17 research outputs found
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Peak fitting applied to low-resolution enrichment measurements
Materials accounting at bulk processing facilities that handle low enriched uranium consists primarily of weight and uranium enrichment measurements. Most low enriched uranium processing facilities draw separate materials balances for each enrichment handled at the facility. The enrichment measurement determines the isotopic abundance of the {sup 235}U, thereby determining the proper strata for the item, while the weight measurement generates the primary accounting value for the item. Enrichment measurements using the passive gamma radiation from uranium were developed for use in US facilities a few decades ago. In the US, the use of low-resolution detectors was favored because they cost less, are lighter and more robust, and don`t require the use of liquid nitrogen. When these techniques were exported to Europe, however, difficulties were encountered. Two of the possible root causes were discovered to be inaccurate knowledge of the container wall thickness and higher levels of minor isotopes of uranium introduced by the use of reactor returns in the enrichment plants. the minor isotopes cause an increase in the Compton continuum under the 185.7 keV assay peak and the observance of interfering 238.6 keV gamma rays. The solution selected to address these problems was to rely on the slower, more costly, high-resolution gamma ray detectors when the low-resolution method failed. Recently, these gamma ray based enrichment measurement techniques have been applied to Russian origin material. The presence of interfering gamma radiation from minor isotopes was confirmed. However, with the advent of fast portable computers, it is now possible to apply more sophisticated analysis techniques to the low-resolution data in the field. Explicit corrections for Compton background, gamma rays from {sup 236}U daughters, and the attenuation caused by thick containers can be part of the least squares fitting routine. Preliminary results from field measurements in Kazakhstan will be discussed
Oncostatin M promotes STAT3 activation, VEGF production, and invasion in osteosarcoma cell lines
<p>Abstract</p> <p>Background</p> <p>We have previously demonstrated that both canine and human OSA cell lines, as well as 8 fresh canine OSA tumor samples, exhibit constitutive phosphorylation of STAT3, and that this correlates with enhanced expression of matrix metalloproteinase-2 (MMP2). While multiple signal transduction pathways can result in phosphorylation of STAT3, stimulation of the cytokine receptor gp130 through either IL-6 or Oncostatin M (OSM) is the most common mechanism through which STAT3 is activated. The purpose of this study was to evaluate the role of IL-6 and OSM stimulation on both canine and human OSA cell lines to begin to determine the role of these cytokines in the biology of OSA.</p> <p>Methods</p> <p>RT-PCR and Western blotting were used to interrogate the consequences of OSM and IL-6 stimulation of OSA cell lines. OSA cells were stimulated with OSM and/or hepatocyte growth factor (HGF) and the effects on MMP2 activity (gel zymography), proliferation (CyQUANT), invasion (Matrigel transwell assay), and VEGF production (Western blotting, ELISA) were assessed. The small molecule STAT3 inhibitor LLL3 was used to investigate the impact of STAT3 inhibition following OSM stimulation of OSA cells.</p> <p>Results</p> <p>Our data demonstrate that the OSM receptor (OSMR), but not IL-6 or its receptor, is expressed by all human and canine OSA cell lines and canine OSA tumor samples; additionally, OSM expression was noted in all tumor samples. Treatment of OSA cell lines with OSM induced phosphorylation of STAT3, Src, and JAK2. OSM stimulation also resulted in a dose dependent increase in MMP2 activity and VEGF expression that was markedly reduced following treatment with the small molecule STAT3 inhibitor LLL3. Lastly, OSM stimulation of OSA cell lines enhanced invasion through Matrigel, particularly in the presence of rhHGF. In contrast, both OSM and HGF stimulation of OSA cell lines did not alter their proliferative capacity.</p> <p>Conclusions</p> <p>These data indicate OSM stimulation of human and canine OSA cells induces STAT3 activation, thereby enhancing the expression/activation of MMP2 and VEGF, ultimately promoting invasive behavior and tumor angiogenesis. As such, OSM and its receptor may represent a novel target for therapeutic intervention in OSA.</p