Genesis of intimal thickening due to hemodynamical shear stresses.

This paper investigates intimal growth in arteries, induced by hemodynamical shear stress, through finite element simulation using the FEniCS computational environment. In our model, the growth of the intima depends on cross-section geometry and shear stress. In this work, the arterial wall is modeled as three distinct layers: the intima, the media and the adventitia, each with different mechanical properties.

Shear stress regulation in cylindrical arteries through medial growth and nitric oxide release.

The mechanisms employed by blood vessels in order to adapt to their hemodynamic environment are important for our general understanding of disease and development. Changes in arterial geometry are generally induced by two effects: vasodilation and/or constriction; and growth and remodeling ("G &R"). The first can occur over short periods of a few minutes, while the second usually occurs over timescales of weeks or months.

A new approach to calculating fiber fields in 2D vessel cross sections using conformal maps.

An arterial vessel has three layers, namely, the intima, the media and the adventitia. Each of these layers is modeled to have two families of strain-stiffening collagen fibers that are transversely helical. In an unloaded configuration, these fibers are coiled up.

Medial Arterial Calcification: JACC State-of-the-Art Review.

Medial arterial calcification (MAC) is a chronic systemic vascular disorder distinct from atherosclerosis that is frequently but not always associated with diabetes mellitus, chronic kidney disease, and aging. MAC is also a part of more complex phenotypes in numerous less common diseases. The hallmarks of MAC include disseminated and progressive precipitation of calcium phosphate within the medial layer, a prolonged and clinically silent course, and compromise of hemodynamics associated with chronic limb-threatening ischemia.

Simple model of atherosclerosis in cylindrical arteries: impact of anisotropic growth on Glagov remodeling.

In 1987, Seymour Glagov observed that arteries went through a two-stage remodeling process as a result of plaque growth: first, a compensatory phase where the lumen area remains approximately constant and second, an encroachment phase where the lumen area decreases over time. In this paper, we investigate the effect of growth anisotropy on Glagov remodeling in five different cases: pure radial, pure circumferential, pure axial, isotropic and general anisotropic growth where the elements of the growth tensor are chosen to minimize the total energy. We suggest that the nature of anisotropy is inclined towards the growth direction that requires the least amount of energy.

An integrated approach to simulating the vulnerable atherosclerotic plaque.

Analyses of individual atherosclerotic plaques are mostly descriptive, relying, for example, on histological classification by spectral analysis of ultrasound waves or staining and observing particular cellular components. Such passive methods have proved useful for characterizing the structure and vulnerability of plaques but have little quantitative predictive power. Our aim is to introduce and discuss a computational framework to provide insight to clinicians and help them visualize internal plaque dynamics.

Media sclerosis drives and localizes atherosclerosis in peripheral arteries.

Media sclerosis (MS) and peripheral artery disease (PAD) may coincide, particularly in type 2 diabetics (T2D) and in patients with chronic kidney disease (CKD). In contrast to non-diabetics, in T2D PAD is more severe and more distal. Although MS is suspected to play a role, the underlying pathophysiological reasons for the differences still remain elusive today.

Multi-Layer Mechanical Model of Glagov Remodeling in Coronary Arteries: Differences between In-Vivo and Ex-Vivo Measurements.

When blood vessels undergo remodeling because of the buildup of atherosclerotic plaque, it is thought that they first undergo compensatory or outward remodeling, followed by inward remodeling: the lumen area stays roughly constant or increases slightly and then decreases rapidly. The second phase of remodeling is supposed to start after the plaque burden exceeds about 40%. These changes in the vessel were first observed by S.

A biochemical and mechanical model of injury-induced intimal thickening.

In this paper, we investigate an axisymmetric model of intimal thickening using hyperelasticity theory. Our model describes the growth of the arterial intima due to cell proliferation which, in turn, is driven by the release of a cytokine such as platelet-derived growth factor (PDGF). With the growth rate tied to both local stress and the local concentration of PDGF, we derive a quadruple free boundary problem with different regions of the vessel wall characterized by different homeostatic stress.

Bayesian Uncertainty Quantification for Bond Energies and Mobilities Using Path Integral Analysis.

Dynamic single-molecule force spectroscopy is often used to distort bonds. The resulting responses, in the form of rupture forces, work applied, and trajectories of displacements, are used to reconstruct bond potentials. Such approaches often rely on simple parameterizations of one-dimensional bond potentials, assumptions on equilibrium starting states, and/or large amounts of trajectory data.

Simulation of a pulsatile non-Newtonian flow past a stenosed 2D artery with atherosclerosis.

Atherosclerotic plaque can cause severe stenosis in the artery lumen. Blood flow through a substantially narrowed artery may have different flow characteristics and produce different forces acting on the plaque surface and artery wall. The disturbed flow and force fields in the lumen may have serious implications on vascular endothelial cells, smooth muscle cells, and circulating blood cells.

Mathematical model of intimal thickening in atherosclerosis: vessel stenosis as a free boundary problem.

Atherosclerosis is an inflammatory disease of the artery characterized by an expansion of the intimal region. Intimal thickening is usually attributed to the migration of smooth muscle cells (SMCs) from the surrounding media and proliferation of SMCs already present in the intima. Intimal expansion can give rise to dangerous events such as stenosis (leading to stroke) or plaque rupture (leading to myocardial infarction).

Growth of necrotic cores in atherosclerotic plaque.

Plaques are fatty deposits that grow mainly in arteries and develop as a result of a chronic inflammatory response. Plaques are characterized as 'vulnerable' when they have large internal regions of necrosis and are heavily infiltrated by macrophages. The particular composition of a vulnerable plaque renders it susceptible to rupture, which releases thrombogenic agents into the bloodstream and can result in myocardial infarction.

Accelerated search kinetics mediated by redox reactions of DNA repair enzymes.

A charge transport (CT) mechanism has been proposed in several articles to explain the localization of base excision repair (BER) enzymes to lesions on DNA. The CT mechanism relies on redox reactions of iron-sulfur cofactors that modify the enzyme's binding affinity. These redox reactions are mediated by the DNA strand and involve the exchange of electrons between BER enzymes along DNA.

Charge-transport-mediated recruitment of DNA repair enzymes.

Damaged or mismatched bases in DNA can be repaired by base excision repair enzymes (BER) that replace the defective base. Although the detailed molecular structures of many BER enzymes are known, how they colocalize to lesions remains unclear. One hypothesis involves charge transport (CT) along DNA [Yavin et al.

Dynamic boundaries in asymmetric exclusion processes.

We investigate the dynamics of a one-dimensional asymmetric exclusion process with Langmuir kinetics and a fluctuating wall. At the left-hand boundary, particles are injected onto the lattice; from there, the particles hop to the right. Along the lattice, particles can adsorb or desorb, and the right-hand boundary is defined by a wall particle.

Continuum theory of nanostructure decay via a microscale condition.

The morphological relaxation of faceted crystal surfaces is studied via a continuum approach. Our formulation includes (i) an evolution equation for the surface slope that describes step line tension, g1, and step repulsion energy, g3; and (ii) a condition at the facet edge (a free boundary) that accounts for discrete effects via the collapse times, t(n), of top steps. For initial cones and t(n) approximately t(n)4, we use t(g) from step simulations and predict self-similar slopes in agreement with simulations for any g = g3/g1 > 0.