• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.7
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• pp.140-148
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• 2017

The purpose of this study was to examine the effects of acute aerobic exercise at different intensities on the blood pressure, blood lipids and fibrinolytic markers in pre-hypertension college-aged males. Six subjects performed an acute running exercise at three different intensities(low intensity(LI): 50-60% heart rate reserve(HRR), moderate intensity(MI): 60-70%HRR, and high intensity(HI): 70-80%HRR). The blood pressure(systolic(SBP) and diastolic blood pressure(DBP), blood lipids(total cholesterol(TC) and high-density lipoprotein cholesterol(HDL-C)) and fibrinolytic markers(tissue plasminogen activator(tPA) and plasminogen activator inhibitor-1(PAI-1)) were determined before(PRE), immediately after(POST) and 60minutes after the exercise(60 POST). Results: the SBP in the LI group was significantly increased at POST(p=0.013). The ES levels for the SBP in the MI and HI groups were reduced (-1.33 and -1.23, respectively), though the differences were not significant. The HDL in the MI(p=0.003) and HI(p=0.002) groups were significantly increased at 60 POST. Also, the tPA in the MI(p=0.021) and HI(p=0.042) groups were significantly increased at POST.

• Journal of Life Science
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• v.19 no.2
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• pp.289-298
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• 2009

Effects of Nattokinase fibrinol (NKF), defined as a fibrinolytic product, on fibrinolytic and atherogenetic markers were studied for healthy adults (20-31 years old), who is smoking more than 20 cigarettes per day. Subjects were divided into 29 for NKF group and 10 for placebo group in a short term study. They were given 2 tablets of NKF (4,000 unit) or placebo tablet and thereafter blood samples were collected at 0, 2, 4 hr prerid. For a 4-week long term study, 15 subjects for NFK group and 10 subjects for placebo group were supplemented one tablet of each NKF (2,000 unit) and placebo per day, respectively. Blood samples were collected at 0, 1, 2, 4 weeks later. The short-term experimental trial showed that NKF remarkably increased fibrinolytic activity at 2hr after consumption, which was maintained up to 4 hr, relative to that of placebo, while NKF reduced the euglobulin clot lysis time (ECLT) and retarded the activated partial thromboplastin time (aPTT), as compared to placebo group. NKF supplementation for 4 weeks elevated fibrinolytic activity, shortened ECLT and retarded aPTT. Furthermore, NKF supplementation increased anti-atherogenic index by decreasing triglyceride (TG) and elevating high-density lipiprotein (HDL)-cholesterol. These results indicate that NKF supplementation for short term or long term might have beneficial effects on preventing and treating cardiovascular disease by increasing fibrinolytic activity and improving atherogenic markers such as hyperlipidemia.

• Clinical and Experimental Pediatrics
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• v.50 no.2
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• pp.205-208
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• 2007

Purpose : Vascular endothelial cell damage and alteration of a fibrinolytic system was suggested to play a role in the development of coronary artery abnormalities in Kawasaki disease (KD). D-dimer is one of the markers of endothelial damage and fibrinolysis. We evaluated the clinical usefulness of D-dimer to differentiate KD from other febrile diseases and predict coronary artery abnormalities in KD. Methods : Sixty eight patients diagnosed as KD and twenty eight patients presented with acute febrile illnesses other than KD from September 2005 to July 2006 were included. Blood levels of D-dimer and various inflammatory markers were measured before treatment and the clinical course of KD was followed. Serial echocardiography was performed at the onset of disease and thereafter at a monthly interval for at least 2 months. Results : KD patients showed a higher D-dimer level than febrile controls, but the difference was not significant ($1.21{\pm}0.77{\mu}g/mL$ vs $0.92{\pm}0.71{\mu}g/mL$, P=0.083). Neither was the difference between KD patients who had coronary artery abnormalities and those who had not ($1.49{\pm}0.98{\mu}g/mL$ vs $1.15{\pm}0.71{\mu}g/mL$, P=0.169). D-dimer was significantly correlated with other inflammatory markers, such as C-reactive protein and erythrocyte sedimentation rate in both KD patients and febrile controls. Conclusion : D-dimer was not specific for KD. But it may be useful as an inflammatory marker to assess the severity of KD.

• Tuberculosis and Respiratory Diseases
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• v.60 no.6
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• pp.625-630
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• 2006

Background: Pulmonary hypertension in COPD patients is the result of a direct effect of tobacco smoke on the intrapulmonary vessels with the abnormal production of the mediators that control vasoconstriction, vasodilatation, and vascular cell proliferation, which ultimately lead to aberrant vascular remodeling and physiology. COPD patients are prone to the developmint of an acute and chronic thromboembolism with an elevation of the plasma procoagulant and fibrinolytic markers However, the roles of the coagulation and fibrinolysis system on the right ventricular dysfunction in COPD patients are not well defined. We examined the alteration of the coagulation and fibrinolysis system in COPD patients according to the right ventricular function measured using cardiac multidetector computed tomography (MDCT). Methods: The right ventricular ejection fraction (RVEF) was measured using cardiac MDCT in 26 patients who were diagnosed with COPD according to the definition of the GOLD guideline. The plasma level of thrombin antithrombin (TAT) and plasminogen activator inhibitor (PAI)-1 were measured using an enzyme linked immunoassay. Results: The plasma TAT was markedly elevated in COPD patients ($10.5{\pm}19.8{\mu}g/L$) compared with those of the control ($3.4{\pm}2.5{\mu}g/L$) (p<0.01). However, the plasma PAI-1 in COPD patients ($29.6{\pm}20.7ng/mL$) was similar to that in the controls. The plasma TAT showed a significant inverse relationship with the RVEF measured by the cardiac MDCT in COPD patients (r=-0.645, p<0.01). However, the plasma PAI-1 did not show a relationship with the RVEF (r=0.022, p=0.92). Conclusion: These results suggest that the coagulation system in COPD patients is markedly activated, and that the plasma level of TAT might be a marker of a right ventricular dysfunction in COPD patients.