• Korean Journal of Clinical Laboratory Science
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• v.47 no.1
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• pp.28-34
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• 2015

Pulse wave velocity (PWV) is used to non-invasively estimate the severity of arteriosclerosis by measuring arterial stiffness. Increased arterial stiffness measured by PWV stands for progressive arteriosclerosis and is caused by atherosclerotic risk factors. This study is focused on how brachial-ankle pulse wave velocity (baPWV) is related to the leading risk factors for arteriosclerosis or atherosclerosis. Subjects were 114, 69 males and 45 females who are in 60's and had baPWV test for acute stroke. The results are as follows: the group with increased arterial stiffness showed significant increase in HbA1c, total cholesterol, BSBP (brachial artery systolic blood pressure), BDBP (brachial artery diastolic blood pressure), CSBP (central artery systolic blood pressure), CDBP (central artery diastolic blood pressure), augmentation index (AIx) and diabetes mellitus. Correlation analysis between baPWV and atherosclerotic risk factor showed significant relationship in age, HbA1c, LDL cholesterol, BSBP, BDBP, CSBP, CDBP and augmentation index. baPWV was independently related to age and BSBP in multiple linear regression analysis. The group with increased arterial stiffness was independently related to BDBP in multiple logistic regression analysis. This study might be meaningful in evaluating the relationship between arterial stiffness and atherosclerotic risk factor in a new way, and be helped to make various studies for cardiovascular disease.

• IMMUNE NETWORK
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• v.4 no.2
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• pp.116-122
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• 2004

Background: LIGHT (TNFSF14) is a member of tumor necrosis factor superfamily and is the ligand for TR2 (TNFRSF14/HVEM). LIGHT is known to have proinflammatory roles in atherosclerosis. Methods: To find out the expression pattern of LIGHT in atherosclerotic plaques, immunohistochemical analysis was performed on human carotid atherosclerotic plaque specimens. LIGHT induced atherogenic events using human monocytic cell line THP-1 were also investigated. Results: Immunohistochemical analysis revealed expression of LIGHT and TR2 in foam cell rich regions in the atherosclerotic plaques. Double immunohistochemical analysis further confirmed the expression of LIGHT in foam cells. Stimulation of THP-1 cells, which express TR2, with either recombinant LIGHT or immobilized anti-TR2 monoclonal antibody induced interleukin-8 and matrix metalloproteinase(MMP)-9. Electrophoretic mobility shift assay demonstrated that LIGHT induces nuclear localization of transcription factor, nuclear factor $(NF)-{\kappa}B$. LIGHT induced activation of MMP-9 is mediated by $NF-{\kappa}B$, since treatment of THP-1 cells with the $NF-{\kappa}B$ inhibitor PDTC (pyrrolidine dithiocarbamate) completely blocked the activation of MMP-9. Conclusion: These data indicate that LIGHT is expressed in foam cells in atherosclerotic plaques and is involved in atherogenesis through activation of pro-atherogenic cytokine IL-8 and destabilization of plaque by inducing matrix degrading enzyme.

• Preventive Nutrition and Food Science
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• v.19 no.4
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• pp.363-366
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• 2014

Zinc is considered to be involved in maintaining healthy vascular condition. Atherosclerotic calcification of vascular smooth muscle cells (VSMCs) occurs via the mechanism of cell death; therefore, cell viability is a critical factor for preventing VSMC calcification. In this study, we tested whether zinc affected VSMC viability under both normal physiological non-calcifying (0 mM P) and atherosclerotic calcifying conditions (3 and 5 mM P), since VSMC physiological characters change during the VSMC calcification process. The study results showed that an optimal zinc level ($15{\mu}M$) restored the decreased VSMC viability which was induced under low zinc levels (0 and $1{\mu}M$) and calcifying conditions (3 and 5 mM P) at 9 and 15 days culture. This zinc-protecting effect for VSMC viability is more prominent under atherosclerotic calcifying condition (3 and 5 mM P) than normal condition (0 mM P). Also, the increased VSMC viability was consistent with the decreased Ca and P accumulation in VSMC cell layers. The results suggested that zinc could be an effective biomineral for preventing VSMC calcification under atherosclerotic calcifying conditions.

• Biomolecules & Therapeutics
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• v.21 no.2
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• pp.89-96
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• 2013

Atherosclerotic vascular dysfunction is a chronic inflammatory process that spreads from the fatty streak and foam cells through lesion progression. Therefore, its early diagnosis and prevention is unfeasible. Reactive oxygen species (ROS) play important roles in the pathogenesis of atherosclerotic vascular disease. Intracellular redox status is tightly regulated by oxidant and antioxidant systems. Imbalance in these systems causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, and leads to dysregulation. Paradoxically, large clinical trials have shown that non-specific ROS scavenging by antioxidant vitamins is ineffective or sometimes harmful. ROS production can be locally regulated by cellular antioxidant enzymes, such as superoxide dismutases, catalase, glutathione peroxidases and peroxiredoxins. Therapeutic approach targeting these antioxidant enzymes might prove beneficial for prevention of ROS-related atherosclerotic vascular disease. Conversely, the development of specific antioxidant enzyme-mimetics could contribute to the clinical effectiveness.

• Journal of Radiopharmaceuticals and Molecular Probes
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• v.4 no.1
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• pp.26-31
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• 2018

Macrophages play a key role in atherosclerotic plaque formation, but their participation has been discerned largely via ex vivo analyses of atherosclerotic lesions. Therefore, we aimed to identify atherosclerosis on noninvasive in vivo imaging using reporter gene system. This study demonstrated that recruitment of macrophages could be detected in atherosclerotic plaques of Apolipoprotein E knockout (ApoE-/-) mice with a sodium iodide symporter (NIS) gene imaging system using $^{99m}Tc-SPECT$. This novel approach to tracking macrophages to atherosclerotic plaques in vivo could have applications in studies of arteriosclerotic vascular disease.

• Journal of Microbiology
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• v.42 no.4
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• pp.299-304
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• 2004

To investigate the presence of infectious agents in human atherosclerotic arterial tissues. Atherosclerotic plaques were removed from 128 patients undergoing carotid endarterectomy or other bypass proce­dures for occlusive disease, and from twenty normal arterial wall samples, obtained from transplant donors with no history of diabetes, hypertension, smoking, or hyperlipidemia. Using the polymerase chain reaction (PCR) or reverse transcription-PCR, these samples were analyzed for the presence of Chlamydia pneumoniae, cytomegalovirus, enterovirus, adenovirus, herpes simplex viruses types 1 and 2, and Epstein-Barr virus. The amplicons were then sequenced, and phylogenetic analyses were per­formed. Enteroviral RNA was found in 22 of 128 atherosclerotic vascular lesions $(17.2\%),$ and C. pneu­moniae and cytomegalovirus were each found in 2 samples $(1.6\%).$ In contrast, adenovirus, herpes simplex viruses, and Epstein-Barr virus were not identified in any of the atherosclerotic samples. Enterovirus was detected in 6/24 $(25.0\%)$ aortas, 7/33 $(21.2\%)$ carotid arteries, 6/40 $(15.0\%)$ femoral arteries, and 3/31 $(9.7\%)$ radial arteries of patients with chronic renal failure. There were no infectious agents detected in any of the control specimens. Using phylogenetic analysis, the enterovirus isolates were clustered into 3 groups, arranged as echovirus 9 and coxsackieviruses Bl and B3. Enteroviral RNA was detected in $17.2\%$ of atherosclerotic plaques, but was not observed in any of the control spec­imens. This suggests a connection between enteroviral infection and atherosclerosis. These findings dif­fer from those of other studies, which found more frequent incidence of C. pneumoniae and cytomegalovirus infection in atherosclerotic plaques.

• Korean Journal of Adult Nursing
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• v.13 no.4
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• pp.529-538
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• 2001

Purpose: This study purposed to examine the disease-related knowledge level and compliance with good health behavior in patients with myocardial infarction according to the atherosclerotic risk factors. Method: The subjects consisted of 72 patients with myocardial infarction and the data were collected by interviewing the subjects with questionnaires and reviewing their medical records from September, 15, 1999 to July 31, 2000. Data were analyzed using the SAS program. Results: 1) With regard to atherosclerotic risk factors: of the subjects, 91.7% lacked regular exercise, followed by smoking (61.1%). 2) The average knowledge score of the patients was 19.7 and the average compliance score was 53.9. 3) There were no significant differences in the total knowledge scores according to the patients' atherosclerotic risk factors. 4) Non-diabetics were significantly higher in knowledge scores on domain of risk factors than the diabetics. 5) The overweight patients were significantly higher in knowledge score on domain of nature of disease than the normalweight patients. 6) The total compliance scores of the non-smokers were significantly higher than those of the smokers. 7) The total compliance scores of the patients who do regular exercise were significantly higher than those of the patients who forgo regular exercise. 8) The non-smokers were significantly higher in compliance scores on domain of diet than the smokers. 9) The diabetic patients were significantly higher in compliance scores on domain of smoking cessation than the non-diabetics. 10) Patients who do regular exercise were significantly higher in compliance scores on other domains than the patients who forgo regular exercise. Conclusion: According to the above findings, it can be concluded that intensive nursing care and education should be provided to patients who have atherosclerotic risk factors such as smoking, hypertension, diabetes mellitus, lack of exercise, over weight, or hypercholesterolemia to increase disease related knowledge level and to improve compliance with good health behavior.

• Journal of the Korean Society of Radiology
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• v.83 no.1
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• pp.70-83
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• 2022

Acute coronary syndrome (ACS) is mainly caused by atherosclerotic coronary artery disease (CAD); however, it can also occur in patients with non-atherosclerotic CAD. Conventional coronary angiography only shows the lumen of arteries, indicating the presence of stenosis or dilatation. Thus, it has limited value in evaluating the coronary artery wall and offers low specificity for diagnosing CAD. Coronary CT angiography provides additional information, including the depiction of the concerned vessel and the aorta, as well as the pulmonary artery, which permits the diagnosis of non-atherosclerotic CAD and the differentiation of various causes of the disease. In this review, we present the pathophysiology and CT imaging features of non-atherosclerotic CAD.

• Journal of Korean Neurosurgical Society
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• v.56 no.1
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• pp.48-50
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• 2014

A 70-year-old woman presented with headaches and recurrent stroke symptoms. During five years, the patient has been treated for cerebral infarction associated with severe atherosclerotic stenosis of the internal carotid artery. Three-year follow-up magnetic resonance angiography showed a tiny de novo aneurysm arising from the distal part of atherosclerotic internal carotid artery. And 5-year follow-up three-dimensional CT angiogram demonstrated a definite aneurysm enlargement as large as requiring treatment. During dissection of aneurysm, the oculomotor nerve was found to be penetrated with the growing de novo aneurysm. The authors report a case of a de novo aneurysm, which resulted from atherosclerotic stenosis of the internal carotid artery at the supraclinoid portion, that was found to be penetrating the oculomotor nerve with no ocular palsy.

• Journal of Korean Neurosurgical Society
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• v.50 no.1
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• pp.40-44
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• 2011

Objective : To evaluate the prevalence and risk factors of clopidogrel resistance, and association between thromboembolic complications and clopidogrel resistance in patient with stent-assisted angioplasty for atherosclerotic cerebrovascular disease. Methods : Between September 2006 and June 2008, clopidogrel resistance test was performed on 41 patients who underwent stent-assisted angioplasty for atherosclerotic cerebrovascular disease. It was performed before drug administration and about 12 hours after drug administration (loading dose : 300 mg, maintain dose : 75 mg). Two patients were excluded, and 41 patients were included (mean : $67.59{\pm}7.10$ years, age range : 41-79). Among 41 patients, 18 patients had intracranial lesions, and 23 had extracranial lesions. We evaluated the prevalence, risk factors and complications related to clopidogrel resistance. Results : Twenty-one patients (51.2%) showed clopidogrel resistance [intracranial : 10 patients (55.6%), extracranial : 11 patients (47.8%)] and no clopidogrel resistance was seen in 20 patients. Hypercholesterolemia was an indepedent risk factor of clopidogrel resistance. Stent-assisted angioplasty was technically successful in all patients, but acute in-stent thrombosis occurred in 5 patients with intracranial lesions (4 patients with clopidogrel resistance and 1 without clopidogrel resistance). Acute thrombi were completely lysed after intra-arterial infusion of abciximab. Conclusion : There was relatively high prevalence of clopidogrel resistance in patients with atherosclerotic cerebrovascular disease. Hypercholesterolemia was an independent predictive factor of clopidogrel resistance. Acute in-stent thrombosis was more frequently seen in the clopidogrel resistant group. Therefore, clopidogrel resistance test should be performed to avoid thromboembolic complications related to stent-assisted angioplasty for atherosclerotic cerebrovascular disease, especially patients with hypercholeterolemia and intracranial lesion.