Can cosmologically-coupled mass growth of black holes solve the mass gap problem?

Observations of elliptical galaxies suggest that black holes (BHs) might serve as dark energy candidates, coupled to the expansion of the Universe. According to this hypothesis, the mass of a BH could increase as the Universe expands. BH low-mass X-ray binaries (LMXBs) in the Galactic disk were born several gigayears ago, making the coupling effect potentially significant. In this work, we calculate the evolution of BH binaries with a binary population synthesis method to examine the possible influence of cosmologically-coupled growth of BHs, if it really exists. The measured masses of the compact objects in LMXBs show a gap around $\sim 2.5-5~{\rm M_\odot}$, separating the most massive neutron stars from the least massive BHs. Our calculated results indicate that, considering the mass growth seem to (partially) account for the mass gap and the formation of compact BH LMXBs, alleviating the challenges in modeling the formation and evolution of BH LMXBs with traditional theory. However, critical observational evidence like the detection of intermediate-mass black hole binaries is required to test this hypothesis.Comment: 10 pages, 4 figures, 3 tables, accepted for publication in ApJ, comments are welcom

The Role of 7,8-Dihydroxyflavone in Preventing Dendrite Degeneration in Cortex After Moderate Traumatic Brain Injury

Our previous research showed that traumatic brain injury (TBI) induced by controlled cortical impact (CCI) not only causes massive cell death, but also results in extensive dendrite degeneration in those spared neurons in the cortex. Cell death and dendrite degeneration in the cortex may contribute to persistent cognitive, sensory, and motor dysfunction. There is still no approach available to prevent cells from death and dendrites from degeneration following TBI. When we treated the animals with a small molecule, 7,8-dihydroxyflavone (DHF) that mimics the function of brain-derived neurotrophic factor (BDNF) through provoking TrkB activation reduced dendrite swellings in the cortex. DHF treatment also prevented dendritic spine loss after TBI. Functional analysis showed that DHF improved rotarod performance on the third day after surgery. These results suggest that although DHF treatment did not significantly reduced neuron death, it prevented dendrites from degenerating and protected dendritic spines against TBI insult. Consequently, DHF can partially improve the behavior outcomes after TBI