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Results The plant stanol and sterol ester spreads lowered plasma total (−9% and −6%, respectively) and low-density lipoprotein (−12% and −9%) cholesterol but had no effect on red cell cholesterol, high-density lipoprotein cholesterol, or plasma triglycerides.
Our findings indicate cholesterol as a critical determinant for enteroviral replication and outline roles for the endocytic machinery in both the enteroviral life cycle and host cell cholesterol homeostasis.
In the process, high density lipoproteins (HDL) serve as transport particles by which peripheral cell cholesterol can be returned to the liver for catabolism [3].
Since the insulin receptor is found within lipid rafts [64] and insulin signalling is cholesterol dependent [65], [66], prion infection induced changes in cell cholesterol may modify insulin signalling.
Cyclodextrins have long been used to extract plasma membrane cholesterol, which can result in depletion of up to half of the total cell cholesterol content within one hour of treatment [9].
Premature atherosclerosis is related to several HDL-dependent activities that include a diminished cell cholesterol efflux capacity by HDL [ 4].
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The effects of the compounds on cholesterol efflux from cells, cholesterol uptake via lipoprotein endocytosis, and the amount of cholesteryl esters in the cells were investigated.
In epithelial cells, cholesterol is mainly found in the plasma membrane, in macrophages, a significant amount of cholesterol can be found stored in intracellular compartments.
In normal cells, cholesterol levels are tightly regulated by a number of mechanisms that include cholesterol uptake, storage and efflux [15].
Alterations of pancreatic β-cell cholesterol content may contribute to β-cell dysfunction.
Recent evidence suggests that alterations of β-cell cholesterol content may contribute to islet dysfunction and loss of insulin secretion (1).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com