University of North Carolina at Greensboro

About: University of North Carolina at Greensboro is a education organization based out in Greensboro, North Carolina, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 5481 authors who have published 13715 publications receiving 456239 citations. The organization is also known as: UNCG & UNC Greensboro.

The State of the Art of Collaboration on Behalf of Students With Disabilities

Abstract: The need for effective collaboration on behalf of students with disabilities has never been greater. The No Child Left Behind Act of 2001 (NCLB) and the reauthorization of the Individuals with Disa...

How patients and nurses experience the acute care psychiatric environment

Abstract: How patients and nurses experience the acute care psychiatric environment The concept of the therapeutic milieu was developed when patients' hospitalizations were long, medications were few, and one- to-one nurse-patient interactions were the norm. However, it is not clear how the notion of 'therapeutic milieu' is experienced in American acute psychiatric environments today. This phenomenological study explored the experience of patients and nurses in an acute care psychiatric unit in the USA, by asking them, 'What stands out to you about this psychiatric hospital environment?' Three figural themes emerged, contextualized by time, which was a source of stress to both groups: for patients there was boredom, and for nurses, pressure and chaos. Although they shared some themes, nurses and patients experienced them differently. For instance, nurses felt caged-in by the Plexiglas-enclosed nursing station, and patients felt caged-in by the locked doors of the unit. The findings from this US study do not support the existence of the therapeutic milieu as described in the literature. Furthermore, although the nurse-patient relationship was yearned for by nurses, it was nearly absent from patients' descriptions. The caring experienced by patients was mainly derived from interactions with other patients.

Reduction of Fe(III) is required for uptake of nonheme iron by Caco-2 cells

Abstract: Differentiated cultures of Caco-2 human colonic cells were used to examine the importance of reduction of nonheme ferric iron, Fe(III), for transport across the brush border surface. Cultures accumulated approximately 100 pmol Fe/(h.mg protein) when 10 mumol Fe(III) as the nitrilotriacetic acid complex (1Fe:2NTA) was added to the apical compartment. Ascorbic acid enhanced cellular acquisition of iron in a dose-dependent manner, with a concentration as low as 8 mumol/L ascorbate increasing iron uptake by 50%. Similarly, the rate of iron transport from the apical to the basolateral compartment increased 5.6- and 30-fold when 100 and 1000 mumol/L ascorbic acid, respectively, were present in the apical chamber. Ascorbate-mediated stimulation of iron uptake was temperature dependent and required the reduction of Fe(III) to Fe(II), because it was inhibited by ascorbate oxidase and chelators of Fe(II). Moreover, Caco-2 cells recycled dehydroascorbic acid to ascorbic acid. Ferricyanide and Fe(II) chelators also partially inhibited iron uptake from a medium devoid of ascorbic acid. Intact Caco-2 cells exhibited a ferrireductase activity on the apical surface that accounted for the majority of iron accumulated by cells incubated in the absence of exogenous reductant. These data suggest that reduction of Fe(III) within the lumen or at the cell surface is required for transfer of this essential micronutrient across the intestinal brush border surface.

Luteolin protects against vascular inflammation in mice and TNF-alpha-induced monocyte adhesion to endothelial cells via suppressing IΚBα/NF-κB signaling pathway

Abstract: Vascular inflammation plays a significant role in the pathogenesis of atherosclerosis. Luteolin, a naturally occurring flavonoid present in many medicinal plants and some commonly consumed fruits and vegetables, has received wide attention for its potential to improve vascular function in vitro. However, its effect in vivo and the molecular mechanism of luteolin at physiological concentrations remain unclear. Here, we report that luteolin as low as 0.5 μM significantly inhibited tumor necrosis factor (TNF)-α-induced adhesion of monocytes to human EA.hy 926 endothelial cells, a key event in triggering vascular inflammation. Luteolin potently suppressed TNF-α-induced expression of the chemokine monocyte chemotactic protein-1 (MCP-1) and adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), key mediators involved in enhancing endothelial cell-monocyte interaction. Furthermore, luteolin inhibited TNF-α-induced nuclear factor (NF)-κB transcriptional activity, IκBα degradation, expression of IκB kinase β and subsequent NF-κB p65 nuclear translocation in endothelial cells, suggesting that luteolin can inhibit inflammation by suppressing NF-κB signaling. In an animal study, C57BL/6 mice were fed a diet containing 0% or 0.6% luteolin for 3 weeks, and luteolin supplementation greatly suppressed TNF-α-induced increase in circulating levels of MCP-1/JE, CXCL1/KC and sICAM-1 in C57BL/6 mice. Consistently, dietary intake of luteolin significantly reduced TNF-α-stimulated adhesion of monocytes to aortic endothelial cells ex vivo. Histology shows that luteolin treatment prevented the eruption of endothelial lining in the intima layer of the aorta and preserved elastin fibers' delicate organization as shown by Verhoeff-Van Gieson staining. Immunohistochemistry studies further show that luteolin treatment also reduced VCAM-1 and monocyte-derived F4/80-positive macrophages in the aorta of TNF-α-treated mice. In conclusion, luteolin protects against TNF-α-induced vascular inflammation in both in vitro and in vivo models. This anti-inflammatory effect of luteolin may be mediated via inhibition of the NF-κB-mediated pathway.