• The Korean Journal of Physiology and Pharmacology
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• v.11 no.3
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• pp.129-133
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• 2007

There are growing evidences suggesting a pivotal role of oxidative stress in the pathophysiology of preeclampsia. We investigated oxidative stress in the rat model of preeclampsia, and in clinical cases. Pregnant female rats were injected intraperitoneally with deoxycorticosterone acetate (DOCA) and given 0.9% saline as drinking water during their pregnancy. We assessed plasma $F_2-isoprostane(8-iso-PGF_{2{\alpha})$ and malondialdehyde (MDA) in a rat model, and the same markers in the plasma of maternal blood and fetal cord blood in pregnant women with preclampsia. Blood samples from the umbilical arteries and veins were collected separately. The concentrations of MDA were increased in the preeclampsia groups of animal and humans, compared with the control group; it was significantly increased in the umbilical artery and vein of the preeclampsia group. The concentrations of $F_2-isoprostane$ were elevated in the preeclampsia groups of animal and humans, compared with the control group, and the increase in $F_2-isoprostane$ concentration was prominent in the umbilical vein than umbilical artery of the preeclampsia group. Therefore, it appears that the placenta has an important role in the pathophysiology of preeclampsia, and the $F_2-isoprostane$ of the umbilical vein may serve as a relatively reliable marker for ischemic/hypoxic injury to the fetus during the perinatal period.

• Korean Journal of Veterinary Research
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• v.42 no.4
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• pp.437-442
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• 2002

The observations of the anatomical closure of the ductus venosus (DV) and vestige of DV were studied in 22 cattle, ranging from 210-day-old fetus to 3-years old Korean native cattle. Vinylite solution was injected into the hepatic, portal, umbilical veins and caudal vena cavae of 22 specimens for vinylite corrosion casts. The DV originated at the confluence of the umbilical and portal veins and emptied into the left hepatic vein or posterior vena cava. The DVs were persisted in a 210-day-old fetus, a 240-day-old fetus, and a 270-day-old fetus. Two newborns, two 2-year-old and two 3-year-old cattle had no rudimentum of DV (6 cases, 31.58%). However, vestiges of DV in varying sizes were observed in a 14-day-old, a 3O-day-old, two 180-day-old and nine adult cattle (13 cases, 68.42%). The lengths of vestiges of DV were about 4.97~99.66 mm. Therefore, the present study demonstrates that DV in cattle can be degenerated during the late period of a pregnancy.

• Journal of Yeungnam Medical Science
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• v.27 no.2
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• pp.91-97
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• 2010

Endothelial cells play a key role in pathological processes such as cancer cell metastasis, atherosclerosis, and diabetic retinopathy. Vascular smooth muscle cells directly involve in the formation of atheroma in atherosclerosis. Some kinds of the endothelial cells are simply harvested from the umbilical veins, the tunica intima of aortic walls, the retina using various enzymes solutions. Those purely isolated cells provide a powerful tool in vitro studies of the endothelial cell related diseases. In this context, the cultured smooth muscle cells after the isolation from the tunica media of aortic walls are also used for elucidating the pathogenesis of atherosclerosis. Here, I briefly introduce articles that include the isolation of human umbilical vein endothelial cells(HUVEC), aortic endothelial and smooth muscle cells, retinal microvascular endothelial cells(RMEC), as well as the diseases' applications of these cells.

• Journal of the Korean Society of Radiology
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• v.84 no.3
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• pp.586-595
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• 2023

An umbilical venous catheter (UVC) is commonly placed for central venous access in preterm or critically ill full-term neonates to provide total parenteral nutrition (TPN) and medication. However, UVCs can result in complications, including infection, portal vein thrombosis, and hepatic tissue injury. The inadvertent administration of hypertonic fluid through a malpositioned UVC can also cause hepatic parenchymal damage with mass-like fluid collection that simulates a tumorous condition during imaging. Ultrasonography and radiographic examinations play an essential role in detecting UVC-related complications. This pictorial essay aims to present the imaging findings of UVC-related hepatic complications in neonates.

• Journal of Biomedical Engineering Research
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• v.11 no.1
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• pp.131-140
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• 1990

To improve antithrombogenicity of polymer that used in vascular graft and artificial organs, seeding of human endothelial cells on the polyurethane was studied. Human endothelial cells were ismlated from human umbilical veins, using type I collagenase, and identified with goat anti vWF antibodies. Human endothilial cell seeding was tried upon the polyurethane which has good mechanical property and resists stresses. The hydrophobic polyurethane surface was changed hydrophilic by corona discharf:e treatment. Surface hydrophilicity was measured with Wilhemly plate method and the goniometer. To evaluate matrix protein adsorption, fibronectin adsorption test was done. To eveluate cell adhesion, human endothelial cell attachment forces were measured rising a perfusion chamber of , ism diamter. Less cells were detached from the hydrophilically treated polyurethane. This showed that corona discharge on the polyurethane could improve matrix adsorption and endothelial cell attachment.

• Journal of Yeungnam Medical Science
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• v.35 no.1
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• pp.89-93
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• 2018

Idiopathic non-cirrhotic portal hypertension (INCPH) is a disease with an uncertain etiology consisting of non-cirrhotic portal hypertension and portal pressure increase in the absence of liver cirrhosis. In INCPH, patients exhibit normal liver functions and structures. The factors associated with INCPH include the following: Umbilical/portal pyremia, bacterial diseases, prothrombic states, chronic exposure to arsenic, vinyl chloride monomers, genetic disorders, and autoimmune diseases. Approximately 70% of patients present a history of major variceal bleeding, and treatment relies on the prevention of complications related to portal hypertension. Autoimmune disorders associated with INCPH are mainly systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis. To the best of our knowledge, a case of ankylosing spondylitis (AS) associated with INCPH has not been reported thus far. Therfore, we report our experience of a patient with AS accompanied by INCPH, who showed perisplenic varices with patent spleno-portal axis and hepatic veins along with no evidence of cirrhosis on liver biopsy, and provide a brief literature review.

• Archives of Plastic Surgery
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• v.32 no.6
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• pp.689-698
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• 2005

Many studies for verifying angiogenesis have been in progress, especially in the field of abnormal vascular proliferation to explain the pathogenesis and to develop a treatment of several diseases. In our previous experiments, endothelial cell proliferations were induced by DMH stimulation in vitro, and the 177 factors(142 up-regulated and 35 down-regulated factors) were identified. Among the up-regulated factors, 9 substances (EFEMP1, CTGF, CYR61, $ITG{\beta}1$, FHL2, SERPINE1, MYC, PTTG1 and MSH6) were selected, which were related to cell proliferation and showed high signal intensities. The RNA was isolated from HUVECs at the time of 0, 6, 12, 24 hours after the DMH treatment, and RNA of control group HUVECs was also isolated. Genetic information of selected molecules was used to make primer for each, and RT-PCR was performed to analyze both groups. In control and treatment groups, each substance presented variety of manifestation degree according to time differences. EFEMP1, CTGF, CYR61, $ITG{\beta}1$, FHL2 and MYC were related to abnormal vascular proliferation steadily and SERPINE1, PTTG1 and MSH6 were related secondarily. CTGF was related to both normal and abnormal proliferation, but it played a more significant role in abnormal proliferation from earlier stage. EFEMP1, CYR61, $ITG{\beta}1$, FHL2 and MYC were similar to CTGF, although the relation appeared lately. Further study should be performed to analyze the expressions and the interactions of growth factors, which could be utilized in the new therapeutic development.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.256-263
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• 2007

Background: Intimal hyperpiasia is characterized by a proliferation of vascular smooth muscle cells in the intimal layer Epigallocatechin-3-gallate (EGCG) is known to suppress smooth muscle cell proliferation. We propose that EGCG may have a protective effect against the development of intimal hyperplasia through the suppression of smooth muscle cell proliferation. Material and Method: Human umbilical vein endothelial cells (HUVEC) and rat aortic smooth muscle cells (RASMC) were cultured with different concentrations of EGCG, and proliferation and migration speed were measured. In 20 dogs, the autologous jugular veins were interposed into the carotid arteries. For the study group (n=10), the graft was stored for 30 minutes in EGCG solution and 300mM EGCG was applied to the perivascular space after grafting. After 6 weeks, the intimal and medial thickness was measured. Result: The proliferation of RASMC and HUVEC was suppressed with EGCG. The migration of RASMC was suppressed with EGCG, but that of HUVEC was not affected. In the in vivo study, the intimal thickness was thinner in EGCG group than in the control group (p<0.05), but the medial thickness did not show any difference. The intimal/medial thickness ratio was lower in the EGCG group (p<0.05). Conclusion: EGCG suppresses intimal hyperplasia after vascular grafting, and this may be mediated by prevention of migration and proliferation of vascular smooth muscle cells. The use of EGCG may offer new therapeutic modality to prevent intimal hyperplasia.

• Journal of Yeungnam Medical Science
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• v.23 no.2
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• pp.182-192
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• 2006

Background: Atherosclerosis has emerged as the leading cause of death in developed countries. At present, human umbilical vein endothelial cells (HUVEC) are most commonly used for the investigation of Endothelial cells (EC). However, HUVEC are not found in arteries but only in veins. Currently there are many reports on methods used to isolate EC;, most of these methods require special equipment to remove contaminating smooth muscle cells (SMC). Materials and Methods: The method described here may be used to isolate not only ECs but also SMCs;,the approach presented here did not require special equipment. Rat aorta was treated with 2 mg/ml of type II collagenase solution for 45 minutes. The isolated cells from the aorta were incubated in medium G for a week;, only ECs could be separated. After the collagenase treatment, the rest of aorta was cut lengthwise, and left undisturbed to obtain SMCs in the culture dish for 10 days. To verify the purity of the isolated cells, we performed immunofluorescence and evaluated the results with transmission electron microscopy analysis. Results: The immunofluorescence study demonstrated specific expression of CD31 and ${\alpha}$-smooth muscle actin in the isolated ECs and SMCs, respectively. Cultured ECs and SMCs showed their own fine structure characteristics. Conclusion: These results suggest that this method for isolating ECs and SMCs may be especially useful for the study of atherosclerosis.

• Journal of Life Science
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• v.29 no.12
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• pp.1393-1400
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• 2019

In the present study, we examined the effect of mitochondrial K⁺ channel opener diazoxide on the mitochondria-dependent apoptotic signaling in endothelial cells exposed to high glucose (HG) media. Endothelial cells derived from human umbilical veins were exposed to HG media containing 30 mM glucose, and the degree of apoptotic cell death associated with activation of the mitochondria-dependent apoptotic signaling pathway was determined. Exposure to HG media was seen to enhance apoptotic cell death in a time-dependent manner. In these cells, activation of caspases 3, 8, and 9 was observed, and while caspase-3 and -9 inhibitors suppressed the HG-induced apoptotic cell death, a caspase-8 inhibitor did not. The HG-treated cells exhibited disruption of mitochondrial membrane potential, formation of permeability transition pores, and cytosolic release of cytochrome c. Subsequently, diazoxide was seen to attenuate the HG-induced apoptotic cell death; caspase-9 activation was suppressed but caspase 8 was not. Diazoxide also suppressed the depolarization of mitochondrial membrane potential, the formation of mitochondrial permeability transition pores, and the release of cytochrome c. These effects were significantly inhibited by 5-hydroxydecanoate, a selective blocker of ATP-sensitive K⁺ channels (K_ATP). The present results demonstrate that diazoxide exhibits a beneficial effect to ameliorate HG-induced endothelial cell apoptosis. Opening the K_ATP could help preserve the functional integrity of mitochondria and provide an underlying mechanism to suppress HG-triggered apoptotic signaling.