The relaxation of few-body quantum systems can strongly depend on the initial state when the system’s semiclassical phase space is mixed; i.e., regions of chaotic motion coexist with regular islands. ...In recent years, there has been much effort to understand the process of thermalization in strongly interacting quantum systems that often lack an obvious semiclassical limit. The time-dependent variational principle (TDVP) allows one to systematically derive an effective classical (nonlinear) dynamical system by projecting unitary many-body dynamics onto a manifold of weakly entangled variational states. We demonstrate that such dynamical systems generally possess mixed phase space. When TDVP errors are small, the mixed phase space leaves a footprint on the exact dynamics of the quantum model. For example, when the system is initialized in a state belonging to a stable periodic orbit or the surrounding regular region, it exhibits persistent many-body quantum revivals. As a proof of principle, we identify new types of “quantum many-body scars,” i.e., initial states that lead to long-time oscillations in a model of interacting Rydberg atoms in one and two dimensions. Intriguingly, the initial states that give rise to most robust revivals are typically entangled states. On the other hand, even when TDVP errors are large, as in the thermalizing tilted-field Ising model, initializing the system in a regular region of phase space leads to a surprising slowdown of thermalization. Our work establishes TDVP as a method for identifying interacting quantum systems with anomalous dynamics in arbitrary dimensions. Moreover, the mixed phase space classical variational equations allow one to find slowly thermalizing initial conditions in interacting models. Our results shed light on a link between classical and quantum chaos, pointing toward possible extensions of the classical Kolmogorov-Arnold-Moser theorem to quantum systems.
The thermodynamic description of many-particle systems rests on the assumption of ergodicity, the ability of a system to explore all allowed configurations in the phase space. Recent studies on ...many-body localization have revealed the existence of systems that strongly violate ergodicity in the presence of quenched disorder. Here, we demonstrate that ergodicity can be weakly broken by a different mechanism, arising from the presence of special eigenstates in the many-body spectrum that are reminiscent of quantum scars in chaotic non-interacting systems. In the single-particle case, quantum scars correspond to wavefunctions that concentrate in the vicinity of unstable periodic classical trajectories. We show that many-body scars appear in the Fibonacci chain, a model with a constrained local Hilbert space that has recently been experimentally realized in a Rydberg-atom quantum simulator. The quantum scarred eigenstates are embedded throughout the otherwise thermalizing many-body spectrum but lead to direct experimental signatures, as we show for periodic recurrences that reproduce those observed in the experiment. Our results suggest that scarred many-body bands give rise to a new universality class of quantum dynamics, opening up opportunities for the creation of novel states with long-lived coherence in systems that are now experimentally realizable.
Recent realization of a kinetically constrained chain of Rydberg atoms by Bernien et al., Nature (London) 551, 579 (2017) resulted in the observation of unusual revivals in the many-body quantum ...dynamics. In our previous work C. J. Turner et al., Nat. Phys. 14, 745 (2018), such dynamics was attributed to the existence of “quantum scarred” eigenstates in the many-body spectrum of the experimentally realized model. Here, we present a detailed study of the eigenstate properties of the same model. We find that the majority of the eigenstates exhibit anomalous thermalization: the observable expectation values converge to their Gibbs ensemble values, but parametrically slower compared to the predictions of the eigenstate thermalization hypothesis (ETH). Amidst the thermalizing spectrum, we identify nonergodic eigenstates that strongly violate the ETH, whose number grows polynomially with system size. Previously, the same eigenstates were identified via large overlaps with certain product states, and were used to explain the revivals observed in experiment. Here, we find that these eigenstates, in addition to highly atypical expectation values of local observables, also exhibit subthermal entanglement entropy that scales logarithmically with the system size. Moreover, we identify an additional class of quantum scarred eigenstates, and discuss their manifestations in the dynamics starting from initial product states. We use forward scattering approximation to describe the structure and physical properties of quantum scarred eigenstates. Finally, we discuss the stability of quantum scars to various perturbations. We observe that quantum scars remain robust when the introduced perturbation is compatible with the forward scattering approximation. In contrast, the perturbations which most efficiently destroy quantum scars also lead to the restoration of “canonical” thermalization.
The optimal placement of turbines in a wind farm is critical to the maximization of power production. In this paper, we develop a new mathematical programming approach for wind farm layout ...optimization. We use Jensen's wake decay model to represent multi-turbine wake effects. We develop mixed integer linear and quadratic optimization formulations and apply them to several example layout cases in the literature. Compared to previous approaches, our models produce layouts that tend to be more symmetric and that generate slightly more power. Our formulations solve quickly, allowing a decision maker to efficiently explore the impact of different turbine densities in a wind farm.
•We develop a new math programming approach for wind farm layout optimization.•We use Jensen's wake decay model to represent multi-turbine wake effects.•We apply our models to several example layout cases in the literature.•Our layouts tend to be more symmetric and generate slightly more power.•Our models solve quickly, allowing exploration of different turbine densities.
Abstract
We present the star cluster catalogues for 17 dwarf and irregular galaxies in the HST Treasury Program ‘Legacy ExtraGalactic UV Survey’ (LEGUS). Cluster identification and photometry in this ...sub-sample are similar to that of the entire LEGUS sample, but special methods were developed to provide robust catalogues with accurate fluxes due to low cluster statistics. The colours and ages are largely consistent for two widely used aperture corrections, but a significant fraction of the clusters are more compact than the average training cluster. However, the ensemble luminosity, mass, and age distributions are consistent suggesting that the systematics between the two methods are less than the random errors. When compared with the clusters from previous dwarf galaxy samples, we find that the LEGUS catalogues are more complete and provide more accurate total fluxes. Combining all clusters into a composite dwarf galaxy, we find that the luminosity and mass functions can be described by a power law with the canonical index of −2 independent of age and global SFR binning. The age distribution declines as a power law, with an index of ≈− 0.80 ± 0.15, independent of cluster mass and global SFR binning. This decline of clusters is dominated by cluster disruption since the combined star formation histories and integrated-light SFRs are both approximately constant over the last few hundred Myr. Finally, we find little evidence for an upper-mass cut-off (<2σ) in the composite cluster mass function, and can rule out a truncation mass below ≈104.5M⊙ but cannot rule out the existence of a truncation at higher masses.
Sirolimus is a potent antiproliferative agent used clinically to prevent renal allograft rejection. However, little is known about the effects of maintenance immunosuppressive agents on the immune ...response to potentially protective vaccines. Here we show that sirolimus paradoxically increases the magnitude and quality of the CD8+ T‐cell response to vaccinia vaccination in nonhuman primates, fostering more robust recall responses compared to untreated and tacrolimus‐treated controls. Enhancement of both the central and effector memory compartments of the vaccinia‐specific CD8+ T‐cell response was observed. These data elucidate new mechanistic characteristics of sirolimus and suggest immune applications extending beyond its role as an immunosuppressant.
The authors show that sirolimus paradoxically enhances CD8+ T cell responses in non‐human primates, fostering more robust recall responses compared to untreated and tacrolimus‐treated controls, and suggesting immune applications extending beyond its role as an immunosuppressant.
We report the first detection of tetrodotoxins (TTX) in European bivalve shellfish. We demonstrate that TTX is present within the temperate waters of the United Kingdom, along the English Channel, ...and can accumulate in filter-feeding molluscs. The toxin is heat-stable and thus it cannot be eliminated during cooking. While quantified concentrations were low in comparison to published minimum lethal doses for humans, the results demonstrate that the risk to shellfish consumers should not be discarded.
ABSTRACT
The morphology of H ii regions around young star clusters provides insight into the time-scales and physical processes that clear a cluster’s natal gas. We study ∼700 young clusters (≤10 ...Myr) in three nearby spiral galaxies (NGC 7793, NGC 4395, and NGC 1313) using Hubble Space Telescope (HST) imaging from LEGUS (Legacy ExtraGalactic Ultraviolet Survey). Clusters are classified by their H α morphology (concentrated, partially exposed, no-emission) and whether they have neighbouring clusters (which could affect the clearing time-scales). Through visual inspection of the HST images, and analysis of ages, reddenings, and stellar masses from spectral energy distributions fitting, together with the (U− B), (V − I) colours, we find (1) the median ages indicate a progression from concentrated (∼3 Myr), to partially exposed (∼4 Myr), to no H α emission (>5 Myr), consistent with the expected temporal evolution of H ii regions and previous results. However, (2) similarities in the age distributions for clusters with concentrated and partially exposed H α morphologies imply a short time-scale for gas clearing (≲1 Myr). Also, (3) our cluster sample’s median mass is ∼1000 M⊙, and a significant fraction ($\sim 20{{\ \rm per\ cent}}$) contain one or more bright red sources (presumably supergiants), which can mimic reddening effects. Finally, (4) the median E(B − V) values for clusters with concentrated H α and those without H α emission appear to be more similar than expected (∼0.18 versus ∼0.14, respectively), but when accounting for stochastic effects, clusters without H α emission are less reddened. To mitigate stochastic effects, we experiment with synthesizing more massive clusters by stacking fluxes of clusters within each H α morphological class. Composite isolated clusters also reveal a colour and age progression for H α morphological classes, consistent with analysis of the individual clusters.
Skeletal muscle tissue demonstrates global hypermethylation with age. However, methylome changes across the time-course of differentiation in aged human muscle derived cells, and larger coverage ...arrays in aged muscle tissue have not been undertaken. Using 850K DNA methylation arrays we compared the methylomes of young (27 ± 4.4 years) and aged (83 ± 4 years) human skeletal muscle and that of young/aged heterogenous muscle-derived human primary cells (HDMCs) over several time points of differentiation (0, 72 h, 7, 10 days). Aged muscle tissue was hypermethylated compared with young tissue, enriched for; pathways-in-cancer (including; focal adhesion, MAPK signaling, PI3K-Akt-mTOR signaling, p53 signaling, Jak-STAT signaling, TGF-beta and notch signaling), rap1-signaling, axon-guidance and hippo-signalling. Aged cells also demonstrated a hypermethylated profile in pathways; axon-guidance, adherens-junction and calcium-signaling, particularly at later timepoints of myotube formation, corresponding with reduced morphological differentiation and reductions in MyoD/Myogenin gene expression compared with young cells. While young cells showed little alterations in DNA methylation during differentiation, aged cells demonstrated extensive and significantly altered DNA methylation, particularly at 7 days of differentiation and most notably in focal adhesion and PI3K-AKT signalling pathways. While the methylomes were vastly different between muscle tissue and HDMCs, we identified a small number of CpG sites showing a hypermethylated state with age, in both muscle tissue and cells on genes KIF15, DYRK2, FHL2, MRPS33, ABCA17P. Most notably, differential methylation analysis of chromosomal regions identified three locations containing enrichment of 6-8 CpGs in the HOX family of genes altered with age. With HOXD10, HOXD9, HOXD8, HOXA3, HOXC9, HOXB1, HOXB3, HOXC-AS2 and HOXC10 all hypermethylated in aged tissue. In aged cells the same HOX genes (and additionally HOXC-AS3) displayed the most variable methylation at 7 days of differentiation versus young cells, with HOXD8, HOXC9, HOXB1 and HOXC-AS3 hypermethylated and HOXC10 and HOXC-AS2 hypomethylated. We also determined that there was an inverse relationship between DNA methylation and gene expression for HOXB1, HOXA3 and HOXC-AS3. Finally, increased physical activity in young adults was associated with oppositely regulating HOXB1 and HOXA3 methylation compared with age. Overall, we demonstrate that a considerable number of HOX genes are differentially epigenetically regulated in aged human skeletal muscle and HDMCs and increased physical activity may help prevent age-related epigenetic changes in these HOX genes.
DNA methylation, through 5-methyl- and 5-hydroxymethylcytosine (5mC and 5hmC), is considered to be one of the principal interfaces between the genome and our environment, and it helps explain ...phenotypic variations in human populations. Initial reports of large differences in methylation level in genomic regulatory regions, coupled with clear gene expression data in both imprinted genes and malignant diseases, provided easily dissected molecular mechanisms for switching genes on or off. However, a more subtle process is becoming evident, where small (<10 %) changes to intermediate methylation levels are associated with complex disease phenotypes. This has resulted in two clear methylation paradigms. The latter "subtle change" paradigm is rapidly becoming the epigenetic hallmark of complex disease phenotypes, although we are currently hampered by a lack of data addressing the true biological significance and meaning of these small differences. Our initial expectation of rapidly identifying mechanisms linking environmental exposure to a disease phenotype led to numerous observational/association studies being performed. Although this expectation remains unmet, there is now a growing body of literature on specific genes, suggesting wide ranging transcriptional and translational consequences of such subtle methylation changes. Data from the glucocorticoid receptor (NR3C1) has shown that a complex interplay between DNA methylation, extensive 5'UTR splicing, and microvariability gives rise to the overall level and relative distribution of total and N-terminal protein isoforms generated. Additionally, the presence of multiple AUG translation initiation codons throughout the complete, processed mRNA enables translation variability, hereby enhancing the translational isoforms and the resulting protein isoform diversity, providing a clear link between small changes in DNA methylation and significant changes in protein isoforms and cellular locations. Methylation changes in the NR3C1 CpG island alters the NR3C1 transcription and eventually protein isoforms in the tissues, resulting in subtle but visible physiological variability. This review addresses the current pathophysiological and clinical associations of such characteristically small DNA methylation changes, the ever-growing roles of DNA methylation and the evidence available, particularly from the glucocorticoid receptor of the cascade of events initiated by such subtle methylation changes, as well as addressing the underlying question as to what represents a genuine biologically significant difference in methylation.
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