1,105 research outputs found

    Functional Verification through Operation Diagnostics

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    One of the core objectives of the commissioning process is to ensure that the dynamic systems function correctly. Just as important, if not more so, is enabling the correct function of those systems throughout occupancy. While verification strategies vary, it is clear that examination of actual operation produces the most accurate results. This is accomplished through trend logging. With analysis of regularly recorded control point data through visualization (including graphs, charts, etc.), a quick and accurate diagnosis of incorrect or less than optimal operation can be assessed. However, several questions arise regarding this process: What data should be visualized? What form should this visualization take? How can data from several different yet interrelated control points be best compared? Finally, what patterns within a visualization should be sought

    Cosine Contours: a Multipurpose Representation for Melodies

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    Melodic contour is central to our ability to perceive and produce music. We propose to represent melodic contours as a combination of cosine functions, using the discrete cosine transform. The motivation for this approach is twofold: (1) it approximates a maximally informative contour representation (capturing most of the variation in as few dimensions as possible), but (2) it is nevertheless independent of the specifics of the data sets for which it is used. We consider the relation with principal component analysis, which only meets the first of these requirements. Theoretically, the principal components of a repertoire of random walks are known to be cosines. We find, empirically, that the principal components of melodies also closely approximate cosines in multiple musical traditions. We demonstrate the usefulness of the proposed representation by analyzing contours at three levels (complete songs, melodic phrases and melodic motifs) across multiple traditions in three small case studies

    AMP-activated protein kinase is a key regulator of acute neurovascular permeability

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    Many neuronal and retinal disorders are associated with pathological hyperpermeability of the microvasculature. We have used explants of rodent retinae to study acute neurovascular permeability and signal transduction and the role of AMP-activated protein kinase (AMPK). Following stimulation with either vascular endothelial growth factor (VEGF-A) or bradykinin (BK), AMPK was rapidly and strongly phosphorylated and acted as a key mediator of permeability downstream of Ca2+ Accordingly, AMPK agonists potently induced acute retinal vascular leakage. AMPK activation led to phosphorylation of endothelial nitric oxide synthase (eNOS), which in turn increased VE-cadherin phosphorylation on Y685. In parallel, AMPK also mediated phosphorylation of p38 MAP kinase and HSP27, indicating that it regulated paracellular junctions and cellular contractility, both previously associated with endothelial permeability. Endothelial AMPK provided a missing link in neurovascular permeability, connecting Ca2+ transients to the activation of eNOS and p38, irrespective of the permeability-inducing factor used. Collectively, we find that, due to its compatibility with small molecule antagonists/agonists and siRNA, the ex-vivo retina model constitutes a reliable tool to identify and study regulators and mechanism of acute neurovascular permeability

    Hydrostatic pressure does not cause detectable changes to survival of human retinal ganglion

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    Purpose: Elevated intraocular pressure (IOP) is a major risk factor for glaucoma. One consequence of raised IOP is that ocular tissues are subjected to increased hydrostatic pressure (HP). The effect of raised HP on stress pathway signaling and retinal ganglion cell (RGC) survival in the human retina was investigated. Methods: A chamber was designed to expose cells to increased HP (constant and fluctuating). Accurate pressure control (10-100mmHg) was achieved using mass flow controllers. Human organotypic retinal cultures (HORCs) from donor eyes (<24h post mortem) were cultured in serum-free DMEM/HamF12. Increased HP was compared to simulated ischemia (oxygen glucose deprivation, OGD). Cell death and apoptosis were measured by LDH and TUNEL assays, RGC marker expression by qRT-PCR (THY-1) and RGC number by immunohistochemistry (NeuN). Activated p38 and JNK were detected by Western blot. Results: Exposure of HORCs to constant (60mmHg) or fluctuating (10-100mmHg; 1 cycle/min) pressure for 24 or 48h caused no loss of structural integrity, LDH release, decrease in RGC marker expression (THY-1) or loss of RGCs compared with controls. In addition, there was no increase in TUNEL-positive NeuN-labelled cells at either time-point indicating no increase in apoptosis of RGCs. OGD increased apoptosis, reduced RGC marker expression and RGC number and caused elevated LDH release at 24h. p38 and JNK phosphorylation remained unchanged in HORCs exposed to fluctuating pressure (10-100mmHg; 1 cycle/min) for 15, 30, 60 and 90min durations, whereas OGD (3h) increased activation of p38 and JNK, remaining elevated for 90min post-OGD. Conclusions: Directly applied HP had no detectable impact on RGC survival and stress-signalling in HORCs. Simulated ischemia, however, activated stress pathways and caused RGC death. These results show that direct HP does not cause degeneration of RGCs in the ex vivo human retina

    The signed loop approach to the Ising model: foundations and critical point

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    The signed loop method is a beautiful way to rigorously study the two-dimensional Ising model with no external field. In this paper, we explore the foundations of the method, including details that have so far been neglected or overlooked in the literature. We demonstrate how the method can be applied to the Ising model on the square lattice to derive explicit formal expressions for the free energy density and two-point functions in terms of sums over loops, valid all the way up to the self-dual point. As a corollary, it follows that the self-dual point is critical both for the behaviour of the free energy density, and for the decay of the two-point functions.Comment: 38 pages, 7 figures, with an improved Introduction. The final publication is available at link.springer.co
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