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Mechanisms and factors associated with the nanoparticle-mediated modulation of cholesterol crystal behaviour are proposed.
This article introduces a hypothesis on nanoparticle-mediated modulation of cholesterol crystal behaviour in the atherosclerotic plaques.
Thus, after a chronic ingestion of DU, rats experience a modulation of cholesterol catabolism but overcome it, since their cholesterolemia is preserved and no pathology is declared.
The goal of our study was to assess baseline CX3CL1 levels, and after modulation of cholesterol levels by statins to determine if CX3CL1 is linked to cholesterol levels or inflammatory stimuli.
In this study we determined baseline CX3CL1 levels in human subjects without known coronary disease and after modulation of cholesterol levels using different statins to determine if CX3CL1 levels are linked to cholesterol levels or other inflammatory stimuli.
The proposed hypothesis on nanoparticle-mediated modulation of cholesterol crystal behaviour may be relevant to other medical conditions including gallbladder stones, arthritis, and ophthalmological diseases such as synchysis scintillans.
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Whether an alteration of the mTORC1 signalling pathway could participate in the modulation of free cholesterol levels we describe here, is unclear at the moment and deserves further studies.
For modulation of cellular cholesterol, the cells were treated before stimulation with BLP for 1 h with MCD (10 mM, Sigma-Aldrich), a 1∶1 mixture of free MCD and MCD saturated with cholesterol (Sigma-Aldrich), or MCD saturated with cholesterol alone.
In the present study we show that the disruption of intestinal HSL results in a modulation of intestinal cholesterol metabolism.
In the latter case, it is still unclear whether the effects of seladin-1 are an indirect consequence of the modulation of intracellular cholesterol, which has well documented protective effects in vitro and in vivo [ 7- 11].
This pharmacological profile is associated with the modulation of both cholesterol and lipid metabolism regulatory genes, including the sterol response element-binding proteins SREBF1 and SREBF2, and their regulatory proteins INSIG1 and INSIG2, in liver and white adipose tissues.
More suggestions(15)
modification of cholesterol
formulation of cholesterol
manipulation of cholesterol
modulation of pHi
modulation of sunspot
modulation of attention
modulation of apoptosis
modulation of speech
modulation of brain
modulation of grip
modulation of pain
modulation of voice
modulation of inflammation
modulation of music
modulation of activity
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