1,733 research outputs found

    What Matters to Whom? Managing Trust Across Multiple Stakeholder Groups

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    Trust has been widely recognized as a key enabler of organizational success. Prior research on organizational trust, however, has not distinguished between the potentially varying bases of trust across different stakeholder groups (e.g., employees, clients, investors, etc.). We develop a framework that distinguishes among organizational stakeholders along two dimensions: intensity (high or low) and locus (internal or external). The framework also helps to identify which of six potential antecedents of trust (benevolence, integrity, competence, reliability, transparency, and identification) will be relevant to which type of stakeholder. We test the predictions of our framework using survey responses from 1,296 respondents across four stakeholder groups from four different organizations. The results reveal that different antecedents of trust are indeed relevant for different stakeholder types, and provide strong support for the validity of the intensity and locus dimensions. This publication is Hauser Center Working Paper No. 39. The Hauser Center Working Paper Series was launched during the summer of 2000. The Series enables the Hauser Center to share with a broad audience important works-in-progress written by Hauser Center scholars and researchers

    On the Metallicity Gradients in the Galactic Disk using Open Clusters

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    We study the metallicity distribution and evolution in the Galactic disk based on the largest sample of open star clusters in the Galaxy. From the catalogue of 1879 open clusters in the range of Galactocentric distance (R_GC) from 4 to 20 kpc, we investigate the variation of metallicity in the Galactic disk as functions of R_GC, vertical distance (Z), and ages of the clusters. In the direction perpendicular to the Galactic plane, variation in metallicity is found to follow a stepped linear relation. We estimate a vertical metallicity gradient d[Fe/H]/dZ of -0.545+/-0.046 dex/kpc for |Z| < 0.487 kpc, and -0.075+/-0.093 dex/kpc for 0.487 < |Z| < 1.8 kpc. On average, metallicity variations above and below the Galactic plane are found to change at similar rates. The change in metallicity in the radial direction is also found to follow a two-function linear relation. We obtain a radial metallicity gradient d[Fe/H]/d[R_GC] of -0.070+/-0.002 dex/kpc for 4.0<R_GC<12.8 kpc, and -0.005+/-0.018 dex/kpc for 12.8< R_GC < 20.5 kpc which clearly shows a strong variation in the metallicity gradient when moving from the inner to the outer Galactic disk. Age-metallicity relation (AMR) is found to follow a steeper negative slope of -0.031+/-0.006 dex/Gyr for clusters older than 240 Myr, however, there is some hint of positive metallicity age gradient for younger clusters.Comment: Accepted for publication in Frontiers in Astronomy and Space Sciences, 28 pages, 9 figures, 4 table

    Sodium silicate mediated response of antioxidative defense system in Lycopersicon esculentum mill. under water stress

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    The present study was designed to study the effect of water stress on Lycopersicon esculentum Mill. and role of sodium silicate in the protection of tomato plants under water deficit condition.Different biochemical parameters such as photosynthetic pigments, protein, sugar, MDA content, proline, nitrate reductase activity and activities of antioxidant enzymes (SOD, CAT, APX and POX) were examined in tomato leaves at 40 and 60 DAS by the standard methods. The lycopene and β-carotene contentsin tomato fruits were also analyzed at 60, 65 and 70 DAS.Water stress significantly decreased relative water content (RWC), pigment content, sugar and protein contents in tomato leaves at 60 DAS but the accumulation of proline was stimulated in tomato leaves under water deficit condition. The activities of antioxidant enzymes such as SOD, CAT, APX and POX were significantly increased under (3d and 6d) water stress condition at 60 DAS.This study offers first hand information on the water stress-induced oxidative stress in Lycopersicon esculentumand development of antioxidative defense system against drought.The results obtained clearly indicated the positive impact of sodium silicate in protection of tomato plants under water deficit condition

    Regulation of Apical NHE3 Trafficking by Ouabain-Induced Activation of Basolateral Na/K-ATPase Receptor Complex

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    The long-term effects of ouabain on transepithelial Na+ transport involve transcriptional downregulation of apical Na+/H+ exchanger isoform 3 (NHE3). The aim of this study was to determine whether ouabain could acutely regulate NHE3 via a posttranscriptional mechanism in LLC-PK1 cells. We observed that the basolateral, but not apical, application of ouabain for 1 h significantly reduced transepithelial Na+ transport. This effect was not due to changes in the integrity of tight junctions or increases in the intracellular Na+ concentration. Ouabain regulated the trafficking of NHE3 and subsequently inhibited its activity, a process independent of intracellular Na+ concentration. Ouabain-induced NHE3 trafficking was abolished by either cholesterol depletion or Src inhibition. Moreover, ouabain increased the intracellular Ca2+concentration. Pretreatment of cells with the intracellular Ca2+ chelator BAPTA-AM blocked ouabain-induced trafficking of NHE3. Also, blockade of Na+-K+-ATPase endocytosis by a phosphatidylinositol 3-kinase inhibitor was equally effective in attenuating ouabain-induced NHE3 trafficking. These data indicate that ouabain acutely stimulates NHE3 trafficking by activating the basolateral Na+-K+-ATPase signaling complex. Taken together with our previous observations, we propose that ouabain can simultaneously regulate basolateral Na+-K+-ATPase and apical NHE3, leading to inhibition of transepithelial Na+ transport. This mechanism may be relevant to proximal tubular Na+ handling during conditions associated with increases in circulating endogenous cardiotonic steroids

    Hypertonicity: Pathophysiologic Concept and Experimental Studies

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    Disturbances in tonicity (effective osmolarity) are the major clinical disorders affecting cell volume. Cell shrinking secondary to hypertonicity causes severe clinical manifestations and even death. Quantitative management of hypertonic disorders is based on formulas computing the volume of hypotonic fluids required to correct a given level of hypertonicity. These formulas have limitations. The major limitation of the predictive formulas is that they represent closed system calculations and have been tested in anuric animals. Consequently, the formulas do not account for ongoing fluid losses during development or treatment of the hypertonic disorders. In addition, early comparisons of serum osmolality changes predicted by these formulas and observed in animals infused with hypertonic solutions clearly demonstrated that hypertonicity creates new intracellular solutes causing rises in serum osmolality higher than those predicted by the formulas. The mechanisms and types of intracellular solutes generated by hypertonicity and the effects of the solutes have been studied extensively in recent times. The solutes accumulated intracellularly in hypertonic states have potentially major adverse effects on the outcomes of treatment of these states. When hypertonicity was produced by the infusion of hypertonic sodium chloride solutions, the predicted and observed changes in serum sodium concentration were equal. This finding justifies the use of the predictive formulas in the management of hypernatremic states

    Down-regulation of the transcription factor snail in the placentas of patients with preeclampsia and in a rat model of preeclampsia

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    <p>Abstract</p> <p>Background</p> <p>Placental malfunction in preeclampsia is believed to be a consequence of aberrant differentiation of trophoblast lineages and changes in utero-placental oxygenation. The transcription factor Snail, a master regulator molecule of epithelial-mesenchymal transition in embryonic development and in cancer, is shown to be involved in trophoblast differentiation as well. Moreover, Snail can be controlled by oxidative stress and hypoxia. Therefore, we examined the expression of Snail and its downstream target, e-cadherin, in human normal term, preterm and preeclamptic placentas, and in pregnant rats that developed preeclampsia-like symptoms in the response to a 20-fold increase in sodium intake.</p> <p>Methods</p> <p>Western blotting analysis was used for comparative expression of Snail and e- cadherin in total protein extracts. Placental cells expressing Snail and e-cadherin were identified by immunohistochemical double-labeling technique.</p> <p>Results</p> <p>The levels of Snail protein were decreased in human preeclamptic placentas by 30% (<it>p < 0.01) </it>compared to normal term, and in the rat model by 40% (<it>p < 0.001) </it>compared to control placentas. In preterm placentas, the levels of Snail expression varied, yet there was a strong trend toward statistical significance between preterm and preeclamptic placentas. In humans, e-cadherin protein level was 30% higher in preeclamptic <it>(p < 0.05) </it>placentas and similarly, but not significantly <it>(p = 0.1)</it>, high in the preterm placentas compared to normal term. In the rat model of preeclampsia, e-cadherin was increased by 60% (<it>p < 0.01)</it>. Immunohistochemical examination of human placentas demonstrated Snail-positive staining in the nuclei of the villous trophoblasts and mesenchymal cells and in the invasive trophoblasts of the decidua. In the rat placenta, the majority of Snail positive cells were spongiotrophoblasts of the junctional zone, while in the labyrinth, Snail-positive sinusoidal giant trophoblasts cells were found in some focal areas located close to the junctional zone.</p> <p>Conclusion</p> <p>We demonstrated that human preeclampsia and the salt-induced rat model of preeclampsia are associated with the reduced levels of Snail protein in placenta. Down-regulation of the transcription factor Snail in placental progenitor cell lineages, either by intrinsic defects and/or by extrinsic and maternal factors, may affect normal placenta development and function and thus contribute to the pathology of preeclampsia.</p

    Hiding inside? Intracellular expression of non-glycosylated c-kit protein in cardiac progenitor cells

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    Cardiac progenitor cells including c-kit(+) cells and cardiosphere-derived cells (CDCs) play important roles in cardiac repair and regeneration. CDCs were reported to contain only small subpopulations of c-kit(+) cells and recent publications suggested that depletion of the c-kit(+) subpopulation of cells has no effect on regenerative properties of CDCs. However, our current study showed that the vast majority of CDCs from murine heart actually express c-kit, albeit, in an intracellular and non-glycosylated form. Immunostaining and flow cytometry showed that the fluorescent signal indicative of c-kit immunostaining significantly increased when cell membranes were permeabilized. Western blots further demonstrated that glycosylation of c-kit was increased during endothelial differentiation in a time dependent manner. Glycosylation inhibition by 1-deoxymannojirimycin hydrochloride (1-DMM) blocked c-kit glycosylation and reduced expression of endothelial cell markers such as Flk-1 and CD31 during differentiation. Pretreatment of these cells with a c-kit kinase inhibitor (imatinib mesylate) also attenuated Flk-1 and CD31 expression. These results suggest that c-kit glycosylation and its kinase activity are likely needed for these cells to differentiate into an endothelial lineage. In vivo, we found that intracellular c-kit expressing cells are located in the wall of cardiac blood vessels in mice subjected to myocardial infarction. In summary, our work demonstrated for the first time that c-kit is not only expressed in CDCs but may also directly participate in CDC differentiation into an endothelial lineage
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