Constant-Overhead Fault-Tolerant Quantum Computation with Reconfigurable Atom Arrays

Quantum low-density parity-check (qLDPC) codes can achieve high encoding rates and good code distance scaling, providing a promising route to low-overhead fault-tolerant quantum computing. However, the long-range connectivity required to implement such codes makes their physical realization challenging. Here, we propose a hardware-efficient scheme to perform fault-tolerant quantum computation with high-rate qLDPC codes on reconfigurable atom arrays, directly compatible with recently demonstrated experimental capabilities. Our approach utilizes the product structure inherent in many qLDPC codes to implement the non-local syndrome extraction circuit via atom rearrangement, resulting in effectively constant overhead in practically relevant regimes. We prove the fault tolerance of these protocols, perform circuit-level simulations of memory and logical operations with these codes, and find that our qLDPC-based architecture starts to outperform the surface code with as few as several hundred physical qubits at a realistic physical error rate of $10^{-3}$. We further find that less than 3000 physical qubits are sufficient to obtain over an order of magnitude qubit savings compared to the surface code, and quantum algorithms involving thousands of logical qubits can be performed using less than $10^5$ physical qubits. Our work paves the way for explorations of low-overhead quantum computing with qLDPC codes at a practical scale, based on current experimental technologies

Probing many-body noise in a strongly interacting two-dimensional dipolar spin system

The most direct approach for characterizing the quantum dynamics of a strongly-interacting system is to measure the time-evolution of its full many-body state. Despite the conceptual simplicity of this approach, it quickly becomes intractable as the system size grows. An alternate framework is to think of the many-body dynamics as generating noise, which can be measured by the decoherence of a probe qubit. Our work centers on the following question: What can the decoherence dynamics of such a probe tell us about the many-body system? In particular, we utilize optically addressable probe spins to experimentally characterize both static and dynamical properties of strongly-interacting magnetic dipoles. Our experimental platform consists of two types of spin defects in diamond: nitrogen-vacancy (NV) color centers (probe spins) and substitutional nitrogen impurities (many-body system). We demonstrate that signatures of the many-body system's dimensionality, dynamics, and disorder are naturally encoded in the functional form of the NV's decoherence profile. Leveraging these insights, we directly characterize the two-dimensional nature of a nitrogen delta-doped diamond sample. In addition, we explore two distinct facets of the many-body dynamics: First, we address a persistent debate about the microscopic nature of spin dynamics in strongly-interacting dipolar systems. Second, we demonstrate direct control over the spectral properties of the many-body system, including its correlation time. Our work opens the door to new directions in both quantum sensing and simulation.Comment: 10 + 8 + 5 pages; 3 + 5 figure

High-fidelity parallel entangling gates on a neutral atom quantum computer

The ability to perform entangling quantum operations with low error rates in a scalable fashion is a central element of useful quantum information processing. Neutral atom arrays have recently emerged as a promising quantum computing platform, featuring coherent control over hundreds of qubits and any-to-any gate connectivity in a flexible, dynamically reconfigurable architecture. The major outstanding challenge has been to reduce errors in entangling operations mediated through Rydberg interactions. Here we report the realization of two-qubit entangling gates with 99.5% fidelity on up to 60 atoms in parallel, surpassing the surface code threshold for error correction. Our method employs fast single-pulse gates based on optimal control, atomic dark states to reduce scattering, and improvements to Rydberg excitation and atom cooling. We benchmark fidelity using several methods based on repeated gate applications, characterize the physical error sources, and outline future improvements. Finally, we generalize our method to design entangling gates involving a higher number of qubits, which we demonstrate by realizing low-error three-qubit gates. By enabling high-fidelity operation in a scalable, highly connected system, these advances lay the groundwork for large-scale implementation of quantum algorithms, error-corrected circuits, and digital simulations.Comment: 5 pages, 4 figures. Methods: 13 pages, 10 figure

The impact of hypsarrhythmia on infantile spasms treatment response: Observational cohort study from the National Infantile Spasms Consortium

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141801/1/epi13937_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141801/2/epi13937.pd

Association of ultra-rare coding variants with genetic generalized epilepsy: A case\u2013control whole exome sequencing study

Objective: We aimed to identify genes associated with genetic generalized epilepsy (GGE) by combining large cohorts enriched with individuals with a positive family history. Secondarily, we set out to compare the association of genes independently with familial and sporadic GGE. Methods: We performed a case\u2013control whole exome sequencing study in unrelated individuals of European descent diagnosed with GGE (previously recruited and sequenced through multiple international collaborations) and ancestry-matched controls. The association of ultra-rare variants (URVs; in 18 834 protein-coding genes) with epilepsy was examined in 1928 individuals with GGE (vs. 8578 controls), then separately in 945 individuals with familial GGE (vs. 8626 controls), and finally in 1005 individuals with sporadic GGE (vs. 8621 controls). We additionally examined the association of URVs with familial and sporadic GGE in two gene sets important for inhibitory signaling (19 genes encoding \u3b3-aminobutyric acid type A [GABAA] receptors, 113 genes representing the GABAergic pathway). Results: GABRG2 was associated with GGE (p = 1.8  7 10 125), approaching study-wide significance in familial GGE (p = 3.0  7 10 126), whereas no gene approached a significant association with sporadic GGE. Deleterious URVs in the most intolerant subgenic regions in genes encoding GABAA receptors were associated with familial GGE (odds ratio [OR] = 3.9, 95% confidence interval [CI] = 1.9\u20137.8, false discovery rate [FDR]-adjusted p =.0024), whereas their association with sporadic GGE had marginally lower odds (OR = 3.1, 95% CI = 1.3\u20136.7, FDR-adjusted p =.022). URVs in GABAergic pathway genes were associated with familial GGE (OR = 1.8, 95% CI = 1.3\u20132.5, FDR-adjusted p =.0024) but not with sporadic GGE (OR = 1.3, 95% CI =.9\u20131.9, FDR-adjusted p =.19). Significance: URVs in GABRG2 are likely an important risk factor for familial GGE. The association of gene sets of GABAergic signaling with familial GGE is more prominent than with sporadic GGE

Application of rare variant transmission disequilibrium tests to epileptic encephalopathy trio sequence data

The classic epileptic encephalopathies, including infantile spasms (IS) and Lennox–Gastaut syndrome (LGS), are severe seizure disorders that usually arise sporadically. De novo variants in genes mainly encoding ion channel and synaptic proteins have been found to account for over 15% of patients with IS or LGS. The contribution of autosomal recessive genetic variation, however, is less well understood. We implemented a rare variant transmission disequilibrium test (TDT) to search for autosomal recessive epileptic encephalopathy genes in a cohort of 320 outbred patient–parent trios that were generally prescreened for rare metabolic disorders. In the current sample, our rare variant transmission disequilibrium test did not identify individual genes with significantly distorted transmission over expectation after correcting for the multiple tests. While the rare variant transmission disequilibrium test did not find evidence of a role for individual autosomal recessive genes, our current sample is insufficiently powered to assess the overall role of autosomal recessive genotypes in an outbred epileptic encephalopathy population

Ultra-rare genetic variation in common epilepsies: a case-control sequencing study

BACKGROUND:Despite progress in understanding the genetics of rare epilepsies, the more common epilepsies have proven less amenable to traditional gene-discovery analyses. We aimed to assess the contribution of ultra-rare genetic variation to common epilepsies. METHODS:We did a case-control sequencing study with exome sequence data from unrelated individuals clinically evaluated for one of the two most common epilepsy syndromes: familial genetic generalised epilepsy, or familial or sporadic non-acquired focal epilepsy. Individuals of any age were recruited between Nov 26, 2007, and Aug 2, 2013, through the multicentre Epilepsy Phenome/Genome Project and Epi4K collaborations, and samples were sequenced at the Institute for Genomic Medicine (New York, USA) between Feb 6, 2013, and Aug 18, 2015. To identify epilepsy risk signals, we tested all protein-coding genes for an excess of ultra-rare genetic variation among the cases, compared with control samples with no known epilepsy or epilepsy comorbidity sequenced through unrelated studies. FINDINGS:We separately compared the sequence data from 640 individuals with familial genetic generalised epilepsy and 525 individuals with familial non-acquired focal epilepsy to the same group of 3877 controls, and found significantly higher rates of ultra-rare deleterious variation in genes established as causative for dominant epilepsy disorders (familial genetic generalised epilepsy: odd ratio [OR] 2·3, 95% CI 1·7-3·2, p=9·1 × 10-8; familial non-acquired focal epilepsy 3·6, 2·7-4·9, p=1·1 × 10-17). Comparison of an additional cohort of 662 individuals with sporadic non-acquired focal epilepsy to controls did not identify study-wide significant signals. For the individuals with familial non-acquired focal epilepsy, we found that five known epilepsy genes ranked as the top five genes enriched for ultra-rare deleterious variation. After accounting for the control carrier rate, we estimate that these five genes contribute to the risk of epilepsy in approximately 8% of individuals with familial non-acquired focal epilepsy. Our analyses showed that no individual gene was significantly associated with familial genetic generalised epilepsy; however, known epilepsy genes had lower p values relative to the rest of the protein-coding genes (p=5·8 × 10-8) that were lower than expected from a random sampling of genes. INTERPRETATION:We identified excess ultra-rare variation in known epilepsy genes, which establishes a clear connection between the genetics of common and rare, severe epilepsies, and shows that the variants responsible for epilepsy risk are exceptionally rare in the general population. Our results suggest that the emerging paradigm of targeting of treatments to the genetic cause in rare devastating epilepsies might also extend to a proportion of common epilepsies. These findings might allow clinicians to broadly explain the cause of these syndromes to patients, and lay the foundation for possible precision treatments in the future. FUNDING:National Institute of Neurological Disorders and Stroke (NINDS), and Epilepsy Research UK

Auras in generalized epilepsy

OBJECTIVE: We studied the frequency of auras in generalized epilepsy (GE) using a detailed semistructured diagnostic interview. METHODS: In this cross-sectional study, participants with GE were drawn from the Epilepsy Phenome/Genome Project (EPGP). Responses to the standardized diagnostic interview regarding tonic-clonic (grand mal) seizures were then examined. This questionnaire initially required participants to provide their own description of any subjective phenomena before their “grand mal seizures.” Participants who provided answers to these questions were considered to have an aura. All participants were then systematically queried regarding a list of specific symptoms occurring before grand mal seizures, using structured (closed-ended) questions. RESULTS: Seven hundred ninety-eight participants with GE were identified, of whom 530 reported grand mal seizures. Of these, 112 (21.3%) reported auras in response to the open-ended question. Analysis of responses to the closed-ended questions suggested that 341 participants (64.3%) experienced at least one form of aura. CONCLUSIONS: Auras typically associated with focal epilepsy were reported by a substantial proportion of EPGP subjects with GE. This finding may support existing theories of cortical and subcortical generators of GE with variable spread patterns. Differences between responses to the open-ended question and closed-ended questions may also reflect clinically relevant variation in patient responses to history-taking and surveys. Open-ended questions may underestimate the prevalence of specific types of auras and may be in part responsible for the underrecognition of auras in GE. In addition, structured questions may influence participants, possibly leading to a greater representation of symptoms

Auras in generalized epilepsy

ObjectiveWe studied the frequency of auras in generalized epilepsy (GE) using a detailed semistructured diagnostic interview.MethodsIn this cross-sectional study, participants with GE were drawn from the Epilepsy Phenome/Genome Project (EPGP). Responses to the standardized diagnostic interview regarding tonic-clonic (grand mal) seizures were then examined. This questionnaire initially required participants to provide their own description of any subjective phenomena before their "grand mal seizures." Participants who provided answers to these questions were considered to have an aura. All participants were then systematically queried regarding a list of specific symptoms occurring before grand mal seizures, using structured (closed-ended) questions.ResultsSeven hundred ninety-eight participants with GE were identified, of whom 530 reported grand mal seizures. Of these, 112 (21.3%) reported auras in response to the open-ended question. Analysis of responses to the closed-ended questions suggested that 341 participants (64.3%) experienced at least one form of aura.ConclusionsAuras typically associated with focal epilepsy were reported by a substantial proportion of EPGP subjects with GE. This finding may support existing theories of cortical and subcortical generators of GE with variable spread patterns. Differences between responses to the open-ended question and closed-ended questions may also reflect clinically relevant variation in patient responses to history-taking and surveys. Open-ended questions may underestimate the prevalence of specific types of auras and may be in part responsible for the underrecognition of auras in GE. In addition, structured questions may influence participants, possibly leading to a greater representation of symptoms

Auras in generalized epilepsy

ABSTRACT Objective: We studied the frequency of auras in generalized epilepsy (GE) using a detailed semistructured diagnostic interview. Methods: In this cross-sectional study, participants with GE were drawn from the Epilepsy Phenome/Genome Project (EPGP). Responses to the standardized diagnostic interview regarding tonic-clonic (grand mal) seizures were then examined. This questionnaire initially required participants to provide their own description of any subjective phenomena before their "grand mal seizures." Participants who provided answers to these questions were considered to have an aura. All participants were then systematically queried regarding a list of specific symptoms occurring before grand mal seizures, using structured (closed-ended) questions