771 research outputs found

    Engineering of Chern insulators and circuits of topological edge states

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    Impurities embedded in electronic systems induce bound states which under certain circumstances can hybridize and lead to impurity bands. Doping of insulators with impurities has been identified as a promising route towards engineering electronic topological states of matter. In this paper we show how to realize tuneable Chern insulators starting from a three dimensional topological insulator whose surface is gapped and intentionally doped with magnetic impurities. The main advantage of the protocol is that it is robust, and in particular not very sensitive to the impurity configuration. We explicitly demonstrate this for a square lattice of impurities as well as a random lattice. In both cases we show that it is possible to change the Chern number of the system by one through manipulating its topological state. We also discuss how this can be used to engineer circuits of edge channels.Comment: 9 pages, 6 figure

    Wiedemann-Franz law in a non-Fermi liquid and Majorana central charge: Thermoelectric transport in a two-channel Kondo system

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    Quantum dot devices allow one to access the critical point of the two-channel Kondo model. The effective critical theory involves a free Majorana fermion quasiparticle localized on the dot. As a consequence, this critical point shows both the phenomenon of non-Fermi liquid physics and fractionalization. Although a violation of the Wiedemann-Franz law is considered a defining feature of non-Fermi liquid systems, we show by exact calculations that it holds at the critical point, providing a counterexample to this lore. Furthermore, we show that the fractionalized Majorana character of the critical point can be unambiguously detected from the heat conductivity, opening the door to a direct experimental measurement of the elusive Majorana central charge c=12c=\tfrac{1}{2}.Comment: 18 pages, 3 figure

    Assessing the reactive surface area of soils and the association of soil organic carbon with natural oxide nanoparticles using ferrihydrite as proxy

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    Assessment of the surface reactivity of natural metal-(hydr)oxide nanoparticles is necessary for predicting ion adsorption phenomena in soils using surface complexation modeling. Here, we describe how the equilibrium concentrations of PO4, obtained with 0.5 M NaHCO3 extractions at different solution-to-soil ratios, can be interpreted with a state-of-the-art ion adsorption model for ferrihydrite to assess the reactive surface area (RSA) of agricultural top soils. Simultaneously, the method reveals the fraction of reversibly adsorbed soil PO4 (R-PO4). The applied ion-probing methodology shows that ferrihydrite is a better proxy than goethite for consistently assessing RSA and R-PO4. The R-PO4 pool agrees well with ammonium oxalate (AO)-extractable phosphorus, but only if measured as orthophosphate. The RSA varied between ∼2 and 20 m2/g soil. The corresponding specific surface area (SSA) of the natural metal-(hydr)oxide fraction is ∼350–1400 m2/g, illustrating that this property is highly variable and cannot be represented by a single value based on the AO-extractable oxide content. The soil organic carbon (SOC) content of our top soils increases linearly not only with the increase in RSA but remarkably also with the increase in mean particle size (1.5–5 nm). To explain these observations, we present a structural model for organo-mineral associations based on the coordination of SOC particles to metal-(hydr)oxide cores.Universidad de Costa Rica/[]/UCR/Costa RicaUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Agroalimentarias::Centro de Investigaciones Agronómicas (CIA

    Inhibition of Autophagy Does Not Re-Sensitize Acute Myeloid Leukemia Cells Resistant to Cytarabine

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    Elevated activation of the autophagy pathway is currently thought to be one of the survival mechanisms allowing therapy-resistant cancer cells to escape elimination, including for cytarabine (AraC)-resistant acute myeloid leukemia (AML) patients. Consequently, the use of autophagy inhibitors such as chloroquine (CQ) is being explored for the re-sensitization of AraC-resistant cells. In our study, no difference in the activity of the autophagy pathway was detected when comparing AraC-Res AML cell lines to parental AraC-sensitive AML cell lines. Furthermore, treatment with autophagy inhibitors CQ, 3-Methyladenine (3-MA), and bafilomycin A1 (BafA1) did not re-sensitize AraC-Res AML cell lines to AraC treatment. However, in parental AraC-sensitive AML cells, treatment with AraC did activate autophagy and, correspondingly, combination of AraC with autophagy inhibitors strongly reduced cell viability. Notably, the combination of these drugs also yielded the highest level of cell death in a panel of patient-derived AML samples even though not being additive. Furthermore, there was no difference in the cytotoxic effect of autophagy inhibition during AraC treatment in matched de novo and relapse samples with differential sensitivity to AraC. Thus, inhibition of autophagy may improve AraC efficacy in AML patients, but does not seem warranted for the treatment of AML patients that have relapsed with AraC-resistant disease

    The Novel Immune Checkpoint GPR56 Is Expressed on Tumor-Infiltrating Lymphocytes and Selectively Upregulated upon TCR Signaling

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    High levels of tumor-infiltrating lymphocytes (TILs) in the tumor microenvironment (TME) are associated with a survival benefit in various cancer types and the targeted (re)activation of TILs is an attractive therapeutic anti-cancer approach that yields curative responses. However, current T cell targeting strategies directed at known immune checkpoints have not increased objective response rates for all cancer types, including for epithelial ovarian cancer (EOC). For this reason, the identification of new immune checkpoints that regulate T cell immunity remains of great interest. One yet largely uninvestigated checkpoint of potential interest is the G protein-coupled receptor 56 (GPR56), which belongs to the adhesion GPCR family. GPR56 was originally reported to function in cerebral cortical development and in anti-depressant response, but also in cancer. Recently, GPR56 was identified as an inhibitory receptor expressed on human NK cells that by cis-interaction with the tetraspanin CD81 attenuated the cytotoxic activity of NK cells. This NK cell checkpoint could be blocked by an GPR56 antibody, leading to increased cytotoxicity. Interestingly, GPR56 expression has also been reported on cytokine producing memory CD8 T lymphocytes and may thus represent a T cell checkpoint as well. Here, GPR56 mRNA expression was characterized in the context of TILs, with GPR56 expression being detected predominantly in tumor infiltrating CD8 T cells with a cytotoxic and (pre-)exhausted phenotype. In accordance with this mRNA profile, TILs from ovarian cancer patients expressed GPR56 primarily within the effector memory and central memory T cell subsets. On T cells from healthy donors the expression was limited to effector memory and terminally differentiated T cells. Notably, GPR56 expression further increased on TILs upon T cell receptor (TCR)-mediated stimulation in co-cultures with cancer cells, whereas GPR56 expression on healthy primary human T cells did not. Further, the ectopic expression of GPR56 significantly reduced the migration of GPR56-positive T cells. Taken together, GPR56 is a potential immune-checkpoint in EOC found on (pre-)exhausted CD8 TILs that may regulate migratory behavior

    A randomized, placebo-controlled double-blinded comparative clinical study of five over-the-counter non-pharmacological topical analgesics for myofascial pain: single session findings

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    <p>Abstract</p> <p>Objectives</p> <p>To investigate the effects of topical agents for the treatment of Myofascial Pain Syndrome (MPS) and Myofascial Trigger Point (MTRP).</p> <p>Methods</p> <p>Subjects with an identifiable trigger point in the trapezius muscle, age 18-80 were recruited for a single-session randomized, placebo-blinded clinical study. Baseline measurements of trapezius muscle pressure pain threshold (PPT: by pressure algometer) along with right and left cervical lateral flexion (rangiometer) were obtained by a blinded examiner. An assessor blinded to the outcomes assessments applied one of 6 topical formulations which had been placed in identical plastic containers. Five of these topicals were proposed active formulations; the control group was given a non-active formulation (PLA). Five minutes after the application of the formula the outcome measures were re-tested. Data were analyzed with a 5-way ANOVA and Holms-adjusted t-tests with an alpha level of 0.05.</p> <p>Results</p> <p>120 subjects were entered into the study (63 females; ages 16-82); 20 subjects randomly allocated into each group. The pre- and post-treatment results for pressure threshold did show significant intra-group increases for the Ben-Gay Ultra Strength Muscle Pain Ointment (BG), the Professional Therapy MuscleCare Roll-on (PTMC roll-on) and Motion Medicine Cream (MM) with an increased threshold of 0.5 kg/cm<sup>2 </sup>(+/-0.15), 0.72 kg/cm<sup><b>2 </b></sup>(+/-0.17) and 0.47 Kg/cm<sup><b>2 </b></sup>(+/-0.19) respectively. With respect to the inter-group comparisons, PTMC roll-on showed significant increases in pressure threshold compared with Placebo (PLA) (p = 0.002) and Icy Hot Extra Strength Cream (IH) (p = 0.006). In addition, BG demonstrated significant increases in pressure threshold compared with PLA (p = 0.0003).</p> <p>Conclusions</p> <p>With regards to pressure threshold, PTMC roll-on, BG and MM showed significant increases in pain threshold tolerance after a short-term application on a trigger points located in the trapezius muscle. PTMC roll-on and BG were both shown to be superior vs placebo while PTMC was also shown to be superior to IH in patients with trigger points located in the trapezius muscle on a single application.</p> <p>CMCC Research Ethics Board Approval # 1012X01, 2011</p

    Gasdynamic fusion propulsion system for space exploration

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76953/1/AIAA-23876-408.pd
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