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Pediatric Surgery

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    In our division, three faculties performed several clinical and experimental research programs. One of them is to determine the differentiation and development of interstitial cells of Cajal in the human gastrointestinal tract to aid interpretation of pathological specimens. Although interstitial cells of Cajal have been recognized for over a century their roles as pacemakers and mediators of neurotransmission in the gut have only been recently. The discoveries that interstitial cells of Cajal express the tyrosine kinase receptor c-kit and that disruption of the c-kit signalling pathway inhibits differentiation of subpopulation of interstitial cells of Cajal, has allowed rapid progress to be made.

    We also interest in the pathogenesis of atherosclerosis and arterial restenosis. The pathogenesis of atherosclerosis and arterial restenosis is thought to be a complex process that is augmented by many risk factors. There are several lines of evidence from clinical studies and basic research suggest that chronic infections and vascular inflammation are both important for the initiation and progression of atherosclerotic lesions. To evaluate this concept, extended studies using the rat model indicate that rat cytomegalovirus accelerates the development of vascular disease following cardiac allograft transplantation. Another substantial experimental and clinical evidence suggests that the activation of renin-angiotensin system contributes to macrovascular disease in part by promoting atherogenesis and vascular smooth muscle cell remodeling. The angiotensin receptor exerts a variety of its signalling and cellular actions though its effects on protein phosphorylation. A two-dimensional gel electrophoresis-based proteomic analysis of total proteins from rat aortic smooth muscle cells ascertain that heat shock protein represents the major low-molecular-weight phosphorylation target of the angiotensin II/angiotensin type 1 receptor pathway.

    We also study the action mechanism of mizoribine, inhibitor of inosine monophospate dehydrogenase, which are used clinically as immunosuppressive drugs. The study is designed to evaluate the mechanism by which mizoribine exerts the cytotoxic effect on Jurkat T cells. Mizoribine-induced cell death is confirmed as apoptosis characterized by chromatin condensation. We also mascertain mizoribine induced the catalytic activities of caspase-3 protease, caspase-8 protease and caspase-9 protease. Furthermore, mizoribine induced the changes of mitochondrial transmembrane potential (MTP) and the cytosolic release of cytochrome c from mitochondria and the decrease of Bcl-XL expression and increase of Bcl-XS, Bak and Bim are certified. Also, We have screened the expression profile of proteins in Jurkat cells by using two-dimensional gel electrophoresis. Taken together, we are going to confirm that mizoribine functions as inhibitors of inosine monophospate dehydrogenase in apoptosis of Jurkat cells via activation of intrinsic caspase cascades as well as mitochondrial dysfunction.
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    • Jeong, Sang Yeong
    Major :
    Pediatric, Vascular and Transplant..