References: Lecithin
Biomed Biochim Acta. 1989;48(10):849-52.
Inhibition of human lecithin: cholesterol acyltransferase activity by catecholamines in vitro.
Schauer UJ, Schauer I.
Poliklinik fur Innere Medizin, Medizinische Akademie, Erfurt, DDR.
The effects of L-adrenaline and L-noradrenaline on human lecithin: cholesterol acyltransferase (LCAT) activity were investigated in vitro. Both catecholamines are shown to be inhibitors of this enzyme. Despite inter-individual variations in the dose-response relationships calculated for both hormones, significant effects can be expected in the upper physiological range of concentration. Since diminished LCAT activity is known to be followed by a low level of HDL cholesterol and an increased concentration of triglycerides, it is supposed that catecholamine mediated inhibition of LCAT activity may contribute to the development of stress mediated fluctuations in plasma lipoprotein concentrations.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2634963&dopt=Abstract lecithin
Artif Cells Blood Substit Immobil Biotechnol. 1994;22(1):83-9.
Effects of lecithin-emulsified perfluorochemical compounds in ischemic brain injury.
Sakas DE, Crowell RM, Zervas NT.
Massachusetts General Hospital, Department of Surgery, Harvard Medical School, Boston 02114.
A lecithin-emulsified "Pluronic F-68"-free perfluorochemical compound, named F-1,3-DMA, was tested as a new agent in the prevention of central nervous tissue ischemia. A permanent ischemia leading to cerebral infarction was induced after microsurgical exposure and occlusion of the internal carotid, anterior, and middle cerebral arteries in the rabbit. Following arterial occlusion, F-1,3-DMA was administered intravenously, in a solution rendered isotonic to plasma, over a 30 minute period. The F-1,3-DMA was well tolerated. Hemodynamic, cardiovascular and metabolic parameters were not affected by the infusion of F-1,3-DMA. Although PO2 remained virtually unchanged, animals treated with F-1,3-DMA (n = 9), had smaller infarct volume by 61 percent as compared to the control (n = 8) group (P < 0.04, Student's t-test). Histopathology did not reveal any F-1,3-DMA related damage in the non-infarcted brain. These results suggest that F-1,3-DMA has nervous tissue ischemia protective properties possibly because of microflow effects although O2 transport to "local" tissue may be enhanced as well. We believe that further research is necessary in order to make clinical trials of F-1,3-DMA possible.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8055099&dopt=Abstract lecithin
Biochem J. 1995 Dec 15;312 ( Pt 3):795-7.
Partial characterization of regulation of biliary lecithin hydrophobicity: association with organic anion-induced solute cholestasis in rats.
Miura H, Tazuma S, Kajiyama G.
First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
We examined the effects of the depletion of bile salts and of the intravenous infusion of sodium taurocholate (STC) with or without bromosulphophthalein (BSP) in rats on the biliary secretion of lipids to clarify the regulatory mechanism(s). Each rat was equipped with a bile-duct cannula to collect bile. After the endogenous bile salt pool was depleted, STC was infused at a constant rate (160 nmol/min per 100 g body wt.) with or without BSP (50, 100, or 150 nmol/min per 100 g body wt.). BSP reduced the biliary secretion of cholesterol and phospholipids dose-dependently without affecting the secretion of bile salts (uncoupling phenomenon). Compared with the physiological and STC-infused condition, the biliary cholesterol/phospholipid ratio and saturated/unsaturated fatty acid ratio increased under the bile salts depletion and uncoupling phenomenon. Data indicate that the hydrophobicity of biliary lecithin increases with a decrease in the bile salt micelle capacity to induce biliary lipid secretion, resulting in a higher packing density of biliary vesicle. The cholesterol-holding capacity of the biliary vesicle is therefore enhanced during the depletion of bile salts and the uncoupling phenomenon.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8554522&dopt=Abstract lecithin
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