13 research outputs found

    SAOS-2 binding to culture plastic and h-GF.

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    <p>SAOS-2 appeared as dark round cells in photomicrographs (arrow heads), as opposed to the elongated paler h-GF (arrows). h-GF increased SAOS-2 binding compared with culture plastic alone (p<0.001), and this was increased by TNF-α (1.16nM) treatment of the h-GF (p<0.001). (Bars = 50 µm).</p

    TNF-α increased ICAM-1 expression in h-GF and HUVEC, but only increased VCAM-1 in HUVEC.

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    <p>Fluorescence distribution profiles are shown proportionate to the peak incidence of fluorescence in each cell population studied. Background levels of ICAM-1 in both h-GF and HUVEC were appreciably increased following 24 hrs of stimulation with TNF-α (1.16nM). Although a similar effect of the cytokine was seen in HUVEC with regard to VCAM-1 expression, negligible VCAM-1 in h-GF was not significantly increased by TNF-α (1.16nM) stimulation.</p

    Decaying effect of TNF-α stimulation on h-GF binding of SAOS-2.

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    <p>A graph is shown of SAOS-2 binding to h-GF, in which h-GF were first stimulated with TNF-α (1.16nM) for 24 hrs, and then washed before further culture for from 0 to 24 hrs in M199 with BSA (4%), either with or without fresh TNF-α (1.16nM). There was decreased SAOS-2 attachment between 6 hr and 12 hrs post-cytokine stimulation (p<0.005), and this reduced to a plateau by 18 hrs (p<0.001).</p

    ICAM-1 was involved with TNF-α stimulated h-GF binding of SAOS-2.

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    <p>FACS analysis for ICAM-1 expression in h-GF with or without TNF-α (1.16nM) pre-treatment is shown (A), as well as at increasing times over 24 hr of TNF-α (1.16nM) treatment (B), compared with graphs showing the time-course of increased SAOS-2 binding by TNF-α (1.16nM) treated h-GF (C), and a histogram of the effect of blocking antibody against ICAM-1 (D). (A) h-GF expressed ICAM-1 and this was increased by TNF-α with maximal expression by 6 hr of cytokine treatment (B). (C) In an experiment performed at the same time as that shown in (5B), and using h-GF from the same donor, Maximal ICAM-1 expression correlated with maximal binding of SAOS-2 (p<0.001). As seen in the insert (C) examining the first 5 hr of cytokine stimulation in a separate time course experiment, increased SAOS-2 binding occurred between 0.5 and 1 hr of TNF-α (1.16nM) h-GF stimulation, and was maximal by 1.5 hrs (p<0.001). (D) Blocking antibody against ICAM-1 reduced binding of SAOS-2 to both untreated and TNF-α (1.16nM) stimulated h-GF (p<0.04).</p

    Impact of light-dark cycle on plasma glucose enrichment in mice.

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    <p>The fraction of deuterium enrichment of plasma glucose is plotted against time since the start of label modulo 24 h. Data from mice housed under reversed day/night condition is translated by 12h so that for all mice 0h represents the start of light phase (8am for normal conditions, 8pm for reversed day/night conditions). Grey circles represent measurements from individual mice, the line connects the medians, the points plotted at 24h/0h are duplicates of the 0h data.</p

    Total CD4<sup>+</sup> T cell proliferation rates estimated from D<sub>2</sub>-glucose and D<sub>2</sub>O labeling studies in humans.

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    <p>Each symbol represents a different individual, horizontal lines represent the median of the estimates. <b>(A)</b> Proliferation rates estimated using the kinetic heterogeneity model. <b>(B)</b> Proliferation rates estimated after adjusting for saturation (using the multi-exponential model for the nine-week (9w) D<sub>2</sub>O and seven-day (7d) D<sub>2</sub>-glucose labeling, and the kinetic heterogeneity model for one-day (1d) D<sub>2</sub>-glucose labeling). Although correcting for the saturation of rapidly turning over subpopulations helps to bring the estimates closer (by increasing the proliferation rate estimates obtained in the nine-week D<sub>2</sub>O labeling study) significant discrepancies remain.</p

    Estimates of the plateau enrichment of monocytes in humans.

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    <p>The maximum level of label that monocytes can attain (expressed as a percentage) was estimated for a one-day D<sub>2</sub>-glucose labeling study (subjects C02-C10) and a seven-day D<sub>2</sub>-glucose labeling study (subjects C2–C4). Two different models were considered: the “BM”(bone marrow) model and the “delayed obs.” (delayed observation) model (<a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1004355#sec009" target="_blank">Methods</a>). We also calculated the average estimate of the plateau by weighing each fit with the corresponding Akaike weight [<a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1004355#pcbi.1004355.ref024" target="_blank">24</a>]; these estimates are given in the column “weighted”. Estimates are shown ± standard deviation (sd). The sd in the “weighted” column reflects model uncertainty (whereas sd for the specified models assumes the model is correct). For every model the plateau enrichment was significantly higher in the one-day labeling study than in the seven-day labeling study (P = 0.048, P = 0.012, P = 0.012 for the BM, delayed obs. and weighted model respectively, two-tailed Mann-Whitney). In the one-day labeling study virtually all the plateau estimates were higher than 100% (23/24 ≥ 100%, 1/24 <100%); for the seven-day labeling study estimates were evenly distributed either side of 100% (4/9 ≥ 100%, 5/9 < 100%).</p><p>Estimates of the plateau enrichment of monocytes in humans.</p
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