• Tuberculosis and Respiratory Diseases
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• 제64권2호
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• pp.125-132
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• 2008

연구배경: COPD 환자에서 혈청 C-반응단백은 증가하는 것으로 알려져 있으며 이러한 변화는 급성 악화 시 보다 두드러진다. 폐동맥 고혈압은 COPD의 흔한 합병증 중 하나이며, C-반응단백은 전신적 심혈관계 질환 발생 위험과 밀접한 관련이 있다고 알려져 왔다. 하지만, COPD에서 이차적으로 발생하는 폐동맥 고혈압에 대한 C-반응단백의 영향에 대해서는 연구가 미비한 상태이다. 방법: 본 연구는 AECOPD에 대해 입원 치료를 시작한 72명의 환자를 대상으로 전향적으로 연구하였다. 환자들은 AECOPD에 대한 즉각적인 치료를 받았고 입원 2일 또는 3일째 실내 환기 하에서 혈청 C-반응단백, 동맥혈 산소 분압, 폐동맥 고혈압에 대한 이환 여부 등에 대한 검사를 시행 받았다. 결과: 폐동맥 고혈압에 이환된 환자는 47명으로 전체 환자 중 65.3%에 달하였다. COPD의 중증도가 심할수록 폐동맥 고혈압의 이환율과 C-반응단백 평균치가 증가하였고, C-반응단백 평균치가 증가할수록 평균 우심실 수축압 역시 증가하는 것을 관찰할 수 있었다. 폐동맥 고혈압 환자군과 비환자군에서 C-반응단백은 각각 $37.6{\pm}7.4mg/L$ 와 $19.9{\pm}6.6mg/L$ 통계적으로 의미 있게 폐동맥고혈압 환자군에서 높았지만, 동맥혈 산소분압은 양 군간 의미 있는 차이를 보이지 않았다($77.8{\pm}3.6mmHg$ vs. $87.2{\pm}6.0mmHg$). 결론: 본 연구는 COPD의 급성 악화 시 증가된 C-반응 단백은 폐동맥 고혈압의 이환 여부와 밀접한 관련이 있는 것을 보여 주고 있으며, 이는 COPD의 예후에 심혈관계 질환의 이환 여부가 중요하다는 점을 감안할 때 C-반응단백의 COPD에 대한 독립적 예후인자로서의 가능성을 시사해 준다.

• The Korean Journal of Physiology and Pharmacology
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• 제20권6호
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• pp.641-647
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• 2016

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high $K^+$ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-$N^G$-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1999년도 제38차 춘계학술대회
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• pp.205-208
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• 1999

재협착에 관여하는 인자는 매우 다양하다. 평활근 세포의 증식, ECM의 형성, 혈관벽의 초기 혈전형성, 그리고 혈관 재형성 등이 모든 것들이 재협착의 병인에 기여하고 있다. 환자마다 이런 요소들의 기여정도가 다르며 동일 환자에서도 병변에 따른 기여정도가 또한 다르리라 여긴다. 그러나 아직까지 우리는 외막섬유모세포의 역할, 내피세포의 재생, 증식세포의 계획된 죽음 등 재협착의 기전을 불완전하게 이해하고 있고 따라서 보다 완전한 이해를 통해 효과적인 재협착 예방치료가 시행될 수 있을 것이다.

• 대한영상의학회지
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• 제84권2호
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• pp.418-426
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• 2023

목적 경피적 혈관내 시술 시 급격한 분지 각도를 가지는 혈관의 선택적 진입이 어려운 경우에 활용할 수 있는 새로운 guidewire shaping 방법인 folded-loop guidewire remodeling 방법을 소개한다. 대상과 방법 0.014 inch 미세 guidewire tip을 pigtail loop 형태로 만든 후, metal introducer를 이용하여 guidewire를 microcatheter로 진입시킨다. 혈관 내에서 guidewire를 회전시키면 기존의 pigtail loop 형태로 쉽게 guidewire tip을 변형시킬 수 있다. Guidewire를 뒤로 당기면 guidewire tip이 작은 U형으로 변형되면서 분지 혈관으로 쉽게 진입된다. 결과 2019년 12월부터 2022년 1월까지 동맥 색전술 시 기존 방법으로 분지동맥의 선택적 진입이 어려웠던 64명의 환자(남/여, 49/15; 평균나이 66.8 ± 9.5세)에서 본 방법을 시행하였으며, 98%의 성공률을 확인하였다. 색전술의 적응증은 transcatheter arterial chemoembolization, 위장관 출혈, 객혈, 외상출혈, 종양출혈이었다. 결론 Folded-loop guidewire remodeling 방법은 기존의 보편적 방법으로 선택이 어려웠던 급격한 분지 각도를 가지는 혈관의 선택적 진입에 효과적인 방법이다.

• Molecules and Cells
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• 제37권3호
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• pp.196-201
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• 2014

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.

• Clinical and Experimental Pediatrics
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• 제57권11호
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• pp.472-478
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• 2014

Kawasaki disease (KD), an acute vasculitis that primarily affects young children, is the most common acquired paediatric cardiovascular disease in developed countries. While sequelae of arterial inflammation in the acute phase of KD are well documented, its late effects on vascular health are increasingly unveiled. Late vascular dysfunction is characterized by structural alterations and functional impairment in term of arterial stiffening and endothelial dysfunction and shown to involve both coronary and systemic arteries. Further evidence suggests that continuous low grade inflammation and ongoing active remodeling of coronary arterial lesions occur late after acute illness and may play a role in structural and functional alterations of the arteries. Potential importance of genetic modulation on vascular health late after KD is implicated by associations between mannose binding lectin and inflammatory gene polymorphisms with severity of peripheral arterial stiffening and carotid intima-media thickening. The changes in cholesterol and lipoproteins levels late after KD further appear similar to those proposed to be atherogenic. While data on adverse vascular health are less controversial in patients with persistent or regressed coronary arterial aneurysms, data appear conflicting in individuals with no coronary arterial involvements or only transient coronary ectasia. Notwithstanding, concerns have been raised with regard to predisposition of KD in childhood to accelerated atherosclerosis in adulthood. Until further evidence-based data are available, however, it remains important to assess and monitor cardiovascular risk factors and to promote cardiovascular health in children with a history of KD in the long term.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2001년도 추계학술대회논문집B
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• pp.529-532
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• 2001

The purposes of the present study are to investigate hemodynamic characteristics and to define shear-sensitive remodeling in the stenosed coronary models. Two models for the compensatory remodelling used for this research are a pre-stenotic dilation and a post-stenotic dilation models for the computer simulation. The peak wall shear stress on the post-stenotic model is higher than that of the pre-stenotic model. Two recirculation zones are generated in the pre-stenotic model, and the zones in the pre-stenotic model are smaller than those in the post-stenotic model. Variation of the wall shear stress in the pre-stenotic model is lower than that in the post-stenotic model. In computer simulation with the post-stenotic model, higher temporal and spatial shear fluctuation and stress suggested shear-sensitive remodeling. Shear-sensitive remodeling may be associated with the increased risk of plaque rupture, the underlying cause of acute coronary syndromes, and sudden cardiac death.

• BMB Reports
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• 제47권6호
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• pp.311-317
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• 2014

microRNAs (miRNAs) are a class of small, non-coding RNAs that play critical posttranscriptional regulatory roles typically through targeting of the 3'-untranslated region of messenger RNA (mRNA). Mature miRNAs are known to be involved in global cellular processes, such as differentiation, proliferation, apoptosis, and organogenesis, due to their capacity to target multiple mRNAs. Thus, imbalances in the expression and/or activity of miRNAs are involved in the pathogenesis of numerous diseases, including pulmonary arterial hypertension (PAH). PAH is a progressive disease characterized by vascular remodeling due to excessive proliferation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). Recently, studies have evaluated the roles of miRNAs involved in the pathogenesis of PAH in these pulmonary vascular cells. This review provides an overview of recent discoveries on the role of miRNAs in the pathogenesis of PAH and discusses the potential for miRNAs as therapeutic targets and biomarkers of PAH.

• The Korean Journal of Physiology and Pharmacology
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• 제28권1호
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• pp.39-48
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• 2024

Wogonin, extracted from the roots of Scutellaria baicalensis Georgi, has been shown to suppress collagen deposition in spontaneously hypertensive rats (SHRs). This study was performed to investigate the role and mechanism of wogonin underlying vascular remodeling in SHRs. After injection of SHRs with 40 mg/kg of wogonin, blood pressure in rats was measured once a week. Masson's trichrome staining was conducted to observe the changes in aortas and mesenteric arteries. Vascular smooth muscle cells (VSMCs) isolated from rat thoracic aortas were treated with Angiotensin II (Ang II; 100 nM) in the presence or absence of varying concentrations of wogonin. The viability and proliferation of VSMCs were examined using Cell Counting Kit-8 assay and 5-ethynyl-2'-deoxyuridine assay, respectively. The migration of VSMCs was examined using wound healing assay and transwell assay. We found that wogonin administration alleviated hypertension, increased lumen diameter, and reduced the thickness of the arterial media in SHRs. Ang II treatment enhanced the viability of VSMCs, which was inhibited by wogonin in a concentration-dependent manner. Wogonin reversed Ang II-induced increases in the viability, proliferation, and migration of VSMCs. Moreover, wogonin inhibited Ang II-induced activation of mitogen-activated protein kinase (MAPK) signaling in VSMCs. Overall, wogonin repressed the proliferative and migratory capacity of VSMCs by regulating the MAPK signaling pathway, thereby attenuating vascular remodeling in hypertensive rats, indicating that wogonin might be a therapeutic agent for the treatment of vascular diseases.

• Archives of Reconstructive Microsurgery
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• 제13권2호
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• pp.101-106
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• 2004

Purpose : This study evaluated the effect of VEGF in the arterial anastomosis by using light and electron microscopy. Marerials and method : Rats underwent femoral arterial end-to-end anastomosis after transection and topical VEGF treatment. The proximal and distal segments of the femoral arteries was drenched with 1 drop of VEGF $(100ng/100{\mu}l/bottle)$. and when half of the repair was finished, the other 1 drop was drenched and then the repair was continued to complete the anastomosis. Gross and histologic characteristics of arterial wall were assessed after 3 days, 1, 3 and 5 weeks. In the control group, normal saline solution instead of VEGF was dropped with the same method in the anastomosis. Results : The histologic findings of the arterial wall were the vascular remodeling with the infiltration of inflammatory cells at early stages and the tissue fibrosis at lately stages in the anastomotic sites of the control and the VEGF-treated groups. The scanning electron microscopic results were; (1) the anastomotic sites were covered by many irregular cells with long cytoplasmic processes at the early stages. (2) After 1 week, endothelial cells started to cover the anastomotic sites. (3) After 3 weeks, the anastomotic sites were partially covered by endothelial cells in the control group. (4) After 5 weeks, the anastomotic sites were completely covered by endothelial cells in the control and VEGF-treated groups. (5) In the VEGF-treated group, the anastomotic site was completely covered by endothelial cells which directed parallel to longitudinal axis of arteries after 3 weeks. Conclusion : Topical VEGF maintained luminal integrity by decreasing fibrosis and increasing re-endothelialization. These findings suggest that topical VEGF may be a promising new strategy to enhance healing and improve the outcome of vascular anastomosis.