The Quantum Socket: Three-Dimensional Wiring for Extensible Quantum Computing

Quantum computing architectures are on the verge of scalability, a key requirement for the implementation of a universal quantum computer. The next stage in this quest is the realization of quantum error correction codes, which will mitigate the impact of faulty quantum information on a quantum computer. Architectures with ten or more quantum bits (qubits) have been realized using trapped ions and superconducting circuits. While these implementations are potentially scalable, true scalability will require systems engineering to combine quantum and classical hardware. One technology demanding imminent efforts is the realization of a suitable wiring method for the control and measurement of a large number of qubits. In this work, we introduce an interconnect solution for solid-state qubits: The quantum socket. The quantum socket fully exploits the third dimension to connect classical electronics to qubits with higher density and better performance than two-dimensional methods based on wire bonding. The quantum socket is based on spring-mounted micro wires the three-dimensional wires that push directly on a micro-fabricated chip, making electrical contact. A small wire cross section (~1 mmm), nearly non-magnetic components, and functionality at low temperatures make the quantum socket ideal to operate solid-state qubits. The wires have a coaxial geometry and operate over a frequency range from DC to 8 GHz, with a contact resistance of ~150 mohm, an impedance mismatch of ~10 ohm, and minimal crosstalk. As a proof of principle, we fabricated and used a quantum socket to measure superconducting resonators at a temperature of ~10 mK.Comment: Main: 31 pages, 19 figs., 8 tables, 8 apps.; suppl.: 4 pages, 5 figs. (HiRes figs. and movies on request). Submitte

The effect of quasiparticle-self-energy on Cd2Re2O7 superconductor

The magnitude and the temperature dependence of the superconducting order parameter Δ(T) of single-crystals of CdThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Genomic Mismatch at LIMS1 Locus and Kidney Allograft Rejection

Background In the context of kidney transplantation, genomic incompatibilities between donor and recipient may lead to allosensitization against new antigens. We hypothesized that recessive inheritance of gene-disrupting variants may represent a risk factor for allograft rejection. Methods We performed a two-stage genetic association study of kidney allograft rejection. In the first stage, we performed a recessive association screen of 50 common gene-intersecting deletion polymorphisms in a cohort of kidney transplant recipients. In the second stage, we replicated our findings in three independent cohorts of donor-recipient pairs. We defined genomic collision as a specific donor-recipient genotype combination in which a recipient who was homozygous for a gene-intersecting deletion received a transplant from a nonhomozygous donor. Identification of alloantibodies was performed with the use of protein arrays, enzyme-linked immunosorbent assays, and Western blot analyses. Results In the discovery cohort, which included 705 recipients, we found a significant association with allograft rejection at the LIMS1 locus represented by rs893403 (hazard ratio with the risk genotype vs. nonrisk genotypes, 1.84; 95% confidence interval [CI], 1.35 to 2.50; P=9.8x10(-5)). This effect was replicated under the genomic-collision model in three independent cohorts involving a total of 2004 donor-recipient pairs (hazard ratio, 1.55; 95% CI, 1.25 to 1.93; P=6.5x10(-5)). In the combined analysis (discovery cohort plus replication cohorts), the risk genotype was associated with a higher risk of rejection than the nonrisk genotype (hazard ratio, 1.63; 95% CI, 1.37 to 1.95; P=4.7x10(-8)). We identified a specific antibody response against LIMS1, a kidney-expressed protein encoded within the collision locus. The response involved predominantly IgG2 and IgG3 antibody subclasses. Conclusions We found that the LIMS1 locus appeared to encode a minor histocompatibility antigen. Genomic collision at this locus was associated with rejection of the kidney allograft and with production of anti-LIMS1 IgG2 and IgG3