• Journal of Biomedical Engineering Research
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• v.16 no.4
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• pp.463-470
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• 1995

Complete prelining of artificial vascular grafts with autologous endothelial cells may be one of the ideal solutions to obtain a nonthrombogenlc blood-contacting surface. To establish an intact endothelial cell monolayer on a prosthetic surface at the time of implantation,a sufficient number of endothelial cells and adequate propagation condition In cell culture are prerequisites. In this experimental study, endothelial cells from microvessels of adult human oriental adipose tissue were enzymatically harvested, and optimal culture conditions for proliferation of the endothelial cells in cell culture were examined. Human oriental adipose tissue was digested with collagenase and endothelial cells were separated from other stromal elements by mesh filtration method. Cultured cells were identified as endothelial cells by immunofluorescent staining for factor VIII-related antigen. Proliferation in usual 20% fetal bovine serum (FBS) medium or medium containing endothelial cell growth factor (ECGF)(5 ng/ml) and heparin (HEP)(1,000 units/ml) were compared,and the effects of adding compounds that increase intracellular cyclic adenosine monophosphate levels, that is,cholera toxin (CT)(1 $\mu\textrm{g}$/ml) and isobutylmethylxanthine (IBMX)(0.2 ml),were also analyzed. In total,following eight media groups were examined. 1) FBS medium + ECGF + HEP, 2) FBS medium + ECGF + HEP+CT, 3) FBS medium+ECGF+HEP+lBMX, 4) FBS medium+ECGF+HEP+CT+ IBMX, 5) FBSmedium, 6) FBS medium +CT, 7) FBS medium + IBMX, 8) FBS medium + CT + IBMX. It was shown that the medium containing ECGF + HEP with or without cholera toxin was most efficient in Stimulating cell proliferation. IBMX was considered to have antagonistic effect to ECGF. Among experimental groups without ECGF and HEP, the addition of cholera toxin and IBMX was shown to significantly potentiate cell proliferation. This results could provide a practical method for use of cultured human endothelial cells for endothelial cell seeding of cardiovascular prosthetic device, particularly in small-diameter vascular grafts.

• Proceedings of the KSME Conference
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• 2002.08a
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• pp.711-712
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• 2002

A numerical study of a hemodynamical model for the tumor angiogenesis is carried out. The tumor angiogenesis process is comprised of a sequence of events; secretion of tumor angiogenesis factor(TAF) from the solid tumor, degradation of the basement membrane of nearby blood vessels, migration and proliferation of the endothelial cells. The model takes into account the effect of TAF concentration and endothelial cell density, and their conservation equations are represented as a set of one-dimensional initial boundary value problems. These equations are discretized by using a finite difference method in which the second order schemes both in time and in space are used. The effects of the parameters contained in the model are Investigated extensively through the numerical simulation of the discretized model. The result for the typical case compares very well with the known result.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.10
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• pp.178-184
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• 2017

This study was performed on 16 patients diagnosed with tsutsugamushi disease and cerebral infarction from January 2007 to December 2015. An acute cerebral infarction was diagnosed by brain MRI and MRA. Tsutsugamushi disease was diagnosed using a polymerase chain reaction. To distinguish the difference between the generalized cerebral infarction and infarction with tsutsugamushi disease, the blood pressure and body temperature were measured uponadmission. In general, the blood pressure increases during an acute cerebral infarction. Interestingly, in this study, 12 patients showed a systolic blood pressure less than 130 mmHg uponadmission. The location of the cerebral infarction and whether single or multiple cerebral infarction were examined. Thirteen patients had a cerebral infarction in anterior circulation and 3 patients developed in posterior circulation. To evaluate the coagulation disorders, prothrombin time (PT), activated partial thromboplastin time (aPTT), D-dimer, fibrinogen, fibrin degradation product (FDP). D-dimer, which is generally known to increase in an acute cerebral infarction, showed a significant increase in the 13 patients. Fibrin degradation products (FDP) showed a significant increase in 15 patients. The pathophysiological mechanism of tsutsugamushi disease is known as vasculitis, which may result in an endothelial cell injury and proliferation of the endothelial wall, which may lead to a cerebral infarction accompanied by coagulopathy. Without endothelial cell damage and proliferation, a vasospasm caused by vasculitis may cause vasoconstriction and cerebral infarction.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.74-79
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• 2008

Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with $TNF{\alpha}$ for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy ($15\;{\mu}M$ Zn) or Zn-deficiency ($0\;{\mu}M$ Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various $TNF{\alpha}$ (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, $0-30\;{\mu}M$) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-$\alpha$ treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-$\alpha$ and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.12 no.1
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• pp.72-81
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• 1990

Because failure of microvascular flap grafting has sometimes been attributed to vascular obstruction in the anastomotic site, this study investigated the healing process after microvascular anastomoses. The healing process of anastomotic sites were observed by the use of the light and the scanning electron microscope after microvascular anastomoses of the right common carotid artery in rats. The experimental animals were sacrificed on the 4th day, 1st, 2nd, 4th and 6th week. Throughout the whole experimental period, arterial patency rate was 78% (11/14). At the early stage, it was possible to recognize histologically disappearance of endothelial cell and rupture of part of the media. Subintimal hyperplasia and the growth of media appeared around the suture line at the 2nd week. Endothelial cell regeneration occurred and the depth of vessel wall was normalized at the 4th week. By the scanning electron microscope, at the early stage, the anastomotic site was covered with many platelets, red blood cells, fibrins and macrophages. At the 4th week, the insertion site of the thread was completely covered with normal endothelial cells which were parallel to longitudinal axis of vessels and complete reendothelialization over the anastomotic site seemed to take about 6th week.

• YAKHAK HOEJI
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• v.37 no.1
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• pp.41-48
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• 1993

The effect of captopril on the lung angiotensin converting enzyme (ACE) was investigated after 3 weeks oral administration (120~160 mg/kg/day) through drinking water in SpragueDawley rats. On the $^{125}$I-351A, an ACE inhibitor, binding assay in the isolated perpused lungs, the number of ACE molecules at the intrapulmonary endothelial cell surface was significantly decreased (p<0.001), and recovered to the normal level 7 days after discontinuation of captopril treatment. Intrapulmonary conversion ratio of Al to All was also significantly decreased (p<0.05) in the isolated perpused lungs. Bolus intravenous injection of angiotensin I did not showed pressor response in the both of systemic and pulmonary blood pressure of the anesthetized rats. ACE activity of the lung homogenates was also significantly reduced. These data consistently indicate the decrease of functionally active ACE molecule at the pulmonary artery after chronic captopril treatment. However, serum ACE activity was increased three fold in captopril treated rats compared to the normal rats. So, these results suggest that the functionally active ACE molecule at the pulmonary artery was still inhibited, which is directly associated with the antihypertensive effects, even if the total angiotensn converting enzyme induction was resulted after chronic captopril treatment.

• Korean Journal of Microbiology
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• v.44 no.4
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• pp.282-288
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• 2008

Tissue ischemia resulting from the constriction or obstruction of blood vessels leads to an illness that may affect many organs including the heart, brain, and legs. In recent years, considerable progress has been made in the field of therapeutic angiogenesis and the new approaches are expected to cure those "no-option patients" who are unsuited to conventional therapies. Although single angiogenic growth factor may be successful in inducing angiogenesis, combination of multiple growth factors is increasingly sought these days to augment the therapeutic responses. This trend is proper in light of the fact that blood vessel formation is a complex and multi-step process that requires the actions of many different factors. To meet the growing need for functionally significant blood flow recovery in the ischemic tissues, a novel strategy that can provide concerted actions of multiple factors is required. One way to achieve such a goal is to use a transcription factor that can orchestrate the expression of multiple target genes in the ischemic region and thus induce significant level of angiogenesis. Here, a putative transcription factor, cardiac ankyrin repeat protein (CARP), was evaluated in adenoviral vector context for angiogenic activity in human umbilical vein endothelial cells. The results indicated significant increase in proliferation, capillary-like structure formation, and induction of vascular endothelial growth factor, a typical angiogenic gene. Taken together, these results suggest that CARP represents itself as a novel target for therapeutic angiogenesis and warrants further investigation.

• The Korean Journal of Blood Transfusion
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• v.29 no.3
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• pp.229-239
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• 2018

The circulatory system is closely related to the inter-relationship between the anatomy of the heart and blood vessels, and the fluid dynamic properties of blood. The physical properties of blood, which affect blood flow, are called hemorheologic factors. Hemorheologic factors, such as blood viscosity and erythrocyte aggregation, are influenced mainly by hematocrit. A higher hematocrit level results in an increase in blood viscosity, erythrocyte aggregation, which impedes the circulation itself, and tissue oxygenation. An excess of serum ferritin causes injury to vascular endothelial cells and erythrocytes via oxygen free radicals. In addition, an excess of blood can aggravatee the adverse effects of the hemorheologic parameters and induce atherogenesis, microcirculatory disturbances, and major cardiovascular events. A preventive and therapeutic approach with a phlebotomy or blood donation has been stimulated by the knowledge that blood loss, such as regular donations, is associated with significant decreases in key hemorheologic variables, including blood viscosity, erythrocyte aggregation, hematocrit, and fibrinogen. Major cardiovascular events have been improved in regular blood donors by improving blood flow and microcirculation by decreasing the level of oxidative stress, improving the hemorheologic parameters, and reducing the serum ferritin level. Confirmation of the positive preventive and therapeutic effects of blood donations on cardiovascular disease by a well-designed and well-controlled Cohort study may be good news to patients with cardiovascular disease or at risk of these diseases, as well as patients who require a transfusion.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.199.2-200
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• 2003

Choline is an important membrane phospholipid constituent and a neurotransmitter precursor that is minimally synthesized in brain. The long-term maintenance of brain choline concentration is dependent on choline transport from plasma, which occurs via saturable transport system at the blood-brain barrier. In the present study, we examined to elucidate the characteristics of transport of cationic amines, especially choline which is one of cationic amines, to BBS using conditionally immortalized rat brain capillary endothelial cell line (TR-BBB) in vitro. (omitted)

• Biomolecules & Therapeutics
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• v.20 no.2
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• pp.158-164
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• 2012

Inhibiting the bioactivities of circulating endothelial progenitor cells (EPCs) results in significant inhibition of neovessel formation during tumor angiogenesis. To investigate the potential effect of phloroglucinol as an EPC inhibitor, we performed several in vitro functional assays using $CD34^+$ cells isolated from human umbilical cord blood (HUCB). Although a high treatment dose of phloroglucinol did not show any cell toxicity, it specifically induced the cell death of EPCs under serum free conditions through apoptosis. In the EPC colony-forming assay (EPC-CFA), we observed a significant decreased in the small EPC-CFUs for the phloroglucinol group, implying that phloroglucinol inhibited the early stage of EPC commitment. In addition, in the in vitro expansion assay using $CD34^+$ cells, treatment with phloroglucinol was shown to inhibit endothelial lineage commitment, as demonstrated by the decrease in endothelial surface markers of EPCs including $CD34^+$, $CD34^+/CD133^+$, $CD34^+/CD31^+$ and $CD34^+/CXCR4^+$. This is the first report to demonstrate that phloroglucinol can inhibit the functional bioactivities of EPCs, indicating that phloroglucinol may be used as an EPC inhibitor in the development of biosafe anti-tumor drugs that target tumor angiogenesis.