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2
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Ann Biomed Eng. 2015 Jan;43(1):94-106. doi: 10.1007/s10439-014-1155-9. Epub 2014 Oct 15.
3
Human neutrophil cytoskeletal dynamics and contractility actively contribute to trans-endothelial migration.人类中性粒细胞细胞骨架动力学和收缩性积极促进跨内皮迁移。
PLoS One. 2013 Apr 23;8(4):e61377. doi: 10.1371/journal.pone.0061377. Print 2013.
4
Computational fluid dynamics analysis of the effect of plaques in the left coronary artery.左冠状动脉斑块对血流影响的计算流体动力学分析。
Comput Math Methods Med. 2012;2012:504367. doi: 10.1155/2012/504367. Epub 2012 Feb 12.
5
Coronary artery wall shear stress is associated with progression and transformation of atherosclerotic plaque and arterial remodeling in patients with coronary artery disease.冠状动脉壁切应力与冠状动脉疾病患者粥样斑块的进展和转化以及动脉重构有关。
Circulation. 2011 Aug 16;124(7):779-88. doi: 10.1161/CIRCULATIONAHA.111.021824. Epub 2011 Jul 25.
6
Prediction of the localization of high-risk coronary atherosclerotic plaques on the basis of low endothelial shear stress: an intravascular ultrasound and histopathology natural history study.基于低内皮剪切应力预测高危冠状动脉粥样硬化斑块的定位:一项血管内超声和组织病理学自然史研究。
Circulation. 2008 Feb 26;117(8):993-1002. doi: 10.1161/CIRCULATIONAHA.107.695254. Epub 2008 Feb 4.
7
Transendothelial flow inhibits neutrophil transmigration through a nitric oxide-dependent mechanism: potential role for cleft shear stress.跨内皮血流通过一氧化氮依赖机制抑制中性粒细胞迁移:裂隙切应力的潜在作用。
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Multi-cell agent-based simulation of the microvasculature to study the dynamics of circulating inflammatory cell trafficking.基于多细胞代理的微血管模拟,以研究循环炎症细胞运输的动力学。
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9
Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha.富含甘油三酯的脂蛋白使主动脉内皮细胞对肿瘤坏死因子-α产生增强的炎症反应做好准备。
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10
A numerical and experimental investigation of transitional pulsatile flow in a stenosed channel.狭窄通道内过渡性脉动流的数值与实验研究
J Biomech Eng. 2005 Dec;127(7):1147-57. doi: 10.1115/1.2073628.

白细胞捕获对瞬时脉动血流的依赖性。

Dependence of leukocyte capture on instantaneous pulsatile flow.

作者信息

Ciri Umberto, Bhui Rita, Bailon-Cuba Jorge, Hayenga Heather N, Leonardi Stefano

机构信息

Department of Mechanical Engineering, The University of Texas at Dallas, Richardson, TX, USA.

Department of Physics, The University of Texas at Dallas, Richardson, TX, USA.

出版信息

J Biomech. 2018 Jul 25;76:84-93. doi: 10.1016/j.jbiomech.2018.05.044. Epub 2018 Jun 15.

DOI:10.1016/j.jbiomech.2018.05.044
PMID:29914741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6103190/
Abstract

Atherosclerosis, an artery disease, is currently the leading cause of death in the United States in both men and women. The first step in the development of atherosclerosis involves leukocyte adhesion to the arterial endothelium. It is broadly accepted that blood flow, more specifically wall shear stress (WSS), plays an important role in leukocyte capture and subsequent development of an atherosclerotic plaque. What is less known is how instantaneous WSS, which can vary by up to 5 Pa over one cardiac cycle, influences leukocyte capture. In this paper we use direct numerical simulations (DNS), performed using an in-house code, to illustrate that leukocyte capture is different whether as a function of instantaneous or time-averaged blood flow. Specifically, a stenotic plaque is modeled using a computational fluid dynamics (CFD) solver through fully three-dimensional Navier-Stokes equations and the immersed boundary method. Pulsatile triphasic inflow is used to simulate the cardiac cycle. The CFD is coupled with an agent-based leukocyte capture model to assess the impact of instantaneous hemodynamics on stenosis growth. The computed wall shear stress agrees well with the results obtained with a commercial software, as well as with theoretical results in the healthy region of the artery. The analysis emphasizes the importance of the instantaneous flow conditions in evaluating the leukocyte rate of capture. That is, the capture rate computed from mean flow field is generally underpredicted compared to the actual rate of capture. Thus, in order to obtain a reliable estimate, the flow unsteadiness during a cardiac cycle should be taken into account.

摘要

动脉粥样硬化是一种动脉疾病,目前是美国男性和女性的主要死因。动脉粥样硬化发展的第一步涉及白细胞与动脉内皮的粘附。人们普遍认为,血流,更具体地说是壁面剪应力(WSS),在白细胞捕获和随后动脉粥样硬化斑块的形成中起着重要作用。鲜为人知的是,在一个心动周期内可变化高达5帕斯卡的瞬时WSS如何影响白细胞捕获。在本文中,我们使用内部代码进行直接数值模拟(DNS),以说明白细胞捕获作为瞬时或时间平均血流的函数时是不同的。具体而言,使用计算流体动力学(CFD)求解器通过完全三维的纳维-斯托克斯方程和浸入边界法对狭窄斑块进行建模。使用脉动三相流入来模拟心动周期。CFD与基于代理的白细胞捕获模型相结合,以评估瞬时血流动力学对狭窄生长的影响。计算得到的壁面剪应力与商业软件获得的结果以及动脉健康区域的理论结果吻合良好。分析强调了瞬时流动条件在评估白细胞捕获率方面的重要性。也就是说,与实际捕获率相比,从平均流场计算得到的捕获率通常被低估。因此,为了获得可靠的估计,应考虑心动周期中的流动不稳定性。