7 Search Results

We propose an autonomous quantum error correction scheme using squeezed cat (SC) code against excitation loss in continuous-variable systems. Through reservoir engineering, we show that a structured dissipation can stabilize a two-component SC while autonomously correcting the errors. The implementation of such dissipation only requires low-order nonlinear couplings among three bosonic modes or between a bosonic mode and a qutrit. While our proposed scheme is device independent, it is readily implementable with current experimental platforms such as superconducting circuits and trapped-ion systems. Compared to the stabilized cat, the stabilized SC has a much lower dominant error rate and a significantly enhanced noise bias. Furthermore, the bias-preserving operations for the SC have much lower error rates. In combination, the stabilized SC leads to substantially better logical performance when concatenating with an outer discrete-variable code. The surface-SC scheme achieves more than one order of magnitude increase in the threshold ratio between the loss rate κ₁ and the engineered dissipation rate κ₂. Under a practical noise ratio κ₁/κ₂ = 10^-3, the repetition-SC scheme can reach a 10^-15 logical error rate even with a small mean excitation number of 4, which already suffices for practically useful quantum algorithms.

A fundamental problem posed from the study of correlated electron compounds, of which heavy-fermion systems are prototypes, is the need to understand the physics of states near a quantum critical point (QCP). At a QCP, magnetic order is suppressed continuously to zero temperature and unconventional superconductivity often appears. Here, we report pressure (P)-dependent ¹¹⁵In nuclear quadrupole resonance (NQR) measurements on heavy-fermion antiferromagnet CeRh_0.5Ir_0.5In₅. These experiments reveal an antiferromagnetic (AF) QCP at \({P}_{{\rm{c}}}^{{\rm{AF}}}=1.2\) GPa where a dome of superconductivity reaches a maximum transition temperature T_c. Preceding \({P}_{{\rm{c}}}^{{\rm{AF}}}\), however, the NQR frequency ν_Q undergoes an abrupt increase at \({P}_{{\rm{c}}}^{{\rm{* }}}\) = 0.8 GPa in the zero-temperature limit, indicating a change from localized to itinerant character of cerium’s f-electron and associated small-to-large change in the Fermi surface. At \({P}_{{\rm{c}}}^{{\rm{AF}}}\) where T_c is optimized, there is an unusually large fraction of gapless excitations well below T_c that implicates spin-singlet, odd-frequency pairing symmetry.

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KLF5 and nuclear factor κB (NF-κB) regulate cell proliferation and inflammation. Vitamin D signaling through vitamin D receptor (VDR) exerts anti-proliferative and anti-inflammatory actions. However, an actual relationship between KLF5, NF-κB and VDR in the inflammation and proliferation of macrophages is still unclear. Here, we showed that LPS and proinflammatory cytokines stimulate KLF5 gene expression in macrophages, and that 1, 25(OH){sub 2}D{sub 3} suppresses LPS-induced KLF5 expression and cell proliferation via upregulation of VDR expression. Mechanistic studies suggested that KLF5 interacts with p50 subunit of NF-κB to cooperatively induce the expressions of positive cell cycle regulators cyclin B1 and Cdk1/Cdc2 in LPS-treated macrophages. Further studies revealed that 1, 25(OH){sub 2}D{sub 3}-induced interaction of VDR with p50 decreases LPS-induced interaction of KLF5 with p50. Collectively, we identify a novel regulatory pathway in which 1, 25(OH){sub 2}D{sub 3} induces VDR expression and promotes VDR interaction with p50 subunit of NF-κB, which in turn attenuates the association of KLF5 with p50 subunit of NF-κB and thus exerts anti-inflammatory and anti-proliferative effects on macrophages. - Highlights: • 1, 25(OH){sub 2}D{sub 3} suppresses LPS-induced KLF5 expression via upregulation of VDR expression. • KLF5 interacts with NF-κB-p50 to cooperatively induce the expressions of positive cell cycle regulators cyclin B1 and Cdk1/Cdc2 in LPS-treated macrophages. • 1,25(OH){sub 2}D{sub 3} induces interaction of VDR with p50.

The cancer cells residing in the hypoxic layer are resistant to radiation and these are ones responsible for cancer recurrence after radiation therapy. One of the reasons why hypoxic cancer cells acquire radioresistance may be attributable to changes in the gene expression profile by the activation of hypoxia inducible factors (HIFs). However, the details underlying this process remain unknown. In this study, we investigated the effects of knockdown of HIF subunit genes to elucidate how HIF subunit genes may be involved in the radioresistance acquired by HeLa cells following exposure to a hypoxia mimic. Interestingly, HIF-1α and HIF-2α seemed mutually complementary for each other when either of them was suppressed. We thus suppressed the expression of both genes simultaneously. To do this, we developed a short hairpin RNA (shRNA) targeting a high homology region between HIF-1α and HIF-2α. It was shown that the expression of the shRNA effectively suppressed the acquisition of radioresistance following the hypoxia mimic. Moreover, it was confirmed that suppression of both subunits resulted in the downregulation of stem cell markers and the suppression of spheroid formation during the hypoxia mimicking-conditions. This shRNA-mediated knockdown method targeting a common region shared by a family of genes may offer a new candidate cancer treatment. - Highlights: • Incubation with CoCl{sub 2} confers radioresistance to HeLa cells. • Both HIF-1α and HIF-2α are involved in the acquisition of radioresistance. • An shRNA to a homology region of HIF-1α and HIF-2α suppressed the radioresistance. • The shRNA decreased cells with stem cell markers and a stem cell phenotype.