• 방송공학회논문지
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• 제25권1호
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• pp.1-12
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• 2020

의료분야에서 질환별 유병률 차이로 인한 데이터 수적 불균형은 흔하게 발생되는 문제로 인공지능 학습 성능을 저하시켜 개발의 어려움을 초래한다. 최근 이러한 데이터 수적 불균형문제를 해결하기 위한 한 방법으로 적대적 생성 신경망(GAN) 기술이 도입되었고 다양한 분야에 성공적으로 적용되어왔다. 그러나 수적 불균형에 의해 저하된 성능 문제를 해결하는데 있어서 기존 연구들의 영상 해상도가 아직 충분하지 않고 영상 내 구조가 전역적으로 일관성 있게 모델링 되지 않아 좋은 결과를 얻기 어렵다. 본 논문에서는, 흉부 X선 영상 데이터의 수적 불균형문제를 해결하기 위하여 고해상도 영상을 생성할 수 있는 주목 메커니즘 기반 멀티 스케일 조건부 적대적 생성 네트워크를 제안한다. 해당 네트워크는 질환제어 조건변수에 의해 하나의 네트워크만으로 다양한 질환 영상을 생성할 수 있어 각 클래스별로 학습을 하는 비효율성을 줄였고, 자기 주목 메커니즘을 통해 영상 내 장거리 종속성 문제를 해결하였다.

• The Korean Journal of Physiology and Pharmacology
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• 제18권2호
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• pp.177-182
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• 2014

This study was to determine the correlation between endothelial function and neuro-endocrine-immune (NEI) network through observing the changes of NEI network under the different endothelial dysfunction models. Three endothelial dysfunction models were established in male Wistar rats after exposure to homocysteine (Hcy), high fat diet (HFD) and Hcy+HFD. The results showed that there was endothelial dysfunction in all three models with varying degrees. However, the expression of NEI network was totally different. Interestingly, treatment with simvastatin was able to improve vascular endothelial function and restored the imbalance of the NEI network, observed in the Hcy+HFD group. The results indicated that NEI network may have a strong association with endothelial function, and this relationship can be used to distinguish different risk factors and evaluate drug effects.

• BMB Reports
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• 제54권11호
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• pp.569-574
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• 2021

Vascular calcification is the heterotopic accumulation of calcium phosphate salts in the vascular tissue and is highly correlated with increased cardiovascular morbidity and mortality. In this study, we found that the expression of neuromedin B (NMB) and NMB receptor is upregulated in phosphate-induced calcification of vascular smooth muscle cells (VSMCs). Silencing of NMB or treatment with NMB receptor antagonist, PD168368, inhibited the phosphate-induced osteogenic differentiation of VSMCs by inhibiting Wnt/β-catenin signaling and VSMC apoptosis. PD168368 also attenuated the arterial calcification in cultured aortic rings and in a rat model of chronic kidney disease. The results of this study suggest that NMB-NMB receptor axis may have potential therapeutic value in the diagnosis and treatment of vascular calcification.

• Archives of Reconstructive Microsurgery
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• 제10권1호
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• pp.38-43
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• 2001

Introduction : The goal in the management of soft tissue injuries of the lower extremity is to obtain a closed stable wound as soon as possible. Recently, An anatomic study that has shown the role of the vascular axis that follows the superficial sensory nerves in supplying the skin developed the concept of a neuroskin island flap. It has been suggested that skin island flaps supplied by the vascular network of the saphenous nerve is one of the most reliable treatment to skin defect below the knee joint. Purpose : The aim of this article is to present a clinical experience of neuroskin island flaps based on the saphenous nerve and to estimate the clinical utilities of distally based saphenous neuroskin flap. Materials and Methods : From September 1995 to May 2000, a total 12 distally based neuroskin island flaps supplied by the vascular axis of the saphenous nerve were performed to cover defects in pretibial area below the knee. Result : flap necrosis due to reactivation of existing infection developed in a case that skin defect had been on infected nonunion site of tibia. But other 11 cases survived completely without any specific complications. Conclusion : The distally based neuroskin pedicled island flap using the vascular network of the saphenous nerve are versatile and reliable and especially indicated for limited defects in pretibial area below the knee joint which are not good indications for other better-known flaps.

• 한국정밀공학회:학술대회논문집
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• 한국정밀공학회 2010년도 추계학술대회 논문집
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• pp.655-656
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• 2010

• BMB Reports
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• 제56권3호
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• pp.160-165
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• 2023

Vascular calcification is common in cardiovascular diseases including atherosclerosis, and is associated with an increased risk of pathological events and mortality. Some semaphorin family members play an important role in atherosclerosis. In the present study, we show that Semaphorin 4D/Sema4D and its Plexin-B1 receptor were significantly upregulated in calcified aorta of a rat chronic kidney disease model. Significantly higher Sema4D and Plexin-B1 expression was also observed during inorganic phosphate-induced calcification of vascular smooth muscle cells. Knockdown of Sema4D or Plexin-B1 genes attenuated both the phosphate-induced osteogenic phenotype of vascular smooth muscle cells, through regulation of SMAD1/5 signaling, as well as apoptosis of vascular smooth muscle cells, through modulation of the Gas6/Axl/Akt survival pathway. Taken together, our results offer new insights on the role of Sema4D and Plexin-B1 as potential therapeutic targets against vascular calcification.

• Journal of Ginseng Research
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• 제32권3호
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• pp.244-249
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• 2008

Vascular inflammation is an important step in the development of cardiovascular disorder. Since it has not been known whether Korean red ginseng has a role to play on the vascular inflammation, we investigated the effects of Korean red ginseng extract (KRGE) on monocyte adhesion and its underlying signaling mechanism. Monocyte adhesion assay and Western blot were conducted on the human umbilical vein endothelial cells to study monocyte adhesion and the expression of adhesion molecules. Intracellular calcium was measured with Fura-2 fluorescent staining, and superoxide production was measured with lucigenin chemiluminescence in the endothelial cells. KRGE inhibits tumor necrosis factor (TNF)-alpha-induced monocyte adhesion on the endothelial cells at the range of $0.03{\sim}1$ mg/ml. TNF-alpha-induced vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 expression were inhibited by the pretreatment of KRGE in the endothelial cells. KRGE also inhibits TNF-alpha-induced intracellular calcium and the superoxide production in the endothelial cells. This study first demonstrated that KRGE inhibits TNF-alpha-induced monocyte adhesion by inhibiting the adhesion molecule expression, intracellular calcium and superoxide production in the endothelial cells. Therefore, the anti-inflammatory function of KRGE may be contributed to protecting the endothelial dysfunction in the vascular inflammatory disorders.

• 센서학회지
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• 제22권1호
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• pp.76-83
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• 2013

A real-time wireless monitoring and analysis methods using the wearable PPG sensor to estimate cardiovascular condition is studied for ubiquitous healthcare service. A small size and low-power consuming wearable photoplethysmogram (PPG) sensor is designed as a wrist type device and connected with the IP node assigned its own IPv6 address. The measured PPG waveform in the IP node is collected and transferred to a central server PC through the IP-enabled wireless network for storage and analysis purposes. A monitoring and analysis program is designed to process the accelerated plethysmogram (APG) waveform by applying the second order derivatives to analyze systolic waves as well as heart rate variability analysis from the measured PPG waveform. From our results, the features of cardiovascular condition from individual's PPG waveform and estimation of vascular compliance by the comparison of APG-aging index (AI) and ratio of LF/HF are demonstrated.

• Molecules and Cells
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• 제38권12호
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• pp.1064-1070
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• 2015

Translocator protein 18 kDa (TSPO) is a mitochondrial outer membrane protein and is abundantly expressed in a variety of organ and tissues. To date, the functional role of TSPO on vascular endothelial cell activation has yet to be fully elucidated. In the present study, the phorbol 12-myristate 13-acetate (PMA, 250 nM), an activator of protein kinase C (PKC), was used to induce vascular endothelial activation. Adenoviral TSPO overexpression (10-100 MOI) inhibited PMA-induced vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1) expression in a dose dependent manner. PMA-induced VCAM-1 expressions were inhibited by Mito-TEMPO ($0.1-0.5{\mu}m$), a specific mitochondrial antioxidants, and cyclosporin A ($1-5{\mu}m$), a mitochondrial permeability transition pore inhibitor, implying on an important role of mitochondrial reactive oxygen species (ROS) on the endothelial activation. Moreover, adenoviral TSPO overexpression inhibited mitochondrial ROS production and manganese superoxide dismutase expression. On contrasts, gene silencing of TSPO with siRNA increased PMA-induced VCAM-1 expression and mitochondrial ROS production. Midazolam ($1-50{\mu}m$), TSPO ligands, inhibited PMA-induced VCAM-1 and mitochondrial ROS production in endothelial cells. These results suggest that mitochondrial TSPO can inhibit PMA-induced endothelial inflammation via suppression of VCAM-1 and mitochondrial ROS production in endothelial cells.

• Asian Pacific Journal of Cancer Prevention
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• 제13권2호
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• pp.499-503
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• 2012

The present study was based on the unexpected discovery that norcantharidin exerted anti-angiogenesis activity when effects on growth of human colon cancer were studied. The aim was to further verify this finding and explore possible mechanisms using a tumor xenograft model in nude mice. We confirmed that norcantharidin (5 or 15 mg/kg) could inhibit angiogenesis of human colon cancer in vivo. In vitro, crossing river assay, cell adhesion assay and tube formation assay indicated that NCTD could reduce the migration, adhesion and vascular network tube formation ability of HUVECs. At the same time, the expression levels of VEGF and VEGFR-2 proteins which play important roles in angiogenesis were reduced as examined by western blotting analysis. Taken together, the results firstly showed NCTD could inhibit angiogenesis of human colon cancer in vivo, probably associated with effects on migration, adhesion and vascular network tube formation of HUVECs and expression levels of VEGF and VEGFR-2 proteins.