Publications by authors named "C J Packard"
Article Synopsis
- ApoB is the key protein found in LDL and other lipoproteins, playing a major role in their formation and link to atherosclerosis.
- LDL contributes to plaque formation in arteries by entering the wall and triggering inflammatory responses through interaction with other molecules, leading to harmful processes like foam cell formation.
- Research has identified potential interventions to combat atherosclerosis by lowering lipoprotein levels and addressing the inflammatory responses in the arterial wall.
The properties of tissue interfaces - between separate populations of cells, or between a group of cells and its environment - has attracted intense theoretical, computational, and experimental study. Recent work on shape-based models inspired by dense epithelia have suggested a possible "topological sharpening" effect, by which four-fold vertices spatially coordinated along a cellular interface lead to a cusp-like restoring force acting on cells at the interface, which in turn greatly suppresses interfacial fluctuations. We revisit these interfacial fluctuations, focusing on the distinction between short length scale reduction of interfacial fluctuations and long length scale renormalized surface tension.
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- Lipoprotein(a) is a harmful particle that can increase the risk of heart disease and problems with the aortic valve.
- New studies show that Lp(a) is much more dangerous than LDL, which is another type of fat in the blood.
- Learning more about Lp(a) is important because it could help doctors figure out who is at risk and how to better treat heart problems.
Background: Triglyceride-rich lipoproteins and remnants (TRL/remnants) have a causal, but not yet quantified, relationship with coronary heart disease (CHD): myocardial infarction plus revascularization.
Objectives: The authors sought to estimate TRL/remnant per-particle atherogenicity, investigate causal relationships with inflammation, and determine whether differences in the atherogenicity of TRL/remnants and low-density lipoprotein (LDL) impact the causal association of non-high-density lipoprotein cholesterol (non-HDL-C) with CHD.
Methods: Single nucleotide polymorphisms (SNPs) (N = 1,357) identified by genome-wide association in the UK Biobank were ranked into 10 clusters according to the effect on TRL/remnant-C vs LDL-C.
Cardiovascular (CV) disease is the most common cause of death in Europe. Despite proven benefits, use of lipid-lowering therapy remains suboptimal. Treatment goals are often not achieved, even in patients at high risk with atherosclerotic CV disease (ASCVD).
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