24,089 research outputs found

    Cathodoluminescence of shocked quartz at the Cretaceous-Tertiary boundary

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    Empirical studies have documented an association between rock type and the cathodoluminescence color of constituent quartz grains. Quartz from extrusive igneous sources luminesces uniform pale blue. Quartz from intrusive igneous and high-grade metamorphic rocks generally luminesces darker purple-blue, whereas quartz recrystallized under low-grade metamorphic conditions luminesces reddish-brown. Quartz grains in most sandstones luminesce a heterogeneous mixture of these colors because the grains were derived from a variety of ultimate source rocks. If shocked quartz found at the Cretaceous-Tertiary (K-T) boundary is volcanic in origin, its cathodoluminescence should be predominantly pale blue. Alternatively, quartz grains derived from bolide impact upon, and ejection of, mixed igneous, metamorphic, and sedimentary rocks should luminesce a variety of colors. Grain mounts of sand collected at the K-T boundary horizon from the Clear Creek North site in the Raton Basin, Colorado were examined. Shocked quartz luminesced a variety of colors and very few grains luminesced the pale blue color that is typical of volcanic quartz. It was concluded that the shocked quartz was derived from a petrologically diverse source region without substantial volcanic contribution. Most shocked grains apparently were derived from low-grade metamorphic rocks, with a slightly smaller contribution from high-grade metamorphic and intrusive igneous rocks. Rare quartz grains with brown-luminescing rims reflect a minor addition from detrital sedimentary sources. The apparent relative abundances of intrusive (and rare extrusive) igneous, metamorphic, and sedimentary ultimate source rocks suggested by CL colors of shock-deformed quartz at the K-T boundary is consistent with a crustal/supracrustal origin for the grains

    Stress relief as the driving force for self-assembled Bi nanolines

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    Stress resulting from mismatch between a substrate and an adsorbed material has often been thought to be the driving force for the self-assembly of nanoscale structures. Bi nanolines self-assemble on Si(001), and are remarkable for their straightness and length -- they are often more than 400 nm long, and a kink in a nanoline has never been observed. Through electronic structure calculations, we have found an energetically favourable structure for these nanolines that agrees with our scanning tunneling microscopy and photoemission experiments; the structure has an extremely unusual subsurface structure, comprising a double core of 7-membered rings of silicon. Our proposed structure explains all the observed features of the nanolines, and shows that surface stress resulting from the mismatch between the Bi and the Si substrate are responsible for their self-assembly. This has wider implications for the controlled growth of nanostructures on semiconductor surfaces.Comment: 4 pages, 4 figures, submitted to Phys. Rev. Let

    Multiscale modelling of tumour growth and therapy: the influence of vessel normalisation on chemotherapy

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    Following the poor clinical results of antiangiogenic drugs, particularly when applied in isolation, tumour biologists and clinicians are now turning to combinations of therapies in order to obtain better results. One of these involves vessel normalisation strategies. In this paper, we investigate the effects on tumour growth of combinations of antiangiogenic and standard cytotoxic drugs, taking into account vessel normalisation. An existing multiscale framework is extended to include new elements such as tumour-induced vessel dematuration. Detailed simulations of our multiscale framework allow us to suggest one possible mechanism for the observed vessel normalisation-induced improvement in the efficacy of cytotoxic drugs: vessel dematuration produces extensive regions occupied by quiescent (oxygen-starved) cells which the cytotoxic drug fails to kill. Vessel normalisation reduces the size of these regions, thereby allowing the chemotherapeutic agent to act on a greater number of cells

    Manufacture of DPFC-DMS polymer in the SKG range

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    BPFC-DMS block copolymers were synthesized on a pre-pilot scale (i.e., to 5 Kg lots) and subsequently fabricated into clear, colorless films. Details of the synthesis procedures, property determinations, and film casting techniques are presented. Solubility, viscosity and molecular weight characteristics of the resulting product are reported

    The impact of cell crowding and active cell movement on vascular tumour growth

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    A multiscale model for vascular tumour growth is presented which includes systems of ordinary differential equations for the cell cycle and regulation of apoptosis in individual cells, coupled to partial differential equations for the spatio-temporal dynamics of nutrient and key signalling chemicals. Furthermore, these subcellular and tissue layers are incorporated into a cellular automaton framework for cancerous and normal tissue with an embedded vascular network. The model is the extension of previous work and includes novel features such as cell movement and contact inhibition. We presented a detailed simulation study of the effects of these additions on the invasive behaviour of tumour cells and the tumour's response to chemotherapy. In particular, we find that cell movement alone increases the rate of tumour growth and expansion, but that increasing the tumour cell carrying capacity leads to the formation of less invasive dense hypoxic tumours containing fewer tumour cells. However, when an increased carrying capacity is combined with significant tumour cell movement, the tumour grows and spreads more rapidly, accompanied by large spatio-temporal fluctuations in hypoxia, and hence in the number of quiescent cells. Since, in the model, hypoxic/quiescent cells produce VEGF which stimulates vascular adaptation, such fluctuations can dramatically affect drug delivery and the degree of success of chemotherapy

    Bumps and rings in a two-dimensional neural field: splitting and rotational instabilities

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    In this paper we consider instabilities of localised solutions in planar neural field firing rate models of Wilson-Cowan or Amari type. Importantly we show that angular perturbations can destabilise spatially localised solutions. For a scalar model with Heaviside firing rate function we calculate symmetric one-bump and ring solutions explicitly and use an Evans function approach to predict the point of instability and the shapes of the dominant growing modes. Our predictions are shown to be in excellent agreement with direct numerical simulations. Moreover, beyond the instability our simulations demonstrate the emergence of multi-bump and labyrinthine patterns. With the addition of spike-frequency adaptation, numerical simulations of the resulting vector model show that it is possible for structures without rotational symmetry, and in particular multi-bumps, to undergo an instability to a rotating wave. We use a general argument, valid for smooth firing rate functions, to establish the conditions necessary to generate such a rotational instability. Numerical continuation of the rotating wave is used to quantify the emergent angular velocity as a bifurcation parameter is varied. Wave stability is found via the numerical evaluation of an associated eigenvalue problem

    Oscillatory dynamics in a model of vascular tumour growth -- implications for chemotherapy

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    Background\ud \ud Investigations of solid tumours suggest that vessel occlusion may occur when increased pressure from the tumour mass is exerted on the vessel walls. Since immature vessels are frequently found in tumours and may be particularly sensitive, such occlusion may impair tumour blood flow and have a negative impact on therapeutic outcome. In order to study the effects that occlusion may have on tumour growth patterns and therapeutic response, in this paper we develop and investigate a continuum model of vascular tumour growth.\ud Results\ud \ud By analysing a spatially uniform submodel, we identify regions of parameter space in which the combination of tumour cell proliferation and vessel occlusion give rise to sustained temporal oscillations in the tumour cell population and in the vessel density. Alternatively, if the vessels are assumed to be less prone to collapse, stable steady state solutions are observed. When spatial effects are considered, the pattern of tumour invasion depends on the dynamics of the spatially uniform submodel. If the submodel predicts a stable steady state, then steady travelling waves are observed in the full model, and the system evolves to the same stable steady state behind the invading front. When the submodel yields oscillatory behaviour, the full model produces periodic travelling waves. The stability of the waves (which can be predicted by approximating the system as one of λ-ω type) dictates whether the waves develop into regular or irregular spatio-temporal oscillations. Simulations of chemotherapy reveal that treatment outcome depends crucially on the underlying tumour growth dynamics. In particular, if the dynamics are oscillatory, then therapeutic efficacy is difficult to assess since the fluctuations in the size of the tumour cell population are enhanced, compared to untreated controls.\ud Conclusions\ud \ud We have developed a mathematical model of vascular tumour growth formulated as a system of partial differential equations (PDEs). Employing a combination of numerical and analytical techniques, we demonstrate how the spatio-temporal dynamics of the untreated tumour may influence its response to chemotherapy.\ud Reviewers\ud \ud This manuscript was reviewed by Professor Zvia Agur and Professor Marek Kimmel

    Degeneracy measures for the algebraic classification of numerical spacetimes

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    We study the issue of algebraic classification of the Weyl curvature tensor, with a particular focus on numerical relativity simulations. The spacetimes of interest in this context, binary black hole mergers, and the ringdowns that follow them, present subtleties in that they are generically, strictly speaking, Type I, but in many regions approximately, in some sense, Type D. To provide meaning to any claims of "approximate" Petrov class, one must define a measure of degeneracy on the space of null rays at a point. We will investigate such a measure, used recently to argue that certain binary black hole merger simulations ring down to the Kerr geometry, after hanging up for some time in Petrov Type II. In particular, we argue that this hangup in Petrov Type II is an artefact of the particular measure being used, and that a geometrically better-motivated measure shows a black hole merger produced by our group settling directly to Petrov Type D.Comment: 14 pages, 7 figures. Version 2 adds two references

    Derivation of linearized transfer functions for switching-mode regulations. Phase A: Current step-up and voltage step-up converters

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    Small-signal models are derived for the power stage of the voltage step-up (boost) and the current step-up (buck) converters. The modeling covers operation in both the continuous-mmf mode and the discontinuous-mmf mode. The power stage in the regulated current step-up converter on board the Dynamics Explorer Satellite is used as an example to illustrate the procedures in obtaining the small-signal functions characterizing a regulated converter

    Modelling the response of vascular tumours to chemotherapy: A multiscale approach

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    An existing multiscale model is extended to study the response of a vascularised tumour to treatment with chemotherapeutic drugs which target proliferating cells. The underlying hybrid cellular automaton model couples tissue-level processes (e.g. blood flow, vascular adaptation, oxygen and drug transport) with cellular and subcellular phenomena (e.g. competition for space, progress through the cell cycle, natural cell death and drug-induced cell kill and the expression of angiogenic factors). New simulations suggest that, in the absence of therapy, vascular adaptation induced by angiogenic factors can stimulate spatio-temporal oscillations in the tumour's composition.\ud \ud Numerical simulations are presented and show that, depending on the choice of model parameters, when a drug which kills proliferating cells is continuously infused through the vasculature, three cases may arise: the tumour is eliminated by the drug; the tumour continues to expand into the normal tissue; or, the tumour undergoes spatio-temporal oscillations, with regions of high vascular and tumour cell density alternating with regions of low vascular and tumour cell density. The implications of these results and possible directions for future research are also discussed
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