Rydberg-Blockade-Based Parity Quantum Optimization.

We present a scalable architecture for solving higher-order constrained binary optimization (HCBO) problems on current neutral-atom hardware operating in the Rydberg blockade regime. In particular, we formulate the recently developed parity encoding of arbitrary connected HCBO problems as a maximum-weight independent set (MWIS) problem on disk graphs, that are directly encodable on such devices. Our architecture builds from small MWIS modules in a problem-independent way, crucial for practical scalability.

Quantum Optimization via Four-Body Rydberg Gates.

A large ongoing research effort focuses on obtaining a quantum advantage in the solution of combinatorial optimization problems on near-term quantum devices. A particularly promising platform implementing quantum optimization algorithms are arrays of trapped neutral atoms, laser coupled to highly excited Rydberg states. However, encoding combinatorial optimization problems in atomic arrays is challenging due to limited interqubit connectivity of the native finite-range interactions. Here, we present a four-body Rydberg parity gate, enabling a direct and straightforward implementation of the parity architecture, a scalable architecture for encoding arbitrarily connected interaction graphs. Our gate relies on adiabatic laser pulses and is fully programmable by adjusting two hold times during operation. We numerically demonstrate implementations of the quantum approximate optimization algorithm (QAOA) for small-scale test problems. Variational optimization steps can be implemented with a constant number of system manipulations, paving the way for experimental investigations of QAOA beyond the reach of numerical simulations.

Physiological and pharmacological modulation of the embryonic skeletal muscle calcium channel splice variant CaV1.1e.

CaV1.1e is the voltage-gated calcium channel splice variant of embryonic skeletal muscle. It differs from the adult CaV1.1a splice variant by the exclusion of exon 29 coding for 19 amino acids in the extracellular loop connecting transmembrane domains IVS3 and IVS4. Like the adult splice variant CaV1.1a, the embryonic CaV1.1e variant functions as voltage sensor in excitation-contraction coupling, but unlike CaV1.1a it also conducts sizable calcium currents. Consequently, physiological or pharmacological modulation of calcium currents may have a greater impact in CaV1.1e expressing muscle cells. Here, we analyzed the effects of L-type current modulators on whole-cell current properties in dysgenic (CaV1.1-null) myotubes reconstituted with either CaV1.1a or CaV1.1e. Furthermore, we examined the physiological current modulation by interactions with the ryanodine receptor using a chimeric CaV1.1e construct in which the cytoplasmic II-III loop, essential for skeletal muscle excitation-contraction coupling, has been replaced with the corresponding but nonfunctional loop from the Musca channel. Whereas the equivalent substitution in CaV1.1a had abolished the calcium currents, substitution of the II-III loop in CaV1.1e did not significantly reduce current amplitudes. This indicates that CaV1.1e is not subject to retrograde coupling with the ryanodine receptor and that the retrograde coupling mechanism in CaV1.1a operates by counteracting the limiting effects of exon 29 inclusion on the current amplitude. Pharmacologically, CaV1.1e behaves like other L-type calcium channels. Its currents are substantially increased by the calcium channel agonist Bay K 8644 and inhibited by the calcium channel blocker nifedipine in a dose-dependent manner. With an IC50 of 0.37 µM for current inhibition by nifedipine, CaV1.1e is a potential drug target for the treatment of myotonic dystrophy. It might block the excessive calcium influx resulting from the aberrant expression of the embryonic splice variant CaV1.1e in the skeletal muscles of myotonic dystrophy patients.