Tetris: A compilation Framework for VQE Applications

Quantum computing has shown promise in solving complex problems by leveraging the principles of superposition and entanglement. The Variational Quantum Eigensolver (VQE) algorithm stands as a pivotal approach in the realm of quantum algorithms, enabling the simulation of quantum systems on quantum hardware. In this paper, we introduce two innovative techniques, namely "Tetris" and "Fast Bridging," designed to enhance the efficiency and effectiveness of VQE tasks. The "Tetris" technique addresses a crucial aspect of VQE optimization by unveiling cancellation opportunities within the logical circuit phase of UCCSD ansatz. Tetris demonstrates a remarkable reduction up to 20% in CNOT gate counts, about 119048 CNOT gates, and 30% depth reduction compared to the state-of-the-art compiler 'Paulihedral'. In addition to Tetris, we present the "Fast Bridging" technique as an alternative to the conventional qubit routing methods that heavily rely on swap operations. The fast bridging offers a novel approach to qubit routing, mitigating the limitations associated with swap-heavy routing. By integrating the fast bridging into the VQE framework, we observe further reductions in CNOT gate counts and circuit depth. The bridging technique can achieve up to 27% CNOT gate reduction in the QAOA application. Through a combination of Tetris and the fast bridging, we present a comprehensive strategy for enhancing VQE performance. Our experimental results showcase the effectiveness of Tetris in uncovering cancellation opportunities and demonstrate the symbiotic relationship between Tetris and the fast bridging in minimizing gate counts and circuit depth. This paper contributes not only to the advancement of VQE techniques but also to the broader field of quantum algorithm optimization

Microtissues Enhance Smooth Muscle Differentiation and Cell Viability of hADSCs for Three Dimensional Bioprinting

Smooth muscle differentiated human adipose derived stem cells (hADSCs) provide a crucial stem cell source for urinary tissue engineering, but the induction of hADSCs for smooth muscle differentiation still has several issues to overcome, including a relatively long induction time and equipment dependence, which limits access to abundant stem cells within a short period of time for further application. Three-dimensional (3D) bioprinting holds great promise in regenerative medicine due to its controllable construction of a designed 3D structure. When evenly mixed with bioink, stem cells can be spatially distributed within a bioprinted 3D structure, thus avoiding drawbacks such as, stem cell detachment in a conventional cell-scaffold strategy. Notwithstanding the advantages mentioned above, cell viability is often compromised during 3D bioprinting, which is often due to pressure during the bioprinting process. The objective of our study was to improve the efficiency of hADSC smooth muscle differentiation and cell viability of a 3D bioprinted structure. Here, we employed the hanging-drop method to generate hADSC microtissues in a smooth muscle inductive medium containing human transforming growth factor β1 and bioprinted the induced microtissues onto a 3D structure. After 3 days of smooth muscle induction, the expression of α-smooth muscle actin and smoothelin was higher in microtissues than in their counterpart monolayer cultured hADSCs, as confirmed by immunofluorescence and western blotting analysis. The semi-quantitative assay showed that the expression of α-smooth muscle actin (α-SMA) was 0.218 ± 0.077 in MTs and 0.082 ± 0.007 in Controls; smoothelin expression was 0.319 ± 0.02 in MTs and 0.178 ± 0.06 in Controls. Induced MTs maintained their phenotype after the bioprinting process. Live/dead and cell count kit 8 assays showed that cell viability and cell proliferation in the 3D structure printed with microtissues were higher at all time points compared to the conventional single-cell bioprinting strategy (mean cell viability was 88.16 ± 3.98 vs. 61.76 ± 15% for microtissues and single-cells, respectively). These results provide a novel way to enhance the smooth muscle differentiation of hADSCs and a simple method to maintain better cell viability in 3D bioprinting

Disentangling superconducting and magnetic orders in NaFe_1-xNi_xAs using muon spin rotation

Muon spin rotation and relaxation studies have been performed on a "111" family of iron-based superconductors NaFe_1-xNi_xAs. Static magnetic order was characterized by obtaining the temperature and doping dependences of the local ordered magnetic moment size and the volume fraction of the magnetically ordered regions. For x = 0 and 0.4 %, a transition to a nearly-homogeneous long range magnetically ordered state is observed, while for higher x than 0.4 % magnetic order becomes more disordered and is completely suppressed for x = 1.5 %. The magnetic volume fraction continuously decreases with increasing x. The combination of magnetic and superconducting volumes implies that a spatially-overlapping coexistence of magnetism and superconductivity spans a large region of the T-x phase diagram for NaFe_1-xNi_xAs . A strong reduction of both the ordered moment size and the volume fraction is observed below the superconducting T_C for x = 0.6, 1.0, and 1.3 %, in contrast to other iron pnictides in which one of these two parameters exhibits a reduction below TC, but not both. The suppression of magnetic order is further enhanced with increased Ni doping, leading to a reentrant non-magnetic state below T_C for x = 1.3 %. The reentrant behavior indicates an interplay between antiferromagnetism and superconductivity involving competition for the same electrons. These observations are consistent with the sign-changing s-wave superconducting state, which is expected to appear on the verge of microscopic coexistence and phase separation with magnetism. We also present a universal linear relationship between the local ordered moment size and the antiferromagnetic ordering temperature TN across a variety of iron-based superconductors. We argue that this linear relationship is consistent with an itinerant-electron approach, in which Fermi surface nesting drives antiferromagnetic ordering.Comment: 20 pages, 14 figures, Correspondence should be addressed to Prof. Yasutomo Uemura: [email protected]

Benzyl isothiocyanate induces apoptosis and inhibits tumor growth in canine mammary carcinoma via down-regulation of the cyclin B1/Cdk1 pathway

Background: Canine mammary carcinoma is common in female dogs, and its poor prognosis remains a serious clinical challenge, especially in developing countries. Benzyl isothiocyanate (BITC) has attracted great interest because of its inhibitory effect against tumor activity. However, its effect and the underlying mechanisms of action in canine mammary cancer are not well-understood. Here, we show that BITC suppresses mammary tumor growth, both in vivo and in vitro, and reveal some of the potential mechanisms involved. Methods: The effect of BITC on canine mammary cancer was evaluated on CIPp and CMT-7364, canine mammary carcinoma lines. The cell lines were treated with BITC and then subjected to wound healing and invasion assays. Cell cycles and apoptosis were measured using flow cytometry; TUNEL assay; immunohistochemistry (IHC) for caspase 3, caspase 9, and cyclin D1; hematoxylin and eosin (H&E) staining; and/or quantitative polymerase chain reaction (qPCR). Results: BITC showed a strong suppressive effect in both CIPp and CMT-7364 cells by inhibiting cell growth in vitro; these effects were both dose- and time-dependent. BITC also inhibited migration and invasion of CIPp and CMT-7364 cells. BITC induced G2 arrest and apoptosis, decreasing tumor growth in nude mice by downregulation of cyclin B1 and Cdk1 expression. Conclusion: BITC suppressed both invasion and migration of CIPp and CMT-7364 cells and induced apoptosis. BITC inhibited canine mammary tumor growth by suppressing cyclinB1 and Cdk1 expression in nude mice