Efficient Quantum Algorithms for Stabilizer Entropies.

Stabilizer entropies (SEs) are measures of nonstabilizerness or "magic" that quantify the degree to which a state is described by stabilizers. SEs are especially interesting due to their connections to scrambling, localization and property testing. However, applications have been limited so far as previously known measurement protocols for SEs scale exponentially with the number of qubits. Here, we efficiently measure SEs for integer Rényi index n>1 via Bell measurements. The SE of N-qubit quantum states can be measured with O(n) copies and O(nN) classical computational time, where for even n we additionally require the complex conjugate of the state. We provide efficient bounds of various nonstabilizerness monotones that are intractable to compute beyond a few qubits. Using the IonQ quantum computer, we measure SEs of random Clifford circuits doped with non-Clifford gates and give bounds for the stabilizer fidelity, stabilizer extent, and robustness of magic. We provide efficient algorithms to measure Clifford-averaged 4n-point out-of-time-order correlators and multifractal flatness. With these measures we study the scrambling time of doped Clifford circuits and random Hamiltonian evolution depending on nonstabilizerness. Counterintuitively, random Hamiltonian evolution becomes less scrambled at long times, which we reveal with the multifractal flatness. Our results open up the exploration of nonstabilizerness with quantum computers.

Inhibition of Hepatic Stellate Cell Activation Suppresses Tumorigenicity of Hepatocellular Carcinoma in Mice.

Transdifferentiation (or activation) of hepatic stellate cells (HSCs) to myofibroblasts is a key event in liver fibrosis. Activated HSCs in the tumor microenvironment reportedly promote tumor progression. This study analyzed the effect of an inhibitor of HSC activation, retinol-binding protein-albumin domain III fusion protein (R-III), on protumorigenic functions of HSCs. Although conditioned medium collected from activated HSCs enhanced the migration, invasion, and proliferation of the hepatocellular carcinoma cell line Hepa-1c1c7, this effect was not observed in Hepa-1c1c7 cells treated with conditioned medium from R-III-exposed HSCs. In a subcutaneous tumor model, larger tumors with increased vascular density were formed in mice transplanted with Hepa-1c1c7+HSC than in mice transplanted with Hepa-1c1c7 cells alone. Intriguingly, when Hepa-1c1c7+HSC-transplanted mice were injected intravenously with R-III, a reduction in vascular density and extended tumor necrosis were observed. In an orthotopic tumor model, co-transplantation of HSCs enhanced tumor growth, angiogenesis, and regional metastasis accompanied by increased peritumoral lymphatic vessel density, which was abolished by R-III. In vitro study showed that R-III treatment affected the synthesis of pro-angiogenic and anti-angiogenic factors in activated HSCs, which might be the potential mechanism underlying the R-III effect. These findings suggest that the inhibition of HSC activation abrogates HSC-induced tumor angiogenesis and growth, which represents an attractive therapeutic strategy.