Role of Elastic Tissue in Cholesterol Deposition in the Arterial Wall

1973 ◽  
Vol 15 (1-2) ◽  
pp. 46-58 ◽  
Author(s):  
B. Jacotot ◽  
J.L. Beaumont ◽  
G. Monnier ◽  
M. Szigeti ◽  
B. Robert ◽  
...  
Keyword(s):  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yafei Wang ◽  
Erik Brodin ◽  
Kenichiro Nishii ◽  
Hermann B. Frieboes ◽  
Shannon M. Mumenthaler ◽  
...  

AbstractColorectal cancer and other cancers often metastasize to the liver in later stages of the disease, contributing significantly to patient death. While the biomechanical properties of the liver parenchyma (normal liver tissue) are known to affect tumor cell behavior in primary and metastatic tumors, the role of these properties in driving or inhibiting metastatic inception remains poorly understood, as are the longer-term multicellular dynamics. This study adopts a multi-model approach to study the dynamics of tumor-parenchyma biomechanical interactions during metastatic seeding and growth. We employ a detailed poroviscoelastic model of a liver lobule to study how micrometastases disrupt flow and pressure on short time scales. Results from short-time simulations in detailed single hepatic lobules motivate constitutive relations and biological hypotheses for a minimal agent-based model of metastatic growth in centimeter-scale tissue over months-long time scales. After a parameter space investigation, we find that the balance of basic tumor-parenchyma biomechanical interactions on shorter time scales (adhesion, repulsion, and elastic tissue deformation over minutes) and longer time scales (plastic tissue relaxation over hours) can explain a broad range of behaviors of micrometastases, without the need for complex molecular-scale signaling. These interactions may arrest the growth of micrometastases in a dormant state and prevent newly arriving cancer cells from establishing successful metastatic foci. Moreover, the simulations indicate ways in which dormant tumors could “reawaken” after changes in parenchymal tissue mechanical properties, as may arise during aging or following acute liver illness or injury. We conclude that the proposed modeling approach yields insight into the role of tumor-parenchyma biomechanics in promoting liver metastatic growth, and advances the longer term goal of identifying conditions to clinically arrest and reverse the course of late-stage cancer.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Georgia Siasou ◽  
Gerasimos Siasos ◽  
Marilita M Moschos ◽  
Nikolaos Gouliopoulos ◽  
Evangelos Oikonomou ◽  
...  

Introduction: Primary open-angle glaucoma (POAG) is one of the most prevalent causes of irreversible blindness and is associated with endothelial dysfunction and arterial stiffness. Pseudoexfoliative glaucoma (PEG) is another type of glaucoma observed in pseudoexfoliation syndrome. It is characterized by the deposition of pseudoexfoliative material not only to the anterior segment of the eye, but also to the vessels, heart and other organs. Hypothesis: Endothelial function and arterial stiffness are impaired in patients with POAG and PEG supporting the significant role of vascular function impairment in the progression of the disease. Methods: Forty four POAG patients, 22 PEG and 38 healthy subjects (Cl) were included in this study. All subjects were free of cardiovascular or inflammatory diseases. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections Results: Between the three study groups CL, POAG, PEG there was no difference in age (67±10years vs. 70±9years vs. 66±12yeras, p=0.12) or prevalence of male sex (70% vs. 57% vs. 50%, p=0.21). Importantly, there was a linear impairment of FMD (7.35±2.77% vs. 6.58±3.18% vs. 4.88±3.29%, p=0.006), PWV (7.98±1.56m/sec vs. 9.20±1.84m/sec vs. 9.22±2.16m/sec, p=0.004) and AIx (21.29±8.77% vs. 25.14±5.71% vs. 28.20±8.75%, p=0.002) from CL to POAG and PEG. Interestingly post hoc test after Scheffe correction revealed also that PEG subjects had not only significantly impaired FMD, compared to control subjects, but also compared to POAG subjects (4.88±3.29% vs. 6.58±3.18%, p=0.02). Conclusions: Endothelial function and arterial stiffness are significantly impaired in patients with pseudoexfoliative glaucoma. These findings shed some light in the pathophysiology of pseudoexfoliative glaucoma and support the theory that pseudoexfoliative fibrils may also accumulate and damage the arterial wall.


2002 ◽  
Vol 282 (2) ◽  
pp. H389-H394 ◽  
Author(s):  
Edmundo I. Cabrera Fischer ◽  
Ricardo L. Armentano ◽  
Franco M. Pessana ◽  
Sebastián Graf ◽  
Luis Romero ◽  
...  

The role of blood viscosity on arterial wall elasticity before and after deendothelization (DE) was studied. Seven ovine brachiocephalic arteries were studied in vitro under physiological pulsatile flow conditions achieved by a mock circulation loop. Instantaneous pressure and diameter signals were assessed in each arterial segment. Incremental elastic modulus ( E inc) was calculated using the slope of the pure elastic stress-strain relationship. There was no significant difference between E inc values before and after DE (3.11 vs. 3.16 107 dyn/cm2) at a blood viscosity of 2.00 mPa · s. Increases in blood viscosity (2.50, 3.00, 3.50, and 4.00 mPa · s) always resulted in decreases of E inc before DE; inversely, increases in blood viscosity resulted in increases of E inc after DE. These values of E inc, for identical levels of blood viscosity, were always significantly lower ( P< 0.05) before DE than those obtained after DE. Arterial wall elasticity assessed through E inc was strongly influenced by blood viscosity, probably due to presence or absence of endothelium relaxing factors or to direct shear smooth muscle activation when endothelial cells are removed.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Francesco Moroni ◽  
Enrico Ammirati ◽  
Giuseppe Danilo Norata ◽  
Marco Magnoni ◽  
Paolo G. Camici

Atherosclerosis is one of the leading causes of death and disability worldwide. It is a complex disease characterized by lipid accumulation within the arterial wall, inflammation, local neoangiogenesis, and apoptosis. Innate immune effectors, in particular monocytes and macrophages, play a pivotal role in atherosclerosis initiation and progression. Although most of available evidence on the role of monocytes and macrophages in atherosclerosis is derived from animal studies, a growing body of evidence elucidating the role of these mononuclear cell subtypes in human atherosclerosis is currently accumulating. A novel pathogenic role of monocytes and macrophages in terms of atherosclerosis initiation and progression, in particular concerning the role of these cell subsets in neovascularization, has been discovered. The aim of the present article is to review currently available evidence on the role of monocytes and macrophages in human atherosclerosis and in relation to plaque characteristics, such as plaque neoangiogenesis, and patients’ prognosis and their potential role as biomarkers.


2001 ◽  
Vol 82 (4) ◽  
pp. 674-682 ◽  
Author(s):  
Claudio Napoli ◽  
Filomena de Nigris ◽  
Wulf Palinski

2016 ◽  
Vol 88 (4) ◽  
pp. 24
Author(s):  
O. Yu. Druzhilova ◽  
M. A. Druzhilov ◽  
V. V. Otmakhov ◽  
E. S. Andreeva ◽  
T. Yu. Kuznetsova

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