The number of topological defects created in a system driven through a quantum phase transition exhibits a power-law scaling with the driving time. This universal scaling law is the key prediction of the Kibble-Zurek mechanism (KZM), and testing it using a hardware-based quantum simulator is a coveted goal of quantum information science. Here we provide such a test using quantum annealing. Specifically, we report on extensive experimental tests of topological defect formation via the one-dimensional transverse-field Ising model on two different D-Wave quantum annealing devices. We find that the quantum simulator results can indeed be explained by the KZM for open-system quantum dynamics with phase-flip errors, with certain quantitative deviations from the theory likely caused by factors such as random control errors and transient effects. In addition, we probe physics beyond the KZM by identifying signatures of universality in the distribution and cumulants of the number of kinks and their decay, and again find agreement with the quantum simulator results. This implies that the theoretical predictions of the generalized KZM theory, which assumes isolation from the environment, applies beyond its original scope to an open system. We support this result by extensive numerical computations. To check whether an alternative, classical interpretation of these results is possible, we used the spin-vector Monte Carlo model, a candidate classical description of the D-Wave device. We find that the degree of agreement with the experimental data from the D-Wave annealing devices is better for the KZM, a quantum theory, than for the classical spin-vector Monte Carlo model, thus favoring a quantum description of the device. Our work provides an experimental test of quantum critical dynamics in an open quantum system, and paves the way to new directions in quantum simulation experiments.

Patients with APDS1 showed variable clinical manifestations. Life-threatening progressive combined immunodeficiency and massive lymphoproliferation were common indications for HSCT. Fludarabine-based reduced-intensity conditioning-HSCT ameliorated clinical symptoms, but transplantation-related complications were frequent, including graft failure.

Haploinsufficiency of TNFAIP3 (A20) by a germline heterozygous mutation leads to the ALPS phenotype.

Steroid pulse therapy was useful to reduce the fever duration and medical costs for patients with Kawasaki disease. Steroid pulse therapy and additional IVIG treatment were not significantly different in terms of preventing the development of coronary artery aneurysm.

Fecal microflora and lactate concentrations in blood and feces obtained from a patient (a 5 year-old boy) with short-bowel syndrome (SBS) were compared during acidosis to results for the normal condition (no SBS symptoms). The taxonomical position of the lactobacilli found predominantly in the feces sample obtained 2 days before the fifth attack was also studied. The D-lactate level in serum obtained 1 day after the fourth attack was 10-fold higher than that for the normal condition, although there was not a great difference in L-lactate levels. D-Lactate (3.91 mM) and L-lactate (2.86 mM) were also detected in the feces samples collected 2 days before the fifth attack, while no lactate was detected in the feces sample for the normal condition. The counts of total fecal bacteria, especially anaerobic bacteria such as members of the family Bacteroidaceae, were found to be low. The counts of lactobacilli and the total population of lactobacilli relative to total fecal bacteria in the feces 2 days before the fifth attack (40.4%) were extremely high. In this case, a majority of the lactobacilli were D-lactate producers as determined by homolactic fermentation. These lactobacilli were identified as Lactobacillus delbrueckii subsp. lactis. The percentages of bifidobacteria relative to total fecal bacteria in feces samples obtained both 2 days before the fifth attack (50.9%) and for normal condition (61.9%) were also high, although these bacteria were L-lactate producers. In the feces samples for the normal condition, the D-lactate producers decreased to less than 10 9 per g, while the counts of L-or DL-lactate producers were 100-fold higher than the numbers in feces samples obtained 2 days before the fifth attack. These results suggested that an increase in the level of D-lactate producers, such as L. delbrueckii subsp. lactis, in the colon may be associated with the clinical expression of metabolic acidosis.