Quantum gate control of polar molecules with machine learning.

We propose a scheme for achieving basic quantum gates using ultracold polar molecules in pendular states. The qubits are encoded in the YbF molecules trapped in an electric field with a certain gradient and coupled by the dipole-dipole interaction. The time-dependent control sequences consisting of multiple pulses are considered to interact with the pendular qubits. To achieve high-fidelity quantum gates, we map the control problem for the coupled molecular system into a Markov decision process and deal with it using the techniques of deep reinforcement learning (DRL). By training the agents over multiple episodes, the optimal control pulse sequences for the two-qubit gates of NOT, controlled NOT, and Hadamard are discovered with high fidelities. Moreover, the population dynamics of YbF molecules driven by the discovered gate sequences are analyzed in detail. Furthermore, by combining the optimal gate sequences, we successfully simulate the quantum circuit for entanglement. Our findings could offer new insights into efficiently controlling molecular systems for practical molecule-based quantum computing using DRL.

Protein Activity Regulation: Inhibition by Closed-Loop Aptamer-Based Structures and Restoration by Near-IR Stimulation.

Regulation of protein activity is vital for understanding the molecular mechanism of biological activities. In this work, protein activity is suppressed by proximity-dependent surface hybridization and subsequently restored by near-infrared (NIR) light stimulation. Specifically, by constructing closed-loop structures with two aptamer-based affinity ligands, significantly enhanced inhibition of thrombin activity is achieved compared to traditional single affinity ligand based inhibitors. Furthermore, the activity of inhibited thrombin is efficiently recovered under NIR light stimulation by using gold nanorods (AuNRs) as photothermal agents to disrupt the closed-loop structures. Real-time and in situ monitoring of the conversion of fibrinogen into fibrin catalyzed by both inhibited and recovered thrombin was performed with light scattering spectroscopy and laser scanning confocal microscopy (LSCM). Thrombin trapped in the closed-loop structures shows slow reaction kinetics, while the photothermally liberated thrombin displays largely recovered catalytic activity. Human plasma was further employed to demonstrate that both the inhibited and restored thrombin can be applied to clotting reaction in reality. This strategy provides protein activity regulation for studying the molecular basis of biological activities and can be further applied to potential areas such as metabolic pathway regulation and the development of protein-inhibitor pharmaceuticals.

Polymorphisms in the human glutathione transferase zeta promoter.

OBJECTIVES: The zeta-class glutathione transferase GSTZ1-1 catalyses the glutathione-dependent isomerization of maleylacetoacetate to fumarylacetoacetate in the tyrosine catabolic pathway and the biotransformation of alpha-halo acids, including dichloroacetic acid (DCA). Genetic polymorphisms in the coding sequence of GSTZ1 result in significant changes in enzyme function, and deficiency of GSTZ1-1 in mice causes induction of a range of Phase-II enzymes. In this study, the potential for polymorphisms in regulatory sequences to alter gene transcription was investigated. METHODS: A total of 10 single-nucleotide polymorphisms (SNP) were identified in African and Australian European subjects in a region extending 1.5-kb upstream of the GSTZ1 start of transcription. These SNPs formed at least 10 haplotypes and only two were shared between the two population samples. The effect of these SNPs on gene expression was evaluated by the transient expression of specific alleles fused to a luciferase reporter gene. RESULTS: Of the 10 SNPs identified, only -1002 G>A and -289 C>T caused significant changes in promoter activity. The -1002 G>A SNP converts a v-Myb site to a S8 homeodomain (Prx2) site, and the -289 C>T SNP abolishes an Egr1 binding site. CONCLUSION: These SNPs may alter GSTZ1 expression, which may alter the pharmacokinetics of DCA, which is used therapeutically for the treatment of lactic acidosis.

Defective NF-kappaB activation in virus-infected neuronal cells is restored by genetic complementation.

The interferon-beta (IFNbeta) gene is not inducible in neuronal cells in response to measles virus (MV) due to lack of nuclear factor kappa B (NF-kappaB) activation. NF-kappaB is normally sequestered in the cytoplasm by an inhibitor (IkappaBalpha). Previously, the authors demonstrated that the failure to activate neuronal NF-kappaB by MV was due to the inability to phosphorylate and degrade its inhibitor, IkappaBalpha. Here the authors demonstrate that transient transfection of a brain cDNA library into neuronal cells restores the ability of MV to activate NF-kappaB. In addition, tumor necrosis factor-alpha (TNFalpha), but not interleukin-1 (IL-1) or lipopolysaccharide (LPS), stimulation resulted in IkappaBalpha phosphorylation and degradation in two neuronal cell lines. These results indicate that failure of MV to activate neuronal NF-kappaB is due to a signaling defect and that MV utilizes an NF-kappaB signaling pathway distinct from that of TNFalpha, but may overlap with that for IL-1 and LPS.