ABSTRACT
Quantum low density parity check (LDPC) codes may provide a path to build low-overhead fault-tolerant quantum computers. However, as general LDPC codes lack geometric constraints, naïve layouts couple many distant qubits with crossing connections which could be hard to build in hardware and could result in performance-degrading crosstalk. We propose a 2D layout for quantum LDPC codes by decomposing their Tanner graphs into a small number of planar layers. Each layer contains long-range connections which do not cross. For any Calderbank-Shor-Steane code with a degree-δ Tanner graph, we design stabilizer measurement circuits with depth at most (2δ+2) using at most âδ/2â layers. We observe a circuit-noise threshold of 0.28% for a positive-rate code family using 49 physical qubits per logical qubit. For a physical error rate of 10^{-4}, this family reaches a logical error rate of 10^{-15} using fourteen times fewer physical qubits than the surface code.
ABSTRACT
Insulin-like 3 (INSL3), a Leydig cell-specific hormone, is essential for testis descent during foetal life and bone metabolism in adults. Despite its essential roles in male reproductive and bone health, very little is known regarding its transcriptional regulation in Leydig cells. To date, few transcription factors have been shown to activate INSL3 promoter activity: the nuclear receptors AR, NUR77, COUP-TFII and SF1. To identify additional regulators, we have isolated and performed a detailed analysis of a 1.1 kb human INSL3 promoter fragment. Through 5' progressive deletions and site-directed mutagenesis, we have mapped a 10 bp element responsible for about 80% of INSL3 promoter activity in Leydig cells. This element is identical to the CPE element of the placental-specific glycoprotein-5 (PSG5) promoter that is recognized by the developmental regulator Krüppel-like factor 6 (KLF6). Using PCR and western blotting, we found that KLF6 is expressed in several Leydig and Sertoli cell lines. Furthermore, immunohistochemistry on adult mouse testis revealed the presence of KLF6 in the nuclei of both Leydig and Sertoli cells. KLF6 binds to the 10 bp KLF element at -108 bp and activates the -1.1 kb human, but not the mouse, INSL3 promoter. KLF6-mediated activation of the human INSL3 promoter required an intact KLF element as well as Leydig/Sertoli-enriched factors because KLF6 did not stimulate the human INSL3 promoter activity in CV-1 fibroblast cells. Consistent with this, we found that KLF6 transcriptionally cooperates with NUR77 and SF1. Collectively, our results identify KLF6 as a regulator of human INSL3 transcription.
