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Abstract An important parameter in the theory of hot accretion flows around black holes is δ , which describes the fraction of “viscously” dissipated energy in the accretion flow that goes directly into heating electrons. For a given mass accretion rate, the radiative efficiency of a hot accretion flow is determined by δ . Unfortunately, the value of δ is hard to determine from first principles. The recent Event Horizon Telescope Collaboration (EHTC) results on M87* and Sgr A* provide us with a different way of constraining δ . By combining the mass accretion rates in M87* and Sgr A* estimated by the EHTC with the measured bolometric luminosities of the two sources, we derive good constraints on the radiative efficiencies of the respective accretion flows. In parallel, we use a theoretical model of hot magnetically arrested disks (MADs) to calculate the expected radiative efficiency as a function of δ (and accretion rate). By comparing the EHTC-derived radiative efficiencies with the theoretical results from MAD models, we find that Sgr A* requires δ ≳ 0.3. A similar comparison in the case of M87* gives inconclusive results as there is still a large uncertainty in the accretion rate in this source. 

Alzheimer’s Disease (AD) is a neuroinflammatory disease characterized partly by the inability to clear, and subsequent build-up, of amyloid-beta (Aβ). AD has a bi-directional relationship with circadian disruption (CD) with sleep disturbances starting years before disease onset. However, the molecular mechanism underlying the relationship of CD and AD has not been elucidated. Myeloid-based phagocytosis, a key component in the metabolism of Aβ, is circadianly-regulated, presenting a potential link between CD and AD. In this work, we revealed that the phagocytosis of Aβ42 undergoes a daily circadian oscillation. We found the circadian timing of global heparan sulfate proteoglycan (HSPG) biosynthesis was the molecular timer for the clock-controlled phagocytosis of Aβ and that both HSPG binding and aggregation may play a role in this oscillation. These data highlight that circadian regulation in immune cells may play a role in the intricate relationship between the circadian clock and AD. 

In budding yeast, the transcription factors SBF and MBF activate a large program of gene expression in late G1 phase that underlies commitment to cell division, termed Start. SBF/MBF are limiting with respect to target promoters in small G1 phase cells and accumulate as cells grow, raising the questions of how SBF/MBF are dynamically distributed across the G1/S regulon and how this impacts the Start transition. Super-resolution Photo-Activatable Localization Microscopy (PALM) mapping of the static positions of SBF/MBF subunits in fixed cells revealed each transcription factor was organized into discrete clusters containing approximately eight copies regardless of cell size and that the total number of clusters increased as cells grew through G1 phase. Stochastic modeling using reasonable biophysical parameters recapitulated growth-dependent SBF/MBF clustering and predicted TF dynamics that were confirmed in live cell PALM experiments. This spatio-temporal organization of SBF/MBF may help coordinate activation of G1/S regulon and the Start transition.