Eigenstate Thermalization in Long-Range Interacting Systems

Motivated by recent ion experiments on tunable long-range interacting quantum systems [B.Neyenhuis et al., Sci.Adv.3, e1700672 (2017, https://doi.org/10.1126/sciadv.1700672 )], we test the strong eigenstate thermalization hypothesis (ETH) for systems with power-law interactions $\sim 1/r^{\alpha}$. We numerically demonstrate that the strong ETH typically holds at least for systems with $\alpha\geq 0.6$, which include Coulomb, monopole-dipole, and dipole-dipole interactions. Compared with short-range interacting systems, the eigenstate expectation value of a generic local observable is shown to deviate significantly from its microcanonical ensemble average for long-range interacting systems. We find that Srednicki's ansatz breaks down for $\alpha \lesssim 1.0$ at least for relatively large system sizes.Comment: 7 pages, 4 figures, supplemental material with 22 pages and 13 figures. The readability of the manuscript (especially the setup section)is improved. Hyperlinks are embedde

Eigenstate Thermalisation Hypothesis for Translation Invariant Spin Systems

We prove the Eigenstate Thermalisation Hypothesis (ETH) for local observables in a typical translation invariant system of quantum spins with mean field interaction. This mathematically verifies the observation made in [L.Santos and M.Rigol, Phys.Rev.E 82, 031130 (2010, https://journals.aps.org/pre/abstract/10.1103/PhysRevE.82.031130)] that ETH may hold for systems with additional translation symmetries for a naturally restricted class of observables. We also present numerical support for the same phenomenon for Hamiltonians with local interactions.Comment: 23 pages, 2 figure

Eigenstate thermalisation hypothesis for translation invariant spin systems

We prove the Eigenstate Thermalisation Hypothesis (ETH) for local observables in a typical translation invariant system of quantum spins with L-body interactions, where L is the number of spins. This mathematically verifies the observation first made by Santos and Rigol (Phys Rev E 82(3):031130, 2010, https://doi.org/10.1103/PhysRevE.82.031130) that the ETH may hold for systems with additional translational symmetries for a naturally restricted class of observables. We also present numerical support for the same phenomenon for Hamiltonians with local interaction

Leukotriene receptor antagonist attenuated airway inflammation and hyperresponsiveness in a double-stranded RNA-induced asthma exacerbation model

Background: Viral infections are the most common triggers of asthma exacerbation, but the key molecules involved in this process have not been fully identified. Although cysteinyl leukotrienes (cysLTs) have been postulated as the key mediators, their precise roles remain largely unclear. To investigate the roles of cysLTs in virus-induced asthma exacerbation, we developed a murine model using a viral double-stranded RNA analog, polyinosinic–polycytidylic acid (poly I:C), and analyzed the effect of leukotriene receptor antagonist (LTRA) administration. Methods: A/J mice were immunized with ovalbumin (OVA) + alum (days 0, 28, 42, and 49), followed by intranasal challenge with OVA (phase 1: days 50–52) and poly I:C (phase 2: days 53–55). Montelukast was administered during poly I:C challenge (phase 2) in the reliever model or throughout the OVA and poly I:C challenges (phases 1 and 2) in the controller model. Airway responsiveness to acetylcholine chloride was assessed, and bronchoalveolar lavage (BAL) was performed on day 56. Results: Administration of poly I:C to OVA-sensitized and -challenged mice increased the number of eosinophils and levels of IL-13, IL-9, CCL3, and CXCL1 in BAL fluid (BALF) and tended to increase airway responsiveness. Montelukast significantly attenuated the poly I:C-induced increase in the number of eosinophils and levels of IL-13, IL-9, and CCL3 in BALF and airway hyperresponsiveness in both the reliever and controller models. Conclusions: This is the first report showing that LTRA functionally suppressed the pathophysiology of a virus-induced asthma exacerbation model, suggesting the importance of cysLTs as a potential treatment target