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Adaptive quantum circuits—where a quantum many-body state is controlled using measurements and conditional unitary operations—are a powerful paradigm for state preparation and quantum error-correction tasks. They can support two types of nonequilibrium quantum phase transitions: measurement-induced transitions between volume- and area-law-entangled steady states and control-induced transitions where the system falls into an absorbing state or, more generally, an orbit visiting several absorbing states. Within this context, nonlocal conditional operations can alter the critical properties of the two transitions and the topology of the phase diagram. Here, we consider the scenario where the measurements are , in order to engineer efficient control onto dynamical trajectories. Motivated by Rydberg-atom arrays, we consider a locally constrained model with global sublattice magnetization measurements and local correction operations to steer the system’s dynamics onto a many-body orbit with finite recurrence time. The model has a well-defined classical limit, which we leverage to aid our analysis of the control transition. As a function of the density of local correction operations, we find control and entanglement transitions with continuously varying critical exponents. For sufficiently high densities of local correction operations, we find that both transitions acquire a dynamical critical exponent $z<1$, reminiscent of criticality in long-range power-law interacting systems. At low correction densities, we find that the criticality reverts to a short-range nature with $z\gtrsim 1$. In the long-range regime, the control and entanglement transitions are indistinguishable to within the resolution of our finite-size numerics, while in the short-range regime we find evidence that the transitions become distinct. We conjecture that the effective long-range criticality mediated by collective measurements is essential in driving the two transitions together. Published by the American Physical Society2025 

Abstract The rare earth elements (REEs) are critical resources for many clean energy technologies, but are difficult to obtain in their elementally pure forms because of their nearly identical chemical properties. Here, an analogue of macropa, G‐macropa, was synthesized and employed for an aqueous precipitation‐based separation of Nd³⁺and Dy³⁺. G‐macropa maintains the same thermodynamic preference for the large REEs as macropa, but shows smaller thermodynamic stability constants. Molecular dynamics studies demonstrate that the binding affinity differences of these chelators for Nd³⁺and Dy³⁺is a consequence of the presence or absence of an inner‐sphere water molecule, which alters the donor strength of the macrocyclic ethers. Leveraging the small REE affinity of G‐macropa, we demonstrate that within aqueous solutions of Nd³⁺, Dy³⁺, and G‐macropa, the addition of HCO₃⁻selectively precipitates Dy₂(CO₃)₃, leaving the Nd³⁺−G‐macropa complex in solution. With this method, remarkably high separation factors of 841 and 741 are achieved for 50 : 50 and 75 : 25 mixtures. Further studies involving Nd³⁺:Dy³⁺ratios of 95 : 5 in authentic magnet waste also afford an efficient separation as well. Lastly, G‐macropa is recovered via crystallization with HCl and used for subsequent extractions, demonstrating its good recyclability. 

Abstract The mitochondrial calcium uniporter (MCU) is a transmembrane protein that is responsible for mediating mitochondrial calcium (mCa²⁺) uptake. Given this critical function, the MCU has been implicated as an important target for addressing various human diseases. As such, there has a been growing interest in developing small molecules that can inhibit this protein. To date, metal coordination complexes, particularly multinuclear ruthenium complexes, are the most widely investigated MCU inhibitors due to both their potent inhibitory activities as well as their longstanding use for this application. Recent efforts have expanded the metal‐based toolkit for MCU inhibition. This concept paper summarizes the development of new metal‐based inhibitors of the MCU and their structure‐activity relationships in the context of improving their potential for therapeutic use in managing human diseases related tomCa²⁺dysregulation. 

Ischemia-reperfusion injury (IRI), which describes the cell damage and death that occurs after blood and oxygen are restored to ischemic or hypoxic tissue, is a significant factor within the mortality rates of heart disease and stroke patients. At the cellular level, the return of oxygen triggers an increase in reactive oxygen species (ROS) and mitochondrial calcium (mCa2+) overload, which both contribute to cell death. Despite the widespread occurrence of IRI in different pathological conditions, there are currently no clinically approved therapeutic agents for its management. In this Perspective, we will briefly discuss the current therapeutic options for IRI and then describe in great detail the potential role and arising applications of metal-containing coordination and organometallic complexes for treating this condition. This Perspective categorizes these metal compounds based on their mechanisms of action, which include their use as delivery agents for gasotransmitters, inhibitors of mCa2+ uptake, and catalysts for the decomposition of ROS. Lastly, the challenges and opportunities for inorganic chemistry approaches to manage IRI are discussed. 

Abstract The mitochondrial calcium uniporter (MCU) mediates uptake of calcium ions (Ca²⁺) into the mitochondria, a process that is vital for maintaining normal cellular function. Inhibitors of the MCU, the most promising of which are dinuclear ruthenium coordination compounds, have found use as both therapeutic agents and tools for studying the importance of this ion channel. In this study, six Co³⁺cage compounds with sarcophagine‐like ligands were assessed for their abilities to inhibit MCU‐mediated mitochondrial Ca²⁺uptake. These complexes were synthesized and characterized according to literature procedures and then investigated in cellular systems for their MCU‐inhibitory activities. Among these six compounds, [Co(sen)]³⁺(3, sen=5‐(4‐amino‐2‐azabutyl)‐5‐methyl‐3,7‐diaza‐1,9‐nonanediamine) was identified to be a potent MCU inhibitor, with IC₅₀values of inhibition of 160 and 180 nM in permeabilized HeLa and HEK293T cells, respectively. Furthermore, the cellular uptake of compound3was determined, revealing moderate accumulation in cells. Most notably,3was demonstrated to operate in intact cells as an MCU inhibitor. Collectively, this work presents the viability of using cobalt coordination complexes as MCU inhibitors, providing a new direction for researchers to investigate. 

An analogue of the mitochondrial calcium uniporter (MCU) inhibitor Ru265 containing axial ferrocenecarboxylate ligands is reported. This new complex exhibits enhanced cellular uptake compared to the parent compound Ru265.