Finite-element modeling and measurements of flux and eddy current distribution in toroidal cores wound from electrical steel

Despite the apparent relative simplicity of the wound toroidal geometry, numerical modeling techniques are very difficult to implement due to the inherent large mesh size required to model a laminated core or spiral geometry. Recent advancements in computing capabilities have made the simulation and the study of such devices more feasible. Finite-element modeling of toroidal cores wound from grain-oriented electrical steel was conducted to accurately represent their magnetic circuits in order to calculate the internal magnetic flux distribution, its interaction with core geometry, and to be able to predict the associated magnetic losses. The general flux distribution trends agree with measured results from identical cores. The interlaminar flux and the associated induced planar eddy currents were also calculated. The measurements were performed using a series of search coils enclosing every five turns. In each case, the core was magnetized at 50 and 400 Hz under controlled sinusoidal flux density up to 1.5 T

Nuclear Factor of Activated T Cells Is Activated in the Endothelium of Retinal Microvessels in Diabetic Mice

The pathogenesis of diabetic retinopathy (DR) remains unclear but hyperglycemia is an established risk factor. Endothelial dysfunction and changes in Ca2+ signaling have been shown to precede the onset of DR. We recently demonstrated that high extracellular glucose activates the Ca(2+)/calcineurin-dependent transcription factor NFAT in cerebral arteries and aorta, promoting the expression of inflammatory markers. Here we show, using confocal immunofluorescence, that NFAT is expressed in the endothelium of retinal microvessels and is readily activated by high glucose. This was inhibited by the NFAT blocker A-285222 as well as by the ectonucleotidase apyrase, suggesting a mechanism involving the release of extracellular nucleotides. Acute hyperglycemia induced by an IP-GTT (intraperitoneal glucose tolerance test) resulted in increased NFATc3 nuclear accumulation and NFAT-dependent transcriptional activity in retinal vessels of NFAT-luciferase reporter mice. In both Akita (Ins2(+/-) ) and streptozotocin- (STZ-) induced diabetic mice, NFAT transcriptional activity was elevated in retinal vessels. In vivo inhibition of NFAT with A-285222 decreased the expression of OPN and ICAM-1 mRNA in retinal vessels, prevented a diabetes driven downregulation of anti-inflammatory IL-10 in retina, and abrogated the increased vascular permeability observed in diabetic mice. Results identify NFAT signaling as a putative target for treatment of microvascular complications in diabetes