Liquid phase immunoassay utilizing magnetic marker and high Tc superconducting quantum interference device

We have developed a liquid phase immunoassay system utilizing a magnetic marker and a superconducting quantum interference device (SQUID). In this system, the magnetic marker was used to detect the biological material called antigen. The magnetic marker was designed so as to generate a remanence, and the remanence field of the markers that bound to the antigens was measured with the SQUID. The measurement was performed in a solution that contained both the bound and free (or unbound) markers, i.e., without using the so-called bound/free (BF) separation process. The Brownian rotation of the free markers in the solution was used to distinguish the bound markers from the free ones. Using the system, we conducted the detection of biological material called IgE without BF separation. At present, we could detect the IgE down to 7 pg (or 39 amol

Extracting higher central charge from a single wave function

A (2+1)D topologically ordered phase may or may not have a gappable edge, even if its chiral central charge $c_-$ is vanishing. Recently, it is discovered that a quantity regarded as a ``higher'' version of chiral central charge gives a further obstruction beyond $c_-$ to gapping out the edge. In this Letter, we show that the higher central charges can be characterized by the expectation value of the \textit{partial rotation} operator acting on the wavefunction of the topologically ordered state. This allows us to extract the higher central charge from a single wavefunction, which can be evaluated on a quantum computer. Our characterization of the higher central charge is analytically derived from the modular properties of edge conformal field theory, as well as the numerical results with the $\nu=1/2$ bosonic Laughlin state and the non-Abelian gapped phase of the Kitaev honeycomb model, which corresponds to $\mathrm{U}(1)_2$ and Ising topological order respectively. The letter establishes a numerical method to obtain a set of obstructions to the gappable edge of (2+1)D bosonic topological order beyond $c_-$. We also point out that the expectation values of the partial rotation on a single wavefunction put a constraint on the low-energy spectrum of the bulk-boundary system of (2+1)D bosonic topological order, reminiscent of the Lieb-Schultz-Mattis type theorems.Comment: 16 pages, 12 figure

Universal tripartite entanglement in one-dimensional many-body systems

Motivated by conjectures in holography relating the entanglement of purification and reflected entropy to the entanglement wedge cross-section, we introduce two related non-negative measures of tripartite entanglement $g$ and $h$. We prove structure theorems which show that states with nonzero $g$ or $h$ have nontrivial tripartite entanglement. We then establish that in 1D these tripartite entanglement measures are universal quantities that depend only on the emergent low-energy theory. For a gapped system, we argue that either $g\neq 0$ and $h=0$ or $g=h=0$, depending on whether the ground state has long-range order. For a critical system, we develop a numerical algorithm for computing $g$ and $h$ from a lattice model. We compute $g$ and $h$ for various CFTs and show that $h$ depends only on the central charge whereas $g$ depends on the whole operator content.Comment: 5+16 pages, 4+5 figure

Genetic and epigenetic alterations on the short arm of chromosome 11 are involved in a majority of sporadic Wilms' tumours

Wilms' tumour is one of the most common solid tumours of childhood. 11p13 (WT1 locus) and 11p15.5 (WT2 locus) are known to have genetic or epigenetic aberrations in these tumours. In Wilms' tumours, mutation of the Wilms tumour 1 (WT1) gene at the WT1 locus has been reported, and the WT2 locus, comprising the two independent imprinted domains IGF2/H19 and KIP2/LIT1, can undergo maternal deletion or alterations associated with imprinting. Although these alterations have been identified in many studies, it is still not clear how frequently combined genetic and epigenetic alterations of these loci are involved in Wilms' tumours or how these alterations occur. To answer both questions, we performed genetic and epigenetic analyses of these loci, together with an additional gene, CTNNB1, in 35 sporadic Wilms' tumours. Loss of heterozygosity of 11p15.5 and loss of imprinting of IGF2 were the most frequent genetic (29%) and epigenetic (40%) alterations in Wilms' tumours, respectively. In total, 83% of the tumours had at least one alteration at 11p15.5 and/or 11p13. One-third of the tumours had alterations at multiple loci. Our results suggest that chromosome 11p is not only genetically but also epigenetically critical for the majority of Wilms' tumours