• The Korean Journal of Applied Statistics
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• v.26 no.2
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• pp.335-347
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• 2013

There are various types of real world signals. For example, an electrocardiogram(ECG) represents myocardium activities (contraction and relaxation) according to the beating of the heart. ECG can be expressed as the fluctuation of ampere ratings over time. A signal is a composite of various types of signals. An orchestra (which boasts a beautiful melody) consists of a variety of instruments with a unique frequency; subsequently, each sound is combined to form a perfect harmony. Various research on how to to decompose mixed stationary signals have been conducted. In the case of non-stationary signals, there is a limitation to use methodologies for stationary signals. Huang et al. (1998) proposed empirical mode decomposition(EMD) to deal with non-stationarity. EMD provides a data-driven approach to decompose a signal into intrinsic mode functions according to local oscillation through the identification of local extrema. However, due to the repeating process in the construction of envelopes, EMD algorithm is not efficient and not robust to a noise, and its computational complexity tends to increase as the size of a signal grows. In this research, we propose a new method to extract a local oscillation embedded in a signal by utilizing the second derivative.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.9-14
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• 2016

Adenosine 3',5'-cyclic monophosphate (cAMP) participates in the regulation of numerous cellular functions, including the $Na^+-K^+$-ATPase (sodium pump). Ouabain, used in the treatment of several heart diseases, is known to increase cAMP levels but its effects on the atrium are not understood. The aim of the present study was to examine the effect of ouabain on the regulation of atrial cAMP production and its roles in atrial endothelin-1 (ET-1) secretion in isolated perfused beating rabbit atria. Our results showed that ouabain ($3.0{\mu}mol/L$) significantly increased atrial dynamics and cAMP levels during recovery period. The ouabain-increased atrial dynamics was blocked by KB-R7943 ($3.0{\mu}mol/L$), an inhibitor for reverse mode of $Na^+-Ca^{2+}$ exchangers (NCX), but did not by L-type $Ca^{2+}$ channel blocker nifedipine ($1.0{\mu}mol/L$) or protein kinase A (PKA) selective inhibitor H-89 ($3.0{\mu}mol/L$). Ouabain also enhanced atrial intracellular cAMP production in response to forskolin and theophyline ($100.0{\mu}mol/L$), an inhibitor of phosphodiesterase, potentiated the ouabain-induced increase in cAMP. Ouabain and 8-Bromo-cAMP ($0.5{\mu}mol/L$) markedly increased atrial ET-1 secretion, which was blocked by H-89 and by PD98059 ($30{\mu}mol/L$), an inhibitor of extracellular-signal-regulated kinase (ERK) without changing ouabain-induced atrial dynamics. Our results demonstrated that ouabain increases atrial cAMP levels and promotes atrial ET-1 secretion via the mitogen-activated protein kinase (MAPK)/ERK signaling pathway. These findings may explain the development of cardiac hypertrophy in response to digitalis-like compounds.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.35 no.2A
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• pp.202-208
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• 2010

The performance of upstream transmission in SCM-PON is generally limited by the presence of OBI which is caused by the beating of two or more lasers. In this paper, we propose a novel approach for reducing OBI problem by using heterodyne detection with an additional LD as a local oscillator, resulting that the RF signal is shifted to the other spectal band. In addition, it is possible that the proposed method can provide the cost-effective solution thanks to the loop-back mechanism using R-SOA in ONUs. The performance is superior when the spectral width of LD is smaller and the power difference between the transmission LD and the oscillation LD is bigger. System configuration and design consideration are discussed. Performance of the systems is evaluated by simulator called OptSim. It is expected to provide WDM/SCM-PON system not only cost-effective but also efficient in increasing the number of subscribers.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.6
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• pp.667-674
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• 2017

Angiotensin II (Ang II) is metabolized from N-terminal by aminopeptidases and from C-terminal by Ang converting enzyme (ACE) to generate several truncated angiotensin peptides (Angs). The truncated Angs have different biological effects but it remains unknown whether Ang-(4-8) is an active peptide. The present study was to investigate the effects of Ang-(4-8) on hemodynamics and atrial natriuretic peptide (ANP) secretion using isolated beating rat atria. Atrial stretch caused increases in atrial contractility by 60% and in ANP secretion by 70%. Ang-(4-8) (0.01, 0.1, and $1{\mu}M$) suppressed high stretch-induced ANP secretion in a dose-dependent manner. Ang-(4-8) ($0.1{\mu}M$)-induced suppression of ANP secretion was attenuated by the pretreatment with an antagonist of Ang type 1 receptor ($AT_1R$) but not by an antagonist of $AT_2R$ or $AT_4R$. Ang-(4-8)-induced suppression of ANP secretion was attenuated by the pretreatment with inhibitor of phospholipase (PLC), inositol triphosphate ($IP_3$) receptor, or nonspecific protein kinase C (PKC). The potency of Ang-(4-8) to inhibit ANP secretion was similar to Ang II. However, Ang-(4-8) $10{\mu}M$ caused an increased mean arterial pressure which was similar to that by 1 nM Ang II. Therefore, we suggest that Ang-(4-8) suppresses high stretch-induced ANP secretion through the $AT_1R$ and $PLC/IP_3/PKC$ pathway. Ang-(4-8) is a biologically active peptide which functions as an inhibition mechanism of ANP secretion and an increment of blood pressure.