资源环境科技发展态势分析平台

Interactions between light and an ensemble of strontium atoms in an optical cavity can serve as a testbed for studying dynamical phase transitions, which are currently not well understood.

Interactions between atoms and light in optical cavities provide a means of investigating collective (many-body) quantum physics in controlled environments. Such ensembles of atoms in cavities have been proposed for studying collective quantum spin models, where the atomic internal levels mimic a spin degree of freedom and interact through long-range interactions tunable by changing the cavity parameters(1-4). Non-classical steady-state phases arising from the interplay between atom-light interactions and dissipation of light from the cavity have previously been investigated(5-11). These systems also offer the opportunity to study dynamical phases of matter that are precluded from existence at equilibrium but can be stabilized by driving a system out of equilibrium(12-16), as demonstrated by recent experiments(17-22). These phases can also display universal behaviours akin to standard equilibrium phase transitions(8,23,24). Here, we use an ensemble of about a million strontium-88 atoms in an optical cavity to simulate a collective Lipkin-Meshkov-Glick model(25,26), an iconic model in quantum magnetism, and report the observation of distinct dynamical phases of matter in this system. Our system allows us to probe the dependence of dynamical phase transitions on system size, initial state and other parameters. These observations can be linked to similar dynamical phases in related systems, including the Josephson effect in superfluid helium(27), or coupled atomic(28) and solid-state polariton(29) condensates. The system itself offers potential for generation of metrologically useful entangled states in optical transitions, which could permit quantum enhancement in state-of-the-art atomic clocks(30,31).

Environmental change is rapidly accelerating, and many species will need to adapt to survive(1). Ensuring that protected areas cover populations across a broad range of environmental conditions could safeguard the processes that lead to such adaptations(1-3). However, international conservation policies have largely neglected these considerations when setting targets for the expansion of protected areas(4). Here we show that-of 19,937 vertebrate species globally(5-8)-the representation of environmental conditions across their habitats in protected areas (hereafter, niche representation) is inadequate for 4,836 (93.1%) amphibian, 8,653 (89.5%) bird and 4,608 (90.9%) terrestrial mammal species. Expanding existing protected areas to cover these gaps would encompass 33.8% of the total land surface-exceeding the current target of 17% that has been adopted by governments. Priority locations for expanding the system of protected areas to improve niche representation occur in global biodiversity hotspots(9), including Colombia, Papua New Guinea, South Africa and southwest China, as well as across most of the major land masses of the Earth. Conversely, we also show that planning for the expansion of protected areas without explicitly considering environmental conditions would marginally reduce the land area required to 30.7%, but that this would lead to inadequate niche representation for 7,798 (39.1%) species. As the governments of the world prepare to renegotiate global conservation targets, policymakers have the opportunity to help to maintain the adaptive potential of species by considering niche representation within protected areas(1,2).

Protected areas would need to expand to 33.8% of the total land surface to adequately represent environmental conditions across the habitats of amphibians, birds and terrestrial mammals, far exceeding the current 17% target.

An HLA- and gluten-dependent mouse model of coeliac disease with villous atrophy provides evidence for the cooperative role of IL-15 and gluten-specific CD4(+) T cells in licensing the full activation of cytotoxic T cells that are necessary for inducing epithelial damage.

Coeliac disease is a complex, polygenic inflammatory enteropathy caused by exposure to dietary gluten that occurs in a subset of genetically susceptible individuals who express either the HLA-DQ8 or HLA-DQ2 haplotypes(1,2). The need to develop non-dietary treatments is now widely recognized(3), but no pathophysiologically relevant gluten- and HLA-dependent preclinical model exists. Furthermore, although studies in humans have led to major advances in our understanding of the pathogenesis of coeliac disease(4), the respective roles of disease-predisposing HLA molecules, and of adaptive and innate immunity in the development of tissue damage, have not been directly demonstrated. Here we describe a mouse model that reproduces the overexpression of interleukin-15 (IL-15) in the gut epithelium and lamina propria that is characteristic of active coeliac disease, expresses the predisposing HLA-DQ8 molecule, and develops villous atrophy after ingestion of gluten. Overexpression of IL-15 in both the epithelium and the lamina propria is required for the development of villous atrophy, which demonstrates the location-dependent central role of IL-15 in the pathogenesis of coeliac disease. In addition, CD4(+) T cells and HLA-DQ8 have a crucial role in the licensing of cytotoxic T cells to mediate intestinal epithelial cell lysis. We also demonstrate a role for the cytokine interferon-gamma (IFN gamma) and the enzyme transglutaminase 2 (TG2) in tissue destruction. By reflecting the complex interaction between gluten, genetics and IL-15-driven tissue inflammation, this mouse model provides the opportunity to both increase our understanding of coeliac disease, and develop new therapeutic strategies.