15 research outputs found

    , , and for the hypothetical segregation patterns listed in Table 3.

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    <p>‘na’ indicates that the value is not available in that paper. The results are rounded to the second decimal place.</p><p>, , and for the hypothetical segregation patterns listed in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113767#pone-0113767-t003" target="_blank">Table 3</a>.</p

    Relationship between the computation time and the number of measurement points for spseg().

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    <p>Relationship between the computation time and the number of measurement points for spseg().</p

    Computation time of the implemented functions for different input size.

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    <p>As the number of spatial units increases, the computation time also increases for all functions but at a different rate. The functions tested here are: dissim() (A), conprof() (B), isp() (C), spseg() (D), and deseg() (E).</p

    Computational flow of the spseg() function.

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    <p>It calls a series of subfunctions to calculate the spatial segregation measures. In this diagram, the curved-rectangles represent R functions and processes, the parallelograms refer to R objects, and the diamonds indicate the user options. Among the rectangles, only the shaded ones are user-level functions.</p

    A list of segregation measures currently implemented in the seg package.

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    <p>The mathematical definitions of and are given in this paper. For the other measures, see the corresponding papers cited in the table.</p><p>A list of segregation measures currently implemented in the seg package.</p

    , and the surface-based spatial segregation measures for the hypothetical segregation patterns listed in Table 3.

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    <p> is the exposure of the minority group (i.e., the black cells in the figures) to the majority group (i.e., the white cells), and is that of the majority group to the minority group. All calculations were done with default settings, except that KDE was used for the spatial segregation measures. The results are rounded to the second decimal place.</p><p>, and the surface-based spatial segregation measures for the hypothetical segregation patterns listed in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113767#pone-0113767-t003" target="_blank">Table 3</a>.</p

    Available methods for SegDecomp.

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    <p>SegDecomp is a custom defined S4 class, containing the measured segregation from deseg().</p

    A sample pattern of segregation.

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    <p>The white and black cells are where the minority population comprises 0% and 100% of the local population, respectively. The numbers inside of the cells indicate the cell ID, and the letters denote the edges.</p

    Available methods for SegSpatial and SegLocal.

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    <p>SegSpatial is a S4 class that stores results from the spseg() function. It inherits from another S4 class SegLocal.</p

    Treatment with the Antipsychotic Agent, Risperidone, Reduces Disease Severity in Experimental Autoimmune Encephalomyelitis

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    <div><p>Recent studies have demonstrated that atypical antipsychotic agents, which are known to antagonize dopamine D2 and serotonin 5-HT<sub>2a</sub> receptors, have immunomodulatory properties. Given the potential of these drugs to modulate the immune system both peripherally and within the central nervous system, we investigated the ability of the atypical anti-psychotic agent, risperidone, to modify disease in the animal model of multiple sclerosis (MS)<sup>4</sup>, experimental autoimune encephalomyelitis (EAE). We found that chronic oral administration of risperidone dose-dependently reduced the severity of disease and decreased both the size and number of spinal cord lesions. Furthermore, risperidone treatment substantially reduced antigen-specific interleukin (IL)-17a, IL-2, and IL-4 but not interferon (IFN)-γ production by splenocytes at peak disease and using an <i>in vitro</i> model, we show that treatment of macrophages with risperidone alters their ability to bias naïve T cells. Another atypical antipsychotic agent, clozapine, showed a similar ability to modify macrophages <i>in vitro</i> and to reduce disease in the EAE model but this effect was not due to antagonism of the type 1 or type 2 dopamine receptors alone. Finally, we found that while risperidone treatment had little effect on the <i>in vivo</i> activation of splenic macrophages during EAE, it significantly reduced the activation of microglia and macrophages in the central nervous system. Together these studies indicate that atypical antipsychotic agents like risperidone are effective immunomodulatory agents with the potential to treat immune-mediated diseases such as MS.</p></div
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