• 대한한의학원전학회지
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• 제24권5호
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• pp.131-145
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• 2011

I had come at the conclusion of the development history of Disease Bi(痞病) reflected in Yi Cheon (李梴)'s work, "Euhakibmun(醫學入門)" in the respects of the causes, mechanism, symptoms, differential diagnosis and treatments. The causes of Disease Bi(痞病) mentioned at "Euhakibmun(醫學入門)" followed the Ju Dan-Gyeo(朱丹溪)'s theory. The mechanism of it went after the viewpoints of "Nae-Gyeong(內經)", Jang Jung-Gyeong(張仲景), Yi Dong-Won(李東垣) and Wang Ho-Go(王好古). The symptoms of it kept the Ju Dan-Gyeo(朱丹溪)'s theory. Yi Cheon distinguished Disease Bi(痞病) from Gyeol-Hyung(結胸) according to Jang Jung-Gyeong's theory. He knew it from abdominal dropsy(脹滿) according to Ju Dan-Gyeo's theory. He also divided it into two respects of deficiency(虛) and excessive(實) from Yi Dong-Won's viewpoint. Jang Jung-Gyeong first suggested that treatments of it could be selected according to the difference of deficiency, excessive(實), cold(寒), hot(熱), sputum(痰), fluid(飮), blood(血) and food(食). Yi Dong-Won insisted many doctors could make a mistake because they only used herbs for Gi(氣藥) instead of herbs for blood(血藥) together. Wang Ho-Go(王好古) maintained his opinion that treatments of both digestion(消導) and assistance(補益), remedies of bitter and hot herbs can recover patients from Disease Bi(痞病). Yi Cheon followed their theories properly.

• Biomolecules & Therapeutics
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• 제24권4호
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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.