• Clinical and Experimental Pediatrics
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• v.57 no.1
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• pp.19-25
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• 2014

Recently, surgical outcomes of repair of tetralogy of Fallot (TOF) have improved. For patients with TOF older than 3 months, primary repair has been advocated regardless of symptoms. However, a surgical approach to symptomatic TOF in neonates or very young infants remains elusive. Traditionally, there have been two surgical options for these patients: primary repair versus an initial aortopulmonary shunt followed by repair. Early primary repair provides several advantages, including avoidance of shunt-related complications, early relief of hypoxia, promotion of normal lung development, avoidance of ventricular hypertrophy and fibrosis, and psychological comfort to the family. Because of advances in cardiopulmonary bypass techniques and accumulated experience in neonatal cardiac surgery, primary repair in neonates with TOF has been performed with excellent early outcomes (early mortality<5%), which may be superior to the outcomes of aortopulmonary shunting. A remaining question regarding surgical options is whether shunts can preserve the pulmonary valve annulus for TOF neonates with pulmonary stenosis. Symptomatic neonates and older infants have different anatomies of right ventricular outflow tract (RVOT) obstructions, which in neonates are nearly always caused by a hypoplastic pulmonary valve annulus instead of infundibular obstruction. Therefore, a shunt is less likely to preserve the pulmonary valve annulus than is primary repair. Primary repair of TOF can be performed safely in most symptomatic neonates. Patients who have had primary repair should be closely followed up to evaluate the RVOT pathology and right ventricular function.

• Korean Journal of Veterinary Pathology
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• v.1 no.2
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• pp.157-160
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• 1997

Two 2 and 7 months-old holstin and one 3 months-old native Korean calf suffering from respiratory illness were submitted to the National Veterinary Research Institute for euthanasia and pathologic examination. At necropsy diffuse lobar pneumonia was present in apical cardiac and diaphragmatic lobes in all calves. Microscopically acute multifocal bronchiolitis and interstitial syncytial cell formation were frequently observed. in addition occlusion of bronchiolar lumen due to cellular proliferation and fibrosis accompanied by interlobular septal emphysema were also present. Immunohistochemically bovine respiratory syncytial virus antigen were positively identified in lung lesions including bronchial and bronchiolar epithelium alveolar macrophages and lymphocytes.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.5 no.2
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• pp.192-198
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• 2002

Alagille syndrome is characterized by paucity of interlobular bile ducts, chronic cholestasis, characteristic facial abnormalities, cardiovascular abnormalities, posterior embryotoxon, vertebral arch defects, skeletal abnormalities, and glomerular renal involvement. We experienced a case of Alagille syndrome in a 10 month-old male presenting with jaundice. He had chronic cholestasis, characteristic face, cardiovascular abnormalities (aortic stenosis, dextrocardia, double chamber of left ventricle), and situs inversus. Histological examination of liver biopsy specimen revealed paucity of interlobular bile ducts with septal fibrosis, cirrhotic transformation and severe cholestasis. He underwent liver transplantation, but died of cardiopulmonary arrest associated with cardiac anomaly.

• Molecules and Cells
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• v.45 no.3
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• pp.122-133
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• 2022

The aim of this study was to investigating whether lncRNA H19 promotes myocardial fibrosis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-β axis. Patients with atrial fibrillation (AF) and healthy volunteers were included in the study, and their biochemical parameters were collected. In addition, pcDNA3.1-H19, si-H19, and miR-29a/b-3p mimic/inhibitor were transfected into cardiac fibroblasts (CFs), and proliferation of CFs was detected by MTT assay. Expression of H19 and miR-29a/b-3p were detected using real-time quantitative polymerase chain reaction, and expression of α-smooth muscle actin (α-SMA), collagen I, collagen II, matrix metalloproteinase-2 (MMP-2), and elastin were measured by western blot analysis. The dual luciferase reporter gene assay was carried out to detect the sponging relationship between H19 and miR-29a/b-3p in CFs. Compared with healthy volunteers, the level of plasma H19 was significantly elevated in patients with AF, while miR-29a-3p and miR-29b-3p were markedly depressed (P < 0.05). Serum expression of lncRNA H19 was negatively correlated with the expression of miR-29a-3p and miR-29b-3p among patients with AF (r_s = -0.337, r_s = -0.236). Moreover, up-regulation of H19 expression and down-regulation of miR-29a/b-3p expression facilitated proliferation and synthesis of extracellular matrix (ECM)-related proteins. SB431542 and si-VEGFA are able to reverse the promotion of miR-29a/b-3p on proliferation of CFs and ECM-related protein synthesis. The findings of the present study suggest that H19 promoted CF proliferation and collagen synthesis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-β axis, and provide support for a potential new direction for the treatment of AF.

• Journal of Chest Surgery
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• v.19 no.2
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• pp.225-231
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• 1986

Pericardial adhesions following open heart surgery pose a special problems, increasing the risk of cardiac reoperation because of the danger of damaging the heart, coronary artery and veins, or grafts and also the fibrous tissue may obliterate the pericardial space and eventually constrict the heart. This study was undertaken to evaluate the effect of intrapericardial urokinase and dextran 40 on the formation of pericardial adhesions in an animal model. latrogenic traumas on the pericardium were surgically induced in 30 rabbits, simulating injuries possible during actual surgery. In all rabbits, blood [1 ml] was obtained from an ear vessel and injected into the pericardium. Control group of ten rabbits did not receive any further medication, urokinase group of ten received 15, 000-20, 000 IU of urokinase, and remained ten received 1 ml of 10% dextran 40. All rabbits were sacrificed at 4 weeks. At autopsy, the development of adhesions were graded as none [Grade I], minimal [Grade II], moderate [Grade III], and severe [Grade IV]. Histological studies of the parietal pericardium and epicardium were performed. The results were as follows: 1. Group 1[Control group] showed minimal adhesion in 40%, moderate in 50%, and severe in 10% of the group. Sharp dissections were necessary in 60% of adhesions. 2. Group II [Dextran group] showed no adhesions in 20%, minimal in 60%, and moderate in 20% of the group. 3. Group III [Urokinase group] showed no adhesions in 40%, minimal in 40%, and moderate in 20% of the group. Considering in this group, the adhesion activity was significantly suppressed [60% adhesions] compared to the control group [100% adhesions] [P < 0.05]. 4. Histological findings revealed mild serosal fibrosis in none adherent group, loose fibrous connections between two layers of pericardium in minimal adhesion group, tight fibrous connections in moderate adhesion group, and marked fibrous thickening and close attachment of two surfaces were noted in severe adhesion group. These data have revealed the decreased incidence of pericardial adhesions with urokinase and dextran 40.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.447-456
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• 2018

Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) ($576{\mu}g/kg/day$) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor ($AT_2R$) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as $TNF-{\alpha}$, MCP-1, $IL-1{\beta}$, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via $AT_2R$.

• Journal of Veterinary Science
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• v.22 no.5
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• pp.64.1-64.12
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• 2021

Background: Pituitary pars intermedia dysfunction (PPID), a neurodegenerative disease leading to reduced dopamine production, is a common disease in aged horses. The treatment is based on administration of the dopamine agonist pergolide. This drug has been related to valvular fibrosis in humans, but the cardiovascular effect of this drug has not yet been investigated in horses. Objectives: To determine whether pergolide induces valvular disease in horses or affects the cardiac function. Methods: Standard, tissue Doppler (TDE) and two-dimensional speckle tracking (STE) echocardiography were performed in horses with diagnosed PPID based on adrenocorticotropic hormone dosage. Measurements taken in horses treated with pergolide were compared with those from untreated horses with nonparametric t-tests. Furthermore, measurements from follow-up examinations performed at least three months after the initial exam were compared with a Wilcoxon signed rank test for repeated measurements in each group. Results: Twenty-three horses were included. None of the 12 horses under treatment developed valvular regurgitation. Furthermore, no differences in the measurements of the left ventricular systolic or diastolic function could be seen between the group of horses with treatment and those without treatment. Measurements taken in the follow-up exam did not differ compared to those taken in the initial exam in both groups. Conclusions: No changes of the left ventricular function assessed by TDE and STE could be shown in a small population of horses with confirmed PPID. Treatment with pergolide did not affect the ventricular function nor induce valvular disease.

• Herbal Formula Science
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• v.30 no.3
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• pp.123-135
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• 2022

Oryeongsan (ORS), a formula composed of five herbal medicines, has long been used to treat impairments of the regulation of body fluid homeostasis. The purpose of this study was to determine the antihypertensive and renal protective effects of ORS in rats with hypertension. Spontaneously hypertensive rats (SHR) were divided into two groups with similar mean baseline systolic blood pressure (SBP). Then, 1 mL/kg of vehicle (distilled water) or 1.5, 3 g/kg of ORS extract were administered orally once a day for 4 weeks. SBP and diastolic blood pressure (DBP) were measured at weeks 1, 2, 3 and 4. At the end of the experiment, blood was collected, and heart were removed for histology. By the 2 weeks after initiation of treatment, the ORS treated group had significantly lower SBP than SHR rats. The ORS treatment significantly improved blood pressure and echocardiogram parameters compared to hypertensive rats. Additionally, the left ventricular (LV) remodeling and LV dysfunction were significantly improved in ORS treated group hypertensive rats. Furthermore, an increase in fibrotic area has been observed in SHR rats compared with Wistar-Kyoto rats (WKY). Furthermore, administration of ORS significantly attenuated cardiac fibrosis in hypertensive rats. Therefore, these findings suggest that ORS has a protective effect on heart failure by alleviating hypertensive heart disease and cardiovascular dysfunction in SHR.

• Journal of Ginseng Research
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• v.44 no.4
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• pp.664-671
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• 2020

Background: Ginsenoside compound-Mc1 (Mc1) is a member of the deglycosylated ginsenosides obtained from ginseng extract. Although several ginsenosides have a cardioprotective effect, this has not been demonstrated in ginsenoside Mc1. Methods: We treated H9c2 cells with hydrogen peroxide (H₂O₂) and ginsenoside Mc1 to evaluate the antioxidant effects of Mc1. The levels of antioxidant molecules, catalase, and superoxide dismutase 2 (SOD2) were measured, and cell viability was determined using the Bcl2-associated X protein (Bax):B-cell lymphoma-extra large ratio, a cytotoxicity assay, and flow cytometry. We generated mice with high-fat diet (HFD)-induced obesity using ginsenoside Mc1 and assessed their heart tissues to evaluate the antioxidant effect and the fibrosis-reducing capability of ginsenoside Mc1. Results: Ginsenoside Mc1 significantly increased the level of phosphorylated AMP-activated protein kinase (AMPK) in the H9c2 cells. The expression levels of catalase and SOD2 increased significantly after treatment with ginsenoside Mc1, resulting in a decrease in the production of H₂O₂-mediated reactive oxygen species. Treatment with ginsenoside Mc1 also significantly reduced the H₂O₂-mediated elevation of the Bax:Bcl2 ratio and the number of DNA-damaged cells, which was significantly attenuated by treatment with an AMPK inhibitor. Consistent with the in vitro data, ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax:B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice, resulting in reduced collagen deposition. Conclusion: Ginsenoside Mc1 decreases oxidative stress and increases cell viability in H9c2 cells and the heart tissue isolated from HFD-fed mice via an AMPK-dependent mechanism, suggesting its potential as a novel therapeutic agent for oxidative stress-related cardiac diseases.

• Journal of Chest Surgery
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• v.31 no.4
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• pp.346-352
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• 1998

Rheumatic valvulitis produces at least three distinct pathologic changes, the degree varying widely among the patients: fusion of the valve leaflets at the commissures; fusion and shortening of chordae tendinae: and fibrosis of the leaflets with subsequent stiffening, contraction and calcification. The most extensive changes usually are seen in patients with recurrent attacks of rheumatic fever. We studied on outcome of the surgical treatments of rheumatic valvular diseases that have been experienced for 12 years since 1982 at Pusan National University Hospital. The diagnoses were made by rheumatic fever history, echocardiographic findings, gross operative findings and microscopic findings. Total 502 patients were performed surgery for valvular heart diseases and 440 patients of rheumatic origin have bene analysed. There were more female than male patients as 1.3:1, and the mean age was 37.8 years old. 96.3% of them affected to the mitral valve, 19.8% to aortic valve, 16.3% affected to the tricuspid valve. Most of them underwent valve replacement, and valve repair was done in 3.9% of patients. There were 36 hospital deaths(8.2%) mainly from low cardiac output syndrome, and 15 late deaths equally due to embolism and hemorrhage. Follow up was 90.1% completed(2890 patient- year). Linealized rates of late complication events are follows : thromboembolism 1.3% per patient year; anticoagulant related hemorrhage 0.8% per patient year. Overall actuarial survival including hospital mortality was 92.7＋/-2.9% in 1 year, 88.0＋/-4.5% in 5 year, 82.3＋/-7.7% in 10 year. We conclude that the rheumatic disease is still the most frequent and the most important cause of heart valve disease. So more intensive study is needed in spite of the abrupt decreasing rate of rheumatic fever in U.S.A. and other industrial country.