21,205 research outputs found

    Polar communications: Status and recommendations. Report of the Science Working Group

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    The capabilities of the existing communication links within the polar regions, as well as between the polar regions and the continental United States, are summarized. These capabilities are placed in the context of the principal scientific disciplines that are active in polar research, and in the context of how scientists both utilize and are limited by present technologies. Based on an assessment of the scientific objectives potentially achievable with improved communication capabilities, a list of requirements on and recommendations for communication capabilities necessary to support polar science over the next ten years is given

    On non-normality and classification of amplification mechanisms in stability and resolvent analysis

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    We seek to quantify non-normality of the most amplified resolvent modes and predict their features based on the characteristics of the base or mean velocity profile. A 2-by-2 model linear Navier-Stokes (LNS) operator illustrates how non-normality from mean shear distributes perturbation energy in different velocity components of the forcing and response modes. The inverse of their inner product, which is unity for a purely normal mechanism, is proposed as a measure to quantify non-normality. In flows where there is downstream spatial dependence of the base/mean, mean flow advection separates the spatial support of forcing and response modes which impacts the inner product. Success of mean stability analysis depends on the normality of amplification. If the amplification is normal, the resolvent operator written in its dyadic representation reveals that the adjoint and forward stability modes are proportional to the forcing and response resolvent modes. If the amplification is non-normal, then resolvent analysis is required to understand the origin of observed flow structures. Eigenspectra and pseudospectra are used to characterize these phenomena. Two test cases are studied: low Reynolds number cylinder flow and turbulent channel flow. The first deals mainly with normal mechanisms and quantification of non-normality using the inverse inner product of the leading forcing and response modes agrees well with the product of the resolvent norm and distance between the imaginary axis and least stable eigenvalue. In turbulent channel flow, structures result from both normal and non-normal mechanisms. Mean shear is exploited most efficiently by stationary disturbances while bounds on the pseudospectra illustrate how non-normality is responsible for the most amplified disturbances at spatial wavenumbers and temporal frequencies corresponding to well-known turbulent structures

    Surgery and the Spectrum of the Dirac Operator

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    We show that for generic Riemannian metrics on a simply-connected closed spin manifold of dimension at least 5 the dimension of the space of harmonic spinors is no larger than it must be by the index theorem. The same result holds for periodic fundamental groups of odd order. The proof is based on a surgery theorem for the Dirac spectrum which says that if one performs surgery of codimension at least 3 on a closed Riemannian spin manifold, then the Dirac spectrum changes arbitrarily little provided the metric on the manifold after surgery is chosen properly.Comment: 23 pages, 4 figures, to appear in J. Reine Angew. Mat

    Secondary acute lymphoblastic leukemia is a distinct clinical entity with prognostic significance.

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    The effect of prior malignancy on the risk of developing, and prognosis of, acute lymphoblastic leukemia (ALL) is unknown. This observational study utilized the California Cancer Registry to estimate the risk of developing ALL after a prior malignancy using standardized incidence ratios (SIRs, 95% confidence intervals). ALL occurring after a malignancy with an SIR>1 (increased-risk (IR) malignancies) was considered secondary ALL (s-ALL). Adjusted hazard ratios (aHRs, 95% confidence intervals) compared the effect of s-ALL with de novo ALL on overall survival. A total of 14 481 patients with ALL were identified (1988-2012) and 382 (3%) had a known prior malignancy. Any prior malignancy predisposed patients to developing ALL: SIR 1.62 (1.45-1.79). Hematologic malignancies (SIR 5.57, 4.38-6.98) and IR-solid tumors (SIR 2.11, 1.73-2.54) increased the risk of developing ALL. s-ALL increased the risk of death compared with de novo ALL (aHR 1.38 (1.16-1.63)) and this effect was more pronounced among younger patients (age<40 years: aHR 4.80 (3.15-7.30); age⩾40 years: aHR 1.40 (1.16-1.69)) (interaction P<0.001). This population-based study demonstrates that s-ALL is a distinct entity that occurs after specific malignancies and carries a poor prognosis compared with de novo ALL, particularly among patients <40 years of age

    Shock compression of feldspars

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    Hugoniot data for oligoclase and microcline to 670 and 580 kb and release adiabat data for oligoclase were obtained by means of the inclined mirror and immersed-foil-reflected-light techniques, respectively. Oligoclase and microcline have Hugoniot elastic limits in the range of 40–55 and 80–85 kb. These limits increase slightly with increasing driving shock pressure. Above the elastic limit, extending to ∼300 and ∼400 kb, transition regions of anomalously high compression are observed for microcline and oligoclase. These data and the data of McQueen, Marsh, and Fritz for albitite and anorthosite indicate that at successively higher shock pressures within this region, the feldspars gradually transform to a high-pressure, high-density polymorph. This polymorph probably corresponds to the rutile-like hollandite structure obtained in high-pressure quenching experiments by Kume, Matsumoto, and Koizumi (in KAlGe_3O_8) and by Ringwood, Reid, and Wadsley (in KAlSo_3O_8, microcline). In the hollandite structure germanium or silicon is in octahedral coordination with oxygen. The zero-pressure density and the Birch-Murnaghan equation of state parameters for the adiabat and isotherm are calculated for the high-pressure polymorphs of oligoclase, microcline, anorthosite, and albitite. The release adiabat centered at 180 kb indicates that at this shock pressure some (∼15%) of the hollandite phase forms but apparently reverts to a lower-density phase on pressure release. Release adiabat curves centered at 272 and 417 kb and calculated postshock temperatures indicate that material of feldspar composition recovered from meteorite and laboratory impacts is converted to the hollandite structure upon shock compression; upon pressure release this material probably reverts to the low-density maskelynite form

    Principal infinity-bundles - General theory

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    The theory of principal bundles makes sense in any infinity-topos, such as that of topological, of smooth, or of otherwise geometric infinity-groupoids/infinity-stacks, and more generally in slices of these. It provides a natural geometric model for structured higher nonabelian cohomology and controls general fiber bundles in terms of associated bundles. For suitable choices of structure infinity-group G these G-principal infinity-bundles reproduce the theories of ordinary principal bundles, of bundle gerbes/principal 2-bundles and of bundle 2-gerbes and generalize these to their further higher and equivariant analogs. The induced associated infinity-bundles subsume the notions of gerbes and higher gerbes in the literature. We discuss here this general theory of principal infinity-bundles, intimately related to the axioms of Giraud, Toen-Vezzosi, Rezk and Lurie that characterize infinity-toposes. We show a natural equivalence between principal infinity-bundles and intrinsic nonabelian cocycles, implying the classification of principal infinity-bundles by nonabelian sheaf hyper-cohomology. We observe that the theory of geometric fiber infinity-bundles associated to principal infinity-bundles subsumes a theory of infinity-gerbes and of twisted infinity-bundles, with twists deriving from local coefficient infinity-bundles, which we define, relate to extensions of principal infinity-bundles and show to be classified by a corresponding notion of twisted cohomology, identified with the cohomology of a corresponding slice infinity-topos. In a companion article [NSSb] we discuss explicit presentations of this theory in categories of simplicial (pre)sheaves by hyper-Cech cohomology and by simplicial weakly-principal bundles; and in [NSSc] we discuss various examples and applications of the theory.Comment: 46 pages, published versio

    Contribution of Matrix Metalloproteinase-9 to Cerebral Edema and Functional Outcome following Experimental Subarachnoid Hemorrhage

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    Background: Cerebral edema is an important risk factor for death and poor outcome following subarachnoid hemorrhage (SAH). However, underlying mechanisms are still poorly understood. Matrix metalloproteinase (MMP)-9 is held responsible for the degradation of microvascular basal lamina proteins leading to blood-brain barrier dysfunction and, thus, formation of vasogenic cerebral edema. The current study was conducted to clarify the role of MMP-9 for the development of cerebral edema and for functional outcome after SAH. Methods: SAH was induced in FVB/N wild-type (WT) or MMP-9 knockout (MMP-9(-/-)) mice by endovascular puncture. Intracranial pressure (ICP), regional cerebral blood flow (rCBF), and mean arterial blood pressure (MABP) were continuously monitored up to 30 min after SAH. Mortality was quantified for 7 days after SAH. In an additional series neurological function and body weight were assessed for 3 days after SAH. Subsequently, ICP and brain water content were quantified. Results: Acute ICP, rCBF, and MABP did not differ between WT and MMP-9(-/-) mice, while 7 days' mortality was lower in MMP-9(-/-) mice (p = 0.03; 20 vs. 60%). MMP-9(-/-) mice also exhibited better neurological recovery, less brain edema formation, and lower chronic ICP. Conclusions: The results of the current study suggest that MMP-9 contributes to the development of early brain damage after SAH by promoting cerebral edema formation. Hence, MMP-9 may represent a novel molecular target for the treatment of SAH. Copyright (C) 2011 S. Karger AG, Base
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