Establishing a reliable method to form scalable neutral-atom platforms is an essential cornerstone for quantum computation, quantum simulation and quantum many-body physics. Here we demonstrate a real-time transport of single atoms using holographic microtraps controlled by a liquid-crystal spatial light modulator. For this, an analytical design approach to flicker-free microtrap movement is devised and cold rubidium atoms are simultaneously rearranged with 2N motional degrees of freedom, representing unprecedented space controllability. We also accomplish an in situ feedback control for single-atom rearrangements with the high success rate of 99% for up to 10 μm translation. We hope this proof-of-principle demonstration of high-fidelity atom-array preparations will be useful for deterministic loading of N single atoms, especially on arbitrary lattice locations, and also for real-time qubit shuttling in high-dimensional quantum computing architectures.

Photoelectron circular dichroism (PECD) is a highly sensitive enantiospecific spectroscopy for studying chiral molecules in the gas phase using either single-photon ionization or multiphoton ionization. In the short pulse limit investigated with femtosecond lasers, resonance-enhanced multiphoton ionization (REMPI) is rather instantaneous and typically occurs simultaneously via more than one vibrational or electronic intermediate state due to limited frequency resolution. In contrast, vibrational resolution in the REMPI spectrum can be achieved using nanosecond lasers. In this work, we follow the high-resolution approach using a tunable narrow-band nanosecond laser to measure REMPI-PECD through distinct vibrational levels in the intermediate 3s and 3p Rydberg states of fenchone. We observe the PECD to be essentially independent of the vibrational level. This behaviour of the chiral sensitivity may pave the way for enantiomer specific molecular identification in multi-component mixtures: one can specifically excite a sharp, vibrationally resolved transition of a distinct molecule to distinguish different chiral species in mixtures.

Background: Although the clinical importance of heart failure with preserved ejection fraction (HFpEF) has been extensively explored, most therapeutic regimens, including nitric oxide (NO) donors, lack therapeutic benefit. Although the clinical characteristics of HFpEF are somewhat heterogeneous, diastolic dysfunction (DD) is one of the most important features. Here we report that neuronal nitric oxide synthase (nNOS) induces DD by S-nitrosylation of histone deacetylase 2 (HDAC2). Methods: Two animal models of DD—SAUNA (SAlty drinking water/Unilateral Nephrectomy/Aldosterone) and mild transverse aortic constriction (mTAC) mice— as well as human heart samples from left ventricular hypertrophy (LVH) patients were used. Genetically modified mice that were either nNOS-ablated or HDAC2 S-nitrosylation-resistant were also challenged. N(ω)-propyl-L-arginine (NPLA), an nNOS selective inhibitor, and dimethyl fumarate (DMF), an NRF2 inducer, were used. Molecular events were further checked in human left ventricle specimens. Results: SAUNA or mTAC stress impaired diastolic function and exercise tolerance without overt systolic failure. Among the post-translational modifications tested, S-nitrosylation was most dramatically increased in both models. Utilizing heart samples from both mice and humans, we observed increases in nNOS expression and NO production. NPLA alleviated the development of DD in vivo . Similarly, nNOS knock out mice were resistant to SAUNA stress. nNOS-induced S-nitrosylation of HDAC2 was relayed by transnitrosylation of GAPDH. HDAC2 S-nitrosylation was confirmed in both DD mouse and human LVH. S-Nitrosylation of HDAC2 took place at C262 and C274. When DD was induced, HDAC2 S-nitrosylation was detected in wild type mouse, but not in HDAC2 knock-in mouse heart that expressed HDAC2 C262A/C274A. In addition, HDAC2 C262A/C274A mice maintained normal diastolic function under DD stimuli. Gene delivery with AAV9-NRF2, a putative denitrosylase of HDAC2, or pharmacologic intervention by DMF successfully induced HDAC2 denitrosylation and mitigated DD in vivo . Conclusions: Our observations are the first to demonstrate a new mechanism underlying DD pathophysiology. Our results provide theoretical and experimental evidence to explain the ineffectiveness of conventional NO-enhancement trials for improving DD with heart failure symptoms. More importantly, our results suggest that reduction of NO or denitrosylation of HDAC2 may provide a new therapeutic platform for the treatment of refractory HFpEF.

Flavonoids are widely distributed secondary metabolites in plants that have a variety biological functions, as well as beneficial biological and pharmacological activities. In barley (Hordeum vulgare L.), for example, high levels of saponarin accumulate during primary leaf development. However, the effect of saponarin biosynthetic pathway genes on the accumulation of saponarin in barley is poorly understood. Accordingly, the aim of the present study was to examine the saponarin contents and expression levels of saponarin biosynthetic pathway genes [chalcone synthase (CHS), chalcone isomerase (CHI), and UDP-Glc:isovitexin 7-O-glucosyltransferase (OGT)] during early seedling developmental and under several abiotic stress conditions. Interestingly, the upregulation of HvCHS, HvCHI, and HvOGT during early development was associated with saponarin accumulation during later stages. In addition, exposure to abiotic stress conditions (e.g., light/dark transition, drought, and low or high temperature) significantly affected the expression of HvCHS and HvCHI but failed to affect either HvOGT expression or saponarin accumulation. These findings suggested that the expression of HvOGT, which encodes an enzyme that catalyzes the final step of saponarin biosynthesis, is required for saponarin accumulation. Taken together, the results of the present study provide a basis for metabolic engineering in barley plants, especially in regards to enhancing the contents of useful secondary metabolites, such as saponarin.