The stranglehold of low temperatures on fascinating quantum phenomena in one-dimensional quantum magnets has been challenged recently by the discovery of anomalous spin transport at high temperatures. Whereas both regimes have been investigated separately, no study has attempted to reconcile them. For instance, the paradigmatic quantum Heisenberg spin-1/2 chain falls at low temperature within the Tomonaga-Luttinger liquid framework, while its high-temperature dynamics is superdiffusive and relates to the Kardar-Parisi-Zhang universality class in 1+1 dimensions. This Letter aims at reconciling the two regimes. Building on large-scale matrix product state simulations, we find that they are connected by a temperature-dependent spatiotemporal crossover. As the temperature T is reduced, we show that the onset of superdiffusion takes place at longer length and timescales ∝1/T. This prediction has direct consequences for experiments including nuclear magnetic resonance: it is consistent with earlier measurements on the nearly ideal Heisenberg S=1/2 chain compound Sr_{2}CuO_{3}, yet calls for new and dedicated experiments.

The stranglehold of low temperatures on fascinating quantum phenomena in one-dimensional quantum magnets has been challenged recently by the discovery of anomalous spin transport at high temperatures. Whereas both regimes have been investigated separately, no study has attempted to reconcile them. For instance, the paradigmatic quantum Heisenberg spin-$1/2$ chain falls at low temperature within the Tomonaga-Luttinger liquid framework, while its high-temperature dynamics is superdiffusive and relates to the Kardar-Parisi-Zhang universality class in $1+1$ dimensions. This Letter aims at reconciling the two regimes. Building on large-scale matrix product state simulations, we find that they are connected by a temperature-dependent spatiotemporal crossover. As the temperature $T$ is reduced, we show that the onset of superdiffusion takes place at longer length and timescales $\propto 1/T$. This prediction has direct consequences for experiments including nuclear magnetic resonance: it is consistent with earlier measurements on the nearly ideal Heisenberg $S=1/2$ chain compound Sr$_2$CuO$_3$, yet calls for new and dedicated experiments.

Spectral probes, such as neutron scattering, are crucial for characterizing excitations in quantum many-body systems and the properties of quantum materials. Among the most elusive phases of matter are quantum spin liquids, which have no long-range order even at zero temperature and host exotic fractionalized excitations with nontrivial statistics. These phases can occur in frustrated quantum magnets, such as the paradigmatic Heisenberg model with nearest- and next-nearest-neighbor exchange interactions on the triangular lattice, the so-called J1-J2 model. In this work, we compute the spectral function using large-scale matrix product state simulations across the three different phases of this model's phase diagram, including a quantum spin-liquid phase at intermediate J2/J1. Despite a plethora of theoretical and experimental studies, the exact nature of this phase is still contested, with the dominant candidates being a gapped Z2, a gapless U(1) Dirac, and a spinon Fermi surface quantum spin-liquid state. We find a V-shaped spectrum near the center of the Brillouin zone (Γ point), a key signature of a spinon Fermi surface, observed in prior neutron scattering experiments. However, we find a small gap near the Γ point, ruling out such a phase. Furthermore, we find localized gapless excitations at the corner of the Brillouin zone boundary (K point) and the middle of the edge of the Brillouin zone boundary (M point), ruling out the gapped Z2 spin-liquid phase. Our results imply that the intermediate spin-liquid phase is a gapless U(1) Dirac spin liquid, and provide clear signatures to detect this phase in future neutron scattering experiments.

Multipartite entanglement refers to the simultaneous entanglement between multiple subsystems of a many-body quantum system. While multipartite entanglement can be difficult to quantify analytically, it is known that it can be witnessed through the quantum Fisher information (QFI), a quantity that can also be related to dynamical Kubo response functions. In this work, we first show that the finite temperature QFI can generally be expressed in terms of a static structure factor of the system, plus a correction that vanishes as T→0. This implies that the static structure factor witnesses multipartite entanglement near quantum critical points at temperatures below a characteristic energy scale of the system. Therefore, in systems with a known static structure factor, we can deduce finite temperature scaling of multipartite entanglement and low temperature entanglement depth without knowledge of the full dynamical response function of the system. This is particularly useful to study 1D quantum critical systems in which sub-power-law divergences can dominate entanglement growth, where the conventional scaling theory of the QFI breaks down. The 1D spin-12 antiferromagnetic Heisenberg model is an important example of such a system, and we show that multipartite entanglement in the Heisenberg chain diverges nontrivially as ∼ln(1/T)3/2. We verify these predictions with calculations of the QFI using conformal field theory and matrix product state simulations. Finally we discuss the implications of our results for experiments to probe entanglement in quantum materials, comparing to neutron scattering data in KCuF3, a material well described by the Heisenberg chain.

Rap1 GTPase drives assembly of the Mig-10/RIAM/Lamellipodin (MRL protein)-integrin-talin (MIT) complex that enables integrin-dependent lymphocyte functions. Here we used tandem affinity tag-based proteomics to isolate and analyze the MIT complex and reveal that Phostensin (Ptsn), a regulatory subunit of protein phosphatase 1, is a component of the complex. Ptsn mediates dephosphorylation of Rap1, thereby preserving the activity and membrane localization of Rap1 to stabilize the MIT complex. CRISPR/Cas9-induced deletion of PPP1R18, which encodes Ptsn, markedly suppresses integrin activation in Jurkat human T cells. We generated apparently healthy Ppp1r18-/- mice that manifest lymphocytosis and reduced population of peripheral lymphoid tissues ascribable, in part, to defective activation of integrins αLβ2 and α4β7. Ppp1r18-/- T cells exhibit reduced capacity to induce colitis in a murine adoptive transfer model. Thus, Ptsn enables lymphocyte integrin-mediated functions by dephosphorylating Rap1 to stabilize the MIT complex. As a consequence, loss of Ptsn ameliorates T cell-mediated colitis.