellar type, with $t_{\rm peak} = \left(23.2\pm4.0\textrm{ days}\right)\left(M_{\bullet}/10^6M_{\odot}\right)^{1/2}$ for $0.2\le M_{\star}/M_{\odot} \le 5$, while $t_{\rm peak} = \left(29.8\pm3.6\textrm{ days}\right)\left(M_{\bullet}/10^6M_{\odot}\right)^{1/2}$ for a Kroupa initial mass function truncated at $1.5 M_{\odot}$. This second estimate also agrees closely with hydrodynamical simulations, while the frozen-in model is discrepant by orders of magnitude. We conclude that (1) the time to peak luminosity in complete TDEs is almost exclusively determined by SMBH mass, and (2) massive-star TDEs power the largest accretion luminosities. Consequently, (a) decades-long extra-galactic outbursts cannot be powered by complete TDEs, including massive-star disruptions, and (b) the most highly super-Eddington TDEs are powered by the complete disruption of massive stars, which -- if responsible for producing jetted TDEs -- would explain the rarity of jetted TDEs and their preference for young and star-forming host galaxies.Comment: 10 pages, 4 figures, ApJL accepte

The Peak of the Fallback Rate from Tidal Disruption Events: Dependence on Stellar Type

A star completely destroyed in a tidal disruption event (TDE) ignites a luminous flare that is powered by the fallback of tidally stripped debris to a supermassive black hole (SMBH) of mass M•. We analyze two estimates for the peak fallback rate in a TDE, one being the “frozen-in” model, which predicts a strong dependence of the time to peak fallback rate, tpeak, on both stellar mass and age, with 15 days ≲ tpeak ≲ 10 yr for main sequence stars with masses 0.2 ≤ M⋆/M⊙ ≤ 5 and M• = 106M⊙. The second estimate, which postulates that the star is completely destroyed when tides dominate the maximum stellar self-gravity, predicts that tpeak is very weakly dependent on stellar type, with t MM peak • = (23.2 +4.0 days) (M./10 6M⊙) 1/2 for 0.2 ≤ M⋆/M⊙ ≤ 5, while tpeak = (29.8 +3.6 days) (M./10 6M⊙) 1/2 for a Kroupa initial mass function truncated at 1.5M⊙. This second estimate also agrees closely with hydrodynamical simulations, while the frozen-in model is discrepant by orders of magnitude. We conclude that (1) the time to peak luminosity in complete TDEs is almost exclusively determined by SMBH mass, and (2) massive-star TDEs power the largest accretion luminosities. Consequently, (a) decades-long extra-galactic outbursts cannot be powered by complete TDEs, including massive-star disruptions, and (b) the most highly super-Eddington TDEs are powered by the complete disruption of massive stars, which—if responsible for producing jetted TDEs—would explain the rarity of jetted TDEs and their preference for young and star-forming host galaxies

Associative DNA methylation changes in children with prenatal alcohol exposure

Aim: Prenatal alcohol exposure (PAE) can cause fetal alcohol spectrum disorders (FASD). Previously, we assessed PAE in brain tissue from mouse models, however whether these changes are present in humans remains unknown. Materials & methods: In this report, we show some identical changes in DNA methylation in the buccal swabs of six children with FASD using the 450K array. Results: The changes occur in genes related to protocadherins, glutamatergic synapses, and hippo signaling. The results were found to be similar in another heterogeneous replication group of six FASD children. Conclusion: The replicated results suggest that children born with FASD have unique DNA methylation defects that can be influenced by sex and medication exposure. Ultimately, with future clinical development, assessment of DNA methylation from buccal swabs can provide a novel strategy for the diagnosis of FASD