• Anatomy and Cell Biology
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• v.55 no.4
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• pp.467-474
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• 2022

At birth, the umbilical cord contains various types of thin vessels that are near and outside the umbilicus and separate from the umbilical arteries and vein. These vessels are regarded as the remnant "vitelline vessels" and are often called "umbilical vessels", although this terminology could lead to confusion with the true umbilical arteries and vein. No study has yet comprehensively examined these vessels using histological sections. Our examination of these vessels in 25 midterm fetuses (gestational age: 10-16 weeks) led to five major findings: (i) all specimens had umbilical branches of the inferior epigastric artery; (ii) 5 specimens had vitelline vein remnants; (iii) 4 specimens had a thin artery originating from the left hepatic artery that ran along the umbilical vein; (iv) 2 specimens had a so-called "para-umbilical vein" that was along the umbilical vein and reached the umbilicus; and (v) all specimens had lymphatic vessels originating from the umbilicus that ran caudally along the umbilical artery. The pelvic vein tributaries were well developed along the intra-abdominal umbilical artery, but did not reach the umbilicus. The lymphatic vessel was distinguished from the veins by an intraluminar cluster of lymphocytes attaching to the endothelium. The arterial branch in the umbilical cord did not accompany veins and lymphatic vessels, in contrast to the mother artery in the rectus abdominis. All these thin vessels seemed to be obliterated when the fibrous umbilical ring grew during late-term. The para-umbilical collateral vein in adults might develop outside the fibrous umbilical ring after birth.

• 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.

• BMB Reports
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• v.55 no.7
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• pp.336-341
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• 2022

Narrowing of arteries supplying blood to the limbs provokes critical hindlimb ischemia (CLI). Although CLI results in irreversible sequelae, such as amputation, few therapeutic options induce the formation of new functional blood vessels. Based on the proangiogenic potentials of stem cells, in this study, it was examined whether a combination of dental pulp stem cells (DPSCs) and human umbilical vein endothelial cells (HUVECs) could result in enhanced therapeutic effects of stem cells for CLI compared with those of DPSCs or HUVECs alone. The DPSCs+ HUVECs combination therapy resulted in significantly higher blood flow and lower ischemia damage than DPSCs or HUVECs alone. The improved therapeutic effects in the DPSCs+ HUVECs group were accompanied by a significantly higher number of microvessels in the ischemic tissue than in the other groups. In vitro proliferation and tube formation assay showed that VEGF in the conditioned media of DPSCs induced proliferation and vessel-like tube formation of HUVECs. Altogether, our results demonstrated that the combination of DPSCs and HUVECs had significantly better therapeutic effects on CLI via VEGF-mediated crosstalk. This combinational strategy could be used to develop novel clinical protocols for CLI proangiogenic regenerative treatments.

• Archives of Plastic Surgery
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• v.37 no.4
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• pp.391-395
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• 2010

Purpose: Given that the critical nature of the microvascular anastomosis to what is often a long and difficult reconstructive operation, trainees need to have a high level of microsurgical competence before being allowed to perform microsurgery on patients. Some artificial substitutes and dead or live animal models have been used to improve manual dexterity under the operating microscope. Yet, most surgeons are not equipped with such models, so search for easy available and appropriate microsurgical practice model have been an issue. Umbilical artery, placental vessels and gastroepiploic arteries have been previously suggested as a microsurgical training model, which involves other surgical departments. The purpose of this article is to introduce that saphenous vein specimen obtained from varicose vein surgery is useful and has many advantages as training model for the practice of microvascular anastomosis. Methods: The conventional technique using perforation/inversion method with a metallic stripper is widely performed for varicose vein patients. The stripper is inserted through disconnected safeno-femoral junction and retrieved at the knee or the medial side of ankle. The length of saphenous vein specimens removed is about that of one's leg and inversed from inside out. Obtained saphenous vein specimens are re-inversed and cleansed with normal saline, to be readily available for microsurgical practice. Preserved in a squeezed wet saline gauze and refrigerated, frozen or glycerated specimens were investigated into their comparative quality for microsurgical practice. Results: Varicose vein surgery remains one of the common operations performed in the field of plastic surgery. Convenient informed consent regarding the vessel donation can be easily signed. The diameter of the obtained saphenous vein is as variable as 1.5 to 6 mm, which is already stripped, and is in sufficient length corresponding to that of patient's leg. Vessels specimens were available for microsurgical practice within 1 week period when preserved with squeezed wet saline gauze, and the preservation period could be extended monthly by freezing it. Conclusion: Saphenous vein obtained from varicose vein patients provide with variable size of vessel lumen with sufficient length. The practice can be cost effective and does not require microsurgical laboratory. Additionally there is no need of involving other surgical departments in acquiring vessel specimens. Furthermore, simple preservation method of refrigerating for a week or freezing with squeezed wet saline gauze for a month period, allow the saphenous vein obtained after varicose vein surgery as an excellent model for the microsurgical practice.

• BioChip Journal
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• v.12 no.4
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• pp.294-303
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• 2018

Shear stress occurs in flowing liquids, especially at the interface of a flowing liquid and a stationary solid phase. Thus, it occurs inside the artery system of the human body, where it is responsible for a number of biological functions. The shear stress level generally remains less than $70dyne/cm^2$ in the whole circulatory system, but in the stenotic arteries, which are constricted by 95%, a shear stress greater than $1,000dyne/cm^2$ can be reached. Methods of researching the effects of shear stress on cells are of large interest to understand these processes. Here, we show the development of a microfluidic device for generating shear stress gradients. The performance of the shear stress gradient generator was theoretically simulated prior to experiments. Through simple manipulations of the liquid flow, the shape and magnitude of the shear stress gradients can be manipulated. Our microfluidic device consisted of five portions divided by arrays of micropillars. The generated shear stress gradient has five distinct levels at 8.38, 6.55, 4.42, 2.97, and $2.24dyne/cm^2$. Thereafter, an application of the microfluidic device was demonstrated testing the effect of shear stress on human umbilical vein endothelial cells.

• 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 Chest Surgery
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• v.37 no.3
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• pp.210-219
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• 2004

Extracellular $K^{+}$ concentration ([ $K^{+}$]$_{0}$ ) can be increased within several mM by the efflux of intracellular $K^{+}$. To investigate the effect of an increase in [ $K^{+}$]$_{0}$ on vascular contractility, we attempted to examine whether extracellular $K^{+}$ might modulate vascular contractility, endothelium-dependent relaxation (EDR) and intracellular $Ca^2$$^{+}$ concentration ([C $a^2$$^{+}$]$_{i}$ ) in endothelial cells (EC). We observed isometric contractions in rabbit carotid, superior mesenteric, basilar arteries and movse aorta. [C $a^2$$^{+}$]$_{i}$ was recorded by microfluorimeter using Fura-2/AM in EC. No change in contractility was recorded by the increase in [ $K^{+}$]$_{0}$ from 6 to 12 mM in conduit artery such as rabbit carotid artery. whereas resistant vessels, such as basilar and branches of superior mesenteric arteries (SMA), were relaxed by the increase. In basilar artery, the relaxation by the increase in [ $K^{+}$]$_{0}$ to from 1 to 3 mM was bigger than that by the increase from 6 to 12 mM. In contrast, in branches of SMA, the relaxation by the increase in [ $K^{+}$]$_{0}$ to from 6 to 12 mM is bigger than that by the increase from 1 to 3 mM. $Ba^2$$^{+}$ (30 $\mu$M) did not inhibit the relaxation by the increase in [ $K^{+}$]$_{0}$ from 1 to 3 mM but did inhibit the relaxation by the increase from 6 to 12 mM. In the mouse aorta without the endothelium or treated with $N^{G}$_nitro-L-arginine (30 $\mu$M), nitric oxide synthesis blocker, the increase in [ $K^{+}$]$_{0}$ from 6 to 12 mM did not change the magnitude of contraction induced either norepinephrine or prostaglandin $F_2$$_{\alpha}$. The increase in [ $K^{+}$]$_{0}$ up to 12 mM did not induce contraction of mouse aorta but the increase more than 12 mM induced contraction. In the mouse aorta, EDR was completely inhibited on increasing [ $K^{+}$]$_{0}$ from 6 to 12 mM. In cultured mouse aorta EC, [C $a^2$$^{+}$]$_{i}$ , was increased by acetylcholine or ATP application and the increased [C $a^2$$^{+}$]$_{i}$ , was reduced by the increase in [ $K^{+}$]$_{0}$ reversibly and concentration-dependently. In human umbilical vein EC, similar effect of extracellular $K^{+}$ was observed. Ouabain, a N $a^{+}$ - $K^{+}$ pump blocker, and N $i^2$$^{+}$, a N $a^{+}$ - $Ca^2$$^{+}$ exchanger blocker, reversed the inhibitory effect of extracellular $K^{+}$. In resistant arteries, the increase in [ $K^{+}$]$_{0}$ relaxes vascular smooth muscle and the underlying mechanisms differ according to the kinds of the arteries; $Ba^2$$^{+}$-insensitive mechanism in basilar artery and $Ba^2$$^{+}$ -sensitive one in branches of SMA. It also inhibits [C $a^2$$^{+}$]$_{i}$ , increase in EC and thereby EDR. The initial mechanism of the inhibition may be due to the activation of N $a^{+}$ - $K^{+}$pump. activation of N $a^{+}$ - $K^{+}$pump.p.p.p.