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  1. Sun Z, Ng CKC, Wong YH, Yeong CH
    Biomolecules, 2021 09 03;11(9).
    PMID: 34572520 DOI: 10.3390/biom11091307
    The diagnostic value of coronary computed tomography angiography (CCTA) is significantly affected by high calcification in the coronary arteries owing to blooming artifacts limiting its accuracy in assessing the calcified plaques. This study aimed to simulate highly calcified plaques in 3D-printed coronary models. A combination of silicone + 32.8% calcium carbonate was found to produce 800 HU, representing extensive calcification. Six patient-specific coronary artery models were printed using the photosensitive polyurethane resin and a total of 22 calcified plaques with diameters ranging from 1 to 4 mm were inserted into different segments of these 3D-printed coronary models. The coronary models were scanned on a 192-slice CT scanner with 70 kV, pitch of 1.4, and slice thickness of 1 mm. Plaque attenuation was measured between 1100 and 1400 HU. Both maximum-intensity projection (MIP) and volume rendering (VR) images (wide and narrow window widths) were generated for measuring the diameters of these calcified plaques. An overestimation of plaque diameters was noticed on both MIP and VR images, with measurements on the MIP images close to those of the actual plaque sizes (<10% deviation), and a large measurement discrepancy observed on the VR images (up to 50% overestimation). This study proves the feasibility of simulating extensive calcification in coronary arteries using a 3D printing technique to develop calcified plaques and generate 3D-printed coronary models.
    Matched MeSH terms: Plaque, Atherosclerotic/pathology*
  2. Molinari F, Raghavendra U, Gudigar A, Meiburger KM, Rajendra Acharya U
    Med Biol Eng Comput, 2018 Sep;56(9):1579-1593.
    PMID: 29473126 DOI: 10.1007/s11517-018-1792-5
    Atherosclerosis is a type of cardiovascular disease which may cause stroke. It is due to the deposition of fatty plaque in the artery walls resulting in the reduction of elasticity gradually and hence restricting the blood flow to the heart. Hence, an early prediction of carotid plaque deposition is important, as it can save lives. This paper proposes a novel data mining framework for the assessment of atherosclerosis in its early stage using ultrasound images. In this work, we are using 1353 symptomatic and 420 asymptomatic carotid plaque ultrasound images. Our proposed method classifies the symptomatic and asymptomatic carotid plaques using bidimensional empirical mode decomposition (BEMD) and entropy features. The unbalanced data samples are compensated using adaptive synthetic sampling (ADASYN), and the developed method yielded a promising accuracy of 91.43%, sensitivity of 97.26%, and specificity of 83.22% using fourteen features. Hence, the proposed method can be used as an assisting tool during the regular screening of carotid arteries in hospitals. Graphical abstract Outline for our efficient data mining framework for the characterization of symptomatic and asymptomatic carotid plaques.
    Matched MeSH terms: Plaque, Atherosclerotic/pathology*
  3. Ooi BK, Phang SW, Yong PVC, Chellappan DK, Dua K, Khaw KY, et al.
    Life Sci, 2021 Aug 01;278:119658.
    PMID: 34048809 DOI: 10.1016/j.lfs.2021.119658
    AIMS: Maslinic acid (MA) is a naturally occurring pentacyclic triterpene known to exert cardioprotective effects. This study aims to investigate the involvement of nuclear factor erythroid 2-related factor 2 (Nrf2) for MA-mediated anti-inflammatory effects in atheroma pathogenesis in vitro, including evaluation of tumor necrosis factor-alpha (TNF-α)-induced monocyte recruitment, oxidized low-density lipoprotein (oxLDL)-induced scavenger receptors expression, and nuclear factor-kappa B (NF-ĸB) activity in human umbilical vein endothelial cells (HUVECS) and human acute monocytic leukemia cell line (THP-1) macrophages.

    MATERIALS AND METHODS: An in vitro monocyte recruitment model utilizing THP-1 and HUVECs was developed to evaluate TNF-α-induced monocyte adhesion and trans-endothelial migration. To study the role of Nrf2 for MA-mediated anti-inflammatory effects, Nrf2 inhibitor ML385 was used as the pharmacological inhibitor. The expression of Nrf2, monocyte chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1), cluster of differentiation 36 (CD36), and scavenger receptor type A (SR-A) in HUVECs and THP-1 macrophages were investigated using RT-qPCR and Western blotting. The NF-κB activity was determined using NF-κB (p65) Transcription Factor Assay Kit.

    KEY FINDINGS: The results showed opposing effects of MA on Nrf2 expression in HUVECs and THP-1 macrophages. MA suppressed TNF-α-induced Nrf2 expression in HUVECs, but enhanced its expression in THP-1 macrophages. Combined effects of MA and ML385 suppressed MCP-1, VCAM-1, and SR-A expressions. Intriguingly, at the protein level, ML385 selectively inhibited SR-A but enhanced CD36 expression. Meanwhile, ML385 further enhanced MA-mediated inhibition of NF-κB activity in HUVECs. This effect, however, was not observed in THP-1 macrophages.

    SIGNIFICANCE: MA attenuated foam cell formation by suppressing VCAM-1, MCP-1, and SR-A expression, as well as NF-κB activity, possibly through Nrf2 inhibition. The involvement of Nrf2 for MA-mediated anti-inflammatory effects however differs between HUVECs and macrophages. Future investigations are warranted for a detailed evaluation of the contributing roles of Nrf2 in foam cells formation.

    Matched MeSH terms: Plaque, Atherosclerotic/pathology
  4. Gopal K, Nagarajan P, Jedy J, Raj AT, Gnanaselvi SK, Jahan P, et al.
    PLoS One, 2013;8(6):e67098.
    PMID: 23826202 DOI: 10.1371/journal.pone.0067098
    Abdominal aortic aneurysm (AAA) is a common chronic degenerative disease characterized by progressive aortic dilation and rupture. The mechanisms underlying the role of α-tocopherol and β-carotene on AAA have not been comprehensively assessed. We investigated if α-tocopherol and β-carotene supplementation could attenuate AAA, and studied the underlying mechanisms utilized by the antioxidants to alleviate AAA. Four-months-old Apoe(-/-) mice were used in the induction of aneurysm by infusion of angiotensin II (Ang II), and were orally administered with α-tocopherol and β-carotene enriched diet for 60 days. Significant increase of LDL, cholesterol, triglycerides and circulating inflammatory cells was observed in the Ang II-treated animals, and gene expression studies showed that ICAM-1, VCAM-1, MCP-1, M-CSF, MMP-2, MMP-9 and MMP-12 were upregulated in the aorta of aneurysm-induced mice. Extensive plaques, aneurysm and diffusion of inflammatory cells into the tunica intima were also noticed. The size of aorta was significantly (P = 0.0002) increased (2.24±0.20 mm) in the aneurysm-induced animals as compared to control mice (1.17±0.06 mm). Interestingly, β-carotene dramatically controlled the diffusion of macrophages into the aortic tunica intima, and circulation. It also dissolved the formation of atheromatous plaque. Further, β-carotene significantly decreased the aortic diameter (1.33±0.12 mm) in the aneurysm-induced mice (β-carotene, P = 0.0002). It also downregulated ICAM-1, VCAM-1, MCP-1, M-CSF, MMP-2, MMP-9, MMP-12, PPAR-α and PPAR-γ following treatment. Hence, dietary supplementation of β-carotene may have a protective function against Ang II-induced AAA by ameliorating macrophage recruitment in Apoe(-/-) mice.
    Matched MeSH terms: Plaque, Atherosclerotic/pathology
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