A series of short screencast videos to introduce synthetic mechanisms

AB - Cholesteryl ester-rich particles extracted from human atherosclerotic plaques were shown to increase the rate of incorporation of [ 14C]oleate into cholesteryl [ 14C]oleate and to cause massive accumulation of cholesteryl esters in monolayers of mouse peritoneal macrophages. This stimulation showed saturation kinetics and susceptibility to competition by polyanions (polyinosinic acid, fucoidin, dextran sulfate), suggesting that cell surface binding was required. Cellular uptake and lysosomal hydrolysis of the cholesteryl esters were also required, as indicated by the finding that stimulation of cholesterol ester formation was prevented by the lysosomal inhibitor, chloroquine. The cholesterol esterification-stimulating activity of the aortic extracts was excluded on a 2% agarose column and floated in the density range of 1.006 to 1.063 g/ml. Cholesterol-rich extracts from human adrenal glands and liver did not stimulate cholesteryl ester formation in macrophages, The aortic extracts did not stimulate cholesteryl ester synthesis in human fibroblasts. Complexes of 125I-labeled albumin and cholesteryl linoleate formed in vivo were taken up and degraded in macrophages but not in fibroblasts, by a process resembling the uptake of the aortic extracts. The current data suggest that macrophages express mechanisms for internalizing certain types of cholesteryl ester-rich lipid/protein complexes, including those present in atherosclerotic plaques.

Includes mechanisms and a detailed description of the synthesis of ..

Organic Reaction Intermediates and Mechanisms; 159193; Ester Synthesis and Reaction Problems

Mechanisms involved in the Synthesis of Dimedone

N2 - Cholesteryl ester-rich particles extracted from human atherosclerotic plaques were shown to increase the rate of incorporation of [ 14C]oleate into cholesteryl [ 14C]oleate and to cause massive accumulation of cholesteryl esters in monolayers of mouse peritoneal macrophages. This stimulation showed saturation kinetics and susceptibility to competition by polyanions (polyinosinic acid, fucoidin, dextran sulfate), suggesting that cell surface binding was required. Cellular uptake and lysosomal hydrolysis of the cholesteryl esters were also required, as indicated by the finding that stimulation of cholesterol ester formation was prevented by the lysosomal inhibitor, chloroquine. The cholesterol esterification-stimulating activity of the aortic extracts was excluded on a 2% agarose column and floated in the density range of 1.006 to 1.063 g/ml. Cholesterol-rich extracts from human adrenal glands and liver did not stimulate cholesteryl ester formation in macrophages, The aortic extracts did not stimulate cholesteryl ester synthesis in human fibroblasts. Complexes of 125I-labeled albumin and cholesteryl linoleate formed in vivo were taken up and degraded in macrophages but not in fibroblasts, by a process resembling the uptake of the aortic extracts. The current data suggest that macrophages express mechanisms for internalizing certain types of cholesteryl ester-rich lipid/protein complexes, including those present in atherosclerotic plaques.

THE MECHANISM FOR THE ESTERIFICATION REACTION

Altogether, these studies indicate that host lipids govern neutral lipid synthesis in Toxoplasma and that interference with mechanisms of host lipid storage is detrimental to parasite survival in mammalian cells.

26/11/2015 · Acetoacetic Ester Synthesis: Acid Catalyzed Reaction Mechanism
10/03/2009 · In order to elucidate the mechanisms of ester synthesis ..

Fischer Esterification - Organic chemistry

Cholesteryl ester-rich particles extracted from human atherosclerotic plaques were shown to increase the rate of incorporation of [ 14C]oleate into cholesteryl [ 14C]oleate and to cause massive accumulation of cholesteryl esters in monolayers of mouse peritoneal macrophages. This stimulation showed saturation kinetics and susceptibility to competition by polyanions (polyinosinic acid, fucoidin, dextran sulfate), suggesting that cell surface binding was required. Cellular uptake and lysosomal hydrolysis of the cholesteryl esters were also required, as indicated by the finding that stimulation of cholesterol ester formation was prevented by the lysosomal inhibitor, chloroquine. The cholesterol esterification-stimulating activity of the aortic extracts was excluded on a 2% agarose column and floated in the density range of 1.006 to 1.063 g/ml. Cholesterol-rich extracts from human adrenal glands and liver did not stimulate cholesteryl ester formation in macrophages, The aortic extracts did not stimulate cholesteryl ester synthesis in human fibroblasts. Complexes of 125I-labeled albumin and cholesteryl linoleate formed in vivo were taken up and degraded in macrophages but not in fibroblasts, by a process resembling the uptake of the aortic extracts. The current data suggest that macrophages express mechanisms for internalizing certain types of cholesteryl ester-rich lipid/protein complexes, including those present in atherosclerotic plaques.

Includes mechanisms and a detailed description of the synthesis of vanillin

Ester Reaction Mechanisms - Boise State University

Altogether, these studies indicate that host lipids govern neutral lipid synthesis in Toxoplasma and that interference with mechanisms of host lipid storage is detrimental to parasite survival in mammalian cells.AB - The intracellular protozoan Toxoplasma gondii lacks a de novo mechanism for cholesterol synthesis and therefore must scavenge this essential lipid from the host environment.

Specific examples of ketone synthesis using these reagents are presented in the following diagram.

A mechanism for the acid catalysed hydrolysis of esters