Variational Quantum Simulation of Lindblad Dynamics via Quantum State Diffusion.

Quantum simulation of dynamics in open quantum systems is crucial but poses a significant challenge due to the non-Hermitian nature leading to nonunitary evolution and the limited quantum resources on current quantum computers. Here we introduce a variational hybrid quantum-classical algorithm designed for simulating the time evolution governed by the Lindblad master equation. Our approach involves on a stochastic unveiling of the density matrix, transforming the Lindblad equation into a wave function-based quantum state diffusion (QSD) method with the aim of reducing qubit requirements. We then apply variational quantum simulation (VQS) to efficiently capture the nonunitary evolution in QSD. We demonstrate our QSD-VQS algorithm by investigating the quantum dynamics in a two-level system subjected to an amplitude damping channel and a four-level transverse field Ising model within a dissipative environment including time-independent and periodic Hamiltonian cases. The results reveal its promising utility with upcoming hardware in the near future.

Reactive oxygen species-driven mitochondrial injury induces apoptosis by teroxirone in human non-small cell lung cancer cells.

Teroxirone as an anticancer agent is used to treat human lung cancer by inducing apoptotic cell death. Previous studies have demonstrated that the status of the tumor suppressor p53 determined the onset of apoptotic cell death in human non-small cell lung cancer cells (NSCLC). In order to further understand the underlying mechanisms of lung cancer, the present study explored the targets of teroxirone. By including antioxidants, the present study analyzed changes in cell proliferation, cell cycle division, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), expression of apoptosis markers and cytochrome c distribution. Subsequent to a 12 h treatment with low concentrations of teroxirone, MMP was suppressed, followed by ROS production and apoptosis in lung cancer cells carrying wild type p53. N-acetylcysteine inhibited apoptotic cell death. The depleted expression of p53, reduction of apoptosis-associated active caspase-3 and poly ADP-ribose polymerase cleavage with resurgence of the pro-survival signal protein kinase B, all demonstrated an antioxidant-mediated reduction of apoptosis by teroxirone. The diminished ROS intensity inhibited the release of mitochondrial cytochrome c and DNA damage. The present study provided evidence that teroxirone treatment induced the ROS-activated intrinsic apoptotic pathway, which led to cell death in human NSCLC cells.

Teroxirone inhibited growth of human non-small cell lung cancer cells by activating p53.

In this work, we demonstrated that the growth of human non-small-cell-lung-cancer cells H460 and A549 cells can be inhibited by low concentrations of an epoxide derivative, teroxirone, in both in vitro and in vivo models. The cytotoxicity was mediated by apoptotic cell death through DNA damage. The onset of ultimate apoptosis is dependent on the status of p53. Teroxirone caused transient elevation of p53 that activates downstream p21 and procaspase-3 cleavage. The presence of caspase-3 inhibitor reverted apoptotic phenotype. Furthermore, we showed the cytotoxicity of teroxirone in H1299 cells with stable ectopic expression of p53, but not those of mutant p53. A siRNA-mediated knockdown of p53 expression attenuated drug sensitivity. The in vivo experiments demonstrated that teroxirone suppressed growth of xenograft tumors in nude mice. Being a potential therapeutic agent by restraining cell growth through apoptotic death at low concentrations, teroxirone provides a feasible perspective in reversing tumorigenic phenotype of human lung cancer cells.