Quantum Circuit Studies with Two-Level Defects of Aluminum Oxide in a Polycrystalline Phase, Amorphous Phase, and at a Metal Surface

This thesis reports on recent achievements toward understanding the nanoscale two-level systems (TLS) within aluminum oxide layers. I will discuss novel experimental and theoretical methods using superconducting resonator data to characterize the TLSs, which are deleterious to qubit coherence. This includes (1) a traditional power dependent loss, which provides the information of collective TLS effects, (2) spectroscopy of individual TLSs by DC-tuning, and (3) two-tone spectroscopy of ensemble TLSs by a second saturation tone. We find that the behaviors of TLSs in different structural phases have distinguishing features. Utilizing the DC-tuning feature of our sensor, we further extract dipole moments from individual TLSs and provide the moment histograms of the two aluminum oxide film types. We observe polycrystalline oxide has an average dipole moment = 2.6 Debye and a single-peak histogram consistent with a single TLS origin. On the other hand, TLSs in amorphous oxide have a wide spread of dipole moment values probably due to oxygen deficiency. Saturation slopes of TLSs in bulk films (polycrystalline and amorphous phases) show a square root dependence of power indicating an ignorable TLS-TLS interaction. Moreover, TLSs in the polycrystalline phase are more stable in the time domain than TLSs in the amorphous phase. Unlike the previous two bulk TLSs, TLSs at the metal-air interface require an explanation from the model assuming TLS frequencies are under stochastic fluctuations originating from TLS-TLS interaction since we find a weak power dependence. We also demonstrate the first published transmon qubits which are solely made from optical lithography. They have a comparable relaxation time and junction resistance to those made from e-beam lithography

Probing Hundreds of Individual Quantum Defects in Polycrystalline and Amorphous Alumina

Quantum two-level systems (TLSs) are present in the materials of qubits and are considered defects because they limit qubit coherence. For superconducting qubits, the quintessential Josephson junction barrier is made of amorphous alumina, which hosts TLSs. However, TLSs are not understood generally -- either structurally or in atomic composition. In this study, we greatly extend the quantitative data available on TLSs by reporting on the physical dipole moment in two alumina types: polycrystalline γ−Al$_2$O$_3$ and amorphous a−AlO$_x$. To obtain the dipole moments p$_z$, rather from the less-structural coupling parameter g, we tune individual TLSs with an external electric field to extract the p$_z$ of the TLSs in a cavity QED system. We find a clear difference in the dipole moment distribution from the film types, indicating a difference in TLS structures. A large sample of approximately 400 individual TLSs are analyzed from the polycrystalline film type. Their dipoles along the growth direction p$_z$ have a mean value of 2.6±0.3 Debye (D) and standard deviation σ = 1.6±0.2 D . The material distribution fits well to a single Gaussian function. Approximately 200 individual TLSs are analyzed from amorphous films. Both the mean p$_z$ =4.6±0.5 D and σ =2.5±0.3 D are larger. Amorphous alumina also has some very large p$_z$, > 8.6 D, in contrast to polycrystalline which has none of this moment. These large moments agree only with oxygen-based TLS models. Based on data and the candidate models (delocalized O and hydrogen-based TLSs), we find polycrystalline alumina has smaller ratio of O-based to H-based TLS than amorphous alumina

Recombinant VP1, an Akt Inhibitor, Suppresses Progression of Hepatocellular Carcinoma by Inducing Apoptosis and Modulation of CCL2 Production

BACKGROUND: The application of viral elements in tumor therapy is one facet of cancer research. Recombinant capsid protein VP1 (rVP1) of foot-and-mouth disease virus has previously been demonstrated to induce apoptosis in cancer cell lines. Here, we aim to further investigate its apoptotic mechanism and possible anti-metastatic effect in murine models of hepatocellular carcinoma (HCC), one of the most common human cancers worldwide. METHODOLOGY/PRINCIPAL FINDINGS: Treatment with rVP1 inhibited cell proliferation in two murine HCC cell lines, BNL and Hepa1-6, with IC₅₀ values in the range of 0.1-0.2 µM. rVP1 also induced apoptosis in these cells, which was mediated by Akt deactivation and dissociation of Ku70-Bax, and resulted in conformational changes and mitochondrial translocation of Bax, leading to the activation of caspases-9, -3 and -7. Treatment with 0.025 µM rVP1, which did not affect the viability of normal hepatocytes, suppressed cell migration and invasion via attenuating CCL2 production. The production of CCL2 was modulated by Akt-dependent NF-κB activation that was decreased after rVP1 treatment. The in vivo antitumor effects of rVP1 were assessed in both subcutaneous and orthotopic mouse models of HCC in immune-competent BALB/c mice. Intratumoral delivery of rVP1 inhibited subcutaneous tumor growth as a result of increased apoptosis. Intravenous administration of rVP1 in an orthotopic HCC model suppressed tumor growth, inhibited intra-hepatic metastasis, and prolonged survival. Furthermore, a decrease in the serum level of CCL2 was observed in rVP1-treated mice. CONCLUSIONS/SIGNIFICANCE: The data presented herein suggest that, via inhibiting Akt phosphorylation, rVP1 suppresses the growth, migration, and invasion of murine HCC cells by inducing apoptosis and attenuating CCL2 production both in vitro and in vivo. Recombinant protein VP1 thus has the potential to be developed as a new therapeutic agent for HCC

Experimentally revealing anomalously large dipoles in the dielectric of a quantum circuit

Quantum two-level systems (TLSs) intrinsic to glasses induce decoherence in many modern quantum devices, such as superconducting qubits. Although the low-temperature physics of these TLSs is usually well-explained by a phenomenological standard tunneling model of independent TLSs, the nature of these TLSs, as well as their behavior out of equilibrium and at high energies above 1 K, remain inconclusive. Here we measure the non-equilibrium dielectric loss of TLSs in amorphous silicon using a superconducting resonator, where energies of TLSs are varied in time using a swept electric field. Our results show the existence of two distinct ensembles of TLSs, interacting weakly and strongly with phonons, where the latter also possesses anomalously large electric dipole moment. These results may shed new light on the low temperature characteristics of amorphous solids, and hold implications to experiments and applications in quantum devices using time-varying electric fields

Expression of PRDX6 Correlates with Migration and Invasiveness of Colorectal Cancer Cells

Background/Aims: Colorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer-related deaths worldwide. PRDXs are antioxidant enzymes that play an important role in cell differentiation, proliferation and apoptosis and have diverse functions in malignancy development. However, the mechanism of aberrant overexpression of PRDX6 in CRC remains unclear. Methods: Boyden chamber assay, flow cytometry and a lentiviral shRNA targeting PRDX6 and transient transfection with pCMV-6-PRDX6 plasmid were used to examine the role of PRDX6 in the proliferation capacity and invasiveness of CRC cells. Immunohistochemistry (IHC) with tissue array containing 40 paraffin- embedded CRC tissue specimens and Western blot assays were used to detect target proteins. Results: PRDX6 was significantly up-expressed in different comparisons of metastasis of colorectal adenomas in node-positive CRC (P = 0.03). In in vitro HCT-116, PRDX6 silencing markedly suppressed CRC cell migration and invasiveness while also inducing cell cycle arrest as well as the generation of reactive oxygen species (ROS); specific overexpression of PRDX6 had the opposite effect. Mechanistically, the PRDX6 inactivation displayed decreased levels of PRDX6, N-cadherin, β-catenin, Vimentin, Slug, Snail and Twist-1 through the activation of the PI3K/ AKT/p38/p50 pathways, but they were also significantly inhibited by PRDX6 transfectants. There was also increased transcriptional activation of dimethylation of histone H3 lysine 4 (H3K4me3) of PRDX6 promoter via the activation of the PI3K/Akt/NFkB pathways. Conclusion: Our findings demonstrated that PRDX6 expression plays a characteristic growth-promoting role in CRC metastasis. This study suggests that PRDX6 may serve as a biomarker of node-positive status and may have a role as an important endogenous regulator of cancer cell tumorigenicity in CRC. PRDX6 may also be an effective therapeutic target