PubMed · 13759545
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M LAURIJSSENS, J VERSTRAETEN, K VUYLSTEEK. 1960-12-15. [Tuberculous constrictive pericarditis].. https://pubmed.ncbi.nlm.nih.gov/13759545/
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Increased free fatty acid flux, giving rise to increased de novo synthesis of diacylglycerol (DAG) and activation of protein kinase C (PKC) in vascular endothelium, may be largely responsible for the endotheliopathy and increased vascular risk associated with insulin resistance syndrome. This mechanism may also mediate, in large part, the increase in plasminogen activator inhibitor-1 (PAI-1) observed in this syndrome. PKC activation promotes transcription of PAI-1 in endothelial cells and other tissues, apparently by boosting the activity of Sp1 transcription factors that bind to the PAI-1 promoter. Plasma PAI-1 correlates inversely with the ability of insulin infusion to suppress free fatty acid levels. Moreover, infusion of triglycerides with heparin - inducing a marked increase in free fatty acids - has been shown to induce a rapid increase in plasma PAI-1. Alternatively, hyperinsulinemia and hypertriglyceridemia have been suggested as mediators of PAI-1 excess in insulin resistance, inasmuch as insulin and VLDL can stimulate PAI-1 production in cell cultures. However, plasma PAI-1 tends to decline in response to hyperinsulinemic clamps and insulin treatment of type 2 diabetes, and gemfibrozil treatment of hypertriglyceridemia does not decrease PAI-1 - suggesting that elevations of insulin or triglycerides are not likely to mediate PAI-1 excess in vivo. Hypertrophied adipose mass can secrete PAI-1, and is likely to contribute to the plasma PAI-1 pool in obese insulin-resistant subjects, but current evidence suggests that this is not likely to be the primary source of the elevated plasma PAI-1 in insulin resistance syndrome. Plasma PAI-1 can be decreased in insulin resistant subjects by improving adipocyte insulin sensitivity (with weight loss and thiazolidinediones), by consuming a very-low-fat diet that minimizes postprandial free fatty acid flux, and by administering activators of AMP-activated kinase (e.g., metformin), which can be expected to lessen tissue DAG synthesis.
Because of the nature of digital imaging, the number of pixels in a reconstructed image is often unrelated to the actual spatial resolution of the image. Similarly, the number of reconstructed frames of a dynamic or cine examination can be unrelated to the acquired temporal resolution. These discrepancies can result in misinterpretations and inaccuracies when image resolution is reported in the literature. The goal of this report is to clarify the differences between acquired and displayed resolution, both spatial and temporal, in magnetic resonance imaging. The effects of imaging parameters on acquired resolution are discussed, as are the mathematic effects of the reconstruction process on the displayed resolution of the resulting image. Finally, recommendations to authors are offered to promote accurate and unambiguous reporting of spatiotemporal resolution in the literature.
BACKGROUND: Weaning of patients from mechanical cardiac support after myocardial recovery has always involved multiple, interacting factors, particularly the training of the myocardium during reduction of pump flow. Rotary pumps offer training advantages when support flow is reduced, even to nearly zero. We report a computer analysis that evaluates the work required of the heart during partial unloading and removal of rotary pumps. METHODS AND RESULTS: A computer model of the assisted circulation, previously implemented in MATLAB (The MathWorks Inc, Natick, Mass), has been augmented with a model of the MicroMed DeBakey ventricular assist device (MicroMed Technology, Inc, Houston, Tex). Flow, pressure patterns, and external work (pressure-volume area, calculated as the area of the ventricular pressure-volume loop [external work] plus potential energy) were calculated for nonassisted and various continuously assisted patients. Under low-flow conditions, the heart imposes an oscillating forward-backward flow through the non-occlusive rotary pump, causing an increase in ventricular work. Thus, an assist flow of 1 to 1.5 L/min requires work equivalent to that of the unsupported heart. At 60% contractility, the nonassisted pressure-volume area is 1.10 Ws/beat, and the potential energy is 0.38 Ws/beat. At a Qpump of 1 L/min, the pressure-volume area is 1.21 Ws/beat, and the potential energy is 0.37 Ws/beat. At a Qpump of 3 L/min, the pressure-volume area is 0.93 Ws/beat, and the potential energy is 0.29 Ws/beat. These conditions cannot be achieved with pulsatile systems. CONCLUSION: During weaning and retraining, an implanted rotary pump can provide a workload to the heart like that in the nonassisted situation, thus increasing the predictability of weaning and reducing the risk of reiterating heart failure.