• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.363-370
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• 2016

Cardiovascular disease is the most common cause of death in diabetic patients. Hyperglycemia is the primary characteristic of diabetes and is associated with many complications. The role of hyperglycemia in the dysfunction of human cardiac progenitor cells that can regenerate damaged cardiac tissue has been investigated, but the exact mechanism underlying this association is not clear. Thus, we examined whether hyperglycemia could regulate mitochondrial dynamics and lead to cardiac progenitor cell dysfunction, and whether blocking glucose uptake could rescue this dysfunction. High glucose in cardiac progenitor cells results in reduced cell viability and decreased expression of cell cycle-related molecules, including CDK2 and cyclin E. A tube formation assay revealed that hyperglycemia led to a significant decrease in the tube-forming ability of cardiac progenitor cells. Fluorescent labeling of cardiac progenitor cell mitochondria revealed that hyperglycemia alters mitochondrial dynamics and increases expression of fission-related proteins, including Fis1 and Drp1. Moreover, we showed that specific blockage of GLUT1 improved cell viability, tube formation, and regulation of mitochondrial dynamics in cardiac progenitor cells. To our knowledge, this study is the first to demonstrate that high glucose leads to cardiac progenitor cell dysfunction through an increase in mitochondrial fission, and that a GLUT1 blocker can rescue cardiac progenitor cell dysfunction and downregulation of mitochondrial fission. Combined therapy with cardiac progenitor cells and a GLUT1 blocker may provide a novel strategy for cardiac progenitor cell therapy in cardiovascular disease patients with diabetes.

• Journal of Biomedical Engineering Research
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• v.30 no.5
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• pp.355-361
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• 2009

Mitochondria play a key role in maintaining life by producing ATP and heat. Recent researches have demonstrated that degenerative diseases such as heart failure, obesity/diabetes, cardiovascular disease, and psychiatric diseases are accompanied by mitochondria dysfunction. In this sense, mitochondria medicine considers the significance of mitochondria in human pathology and tries to explain degenerative diseases as a fatal consequence of mitochondria dysfunction. Here, I introduce the fundamentals of mitochondria physiology and present examples showing the relationship between mitochondria dysfunction and chronic complex diseases. Although mitochondria medicine uses a molecular biological approach predominantly, a biomedical engineering approach might play a critical role in unveiling the complexity of mitochondria medicine and in its application to the diagnosis and treatment of chronic diseases. Thus, I also briefly review the prospects of research using biomedical engineering methods.

• Journal of Chest Surgery
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• v.49 no.3
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• pp.203-206
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• 2016

Patients with venoarterial extracorporeal membrane oxygenation (ECMO) frequently suffer from pulmonary edema due to left ventricular dysfunction that accompanies left heart dilatation, which is caused by left atrial hypertension. The problem can be resolved by left atrium (LA) decompression. We performed a successful percutaneous LA decompression with an atrial septostomy and placement of an LA venting cannula in a 38-month-old child treated with venoarterial ECMO for acute myocarditis.

• Clinical and Experimental Pediatrics
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• v.46 no.6
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• pp.585-590
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• 2003

Purpose : This study is designed to determine the prevalence of cardiovascular autonomic neuropathy and its relationship to risk factors in adolescents with diabetes mellitus(DM). Methods : Ninety-two diabetic patients(80 with type 1 DM and 12 with type 2 DM), ranging from eight to 26 years of age, were studied for cardiovascular autonomic function, and the relationship to age, duration of diabetes, glycated hemoglobin(HbA1c), urinary albumin excretion, and the presence of diabetic retinopathy and abnormal nerve conduction velocities(NCV) were analysed. Autonomic function was assessed by measuring heart rate variation during valsalva manoeuvre, deep breathing and standing from a lying position(30 : 15 ratio), and postural hypotension. Results : Among patients with type 1 DM, 22.5% had early, 8.7% had definite, and 1.3% had severe autonomic dysfunction, and among patients with type 2 DM, 16.7% had early, 8.3% had definite, and 8.3% had severe autonomic dysfunction. On logistic regression analysis including both type 1 and type 2 diabetic patients, the age of the patient(OR=1.133(1.003-1.279), P<0.05) and duration of diabetes(OR=1.148(1.009-1.307), P<0.05) significantly predicted cardiovascular autonomic dysfunction while HbA1c, blood pressure, urinary albumin excretion, and presence of diabetic retinopathy and abnormal NCV did not. The valsalva ratio was borderline or abnormal in 31.5% of patients, the heart rate variation on deep breathing in 41.3%, the 30 : 15 ratio in 14.1%, and postural hypotension in 9.8% of patients. The valsalva ratio and the heart rate variation on deep breathing significantly predicted cardiovascular autonomic dysfunction, but the 30 : 15 ratio and postural hypotension did not. Conclusion : Cardiovascular autonomic dysfunction was found in 32.6% of diabetic patients and 10.8 % of patients had definite or severe involvement. The risk of cardiovascular autonomic dysfunction increased with the patient's age and the duration of DM. This study suggests that the valsalva ratio and the heart rate variation on deep breathing are the most useful tests in evaluating the cardiovascular autonomic function in children and adolescents with DM.

• Journal of Chest Surgery
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• v.21 no.1
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• pp.164-168
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• 1988

Between November, 1984, and May, 1986, 93 patients underwent combined valvular and coronary artery operation. They were 70 male and 23 female, the age ranging from 29 to 82. From this population 89 patients underwent single valve replacement and 4 patients underwent double valve replacement. Patients with mitral valve disease were in the majority present in the age group between 50 till 70, where as in the group after 60 years, patients with aortic valve disease were dominant. The main indication for aortic valve replacement was aortic stenosis and the indication for mitral valve replacement was equal between mitral stenosis and mitral incompetence, the later was due to papillary dysfunction after myocardial infarction. Dyspnea was a very frequent symptom and it was found in nearly all patients. 28 patients had a previous myocardial infarction and severe left ventricular dysfunction. The grafts were placed prior to valve replacement and periods of myocardial ischemia were kept at a minimum by maintaining coronary perfusion throughout the operation. It is our opinion that simultaneous valve replacement and myocardial revascularization does not increase the risk of cardiac valve replacement substantially.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.129-139
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• 1997

The data collected to date indicate that sleep-related breathing disorders, including sleep-disordered breathing(sleep apnea) and underlying respiratory system diseases, are one of the important risk factors for cardiovascular dysfunction. Sleep-disordered breathing(sleep apnea) is now recognized as one of the leading causes of systemic hypertension, cardiac arrhythmias, coronary heart disease, pulmonary hypertension, right heart failure, and stroke. Sleep may exert a profound effect on breathing in patients with underlying respiratory system disease including bronchopumonary diseases, chest wall abnormalities, central alveolar hypoventilation syndromes or respiratory neuromuscular disorders. Chronic hypoxia and hypercapnia in these patients may accelerate the development of long term cardiovascular complications such as cardiac arrhythmias, pulmonary hypertension, and right heart failure(cor pulmonale). Several recent studies reported that sleep-related breathing disorders are associated with long-term cardiovascular morbidity and mortality. Careful assessment of respiratory and cardiovascular function in these patients is critical. Aggressive and highly effective treatment of sleep-related breathing disorders using tracheostomy, mechanical ventilation, nasal continuous positive airway pressure therapy(nCPAP), intercurrent oxygen therapy or other interventions can reduce the prevalence of cardiovascular dysfunction and the long-term mortality.

• Journal of Chest Surgery
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• v.46 no.3
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• pp.185-191
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• 2013

Background: Cardiopulmonary bypass (CPB) induces variable systemic inflammatory reactions associated with major organ dysfunction via polymorphonuclear neutrophils (PMNs). Ulinastatin, a urinary trypsin inhibitor, inhibits PMN activity and reduces systemic inflammatory responses. The aim of this study is to evaluate the effect of ulinastatin on postoperative blood loss and laboratory changes in patients undergoing open heart surgery. Materials and Methods: Between January 2008 and February 2009, 110 patients who underwent atrioventricular valve surgery through right thoracotomy were divided into two groups. Patients received either 5,000 U/kg ulinastatin (ulinastatin group, n=41) or the equivalent volume of normal saline (control group, n=69) before aortic cross clamping. The primary end points were early coagulation profile changes, postoperative blood loss, transfusion requirements, and duration of intubation and intensive care unit stay. Results: There were no statistically significant differences between the two groups in early coagulation profile, other perioperative laboratory data, and postoperative blood loss with transfusion requirements. Conclusion: Administration of ulinastatin during operation did not improve the early coagulation profile, postoperative blood loss, or transfusion requirements of patients undergoing open heart surgery. In addition, no significant effect of ulinastatin was observed in major organs dysfunction, systemic inflammatory reactions, or other postoperative profiles.

• Asian Journal of Atmospheric Environment
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• v.1 no.1
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• pp.28-35
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• 2007

Accumulated epidemiological and animal studies have suggested that prolonged exposure to ambient particulate matter (PM) is associated with an increased risk of cardiovascular disease and pulmonary dysfunction. While diesel exhaust particles (DEP) contain large variety of compounds, polycyclic aromatic hydrocarbons (PAHs) are a dominant component contaminated in DEP. This article reviews effects of two PAH quinones, 9,10-phenanthraquinone (9,10-PQ) and l,2-naphthoquinone (l,2-NQ), on vascular and respiratory systems.

• Journal of Chest Surgery
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• v.18 no.4
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• pp.746-752
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• 1985

A retrospective clinical observation was made of 40 patients with postoperative cerebral dysfunction among 2634 patients who underwent open-heart operations in Severance Hospital. Yonsei University between 1962, the year the first successful open heart operation was done, and June 1985. Suspected causes of brain damage were reviewed. Brain CT findings were evaluated in 24 patients. There were 15 cerebral infarcts, 4 intracerebral bleedings, 3 ischemic brain damages, 1 infarction with intracerebral hemorrhage and 1 diffuse cortical atrophy from unknown cause. The most frequent site of cerebral infarction was the middle cerebral artery area with no predilection on the right of left.

• Clinical and Experimental Pediatrics
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• v.57 no.11
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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.