Magnetic nanoparticles are promising molecular imaging agents due to their relatively high relaxivity and the potential to modify surface functionality to tailor biodistribution. In this work we describe the synthesis of magnetic nanoparticles using organic solvents with organometallic precursors. This method results in nanoparticles that are highly crystalline and have uniform size and shape.
View Article and Find Full Text PDFMercury is toxic to the kidney, and dental amalgam is a source of mercury exposure. Few studies have evaluated the effects of dental amalgam on kidney function in a longitudinal context in children. Here, we evaluated urinary concentrations of glutathione S-transferases (GSTs) alpha and pi as biomarkers of renal proximal and distal tubular integrity, respectively, and albumin as a biomarker of glomerular integrity in children and adolescents 8-18 years of age over a 7-year course of dental amalgam treatment.
View Article and Find Full Text PDFTo present longitudinal urinary creatinine excretion data for developmentally normal children 9-17 years of age. Only extremely limited data have been presented of a longitudinal nature for this age group. Overall, 507 children who participated in a prospective, randomized, controlled trial of dental materials safety were followed longitudinally for 7 years with renal measures, including creatinine excretion.
View Article and Find Full Text PDFEnviron Health Perspect
October 2007
Background: Urinary mercury concentrations are widely used as a measure of mercury exposure from dental amalgam fillings. No studies have evaluated the relationship of these measures in a longitudinal context in children.
Objective: We evaluated urinary mercury in children 8-18 years of age in relation to number of amalgam surfaces and time since placement over a 7-year course of amalgam treatment.
Numerous studies have demonstrated a central role of renal tubular epithelial cells in the etiology of kidney injury and disease through the elaboration of inflammatory mediators. However, little is known about the cellular signaling mechanisms involved in this process. In this study we employed normal rat kidney epithelial (NRK52E) cells to identify a novel LPS-induced signaling pathway in which RhoA-mediated AP-1 activity promotes expression of cyclooxygenase-2 (COX-2) with consequent feedback inhibition of NF-kappaB activation through IKKbeta.
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