LPL

As already said before the QAP for LPI systems has been developped on a modular basis and can vary with the composition of the LPl system given by the specific inspection process. 

Tire development of the QAP system for the MPI and LPl technique together with a camera system for automated flaw detection can give the following advantages ... 

Increased lipid synthesis/inhibi-tion of lipolysis Activation of lipoprotein lipase (LPL)/induc-tion of fatty acid synthase (FAS)/inactivation of hormone sensitive lipase (HSL) Facilitated uptake of fatty acids by LPL-dependent hydrolysis of triacylglycerol from circulating lipoproteins. Increased lipid synthesis through Akt-mediated FAS-expression. Inhibition of lipolysis by preventing cAMP-dependent activation of HSL (insulin-dependent activation of phosphodiesterases )... 

The three principal PVD subprocesses, evaporation, sputtering, and ion plating, are described belowl lPl... 

Figure 15-6. Transport and fate of major lipid substrates and metabolites. (FFA, free fatty acids LPL, lipoprotein lipase MG, monoacylglycerol TG, triacylglycerol VLDL, very low density lipoprotein.)...

Figure 26-6. Transport of cholesterol between the tissues in humans. (C, unesterified choiesterol CE, cho-iesteryi ester TG, triacyigiyceroi VLDL, very iow density iipoprotein iDL, intermediate-density iipoprotein LDL, iow-density iipoprotein HDL, high-density iipoprotein ACAT, acyi-CoA choiesteroi acyitransferase LCAT, iecithinxhoiesteroi acyitransferase A-i, apoiipoprotein A-i CETP, choiesteryi ester transfer protein LPL, lipoprotein iipase HL, hepatic iipase LRP, LDL receptor-reiated protein.)...

Famiiiai aipha-iipoprotein deficiency Tangier disease Fish-eye disease Apo-A-i deficiencies All have low or near absence of HDL. Tendency toward hypertriacylglycerolemia as a result of absence of apo C-ll, causing inactive LPL. Low LDL levels. Atherosclerosis in the elderly. 

Hyperlipoproteinemias Famiiiai iipoprotein iipase deficiency (type i) Hypertriacylglycerolemia due to deficiency of LPL, abnormal LPL, or apo C-ll deficiency causing inactive LPL. Slow clearance of chylomicrons and VLDL. Low levels of LDL and HDL. No increased risk of coronary disease. 

Figure 27-1. Metabolic interrelationships between adipose tissue, the liver, and extrahepatic tissues. In extrahepatic tissues such as heart, metabolic fuels are oxidized in the following order of preference (1) ketone bodies, (2) fatty acids, (3) glucose. (LPL, lipoprotein lipase FFA, free fatty acids VLDL, very low density lipoproteins.)...

FIGURE 3.2.2 Metabolic pathways of carotenoids such as p-carotene. CM = chylomicrons. VLDL = very low-density lipoproteins. LDL = low-density lipoproteins. HDL = high-density lipoproteins. BCO = p-carotene 15,15 -oxygenase. BCO2 = p-carotene 9, 10 -oxygenase. LPL = lipoprotein lipase. RBP = retinol binding protein. SR-BI = scavenger receptor class B, type I. 

Fig. 9-4). Very low-density lipoprotein particles are released into the circulation where they acquire apolipoprotein E and apolipoprotein C-II from HDL. Very-low density lipoprotein loses its triglyceride content through the interaction with LPL to form VLDL remnant and IDL. Intermediate-density lipoprotein can be cleared from the circulation by hepatic LDL receptors or further converted to LDL (by further depletion of triglycerides) through the action of hepatic lipases (HL). Approximately 50% of IDL is converted to LDL. Low-density lipoprotein particles are cleared from the circulation primarily by hepatic LDL receptors by interaction with apolipoprotein B-100. They can also be taken up by extra-hepatic tissues or enter the arterial wall, contributing to atherogenesis.4,6... 

FIGURE 9. Endogenous lipoprotein metabolism. In liver cells, cholesterol and triglycerides are packaged into VLDL particles and exported into blood where VLDL is converted to IDL. Intermediate-density lipoprotein can be either cleared by hepatic LDL receptors or further metabolized to LDL. LDL can be cleared by hepatic LDL receptors or can enter the arterial wall, contributing to atherosclerosis. Acetyl CoA, acetyl coenzyme A Apo, apolipoprotein C, cholesterol CE, cholesterol ester FA, fatty acid HL, hepatic lipase HMG CoA, 3-hydroxy-3-methyglutaryl coenzyme A IDL, intermediate-density lipoprotein LCAT, lecithin-cholesterol acyltransferase LDL, low-density lipoprotein LPL, lipoprotein lipase VLDL, very low-density lipoprotein. 

Fibrates work by reducing apolipoproteins B, C-III (an inhibitor of LPL), and E, and increasing apolipoproteins A-I and A-II through activation of peroxisome proliferator-activated receptors-alpha (PPAR-a), a nuclear receptor involved in cellular function. The changes in these apolipoproteins result in a reduction in triglyceride-rich lipoproteins (VLDL and IDL) and an increase in HDL. 

The clearing effect of heparin on blood is associated with release of the triglyceride-hydrolyzing enzyme lipoproteinlipase (LPL) from the surface of endothelial cells.458,459 In addition to a number of apparently equivalent lipases from different tissues,459 heparin also releases a hepatic lipase.460,461 As suggested by the results of affinity-chromatography studies, this release is probably associated with binding of the polysaccharide to the enzyme. 62,463 Because other polyanions,464 including the... 

LPL found on the endothelial surfaces of the blood capillaries) to produce chylomicron remnants, which are then removed from the circulation by specific remnant receptors located on parenchymal liver cells. VLDLs are secreted by the liver. Following their secretion in blood, VLDLs undergo metabolism in a way... 

Hallett, Vicky. Alchemist s secret. U.S. News World Report (26 Aug 2002). fhttp //www. highbeam.com/librarv/doc3.asp DOCID=lPl 557341921. 

The Space Shuttle Solid Rocket Boosters. Student Space Awareness — National Web Team, University of Arizona Chapter of Students for the Exploration and Development of Space, http //seds.lpl.arizona.edu/ssa/docs/Space.Shuttle/srb.shtml... 

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