资源环境科技发展态势分析平台

Chirality is ubiquitous in nature, and populations of opposite chiralities are surprisingly asymmetric at fundamental levels(1,2). Examples range from parity violation in the subatomic weak force to homochirality in biomolecules. The ability to achieve chirality-selective synthesis (chiral induction) is of great importance in stereochemistry, molecular biology and pharmacology(2). In condensed matter physics, a crystalline electronic system is geometrically chiral when it lacks mirror planes, space-inversion centres or rotoinversion axes(1). Typically, geometrical chirality is predefined by the chiral lattice structure of a material, which is fixed on formation of the crystal. By contrast, in materials with gyrotropic order(3-6), electrons spontaneously organize themselves to exhibit macroscopic chirality in an originally achiral lattice. Although such order-which has been proposed as the quantum analogue of cholesteric liquid crystals-has attracted considerable interest(3-15), no clear observation or manipulation of gyrotropic order has been achieved so far. Here we report the realization of optical chiral induction and the observation of a gyrotropically ordered phase in the transition-metal dichalcogenide semimetal 1T-TiSe2. We show that shining mid-infrared circularly polarized light on 1T-TiSe2 while cooling it below the critical temperature leads to the preferential formation of one chiral domain. The chirality of this state is confirmed by the measurement of an out-of-plane circular photogalvanic current, the direction of which depends on the optical induction. Although the role of domain walls requires further investigation with local probes, the methodology demonstrated here can be applied to realize and control chiral electronic phases in other quantum materials(4,16).

Optical chiral induction and spontaneous gyrotropic electronic order are realized in the transition-metal chalcogenide 1T-TiSe2 by using illumination with mid-infrared circularly polarized light and simultaneous cooling below the critical temperature.

A quantum dot device designed to host four electrons is used to demonstrate Nagaoka ferromagnetism-a model of itinerant magnetism that has so far been limited to theoretical investigation.

Engineered, highly controllable quantum systems are promising simulators of emergent physics beyond the simulation capabilities of classical computers(1). An important problem in many-body physics is itinerant magnetism, which originates purely from long-range interactions of free electrons and whose existence in real systems has been debated for decades(2,3). Here we use a quantum simulator consisting of a four-electron-site square plaquette of quantum dots(4) to demonstrate Nagaoka ferromagnetism(5). This form of itinerant magnetism has been rigorously studied theoretically(6-9) but has remained unattainable in experiments. We load the plaquette with three electrons and demonstrate the predicted emergence of spontaneous ferromagnetic correlations through pairwise measurements of spin. We find that the ferromagnetic ground state is remarkably robust to engineered disorder in the on-site potentials and we can induce a transition to the low-spin state by changing the plaquette topology to an open chain. This demonstration of Nagaoka ferromagnetism highlights that quantum simulators can be used to study physical phenomena that have not yet been observed in any experimental system. The work also constitutes an important step towards large-scale quantum dot simulators of correlated electron systems.

An in vivo approach to identify proteins whose enrichment near cardiac Ca(V)1.2 channels changes upon beta-adrenergic stimulation finds the G protein Rad, which is phosphorylated by protein kinase A, thereby relieving channel inhibition by Rad and causing an increased Ca2+ current.

Increased cardiac contractility during the fight-or-flight response is caused by beta-adrenergic augmentation of Ca(V)1.2 voltage-gated calcium channels(1-4). However, this augmentation persists in transgenic murine hearts expressing mutant Ca(V)1.2 alpha(1C) and beta subunits that can no longer be phosphorylated by protein kinase A-an essential downstream mediator of beta-adrenergic signalling-suggesting that non-channel factors are also required. Here we identify the mechanism by which beta-adrenergic agonists stimulate voltage-gated calcium channels. We express alpha(1C) or beta(2B) subunits conjugated to ascorbate peroxidase(5) in mouse hearts, and use multiplexed quantitative proteomics(6,7) to track hundreds of proteins in the proximity of Ca(V)1.2. We observe that the calcium-channel inhibitor Rad(8,9), a monomeric G protein, is enriched in the Ca(V)1.2 microenvironment but is depleted during beta-adrenergic stimulation. Phosphorylation by protein kinase A of specific serine residues on Rad decreases its affinity for beta subunits and relieves constitutive inhibition of Ca(V)1.2, observed as an increase in channel open probability. Expression of Rad or its homologue Rem in HEK293T cells also imparts stimulation of Ca(V)1.3 and Ca(V)2.2 by protein kinase A, revealing an evolutionarily conserved mechanism that confers adrenergic modulation upon voltage-gated calcium channels.