• Journal of Biomedical Engineering Research
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• v.36 no.6
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• pp.264-270
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• 2015

A mock circulatory loop system has been developed to construct a simulator for trainees in cardiopulmonary bypass systems or to simulate a test environment for cardiac-assist devices. This paper proposes a computerized mock circulatory loop system whose node is modularized by using a servo control flow regulator to simulate dynamic change of the hemodynamic status. To observe the effect of time-varying resistance, one with hemodynamic properties, the proposed system replicates the planned cross-sectional areas of the outlet of a ventricular assist device in terms of voltage input of a servo valve. The experiment is performed (1) for steady-input commands of selected area sizes and (2) for dynamic commands such as monotonous increase and decrease, and oscillatory functions of the voltage input, and a computer program based on LabVIEW (National Instruments, Austin, USA) processes every measured data and control command to the servo valve. The results show that the pressure and flow at the target points with respect to time-varying resistance match intuitive estimation: the pressure at the outlet and the pressure drop between both sides of the valve increased and the flow at the outlet decreased for increased resistance.

• Restorative Dentistry and Endodontics
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• v.27 no.5
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• pp.543-551
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• 2002

Nitric oxide (NO) is a small molecule (mol. wt. 30 Da) and oxidative free radical. It is uncharged and can therefore diffuse freely within and between cells across membrane. Such characteristics make it a biologically important messenger in physiologic processes such as neurotransmission and the control of vascular tone. NO is also highly toxic and is known to acts as a mediator of cytotoxicity during host defense. NO is synthesized by nitric oxide synthase (NOS) through L-arginine/nitric oxide pathway which is a dioxygenation process. NO synthesis involves several participants, three co-substrates, five electrons, five co-factors and two prosthetic groups. Under normal condition, low levels of NO are synthesized by type I and III NOS for a short period of time and mediates many physiologic processes. Under condition of oxidant stress, high levels of NO are synthesized by type II NOS and inhibits a variety of metabolic processes and can also cause direct damage to DNA. Such interaction result in cytostasis, energy depletion and ultimately cell death. NO has the potential to interact with a variety of intercellular targets producing diverse array of metabolic effects. It is known that NO is involved in hemodynamic regulation, neurogenic inflammation, re-innervation, management of dentin hypersensitivity on teeth. Under basal condition of pulpal blood flow, NO provides constant vasodilator tone acting against sympathetic vasoconstriction. Substance P, a well known vasodilator, was reported to be mediated partly by NO, while calcitonin-gene related peptide has provided no evidence of its relation with NO. This review describes the roles of NO in dental pulp in addition to the known general roles of it.

• Journal of Chest Surgery
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• v.17 no.4
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• pp.703-708
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• 1984

Fibrothorax is the end stage of chronic pathologic processes of pleura such as hemothorax, empyema, or tuberculous effusion. The pleural space become adherent and obliterated, and the lung parenchyma is covered by a thick, fibrous, unexpandable "peel", so the lung function is diminished markedly with impaired ventilation and oxygenation. Constrictive pericarditis is often accompanied fibrothorax, also cardiac and hemodynamic function is deteriorated. Surgical relief of these fibrous peels causes remarkable improvement in pulmonary function, cardiac and hemodynamic function, and subjective symptoms. We experienced a case of bilateral fibrothorax combined with constrictive pericarditis which occured 3 years after bilateral tuberculous effusion. Decortication and percardiectomy were done at the same time through bilateral submammary thoracotomy with sternal transection. Comparing postoperative Peripheral venous pressure, Circulation time, Pulmonary function test, Arterial blood gas analysis, Subjective symptoms with preoperative conditions showed noticeable improvement.provement.

• BMB Reports
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• v.48 no.3
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• pp.131-138
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• 2015

Cardiac hypertrophy is a form of global remodeling, although the initial step seems to be an adaptation to increased hemodynamic demands. The characteristics of cardiac hypertrophy include the functional reactivation of the arrested fetal gene program, where histone deacetylases (HDACs) are closely linked in the development of the process. To date, mammalian HDACs are divided into four classes: I, II, III, and IV. By structural similarities, class II HDACs are then subdivided into IIa and IIb. Among class I and II HDACs, HDAC2, 4, 5, and 9 have been reported to be involved in hypertrophic responses; HDAC4, 5, and 9 are negative regulators, whereas HDAC2 is a pro-hypertrophic mediator. The molecular function and regulation of class IIa HDACs depend largely on the phosphorylation-mediated cytosolic redistribution, whereas those of HDAC2 take place primarily in the nucleus. In response to stresses, posttranslational modification (PTM) processes, dynamic modifications after the translation of proteins, are involved in the regulation of the activities of those hypertrophy-related HDACs. In this article, we briefly review 1) the activation of HDAC2 in the development of cardiac hypertrophy and 2) the PTM of HDAC2 and its implications in the regulation of HDAC2 activity.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2008.04a
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• pp.103-115
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• 2008

Hemodynamic shear stress, the dragging force generated by blood flow, is known as an anti-atherogenic factor. We tested whether lysyl-tRNA synthetase (KRS) will be utilized as an agent controlling shear-sensing systems. KRS was previously known to be secreted as a pro-inflammatory agent. Here we found that KRS inhibited various shear-stimulated signaling pathways. We further found that KRS binds to detergent-resistant membrane (DRM), indicating that KRS binding molecules exist in DRM, specialized regions of the plasma membrane. DRM plays important roles in a variety of cellular processes and consists of gangliosides, signaling molecules and cytoskeletons. We then determined that KRS was colocalized with integrins ${\alpha}4$, ${\alpha}5$ and $av{\beta}3$. In addition, KRS was shown to be associated with sialic acid, existing at the end of gangliosides. Interestingly, the adherent effect of KRS was inhibited by pretreatment with sialic acid. Moreover, treatment of endothelial cells with neuraminidase appeared to inhibit both the KRS adhesion to endothelial cells and shear-stimulated signaling. In conclusion, KRS is likely to be utilized as a vascular regulator.

• Childhood Kidney Diseases
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• v.13 no.2
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• pp.99-117
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• 2009

Diabetic nephropathy is a major cause of chronic renal failure in developing countries, and the prevalence rate has markedly increased during the past decade. Diabetic nephropathy shows various specific histological changes not only in the glomeruli but also in the tubulointerstitial region. In the early stage, the effacement of podocyte foot processes and thickened glomerular basement membrane (GBM) is noticed even at the stage of microalbuminuria. Nodular, diffuse, and exudative lesions, so-called diabetic glomerulosclerosis, are well known as glomerular lesions. Interstitial lesions also exhibit fibrosis, edema, and thickened tubular basement membrane. Diabetic nephropathy is considered to be multifactorial in origin with increasing evidence that one of the major pathways involved in the development and progression of diabetic nephropathy as a result of hyperglycemia. Hyperglycemia induces renal damage directly or through hemodynamic alterations, such as, glomerular hyperfiltration, shear stress, and microalbuminuria. Chronic hyperglycemia also induces nonhemodynamic dysregulations, such as, increased production of advanced glycosylation endproducts, oxidative stress, activation of signal pathway, and subsequent various cytokines. Those pathogenic mechanisms resulted in extracellular matrix deposition including mesangial expansion and GBM thickening, glomerular hypertrophy, inflammation, and proteinuria. In this review, recent opinions on the histopathologic changes and pathophysiologic mechanisms leading to initiation and progression of diabetic nephropathy will be introduced.

• Journal of Chest Surgery
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• v.30 no.7
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• pp.670-676
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• 1997

The structural failure of the glutaraldehyde-treated xenograft valves has been the primary concern about the limited durability as predicted from the begimling of clinical use, and long-term follow-up has shown a significant incidence of primary tissue failure(PTF) from both biological and mechanical reasons. Twenty-seven patients with the low-profile lonescu-Shiley valves explanted from mitral position for PTF(Group III) were studied on the patient characteristics and valve pathology, and the results were compared with the matched observations of the Haycock(Group I) and of the standard-profile lonesiu-Shiley valves(Group II). Patients were aged 16 to 56 years(mean, 38.0$\pm$ 11.0 years), and the size of the failed mitral bioprosthesis was 30.8$\pm$ 1.3 mm. The hemodynamic consequences were stenosis in 29.6%, insufficiency in 44.4%, mixed steno-insufficiency in 14.8%, together with normal function for the rest of patients of prophylactic re-replacement. Pathology revealed calcification with or without tissue damage in 63.0% and tissue damage with or without calcification in 58.l%, in contrast with the observations of predominant tissue damage(76.8%) over calcification in Group I and of calcification(76.1%) over tissue damage in group II. Although dystrophic calcification has long and repeatedly dealt with patient's young age as a determinant of valve durability, such a characteristic evidence was not reached even in patients with calcified valves. Moreover, the prolonged explantation p riods from the studied on the previous report suggested strongly yet possibly evolving destructive processes among the valves in the remaining patients, and awaits further follow-up. In conclusion, PTF of the xenograft valves seems to result from more complicated biologic and metabolic reasons as well as more complex mecharical factors than the reported, and newer generation prostheses, with tissue preservation with glutaraldehyde, do not likely to provide decisive improvement in the occurrence of structural failurebioprostheses is generally limited to the highly aged.