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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.
Echocardiographic Imaging of Myocardial Inflammation
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Endothelial dysfunction is a hallmark of other cardiovascular disease states. Endothelial disease is not limited to the larger epicardial coronary arteries and there is evidence that functional endothelial derangements in atherosclerotic disease extend distally into the microcirculation (20,21). Endothelial dysfunction occurs in the setting of ischemia-reperfusion (22). Crystalloid hyperkalemic cardioplegia infusions result in endothelial disruption (23), and regenerated endothelium after coronary angioplasty exhibits reduced endothelium-dependent relaxation (24). Hypercholesterolemia results in endothelial dysfunction that may reverse with lipid-lowering interventions (25). Heart transplant rejection is associated with the upregulation of leukocyte adhesion molecules (26,27). Thus, functional aberrations in the endothelial lining of the coronary vascular tree underlie a host of cardiovascular disease states encountered in clinical practice.
Effects of cooling or warming of the distal upper limb on skin vascular conductance and brachial artery shear profiles during cycling exercise
Published in Research in Sports Medicine, 2022
Kohei Miura, Hideaki Kashima, Saki Namura, Marina Morimoto, Masako Y. Endo, Anna Oue, Yoshiyuki Fukuba
Cardiovascular diseases are associated with endothelial dysfunction, which is the initial step in the pathogenesis of atherosclerosis (Higashi et al., 2009; Ross, 1999). The endothelium plays a role in the regulation of vascular tone. It is well known that regular aerobic exercise such as leg cycling and walking is effective in lowering the risk of arteriosclerosis (Manson et al., 1999; Paffenbarger et al., 1986). The increase in muscle blood flow (BF) during exercise produces a frictional force on the conduit artery wall, which is called shear stress (SS) (Dawson et al., 2013; Green et al., 2005, 2008; Thijssen et al., 2009). Such elevated SS promotes endothelial adaptation mainly through SS-mediated nitric oxide production and its bioavailability (Green et al., 2017). Accordingly, it is postulated that the accumulation of acute elevation of SS by a single bout of exercise plays an important role that leads to endothelial adaptation in conduit arteries following exercise training (Padilla et al., 2011a).
Assessment of potential cardiovascular risk in trichloroethylene exposure by serum methylated arginine levels
Published in International Journal of Environmental Health Research, 2021
Servet Birgin Iritas, Aybike Dip, Meside Gunduzoz, Lutfiye Tutkun, Vugar Ali Turksoy, Serdar Deniz, Gulsum Tekin, Ozgur Oztan, Ali Unlu
The cardiovascular system basically relies on NOS as principle mediator due to nitric oxide production (Vanhoutte 2009). Nitric oxide, as an antiatherosclerotic molecule, plays critical role in cardiac events. Nitric oxide is responsible for blood pressure regulation, inhibition of platelet aggregation, leukocyte adhesion, and smooth muscle cell proliferation. Decreasing of NO may result in endothelial dysfunction and elevation of risk for cardiovascular diseases. Previous studies have shown that endothelial dysfunction has adverse possible future cardiovascular effects and is a potential precursor of cardiovascular diseases.