1,009 research outputs found

    Decoupling the electronic gap from the spin Chern number in disordered higher-order topological insulators

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    In two-dimensional topological insulators, a disorder induced topological phase transition is typically identified with an Anderson localization transition at the Fermi energy. However, in higher-order, spin-resolved topological insulators it is the spectral gap of the spin-spectrum, in addition to the bulk mobility gap, which protects the non-trivial topology of the ground state. In this work, we show that these two gaps, the bulk electronic and spin gap, evolve distinctly upon introduction of disorder. This decoupling leads to a unique situation in which an Anderson localization transition occurs below the Fermi energy at the topological transition. Furthermore, in the clean limit the bulk-boundary correspondence of such higher-order insulators is dictated by crystalline protected topology, coexisting with the spin-resolved topology. By removing the crystalline symmetry, disorder allows for isolated study of the bulk-boundary correspondence of spin-resolved topology for which we demonstrate the absence of protected edge and corner modes in the Hamiltonian and yet the edge modes in the eigenstates of the projected spin operator survive. Our work shows that a non-zero spin-Chern number, in the absence of a non-trivial Z2\mathbb{Z}_{2} index, does not dictate the existence of protected edge modes, resolving a fundamental question posed in 2009.Comment: 13 pages, 11 figure

    Preliminary catalog of pictures taken on the lunar surface during the Apollo 15 mission

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    Catalog of all pictures taken from lunar module or lunar surface during Apollo 15 missio

    Model Capabilities for In-Situ Oil Shale Recovery

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    Desenvolvimento e Validação da Escala de Literacia Mediática e Informacional para Alunos dos 2º e 3º Ciclos do Ensino Básico em Portugal

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    A comunicação e a partilha de significados num mundo altamente mediatizado requer múltiplas literacias. Independentemente das definições e abordagens, estas literacias têm vindo a abrir debates críticos sobre quais as competências que os cidadãos devem ter e desde quando elas devem ser adquiridas. No presente estudo damos conta do processo de desenvolvimento e validação de uma Escala de Literacia Mediática e Informacional (ELMI) para alunos dos 2º e 3º ciclos do Ensino Básico em Portugal. A validade de construto foi examinada via Análise Fatorial Exploratória (AFE) para uma amostra de 1151 participantes. A AFE revelou uma estrutura trifatorial constituída por 22 itens que explicam 53.23% da variância total. A escala apresenta uma consistência interna global excelente (ωt = .92), com adequada consistência interna para todas as subescalas (α de Cronbach e α Ordinal > .70). Os resultados evidenciam boas qualidades psicométricas da ELMI que poderá ser um instrumentovantajoso para o prognóstico e avaliação de intervenções relacionadas com a literacia mediática. Palavras-Chave: literacia mediática e informacional; validação de escala; educação para os media; 2º e 3º ciclos do ensino básico

    Metabolic reprogramming ensures cancer cell survival despite oncogenic signaling blockade

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    There is limited knowledge about the metabolic reprogramming induced by cancer therapies, and how this contributes to therapeutic resistance. Here we show that although inhibition of PI3K-AKT-mTOR signaling markedly decreased glycolysis and restrained tumor growth, these signaling and metabolic restrictions triggered autophagy, which supplied the metabolites required for the maintenance of mitochondrial respiration and redox homeostasis. Specifically, we found that survival of cancer cells was critically dependent on phospholipase A2 (PLA2) to mobilize lysophospholipids and free fatty acids to sustain fatty acid oxidation and oxidative phosphorylation. Consistent with this, we observed significantly increased lipid droplets, with subsequent mobilization to mitochondria. These changes were abrogated in cells deficient for the essential autophagy gene, ATG5. Accordingly, inhibition of PLA2 significantly decreased lipid droplets, decreased oxidative phosphorylation and increased apoptosis. Together, these results describe how treatment-induced autophagy provides nutrients for cancer cell survival and identifies novel co-treatment strategies to override this survival advantage

    Solving Global Optimization Problems Using MANGO

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    Traditional approaches for solving global optimization problems generally rely on a single algorithm. The algorithm may be hybrid or applied in parallel. Contrary to traditional approaches, this paper proposes to form teams of algorithms to tackle global optimization problems. Each algorithm is embodied and ran by a software agent. Agents exist in a multiagent system and communicate over Our proposed MultiAgent ENvironment for Global Optimization (MANGO). Through Communication and cooperation, the agents complement each other in tasks that they cannot do on their own. This paper gives a formal description of MANGO and Outlines design principles for developing agents to execute Oil MANGO. Our case study shows the effectiveness of multiagent teams in solving global optimization problems

    The prognostic value of p53 mutation in pediatric marrow hypoplasia

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    <p>Abstract</p> <p>Background</p> <p>The tumor suppressor gene p53 is involved in the control of cell proliferation, particularly in stressed cells. p 53 gene mutations are the most frequent genetic event found in human cancers. Fanconi Anemia (FA) is the most common representative of inherited bone marrow failure syndromes (IBMFS) with a leukemic propensity. P 53 DNA alteration has not been studied before in Egyptian children with FA.</p> <p>Patients and methods</p> <p>we investigated p53 mutation in the bone marrow and peripheral blood of forty children, FA (n = 10), acquired aplastic anemia (AAA) (n = 10), and immune thrombocytopenia (ITP) as a control (n = 20), using real-time PCR by TaqMan probe assay</p> <p>Results</p> <p>Mutation of p53 gene was demonstrated in the BM of 90% (9/10) of children with FA, compared to 10% (1/10) in AAA (p < 0.001), while, no p53 DNA mutation was seen in the control group. A positive correlation between DNA breakage and presence of p53 mutation was seen in FA (p < 0.02, r0.81).</p> <p>Conclusion</p> <p>mutation of p53 gene in hypoplastic marrow especially FA may represent an early indicator of significant DNA genetic alteration with cancer propensity.</p

    Differentiation status of primary chronic myeloid leukemia cells affects sensitivity to BCR-ABL1 inhibitors

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    Tyrosine kinase inhibitors (TKI) are the mainstay treatment of BCR-ABL1-positive leukemia and virtually all patients with chronic myeloid leukemia in chronic phase (CP CML) respond to TKI therapy. However, there is limited information on the cellular mechanisms of response and particularly on the effect of cell differentiation state to TKI sensitivity in vivo and ex vivo/in vitro. We used multiple, independent high-throughput drug sensitivity and resistance testing platforms that collectively evaluated 295 oncology compounds to characterize ex vivo drug response profiles of primary cells freshly collected from newly-diagnosed patients with BCR-ABL1positive leukemia (n = 40) and healthy controls (n = 12). In contrast to the highly TKI-sensitive cells from blast phase CML and Philadelphia chromosome-positive acute lymphoblastic leukemia, primary CP CML cells were insensitive to TKI therapy ex vivo. Despite maintaining potent BCR-ABL1 inhibitory activity, ex vivo viability of cells was unaffected by TKIs. These findings were validated in two independent patient cohorts and analysis platforms. All CP CML patients under study responded to TKI therapy in vivo. When CP CML cells were sorted based on CD34 expression, the CD34-positive progenitor cells showed good sensitivity to TKIs, whereas the more mature CD34-negative cells were markedly less sensitive. Thus in CP CML, TKIs predominantly target the progenitor cell population while the differentiated leukemic cells (mostly cells from granulocytic series) are insensitive to BCR-ABL1 inhibition. These findings have implications for drug discovery in CP CML and indicate a fundamental biological difference between CP CML and advanced forms of BCR-ABL1-positive leukemia.Peer reviewe
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