Functional completeness of planar Rydberg blockade structures

The construction of Hilbert spaces that are characterized by local constraints as the low-energy sectors of microscopic models is an important step towards the realization of a wide range of quantum phases with long-range entanglement and emergent gauge fields. Here we show that planar structures of trapped atoms in the Rydberg blockade regime are functionally complete: Their ground state manifold can realize any Hilbert space that can be characterized by local constraints in the product basis. We introduce a versatile framework, together with a set of provably minimal logic primitives as building blocks, to implement these constraints. As examples, we present lattice realizations of the string-net Hilbert spaces that underlie the surface code and the Fibonacci anyon model. We discuss possible optimizations of planar Rydberg structures to increase their geometrical robustness.Comment: 33 pages, 14 figures, v2: fixed typos, added additional references and comment

Epitopes Targeted by Bullous Pemphigoid T Lymphocytes and Autoantibodies Map to the Same Sites on the Bullous Pemphigoid 180 Ectodomain

Bullous pemphigoid is a blistering skin disease characterized by autoantibodies directed against the NC16A domain of bullous pemphigoid 180 (collagen XVII), a transmembrane protein of epidermal basal cells. Passive transfer studies in mice have shown that antibodies that bind to this immunodominant region of bullous pemphigoid 180 are capable of inducing a skin disease that closely mimics bullous pemphigoid, supporting the hypothesis that epitopes within NC16A are involved in the pathogenesis of bullous pemphigoid. In this study, we examined the autoimmune T cell response in bullous pemphigoid patients. T cells from eight of 12 bullous pemphigoid patients, all of whom had circulating anti-bullous pemphigoid 180 autoantibodies, showed a specific proliferative response to recombinant forms of NC16A. T cell lines and clones developed from four of these patients recognize the same NC16A peptides as those targeted by autoantibodies from the corresponding individuals. These NC16A-responding T lymphocytes express alpha/beta T cell receptors and CD4 memory T cell surface markers and exhibited a Th1/Th2 mixed cytokine profile that may support the production of antibodies. This new information will aid in defining the key steps involved in the development of the autoimmune response in bullous pemphigoid

Successful renal re-transplantation in the presence of pre-existing anti-DQ5 antibodies when there was zero mismatch at class I human leukocyte antigen A, B, & C: a case report

<p>Abstract</p> <p>Introduction</p> <p>Hyperacute rejection may be prevented by avoiding the transplantation of kidneys into patients with pre-existing anti-donor Class I human leukocyte antigen antibodies. However, the role of anti-donor-Class II-human leukocyte antigen-DQ antibodies is not established. The question is ever more relevant as more sensitive cross-matching techniques detect many additional antibodies during the final crossmatch. We now report successful renal transplantation of a patient who had pre-existing antibodies against his donor's human leukocyte antigen-DQ5.</p> <p>Case presentation</p> <p>Our patient, a Caucasian man, was 34 years of age when he received his first deceased donor renal transplant. After 8 years, his first transplant failed from chronic allograft dysfunction and an earlier bout of Banff 1A cellular rejection. The second deceased donor kidney transplant was initially allocated to the patient due to a 0 out of 6 mismatch. The B cell crossmatch was mildly positive, while the T Cell crossmatch was negative. Subsequent assays showed that the patient had preformed antibodies for human leukocyte antigen DQ5 against his second donor. Despite having preformed antibodies against the donor, the patient continues to have excellent allograft function two years after his second renal transplant.</p> <p>Conclusion</p> <p>The presence of pre-existing antibodies against human leukocyte antigen DQ5 does not preclude transplantation. The relevance of having other antibodies against class II human leukocyte antigens prior to transplantation remains to be studied.</p

A Large-Scale Rheumatoid Arthritis Genetic Study Identifies Association at Chromosome 9q33.2

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease affecting both joints and extra-articular tissues. Although some genetic risk factors for RA are well-established, most notably HLA-DRB1 and PTPN22, these markers do not fully account for the observed heritability. To identify additional susceptibility loci, we carried out a multi-tiered, case-control association study, genotyping 25,966 putative functional SNPs in 475 white North American RA patients and 475 matched controls. Significant markers were genotyped in two additional, independent, white case-control sample sets (661 cases/1322 controls from North America and 596 cases/705 controls from The Netherlands) identifying a SNP, rs1953126, on chromosome 9q33.2 that was significantly associated with RA (ORcommon = 1.28, trend Pcomb = 1.45E-06). Through a comprehensive fine-scale-mapping SNP-selection procedure, 137 additional SNPs in a 668 kb region from MEGF9 to STOM on 9q33.2 were chosen for follow-up genotyping in a staged-approach. Significant single marker results (Pcomb<0.01) spanned a large 525 kb region from FBXW2 to GSN. However, a variety of analyses identified SNPs in a 70 kb region extending from the third intron of PHF19 across TRAF1 into the TRAF1-C5 intergenic region, but excluding the C5 coding region, as the most interesting (trend Pcomb: 1.45E-06 → 5.41E-09). The observed association patterns for these SNPs had heightened statistical significance and a higher degree of consistency across sample sets. In addition, the allele frequencies for these SNPs displayed reduced variability between control groups when compared to other SNPs. Lastly, in combination with the other two known genetic risk factors, HLA-DRB1 and PTPN22, the variants reported here generate more than a 45-fold RA-risk differential