415 research outputs found

    Continuing Demonstration Project: Library Training Institute: Interim Report, West Virginia

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    1973 interim report on the Library Training Institute of the Continuing Demonstration Project from Huntington, West Virginia submitted by James B. Nelson and Phyllis J. MacVicar

    Tele-methylhistamine 1 distribution in rat brain

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65997/1/j.1471-4159.1979.tb02303.x.pd

    Volume Regulated Anion Channel Currents of Rat Hippocampal Neurons and Their Contribution to Oxygen-and-Glucose Deprivation Induced Neuronal Death

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    Volume-regulated anion channels (VRAC) are widely expressed chloride channels that are critical for the cell volume regulation. In the mammalian central nervous system, the physiological expression of neuronal VRAC and its role in cerebral ischemia are issues largely unknown. We show that hypoosmotic medium induce an outwardly rectifying chloride conductance in CA1 pyramidal neurons in rat hippocampal slices. The induced chloride conductance was sensitive to some of the VRAC inhibitors, namely, IAA-94 (300 µM) and NPPB (100 µM), but not to tamoxifen (10 µM). Using oxygen-and-glucose deprivation (OGD) to simulate ischemic conditions in slices, VRAC activation appeared after OGD induced anoxic depolarization (AD) that showed a progressive increase in current amplitude over the period of post-OGD reperfusion. The OGD induced VRAC currents were significantly inhibited by inhibitors for glutamate AMPA (30 µM NBQX) and NMDA (40 µM AP-5) receptors in the OGD solution, supporting the view that induction of AD requires an excessive Na+-loading via these receptors that in turn to activate neuronal VRAC. In the presence of NPPB and DCPIB in the post-OGD reperfusion solution, the OGD induced CA1 pyramidal neuron death, as measured by TO-PRO-3-I staining, was significantly reduced, although DCPIB did not appear to be an effective neuronal VRAC blocker. Altogether, we show that rat hippocampal pyramidal neurons express functional VRAC, and ischemic conditions can initial neuronal VRAC activation that may contribute to ischemic neuronal damage

    Secreted Phospholipase A2 Involvement in Neurodegeneration: Differential Testing of Prosurvival and Anti-Inflammatory Effects of Enzyme Inhibition

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    There is increased interest in the contribution of secreted phospholipase A2 (sPLA2) enzymes to neurodegenerative diseases. Systemic treatment with the nonapeptide CHEC-9, a broad spectrum uncompetitive inhibitor of sPLA2, has been shown previously to inhibit neuron death and aspects of the inflammatory response in several models of neurodegeneration. A persistent question in studies of sPLA2 inhibitors, as for several other anti-inflammatory and neuroprotective compounds, is whether the cell protection is direct or due to slowing of the toxic aspects of the inflammatory response. To further explore this issue, we developed assays using SY5Y (neuronal cells) and HL-60 (monocytes) cell lines and examined the effects of sPLA2 inhibition on these homogeneous cell types in vitro. We found that the peptide inhibited sPLA2 enzyme activity in both SY5Y and HL-60 cultures. This inhibition provided direct protection to SY5Y neuronal cells and their processes in response to several forms of stress including exposure to conditioned medium from HL-60 cells. In cultures of HL-60 cells, sPLA2 inhibition had no effect on survival of the cells but attenuated their differentiation into macrophages, with regard to process development, phagocytic ability, and the expression of differentiation marker CD36, as well as the secretion of proinflammatory cytokines TNF-α and IL-6. These results suggest that sPLA2 enzyme activity organizes a cascade of changes comprising both cell degeneration and inflammation, processes that could theoretically operate independently during neurodegenerative conditions. The effectiveness of sPLA2 inhibitor CHEC-9 may be due to its ability to affect both processes in isolation. Testing potential anti-inflammatory/neuroprotective compounds with these human cell lines and their conditioned media may provide a useful screening tool prior to in vivo therapeutic applications

    Air quality and urban sustainable development: the application of machine learning tools

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    [EN] Air quality has an efect on a population¿s quality of life. As a dimension of sustainable urban development, governments have been concerned about this indicator. This is refected in the references consulted that have demonstrated progress in forecasting pollution events to issue early warnings using conventional tools which, as a result of the new era of big data, are becoming obsolete. There are a limited number of studies with applications of machine learning tools to characterize and forecast behavior of the environmental, social and economic dimensions of sustainable development as they pertain to air quality. This article presents an analysis of studies that developed machine learning models to forecast sustainable development and air quality. Additionally, this paper sets out to present research that studied the relationship between air quality and urban sustainable development to identify the reliability and possible applications in diferent urban contexts of these machine learning tools. To that end, a systematic review was carried out, revealing that machine learning tools have been primarily used for clustering and classifying variables and indicators according to the problem analyzed, while tools such as artifcial neural networks and support vector machines are the most widely used to predict diferent types of events. The nonlinear nature and synergy of the dimensions of sustainable development are of great interest for the application of machine learning tools.Molina-Gómez, NI.; Díaz-Arévalo, JL.; López Jiménez, PA. (2021). Air quality and urban sustainable development: the application of machine learning tools. 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    Between mediatisation and politicisation: The changing role and position of Whitehall press officers in the age of political spin

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    Despite widespread critiques of ‘political spin’, the way governments engage with the mass media has attracted relatively little empirical attention. There is a small but growing body of research into bureaucracies’ responses to mediatisation from within which have identified tensions between bureaucratic and party political values, but this has not included the United Kingdom. There are concerns that the traditional dividing line between government information and political propaganda has come under increasing pressure as a higher premium is placed on persuasion by both journalists and politicians battling for public attention in an increasingly competitive market. Within Whitehall, the arrival of Labour in 1997 after 18 years in opposition was a watershed for UK government communications, allowing the government to reconfigure its official information service in line with the party political imperative to deploy strategic communications as a defence against increasingly invasive media scrutiny. Public relations, in government as elsewhere, has grown in scale, scope and status, becoming institutionalised and normalised within state bureaucracies, but how has this affected the role, status and influence of the civil servants who conduct media management? Within the system of executive self-regulation of government publicity that is characteristic of Whitehall, government press officers must negotiate a difficult path between the need to inform citizens about the government’s programme, and demands by ministers to deploy privileged information to secure and maintain personal and party advantage in the struggle for power. Taking 1997 as a turning point, and through the voices of the actors who negotiate government news – mainly press officers, but also journalists and special advisers – this article examines the changing role and position of Whitehall press officers in what has become known as the age of political spin, finding that profound and lasting change in the rules of engagement has taken place and is continuing

    Two Distinct Modes of Hypoosmotic Medium-Induced Release of Excitatory Amino Acids and Taurine in the Rat Brain In Vivo

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    A variety of physiological and pathological factors induce cellular swelling in the brain. Changes in cell volume activate several types of ion channels, which mediate the release of inorganic and organic osmolytes and allow for compensatory cell volume decrease. Volume-regulated anion channels (VRAC) are thought to be responsible for the release of some of organic osmolytes, including the excitatory neurotransmitters glutamate and aspartate. In the present study, we compared the in vivo properties of the swelling-activated release of glutamate, aspartate, and another major brain osmolyte taurine. Cell swelling was induced by perfusion of hypoosmotic (low [NaCl]) medium via a microdialysis probe placed in the rat cortex. The hypoosmotic medium produced several-fold increases in the extracellular levels of glutamate, aspartate and taurine. However, the release of the excitatory amino acids differed from the release of taurine in several respects including: (i) kinetic properties, (ii) sensitivity to isoosmotic changes in [NaCl], and (iii) sensitivity to hydrogen peroxide, which is known to modulate VRAC. Consistent with the involvement of VRAC, hypoosmotic medium-induced release of the excitatory amino acids was inhibited by the anion channel blocker DNDS, but not by the glutamate transporter inhibitor TBOA or Cd2+, which inhibits exocytosis. In order to elucidate the mechanisms contributing to taurine release, we studied its release properties in cultured astrocytes and cortical synaptosomes. Similarities between the results obtained in vivo and in synaptosomes suggest that the swelling-activated release of taurine in vivo may be of neuronal origin. Taken together, our findings indicate that different transport mechanisms and/or distinct cellular sources mediate hypoosmotic medium-induced release of the excitatory amino acids and taurine in vivo
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