Greater asymmetric wall shear stress in Sievers' type 1/LR compared with 0/LAT bicuspid aortic valves after valve-sparing aortic root replacement

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.

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Effects of Nasal Cavity and Pharyngeal Regions on Airflow Simulation and Particle Depositions in Lower Generations of the Airways

Volume 3: Biomedical and Biotechnology Engineering ◽

10.1115/imece2016-65305 ◽

2016 ◽

Cited By ~ 2

Author(s):

Shahab Taherian ◽

Hamid Rahai ◽

Diego Aguilar

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Nasal Cavity ◽

High Velocity ◽

Secondary Flows ◽

Lower Airways ◽

Wall Shear ◽

Type 3 ◽

The Impact

This study evaluates the impact of excluding various regions of the upper respiratory system on particle depositions in lower airways. Three types of models were investigated, Type 1 includes nasal cavity, pharyngeal regions, trachea, and lower generations, Type 2 includes pharyngeal regions, trachea and lower generations, and finally Type 3 includes just the trachea and lower generations. Results indicate increased mean velocity, turbulent kinetic energy, and wall shear stress in hypopharynx and trachea regions for Types 1 and 2 models. There are strong secondary flows within the trachea just before the lower generations in these models, moving high velocity toward the wall regions, resulting in large velocity gradients and thus increased wall shear stress. For Type 3 model, only a small region experiences high velocity secondary flow and its distribution is significantly different than those of Type 1 and 2. Although total particle depositions differ between models, results show that for fine particles, the deposition ratios in lower airways are nearly the same.

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Patient-Specific Modelling of Aortic Arch Wall Shear Stress Patterns in Patients With Marfan Syndrome

ASME 2009 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2009-206340 ◽

2009 ◽

Author(s):

Bram Trachet ◽

Daniel Devos ◽

Julie De Backer ◽

Anne De Paepe ◽

Bart L. Loeys ◽

...

Keyword(s):

Shear Stress ◽

Aortic Aneurysm ◽

Wall Shear Stress ◽

Marfan Syndrome ◽

Aortic Root ◽

Arterial System ◽

Patient Specific ◽

Physiological Data ◽

Aneurysm Formation ◽

Wall Shear

Marfan syndrome (MFS) is a genetic connective tissue disorder with a high prevalence of aortic aneurysm formation (a pathological dilatation of the aorta), typically at the aortic root. The disorder is caused by mutations in the gene encoding fibrillin-1 [1]. Recently, it has been shown in mouse models that selected manifestations of MFS, such as aortic aneurysm formation, can be explained by excessive signaling by the transforming growth factor–beta (TGF-beta) family of cytokines [2]. Although the footprint of the disease is clearly genetic, there is still a role for (computational) biomechanics and hemodynamics to elucidate why aneurysms develop preferentially at the level of the aortic root, since the genetic defect affects the entire (arterial) system. One of the most obvious parameters to study is the arterial wall shear stress (WSS). WSS plays an important role in the regulation of the vascular system and is considered a significant factor in the development and progression of cardiovascular disease in humans. Low and/or oscillating values of WSS have been associated with the formation of atherosclerotic lesions [3] and with the growth of aneurysms [4]. It is, however, hard to show a link between low WSS and aneurysm initiation, since in most cases the geometrical and physiological data are lacking during the first and most important stages of the aneurysm development. Furthermore follow-up studies in human patients are difficult, since aneurysms grow very slowly (only 0.9 mm/year in MFS patients treated with beta-blockers) and it will take several years before significant changes will have taken place. Therefore, in this study, we have computed the aortic flow field and WSS patterns for 5 different MFS patients with ages varying from 14 to 54 years old, in order to get an idea about the effect of age on the development of the disease.

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