382 research outputs found

    Ex. 279-US-438

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    A report on the Summary of Stream Surveys in the Upper Sprague River, Klamath Basin, Oregon, 1991-1994

    Ex. 279-US-438

    Get PDF
    A report on the Summary of Stream Surveys in the Upper Sprague River, Klamath Basin, Oregon, 1991-1994

    Can the fast bone loss in osteoporotic and osteopenic patients be stopped with active vitamin D metabolites?

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    The aim of this study was to evaluate whether fast trabecular bone loss in osteoporotic and osteopenic patients can effectively be treated with active vitamin D metabolites. Thirty-one osteoporotic and osteopenic patients were monitored between 4 and 22 months before and between 8 and 18 months during the treatment. Fast bone losers were designated as osteoporotic or osteopenic patients with a loss of trabecular bone density in the radius of 3% or more calculated for 1 year. For this differentiation, the high precise peripheral quantitative computed tomography system (DENSISCAN 1000) was used (reproducability 0.3% in mixed collectives). The pretreatment loss and the "gain” under treatment with active vitamin D metabolites was calculated for 1 year. The treatment consisted of either 0.5 μg calcitriol daily or 1 μg of alfacalcidol daily. Before treatment, the trabecular bone loss in the radius/year was −6.6 ± 0.5% (mean ± SEM). After treatment with vitamin D metabolites, the trabecular bone gain in the radius/year was 0.01 ± 0.6% (mean ± SEM). The difference was highly significant (P < 0.001). In contrast to this, the loss of cortical bone density before treatment was −1.8 ± 0.3% (mean ± SEM) and the reduced loss after treatment −0.2 ± 0.4% (mean ± SEM), both values calculated for 1 year. This difference was less significant (P < 0.05). This study shows that the treatment with active vitamin D metabolites is very effective in slowing fast trabecular bone loss in osteoporotic and osteopenic patient

    GFP for EM: Site-Specific Labeling of Proteins for Electron Microscopy

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    The role of the novel Th17 cytokine IL-26 in intestinal inflammation

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    Background and aims: Interleukin 26 (IL-26), a novel IL-10-like cytokine without a murine homologue, is expressed in T helper 1 (Th1) and Th17 cells. Currently, its function in human disease is completely unknown. The aim of this study was to analyse its role in intestinal inflammation.Methods: Expression studies were performed by reverse transcription-PCR (RT-PCR), quantitative PCR, western blot and immunohistochemistry. Signal transduction was analysed by western blot experiments and ELISA. Cell proliferation was measured by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. IL-26 serum levels were determined by an immunoluminometric assay (ILMA).Results: All examined intestinal epithelial cell (IEC) lines express both IL-26 receptor subunits IL-20R1 and IL-10R2. IL-26 activates extracellular signal-related kinase (ERK)-1/2 and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) mitogen-activated protein (MAP) kinases, Akt and signal transducers and activators of transcription (STAT) 1/3. IL-26 stimulation increases the mRNA expression of proinflammatory cytokines but decreases cell proliferation. In inflamed colonic lesions of patients with Crohn's disease, an elevated IL-26 mRNA expression was found that correlated highly with the IL-8 and IL-22 expression. Immunohistochemical analysis demonstrated IL-26 protein expression in colonic T cells including Th17 cells expressing the orphan nuclear receptor ROR\textgreekgt, with an increased number of colonic IL-26-expressing cells in active Crohn's disease.Conclusion: Intestinal cells express the functional IL-26 receptor complex. IL-26 modulates IEC proliferation and proinflammatory gene expression and its expression is upregulated in active Crohn's disease, indicating a role for this cytokine system in the innate host cell response during intestinal inflammation. For the first time, IL-26 expression is demonstrated in colonic ROR\textgreekgt-expressing Th17 cells in situ, supporting a role for this cell type in the pathogenesis of Crohn's disease

    Evidence for direct control of eye movements during reading.

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    It is well established that fixation durations during reading vary with processing difficulty, but there are different views on how oculomotor control, visual perception, shifts of attention, and lexical (and higher cognitive) processing are coordinated. Evidence for a one-to-one translation of input delay into saccadic latency would provide a much needed constraint for current theoretical proposals. Here, we tested predictions of such a direct-control perspective using the stimulus-onset delay (SOD) paradigm. Words in sentences were initially masked and, upon fixation, were individually unmasked with a delay (0-ms, 33-ms, 66-ms, 99-ms SODs). In Experiment 1, SODs were constant for all words in a sentence; in Experiment 2, SODs were manipulated on target words, while non-targets were unmasked without delay. In accordance with predictions of direct control, non-zero SODs entailed equivalent increases in fixation durations in both experiments. Yet, a population of short fixations pointed to rapid saccades as a consequence of low-level information at non-optimal viewing positions rather than of lexical processing. Implications of these results for theoretical accounts of oculomotor control are discussed
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