• Journal of Chest Surgery
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• v.34 no.10
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• pp.745-753
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• 2001

capillary leak syndrome and organ dysfunction in infants. Removing harmful cytokines and complement anaphylatoxins after cardiopulmonary bypass may attenuate this response. This study was conducted to see if the modified ultrafiltration and postoperative peritoneal dialysis can reduce plasma inflammatory mediators in pediatric cardiac surgery. Material and Method: 30 infants (age 1.1 to 12.6 months) who underwent closures of ventricular septal defect using cardiopulmonary bypass (CPB) were enrolled in this study. These patients were divided into three groups; 10 patients selected randomly underwent modified ultrafiltration (Group U), 10 with small body weights ($\leq$5 kg) received postoperative peritoneal dialysis (Group P), and 10 patients did not undergo modified ultrafiltration nor receivcd peritoneal dialysis (Group C). Serum samples were obtained before and after CPB, and after peritoneal dialysis. Effluents sample were also obtained after modified ultrafiltration or peritoneal dialysis. C3a and interleukin-6 (IL-6) were measured by radioimmunoassay and enzyme-linked immunosorbent assay respectively. Result: There was no differences in CPB time, aortic cross-clamping title, and lowest temperature during CPB. The effluents of peritoneal dialysis contained significant amount of C3a and IL-6, but there was no definitive decrease of serum concentration of C3a and IL-6. The effluents of modified ultrafiltration had some amount of C3a and negligible IL-6, and there was no decrease of serum concentration of these (actors. Conclusion: The effluents of peritoneal dialysis contained significant amount of proinflammatory cytokine, IL-6 and complement, C3a. However this study failed to elucidate the decrease in serum levels of these factors. The modified ultrafiltration also was not able to reduce the serum levels of C3a or IL-6 in our study as well.

• Journal of Ginseng Research
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• v.45 no.2
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• pp.344-353
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• 2021

Background: Korean Red ginseng extract (KRGE) has beneficial effects on the cardiovascular system by improving endothelial cell function. However, its pharmacological effect on endothelial cell senescence has not been clearly elucidated. Therefore, we examined the effect and molecular mechanism of KRGE on the senescence of human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were grown in normal or KRGE-supplemented medium. Furthermore, they were transfected with heme oxygenase-1 (HO-1) gene or treated with its inhibitor, a NF-κB inhibitor, and a miR-155-5p mimic or inhibitor. Senescence-associated characteristics of endothelial cells were determined by biochemical and immunohistochemical analyses. Results: Treatment of HUVECs with KRGE resulted in delayed onset and progression of senescence-associated characteristics, such as increased lysosomal acidic β-galactosidase and decreased telomerase activity, angiogenic dysfunction, and abnormal cell morphology. KRGE preserved the levels of anti-senescent factors, such as eNOS-derived NO, MnSOD, and cyclins D and A: however, it decreased the levels of senescence-promoting factors, such as ROS, activated NF-κB, endothelial cell inflammation, and p21 expression. The beneficial effects of KRGE were due to the induction of HO-1 and the inhibition of NF-κB-dependent biogenesis of miR-155-5p that led to the downregulation of eNOS. Moreover, treatment with inhibitors of HO-1, NF-κB, and miR-155-5p abolished the anti-senescence effects of KRGE. Conclusion: KRGE delayed or prevented HUVEC senescence through a signaling cascade involving the induction of HO-1, the inhibition of NF-κB-dependent miR-155-5p biogenesis, and the maintenance of the eNOS/NO axis activity, suggesting that it may protect against vascular diseases associated with endothelial senescence.

• Journal of Chest Surgery
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• v.30 no.9
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• pp.869-875
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• 1997

Perimembranous ventri ular septal defects(PMVSDS) are the most common type of ventricular septal defects(VSDs) and consist morphologically of deficiency of the membranous septum and variable portions of the adjacent muscular septum. Repair of VSD has begun via a right ventriculotomy. Even with this exposure, however, it mght lead to ventricular dysfunction. Transatrial exposure of VSDs is luiown to a versatile approach to PMVSDS and even malaligunent defects can be repaired by this method. Although transatrial exposure can be improved by taking down'the atrioventricular valve at the annulus, surgeons have been hesitant to do so because of concern for valvular competence. Therefore, this study was undertaken to clarity the effects of transamlular approach of tricuspid valve (TATV) at operation of PMVSD. During last 5 years, twenty eight cases from 96 patients of PMVSD were closed by TATV and follow up study was done from 3 months to 33 months and results were obtained as follows. 1. Age at operation was fr m 4 months to 38 years and most patients(17, 62%) were above 5 years. 2. Preoperative pulmonary-systemic flow ratio(QPIQS) was ranged from 1 to 2.8 and 22 patients(79%) were less than 2. 3. Peak systolic pulmonary artery pressure was below 30mmHg in 8, 30-50mmHg in 17, above 50mmHg in 3 patients and 25 patients(89%) were less than 50mmHg. 4. Preoperative tricuspid regurgitation(TR) is none in 12, trivial in 6, mild in 3, moderate in 5, severe in 2 patients but postoperative TR was none in 18, trivial in 6, mild in 4 patients, so TR in most patients had decreased or not. 5. Indications for operation were based on the presence of a significant shunt. However, in patients with small shunts, indications for operation were included additional factors, tricuspid valve pouch, RVOT obstruction(right ventricular outflow tract obstruction), subacute bacterial endocarditis and associated anomalies. 6. There were no hospital deaths and residual shunts in postoperative echocardiography. Therefore TATV is especially a good method in PMVSn where patients have trcuspid valve pouch. And it is a safe and effective technique that improves exposure for PMVSD repair and does not adversely affect tricuspid valvular competence.

• Journal of Genetic Medicine
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• v.5 no.2
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• pp.105-110
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• 2008

Purpose: Preecalmpsia is a pregnancy-specific disorder that reflects widespread endothelial dysfunction resulting from increases of adhesion molecule expression. Intercellular adhesion molecule-1 (ICAM-1) is involved in the pathogenetic mechanisms responsible for preeclampsia, and ICAM-1 plasma levels and/or function is genetically influenced. Therefore, we evaluated the distribution of ICAM-1 gene K469E polymorphism in pregnant Korean women with preeclampsia and evaluated the association between this polymorphism and preeclampsia. Methods: The K469E polymorphism was analyzed in peripheral blood samples from 197 preeclamptic pregnancies and 193 normotensive pregnancies by a SNapShot kit and an ABI Prism 3100 Genetic analyzer. Results: Genotypic and allelic frequencies of ICAM-1 gene polymorphism (K469E) did not differ between preeclamptic and normotensive pregnancies. The distributions of the KK, KE, and EE genotypes were 40.6%, 43.7%, and 15.7%, respectively, in preeclamptic pregnancies and 38.9%, 45.1%, and 16.1%, respectively, in normotensive pregnancies. The frequencies of K and E alleles were 0.62 and 0.38, respectively, in preeclamptic pregnancies and 0.61 and 0.39, respectively, in normotensive pregnancies. By multiple logistic regression analysis, there was no increased risk of preeclampsia in subjects with ICAM-1 KE (OR, 1.08; P=0.74) or EE (OR, 1.07; P=0.88) genotypes. Conclusion: This study suggests that the ICAM-1 gene K469E polymorphism does not associate with an increased risk of preeclampsia in pregnant Korean women.

• Tuberculosis and Respiratory Diseases
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• v.57 no.1
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• pp.37-46
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• 2004

Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$ $CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.

• Journal of Life Science
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• v.25 no.8
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• pp.889-895
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• 2015

Endothelial dysfunction is an initial step in atherosclerosis. B vitamins (B6, B12, and folate) are important contributing factors to vascular homeostasis. Deficiencies in these B vitamins induce cardiovascular diseases by altering vascular homeostasis. Folate plays important roles in nitric oxide homeostasis in the endothelium. To determine the dose-dependent effect of dietary folate on atherosclerosis, we studied aortic relaxation and hepatic C-reactive protein (CRP) levels in C57BL/6 mice. In this study, a total of 54 male C57BL/6, 8-wk old mice were split into 2 dietary groups (control and Western style diet). Each diet group was divided into 3 subgroups according to dietary folate dosage (0.2, 2, and 8 mg/kg). After 18 months, the relaxation response seen in aortic rings from mice fed 0.2 or 2 mg folate/kg in both diet groups. However, the aortic relaxation response was not seen and no differences were observed in mice fed 8mg folate/kg in either diet group (p<0.05). Hepatic CRP levels at all folate dosages (0.2, 2, 8 mg folate/kg) were higher in the groups fed a Western style diet than in mice fed a control diet (p=0.035). CRP levels were lower in mice fed 0.2 mg folate/kg than in mice fed 2 or 8 mg folate/kg in both diet groups (p<0.05). These results indicate that in C57BL/6 mice 0.2 mg folate/kg may be enough to prevent atherosclerosis by inducing the relaxation responses of the aorta and by reducing levels of hepatic CRP, regardless of dietary style.

• Tuberculosis and Respiratory Diseases
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• v.62 no.5
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• pp.389-397
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• 2007

Background B-type natriuretic peptide (BNP) has been shown to be strong mortality predictors in a wide variety of cardiovascular syndromes. Little is known about BNP in patients with acute respiratory distress syndrome (ARDS). We studied whether BNP can predict mortality in patients with ARDS. Method Echocardiographic study was done to all patients with ARDS, and we excluded patient with low ejection fraction (less than 50%) or showing any features of diastolic dysfunction. 47 patients were enrolled between December, 2003 and February, 2006. Parameters including BNP were obtained within 24h hours at the time of enrollment. Result Mean BNP concentrations and APACHE II scores differed between the survivors and nonsurvivors (BNP, $219.5{\pm}57.7pg/mL$ vs $492.3{\pm}88.8pg/mL$; p=0.013, APACHE II score, $17.4{\pm}1.6$ vs $23.1{\pm}1.3$, p=0.009, respectively). With the use of the threshold value for BNP of 585 pg/mL, the specificity for the prediction of mortality was 94%. The threshold value for APACHE II of 15.5 showed sensitivity of 87%. 'APACHE II + $11{\times}logBNP$' showed sensitivity 63%, and specificity 82%, using threshold value for 46.14. Conclusion BNP concentrations and APCHE II scores were more elevated in nonsurvivors than survivors in patients with ARDS who have normal ejection fraction. BNP can predict mortality. Further study should be done.

• Journal of Chest Surgery
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• v.36 no.3
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• pp.142-149
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• 2003

To know the feasibility of the coronary artery bypass graft (CABG) for multivessel coronary artery disease with purely bilateral internal thoracic arteries (ITAs), we analyzed the short-term clinical results and the coronary angiography of the patients. Material and Method: From March 2001 to June 2002, four hundred and five patients underwent CABG. Purely bilateral ITAs were used in 159 patients (39.3%). We analyzed these patients retrospectively The mean age of these patients was $61.2{\pm}8.5$ (range: 30 ~80) years and there were 123 male patients. The preoperative risk factors were as follows: diabetes in 54 patients (34.0%), history of acute myocardiac infarction within 4 weeks in 29 (18.2%), and emergency operation in 6 (3.8%). Off-pump CABG was carried out in 128 patients (80.5%). Associated procedures were mitral valvuloplasty (5), aortic valve replacement (3), Dor procedure (1), and so on. Result: The mean number of distal anastomoses was $3.1{\pm}0.9$ (range: 2~6), the mean duration of hospital stay was $8.4{\pm}4.5$ days. There was one (0.6%) operative death. Except for one early death, no other patients suffered from low cardiac output. The other postoperative complications were occurred as follows: reoperation due to bleeding in 3 patients, perioperative myocardiac infarction in 1, transient cardiac arrest in 2, transient cognitive dysfunction in 7, and transient ischemic attack in 1, and deep sternal wound infection in 1 patient. Recently, early postoperative angiography was performed in 19 patients who had triple vessel disease. The total number of distal anastomosis was 78 (mean $4.1{\pm}0.8$/patient). All distal anastomosis sites were patent, but competition flow was observed at the bypass sites where the native coronary artery stenosis was not significant. Conclusion: The CABG with purely bilateral ITAs for triple vessel disease was performed safely. The early patency rate was relatively good in small number of patients. However the long-term patency rate and the functional study to evaluate the sites where competition flow was observed should be followed.

• Clinical and Experimental Pediatrics
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• v.51 no.6
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• pp.597-603
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• 2008

Purpose : Obesity is associated with insulin resistance. Insulin resistance and the presence of pro-inflammatory mediators are thought to cause a state of vascular endothelial dysfunction, an abnormal lipid profile, hypertension, and vascular inflammation. These chronic inflammatory responses, which are characterized by abnormal cytokine production, lead to activation of a pro-inflammatory signaling pathway. Leptin is an important mediator of inflammatory processes and immune-mediated diseases. The purpose of this study was to investigate the relationship between leptin and various cytokines associated with obesity in adolescents. Methods : Sixty-six obese adolescents (between 16-17 years of age, obesity index >130%) and 26 normal controls were included in this study. Obesity index and body mass index (BMI) were calculated. Serum lipid profile, AST and ALT were tested after 10 hours of fasting. Tumor necrosis factor alpha (TNF-${\alpha}$) and Interleukin-6 (IL-6) levels were measured by ELISA. Insulin, adiponectin, and leptin levels were estimated by radioimmunoassay. Results : Leptin was significantly higher in the obese adolescents compared to the control adolescents ($12.0{\pm}6.8ng/mL$ vs $6.3{\pm}1.0ng/mL$). TNF-${\alpha}$, IL-6, and insulin were significantly higher in the obese adolescents. Adiponectin was significantly lower in the obese group than the control group ($3.3{\pm}1.9{\mu}g/mL$ vs $5.0{\pm}1.4{\mu}g/mL$). Leptin had positive correlations with obesity index, BMI, and IL-6. Conclusion : In obese adolescents, leptin, TNF-${\alpha}$, IL-6, and insulin might be important mediators of obesity. Further clinical research is necessary to ascertain leptin as a predictor of cardiovascular diseases and to develop a guideline for clinical intervention.

• Journal of radiological science and technology
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• v.36 no.3
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• pp.209-217
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• 2013

Adiponectin (AdipoN), brain-derived nerotrophic factor (BDNF) and leptin (LeP) are mainly secreted from adipose tissue and are known to be involved in regulation of the development of obese. However, there are not many studies on the association between abdominal fat and neuropeptides such as AdipoN, BDNF and LeP. The aim of this study was undertaken to investigate the association between abdominal fat thickness, neuropeptides and cardiovascular disease (CVD) risk factors. The participants in the study were 138 male employees without CVD. This study was approved by the Institutional Review Board of Occupational Safety and Health Research Institute. Written informed consent for the participants in this study was obtained from all individuals. We obtained subcutaneous fat thickness (SFT) and visceral fat thickness (VFT) by using ultrasonography and neuropeptides levels were measured with ELISA kit according to the method suggested by kit manufacturer. The mean SFT and VFT were $1.58{\pm}0.51$ and $4.52{\pm}1.44$ cm. The mean concentrations of AdipoN, BDNF and LeP were $3.14{\pm}3.52$ ng/ml, $24.11{\pm}8.52$ pg/ml and $4.27{\pm}2.38$ ng/ml, respectively. VFT were positively correlated with total cholesterol (r=0.217, p<0.05), LDL-cholesterol (r=0.271, p<0.01), triglyceride (r=0.233, p<0.05) and insulin (r=0.338, p<0.01), but was inversely correlated with HDL-cholesterol (r=-420, p<0.01). AdipoN levels were positively correlated with HDL-cholesterol (r=0.220, p<0.05) and were inversely correlated with total cholesterol (r=-0.196, p<0.05), LDL-cholesterol (r=-0.190, p<0.05), triglyceride (r=-0.199, p<0.05), SFT (r=-0.195, p<0.05) and VFT (r=-0.412, p<0.01). However, LeP levels showed a reverse trend to AdipoN. AdipoN level was significantly higher in non-obese participants (BMI<25 kg/m), but LeP concentration was significantly higher in obese participants (BMI>25 kg/m) than in non-obese. On multiple logistic regression analysis, obese were significantly associated with AdipoN (odds ratio=0.784) and LeP (odds ratio=1.494). These results suggested that AdipoN and LeP concentrations are affected abdominal fat and that dysfunction and/or declination in the production and secretion of neuropeptides might induced ultimately obese and CVD.