We use the poor man's scaling approach to study the phase boundaries of a pair of quantum impurity models featuring a power-law density of states ρ(ε) ∝ |ε| r , either vanishing (for r > 0) or diverging (for r < 0) at the Fermi energy ε = 0, that gives rise to quantum phase transitions between local-moment and Kondo-screened phases. For the Anderson model with a pseudogap (i.e., r > 0), we find the phase boundary for (a) 0 < r < 1/2, a range over which the model exhibits interacting quantum critical points both at and away from particle-hole (p-h) symmetry, and (b) r > 1, where the phases are separated by first-order quantum phase transitions that are accessible only for broken p-h symmetry. For the p-h-symmetric Kondo model with easy-axis or easy-plane anisotropy of the impurity-band spin exchange, the phase boundary and scaling trajectories are obtained for both r > 0 and r < 0. Throughout the regime of weak-to-moderate impurity-band coupling in which poor man's scaling is expected to be valid, the approach predicts phase boundaries in excellent qualitative and good quantitative agreement with the nonperturbative numerical renormalization group, while also establishing the functional relations between model parameters along these boundaries.
Organism aging occurs at the multicellular level; however, how pro-longevity mechanisms slow down aging in different cell types remains unclear. We generated single-cell transcriptomic atlases across the lifespan ofCaenorhabditis elegansunder different pro-longevity conditions (http://mengwanglab.org/atlas). We found cell-specific, age-related changes across somatic and germ cell types and developed transcriptomic aging clocks for different tissues. These clocks enabled us to determine tissue-specific aging-slowing effects of different pro-longevity mechanisms, and identify major cell types sensitive to these regulations. Additionally, we provided a systemic view of alternative polyadenylation events in different cell types, as well as their cell-type-specific changes during aging and under different pro-longevity conditions. Together, this study provides molecular insights into how aging occurs in different cell types and how they respond to pro-longevity strategies.One sentence summarySingle-nucleus transcriptome atlas reveals tissue-specific aging patterns and longevity regulation in a multicellular organism
Proteomic analysis revealed the preservation of many proteins in the Heslington brain (which is at least 2600-year-old brain tissue uncovered within the skull excavated in 2008 from a pit in Heslington, Yorkshire, England). Five of these proteins—“main proteins”: heavy, medium, and light neurofilament proteins (NFH, NFM, and NFL), glial fibrillary acidic protein (GFAP), and myelin basic (MBP) protein—are engaged in the formation of non-amyloid protein aggregates, such as intermediate filaments and myelin sheath. We used a wide spectrum of bioinformatics tools to evaluate the prevalence of functional disorder in several related sets of proteins, such as the main proteins and their 44 interactors, all other proteins identified in the Heslington brain, as well as the entire human proteome (20,317 manually curated proteins), and 10,611 brain proteins. These analyses revealed that all five main proteins, half of their interactors and almost one third of the Heslington brain proteins are expected to be mostly disordered. Furthermore, most of the remaining Heslington brain proteins are expected to contain sizable levels of disorder. This is contrary to the expected substantial (if not complete) elimination of the disordered proteins from the Heslington brain. Therefore, it seems that the intrinsic disorder of NFH, NFM, NFL, GFAP, and MBP, their interactors, and many other proteins might play a crucial role in preserving the Heslington brain by forming tightly folded brain protein aggregates, in which different parts are glued together via the disorder-to-order transitions.
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