4-bit Factorization Circuit Composed of Multiplier Units with Superconducting Flux Qubits toward Quantum Annealing

Prime factorization (P = M*N) is considered to be a promising application in quantum computations. We perform 4-bit factorization in experiments using a superconducting flux qubit toward quantum annealing. Our proposed method uses a superconducting quantum circuit implementing a multiplier Hamiltonian, which provides combinations of M and N as a factorization solution after quantum annealing when the integer P is initially set. The circuit comprises multiple multiplier units combined with connection qubits. The key points are a native implementation of the multiplier Hamiltonian to the superconducting quantum circuit and its fabrication using a Nb multilayer process with a Josephson junction dedicated to the qubit. The 4-bit factorization circuit comprises 32 superconducting flux qubits. Our method has superior scalability because the Hamiltonian is implemented with fewer qubits than in conventional methods using a chimera graph architecture. We perform experiments at 10 mK to clarify the validity of interconnections of a multiplier unit using qubits. We demonstrate experiments at 4.2 K and simulations for the factorization of integers 4, 6, and 9.Comment: Main text (9 pages, 5 figures) and Appendix (8 pages, 7 figures). Submitted in IEEE Transactions on Applied Superconductivity (under review

PCNA–MutSα-mediated binding of MutLα to replicative DNA with mismatched bases to induce apoptosis in human cells

Modified bases, such as O(6)-methylguanines, are produced in cells exposed to alkylating agents and cause apoptosis. In human cells treated with N-methyl-N-nitrosourea, we detected a protein complex composed of MutSα, MutLα and PCNA on damaged DNA by immunoprecipitation method using chromatin extracts, in which protein–protein interactions were stabilized by chemical crosslinking. Time course experiments revealed that MutSα, consisting of MSH2 and MSH6 proteins, and PCNA bind to DNA to form an initial complex, and MutLα, composed of MLH1 and PMS2, binds to the complex when the DNA is damaged. This sequential mode of binding was further confirmed by the findings that the association of PCNA–MutSα complex on chromatin was observed even in the cells that lack MLH1, whereas in the absence of MSH2 no association of MutLα with the chromatin was achieved. Moreover, reduction in the PCNA content by small-interfering RNA or inhibition of DNA replication by aphidicolin, an inhibitor of DNA polymerase, significantly reduced the levels of the PCNA–MutSα–MutLα complex and also suppressed an increase in the caspase-3 activity, a hallmark for the induction of apoptosis. These observations imply that the induction of apoptosis is coupled with the progression of DNA replication through the action of PCNA

Experimental Demonstrations of Native Implementation of Boolean Logic Hamiltonian in a Superconducting Quantum Annealer

Experimental demonstrations of quantum annealing with native implementation of Boolean logic Hamiltonians are reported. As a superconducting integrated circuit, a problem Hamiltonian whose set of ground states is consistent with a given truth table is implemented for quantum annealing with no redundant qubits. As examples of the truth table, NAND and NOR are successfully fabricated as an identical circuit. Similarly, a native implementation of a multiplier comprising six superconducting flux qubits is also demonstrated. These native implementations of Hamiltonians consistent with Boolean logic provide an efficient and scalable way of applying annealing computation to so-called circuit satisfiability problems that aim to find a set of inputs consistent with a given output over any Boolean logic functions, especially those like factorization through a multiplier Hamiltonian. A proof-of-concept demonstration of a hybrid computing architecture for domain-specific quantum computing is described.Comment: 12 pages, 11 figure

Scalable interconnection using a superconducting flux qubit

Abstract Superconducting quantum computers are rapidly reaching scales where bottlenecks to scaling arise from the practical aspects of the fabrication process. To improve quantum computer performance, implementation technology that guarantees the scalability of the number of qubits is essential. Increasing the degrees of freedom in routing by 2.5-dimensional implementation is important for realizing circuit scalability. We report an implementation technology to overcome the scaling bottlenecks using a reliable connection qubit with a demonstration of quantum annealing. The method comprises interconnection based on quantum annealing using a superconducting flux qubit, precise coupling status control, and flip-chip bonding. We perform experiments and simulations with a proof-of-concept demonstration of qubit coupling via interconnection using a flux qubit. The coupling status is strictly controllable by quantum annealing. A low-temperature flip-chip bonding technology is introduced for the 2.5-dimensional interconnection. The superconducting flux qubit, formed across two different chips via bumps, is demonstrated for the first time to show a state transition like that in a conventional qubit. The quantum annealing flux qubit and flip-chip bonding enable new interconnections between qubits. A perspective on the possibility of applying this technology to the connection between gate-type qubits is described

The Identification of a Novel Gene, <em>MAPO2</em>, That Is Involved in the Induction of Apoptosis Triggered by O⁶-Methylguanine

<div><p>O⁶-Methylguanine, one of alkylated DNA bases, is especially mutagenic. Cells containing this lesion are eliminated by induction of apoptosis, associated with the function of mismatch repair (MMR) proteins. A retrovirus-mediated gene-trap mutagenesis was used to isolate new genes related to the induction of apoptosis, triggered by the treatment with an alkylating agent, <em>N</em>-methyl-<em>N</em>-nitrosourea (MNU). This report describes the identification of a novel gene, <em>MAPO2</em> (O⁶-<u>m</u>ethylguanine-induced <u>apo</u>ptosis <u>2</u>), which is originally annotated as <em>C1orf201</em>. The <em>MAPO2</em> gene is conserved among a wide variety of multicellular organisms and encodes a protein containing characteristic PxPxxY repeats. To elucidate the function of the gene product in the apoptosis pathway, a human cell line derived from HeLa MR cells, in which the <em>MAPO2</em> gene was stably knocked down by expressing specific miRNA, was constructed. The knockdown cells grew at the same rate as HeLa MR, thus indicating that MAPO2 played no role in the cellular growth. After exposure to MNU, HeLa MR cells and the knockdown cells underwent cell cycle arrest at G₂/M phase, however, the production of the sub-G₁ population in the knockdown cells was significantly suppressed in comparison to that in HeLa MR cells. Moreover, the activation of BAK and caspase-3, and depolarization of mitochondrial membrane, hallmarks for the induction of apoptosis, were also suppressed in the knockdown cells. These results suggest that the <em>MAPO2</em> gene product might positively contribute to the induction of apoptosis triggered by O⁶-methylguanine.</p> </div