Computing prime factors with a Josephson phase qubit quantum processor

A quantum processor (QuP) can be used to exploit quantum mechanics to find the prime factors of composite numbers[1]. Compiled versions of Shor's algorithm have been demonstrated on ensemble quantum systems[2] and photonic systems[3-5], however this has yet to be shown using solid state quantum bits (qubits). Two advantages of superconducting qubit architectures are the use of conventional microfabrication techniques, which allow straightforward scaling to large numbers of qubits, and a toolkit of circuit elements that can be used to engineer a variety of qubit types and interactions[6, 7]. Using a number of recent qubit control and hardware advances [7-13], here we demonstrate a nine-quantum-element solid-state QuP and show three experiments to highlight its capabilities. We begin by characterizing the device with spectroscopy. Next, we produces coherent interactions between five qubits and verify bi- and tripartite entanglement via quantum state tomography (QST) [8, 12, 14, 15]. In the final experiment, we run a three-qubit compiled version of Shor's algorithm to factor the number 15, and successfully find the prime factors 48% of the time. Improvements in the superconducting qubit coherence times and more complex circuits should provide the resources necessary to factor larger composite numbers and run more intricate quantum algorithms.Comment: 5 pages, 3 figure

Resistance Exercise Reverses Aging in Human Skeletal Muscle

Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training