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Introduction to Cancer
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
Tumor cells are detained at the secondary metastatic sites after surviving in the harsh environment of circulation and extravasate into parenchyma tissue. This process requires transendothelial migration (Zhao et al., 2017; Cui et al., 2018; de Oliveira et al., 2018; Liu et al., 2018; Ward et al., 2018) of cancer cells to the endothelial wall. It is carried out by adhering the cancerous cells to endothelial cells for migration through the endothelial barrier. Endothelial cells can control the adhesion of cancer cells; therefore, they have an essential role in metastatic body formation (Foss et al., 2020).
Vascularized Microfluidic Organ on a Chip and Its Applications
Published in Tuhin S. Santra, Microfluidics and Bio-MEMS, 2020
Qiyue Sun, Jianghua Pei, Qinyu Li, Xiaolin Wang
Besides a better understanding of the basic mechanisms of vascularization, the other promising application of engineered microvessels is in modeling human diseases in vitro. Endothelial dysfunction is a major physiological mechanism that can cause various vascular diseases, such as thrombosis, atherosclerosis, and inflammation [106]. Especially within the field of cancer biology, in vitro tumor models have provided important tools for cancer research and served as low-cost anticancer drug screening platforms. On the basis of the tumor formation type and vascular integration, these models can be broadly classified into four categories: transwell based [107], spheroid based [108], hydrogel droplet embedded culture [109], and vascularized tumor [110]. More than 90% of cancer-related mortality is attributed to cancer metastasis [111], which often involves multiple steps closely associated with vascular pathology, such as tumor angiogenesis [112], intravasation [113], and extravasation [114]. Therefore, engineered vascularized tumor models play an important role in studying cancer metastasis.
Nano-Biomedicine: A Next-Generation Tool for Effective and Safe Therapy
Published in Rajesh Singh Tomar, Anurag Jyoti, Shuchi Kaushik, Nanobiotechnology, 2020
Vikas Shrivastava, Pallavi Singh Chauhan, Rajesh Singh Tomar
The endothelium has an important role in different pathological processes like cancer, inflammation, oxidative stress, and thrombosis. Various studies have reported for controlling the distribution of targeted NPs by specific endothelial cells [41]. Cationic liposomes after entering the circulation are internalized via endosomes and lysosomes.
Advances in the application of computational fluid dynamics in cardiovascular flow
Published in Cogent Engineering, 2023
Nitesh Kumar, Ganesha A, Girish H, Shiva Kumar, Gowrava Shenoy B
Computational Fluid Dynamics (CFD) has been an established tool since many decades to solve and visualize complex flow problems in biomedical applications. A combination of medical image processing, reconstruction of vasculature, and technology to generate computational mesh to calculate hemodynamic parameters can yield temporal and spatial distributions of blood flow (Fujimura et al., 2018). Flow of blood is a critical parameter in formation of arterial stenosis . It plays an important role in stimulation of endothelium and development of inflammatory cells and the corresponding response of the endothelium. Healthy endothelial layer makes sure that the vascular lumen is stable and controls the distribution of anti-inflammatory factors. Imbalance between the flow conditions and endothelium alters the physiological factors of the vessel and initiates the development of atherosclerosis (Gimbrone & Garcia-Cardeña, 2016;, Rafieian-Kopaei et al., 2014).
A free boundary mathematical model of atherosclerosis
Published in Applicable Analysis, 2023
G. Abi Younes, N. El Khatib, V. Volpert
A qualitative change in the arterial surface is a precursor of atherogenesis. A normal artery is composed of three layers: intima, the inner layer, media, the middle layer, and adventitia, the outer layer. A thin matrix layer, called endothelium, lines the interior surface of the vessel, and regulates the exchange between bloodstream and the arterial wall [3]. Endothelium exerts a number of vasoprotective effects, such as vasodilation and inhibition of inflammatory responses. Many of these effects are largely mediated by nitric oxide [4]. A defect in the production or activity of nitric oxide caused by cardiovascular risk factors leads to endothelial dysfunction, the early marker for atherosclerosis. Impaired endothelial function initiates a number of processes including leaky junctions between endothelial cells which result in increased endothelial permeability and leukocyte adhesion [4].
Impact of prolonged sitting interruption strategies on shear rate, flow-mediated dilation and blood flow in adults: A systematic review and meta-analysis of randomized cross-over trials
Published in Journal of Sports Sciences, 2022
Francisco Javier Soto-Rodríguez, Eva Isidoro Cabañas, José Manuel Pérez-Mármol
Endothelial dysfunction is a fundamental factor in basic understanding of the origin of cardiovascular disease. The structural and/or functional alteration of the endothelium has been found to precede and facilitate the development of atherosclerosis (Thosar et al., 2012). In fact, it has been determined that a 1% decrease in endothelial function increases the risk of cardiovascular event by 13% (Inaba et al., 2010). The decrease in flow-mediated vasodilation (FMD) is one of the main factors responsible for this, induced by the reduction of shear stress (Restaino et al., 2016). Shear stress, measured in terms of shear rate (SR), has a fundamental role in the production of nitric oxide in the endothelium and the respective expression of its vasodilator, fibrinolytic, anti-inflammatory and anticoagulant properties (Davignon & Ganz, 2004). In this sense, the reduction in SR and its consequent effect on FMD has an important prognostic value. Low FMD has been reported to be an important predictor of cardiovascular risk (relative risk = 2.66; Brevetti et al., 2003). On the other hand, a meta-analysis conducted by Inaba et al. (Inaba et al., 2010) reported that for each 1% increase in FMD, the relative risk of a cardiovascular event was 0.87.