70 research outputs found

    Are Women in IS Better at Managing Conflict?

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    Long-range ballistic transport of Brown-Zak fermions in graphene superlattices

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    In quantizing magnetic fields, graphene superlattices exhibit a complex fractal spectrum often referred to as the Hofstadter butterfly. It can be viewed as a collection of Landau levels that arise from quantization of Brown-Zak minibands recurring at rational (p/q) fractions of the magnetic flux quantum per superlattice unit cell. Here we show that, in graphene-on-boron-nitride superlattices, Brown-Zak fermions can exhibit mobilities above 106 cm2 V−1 s−1 and the mean free path exceeding several micrometers. The exceptional quality of our devices allows us to show that Brown-Zak minibands are 4q times degenerate and all the degeneracies (spin, valley and mini-valley) can be lifted by exchange interactions below 1 K. We also found negative bend resistance at 1/q fractions for electrical probes placed as far as several micrometers apart. The latter observation highlights the fact that Brown-Zak fermions are Bloch quasiparticles propagating in high fields along straight trajectories, just like electrons in zero field

    The neuropeptidome of the Crown-of-Thorns Starfish, Acanthaster planci

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    This study was supported by funds from the Australian federal government Department of the Environment Reef Rescue ‘Caring for Country’ program for funding the ‘The Crown-of-Thorns secretome: Towards a control technology’ project (M. R. H., S. C.). M.R.E. was supported by grants from the BBSRC (BB/M001644/1) and Leverhulme Trust (RPG-2013-351)

    A subset of platinum-containing chemotherapeutic agents kills cells by inducing ribosome biogenesis stress

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    Cisplatin and its platinum analogs, carboplatin and oxaliplatin, are some of the most widely used cancer chemotherapeutics. Although cisplatin and carboplatin are used primarily in germ cell, breast and lung malignancies, oxaliplatin is instead used almost exclusively to treat colorectal and other gastrointestinal cancers. Here we utilize a unique, multi-platform genetic approach to study the mechanism of action of these clinically established platinum anti-cancer agents, as well as more recently developed cisplatin analogs. We show that oxaliplatin, unlike cisplatin and carboplatin, does not kill cells through the DNA-damage response. Rather, oxaliplatin kills cells by inducing ribosome biogenesis stress. This difference in drug mechanism explains the distinct clinical implementation of oxaliplatin relative to cisplatin, and it might enable mechanistically informed selection of distinct platinum drugs for distinct malignancies. These data highlight the functional diversity of core components of front-line cancer therapy and the potential benefits of applying a mechanism-based rationale to the use of our current arsenal of anti-cancer drugs
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