• Proceedings of the Korean Society of Precision Engineering Conference
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• 2004.10a
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• pp.1176-1179
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• 2004

A new cell-cross bridge mechanics model is proposed to analyze the mechanics of heart muscle. Electrophysiology of a cardiac cell is numerically approximated using the previous model of human ventricular myocyte. Ion transports across cell membrane initiated by action potential induce excitation-contraction mechanism in the cell via cross bridge dynamics. Negroni and Lascano model (NL model) is employed to compute the tension of cross bridge closely related to ion dynamics in cytoplasm.

• Molecules and Cells
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• v.24 no.2
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• pp.224-231
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• 2007

$H_2O_2$, as an example of oxidative stress, induces cardiac myocyte apoptosis. Bcl-2 family proteins are key regulators of the apoptotic response while their functions can be regulated by post-translational modifications including phosphorylation, dimerization or proteolytic cleavage. In this study, we examined the role of various protein kinases in regulating total BAD protein levels in adult rat cardiac myocytes undergoing apoptosis. Stimulation with 0.1 mM $H_2O_2$, which induces apoptosis, resulted in a marked down-regulation of BAD protein, which is attributed to cleavage by caspases since it can be restored in the presence of a general caspase inhibitor. Inhibition of PKC, p38-MAPK, ERK1/2 and PI-3-K did not influence the reduced BAD protein levels observed after stimulation with $H_2O_2$. On the contrary, inhibition of PKA or specifically $PKC{\delta}$ resulted in up-regulation of BAD. Decreased caspase 3 activity was observed in $H_2O_2$ treated cells after inhibition of PKA or $PKC{\delta}$ whereas inhibition of PKA also resulted in improved cell survival. Furthermore, addition of okadaic acid to inhibit selected phosphatases resulted in enhanced BAD cleavage. These data suggest that, during oxidative stress-induced cardiac myocyte apoptosis, there is a caspase-dependent down-regulation of BAD protein, which seems to be regulated by coordinated action of PKA, $PKC{\delta}$ and phosphatases.

• Journal of Mechanical Science and Technology
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• v.20 no.5
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• pp.668-674
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• 2006

In order to develop a cell based robot, we present a micro-mechanical force measurement system for the biological muscle actuators, which utilize glucose as a power source. The proposed measurement system is composed of a micro-manipulator, a force transducer with a glass probe, a signal processor, an inverted microscope and video recording system. Using this measurement system, the contractile force and frequency of the cardiac myocytes were measured in real time and the magnitudes of the contractile force of each cardiac myocyte under different conditions were compared. From the quantitative experimental results, we could estimate that the force of cardiac myocytes is about $20\sim40{\mu}N$, and show that there are differences between the control cells and the micro-patterned cells.

• Proceedings of the KSME Conference
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• 2005.11a
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• pp.70.1-70.1
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• 2005

• 제어로봇시스템학회:학술대회논문집
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• 2005.06a
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• pp.1179-1182
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• 2005

To facilitate the cell based robot research, we presented a micro-mechanical force measurement system for the biological muscle actuators, which utilize glucose as a power source for potential application in a human body or blood vessels. The system is composed of a micro-manipulator, a force transducer with a glass probe, a signal processor, an inverted microscope and video recoding system. Using this measurement system, the contractile force and frequency of the cardiac myocytes were measured in real time and the magnitude of the contractile force of each cardiac myocyte on a different condition was compared. From the quantitative experimental results, we estimated that the force of cardiac myocytes is about $20{\sim}40\;{\mu}$N, and showed that there is difference between the control cells and the micro-patterned cells.

• International Journal of Vascular Biomedical Engineering
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• v.3 no.1
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• pp.23-29
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• 2005

We developed a three dimensional cardiac tissue model based on human cardiac cell and mono-domain approximation for action potential propagation. The human myocyte model proposed by ten Tusscher et al. (TNNP model) (2004) for cell electrophysiology and a mono-domain method for electric wave propagation are used to simulate the cardiac tissue propagation mechanism using a finite element method. To delineate non-homogeneity across cardiac tissue layer, we used three types of cardiac cell models. Ansiotropic effect of action potential propagation is also considered in this study. In this 3D anisotropic cardiac tissue with three cell layers, we generated a reentrant wave using S1-S2 protocol. Computational results showed that the reentrant wave was affected by the anisotropic properties of the cells. To test the reentrant wave under pathological state, we simulated a hypertopic model with non-excitable fibroblasts in stochastic manner. Compared with normal tissue, the hypertropic tissue result showed another center of reentrant wave, indicating that the wave pattern can be more easily changed from regular with a concentric focus to irregular multi-focused reentrant waves in case of patients with hypertrophy.

• Proceedings of the Korean Biophysical Society Conference
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• 1997.07a
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• pp.28-28
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• 1997

Stimulation of $\alpha$$_1$-adrenergic receptor ($\alpha$$_1$-AR) by phenylephrine produced a decrease in intracellular N $a^{＋}$ activity ( $a_{Na}$ $^{i}$ ) in multicellular preparations of cardiac tissues. The role of protein kinase C (PKC) in $\alpha$$_1$-adrenergic regulation of $a_{Na}$ $^{i}$ was studied in single ventricular myocyte isolated from guinea pig hearts. $a_{Na}$ $^{i}$ and membrane potential were measured with N $a^{+}$ indicator, sodium-binding benzofuran isophthalate tetraacetoxy methyl ester (SBFI/AM) and microelectrodes respectively when ventricular myocyte was stimulated at 0.3 Hz.(omitted)d)

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.203-210
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• 2015

AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism. Previous studies have shown that activation of AMPK results in suppression of cardiac myocyte hypertrophy via inhibition of the p70S6 kinase (p70S6K) and eukaryotic elongation factor-2 (eEF2) signaling pathways. Epigallocatechin-3-gallate (EGCG), the major polyphenol found in green tea, possesses multiple protective effects on the cardiovascular system including cardiac hypertrophy. However, the molecular mechanisms has not been well investigated. In this study, we found that EGCG could significantly reduce natriuretic peptides type A (Nppa), brain natriuretic polypeptide (BNP) mRNA expression and decrease cell surface area in H9C2 cardiomyocytes stimulated with phenylephrine (PE). Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy.

• Journal of Chest Surgery
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• v.33 no.1
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• pp.1-6
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• 2000

Background: TNF-$\alpha$ plays a major role in producing left ventricular dysfunction cardio-myopathy pulmonary edema and inhibits the compensatory mechanism of congestive heart failure. IL-6 is an acute reactant of immune reaction and also known to control immune reaction but its function in the myocyte was not clearly investigated. Author's performed this experiment to investigate the contents of TNF-$\alpha$ and IL-6 on the assumption that TNF-$\alpha$ and IL-6 may reside in nonfailing heart that has gone cardiac surgery and play some role in cardiac function. Material and Method : Right auricular tissues were sampled from 12 patients who had undergone total corrective surgery for both congenital and acquired heart diseases from January 1998 to June 1998 in Kosin Universcfy Gospel hospital. The quantitive analysis of TNF-$\alpha$ and IL-6 were assessed by ELISA method in right auricular tissue. Hemodynamic values about the pressure of ventricle atrium aorta pulmonary artery and cardiac index pulmonary and systemic vascular resistance and cardiac output were measured by echocardiography and cardiac catheterization and biochemical analyses of LDH & AST were done before operation. statistical analysis was by Paired Student t-test. Patients were divided into children(under 15 years olds) and adults groups and the data was compared beween two groups. Conclusion: Mild pulmonary hypertension and increased pulmonary vascular resistance were existed in both group. The contents of tissue TNF-$\alpha$ IL-6 in each group were independent of each data.

• Archives of Pharmacal Research
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• v.21 no.5
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• pp.496-502
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• 1998

The present study was carried out to determine the possible use of cTn-I in the cardiac myofibrillar architecture, as a potential target for in vivo radioimmunodetection of cardiac damage in a brain death pig model. Radioiodiantion of the anti-cTn-I 5F4 McAb was carried out by lactoperoxidase method. the percentage iodine incorporation achieved was 70-75%. The radioiodinated McAbs were purified on Sephadex G-25 column and characterised by Paper chromatography, Phast Gel electrophoresis and electroimmunoblotting. Radioiodinated anticTn-I 5F4 McAbs were employed alongside Pyrophosphate($Tc_{99m}$-PPi$) and $Thallium^{201}$ chloride($TI^{201}$) in 24 landrace pigs (brain-dead=18 & sham-operated=6). The percentage cardiac uptake of the radiolabelled antibody injected dose was significantly higher in the brain dead animals(0.196%) as compared to that of sham-operated animals (0.11%). Specific in vivo localization of radiolabelled McAbs in the infarcted cardiac tissue was confirmed by computer-aided reconstruction of 3-D images of the isolated heart. The preliminary results of the study revealed preferential uptake of radiolabelled antibody at the site of myocyte damage resulting from artificially induced brain death.