• 한국전산유체공학회지
• /
• 제14권4호
• /
• pp.78-85
• /
• 2009

Cavitating flow simulation is of practical importance for many engineering systems, such as marine propellers, pump impellers, nozzles, injectors, torpedoes, etc. The present work has focused on the simulation of cavitating flow past cylinders with strong side flows. The governing equation is the Navier-Stokes equation based on the homogeneous mixture model. The momentum and energy equation is in the mixture phase while the continuity equation is solved liquid and vapor phase, separately. An implicit dual time and preconditioning method are employed for computational analysis. For the code validation, the results from the present solver have been compared with experiments and other numerical results. A fairly good agreement with the experimental data and other numerical results have been obtained. After the code validation, the strong side flow was applied to include the wake flow effects of the submarine or ocean tide.

• 한국추진공학회:학술대회논문집
• /
• 한국추진공학회 2008년 영문 학술대회
• /
• pp.260-265
• /
• 2008

A numerical scheme for solid propellant rocket has been studied using preconditioning method to research unsteady combustion processes for the double-base propellant with a converging-diverging nozzle. The Navier-Stokes equation is solved by dualtime stepping method with finite volume method. The turbulence model uses a shear stress transport modeling. The species equation follows up the method of Xinping WI, Mridul Kumar and Kenneth K. Kuo. A preconditioned algorithm is applied to solve incompressible regime inside the combustor and compressible flow at nozzle. Mass flux was evaluated using modified advective upwind splitting method. The simulated result the comparison a fully coupled implicit method and a semi implicit method in terms of accuracy and efficiency. This report shows the result of solid rocket propellant combustion.

• Smart Structures and Systems
• /
• 제23권1호
• /
• pp.45-60
• /
• 2019

This paper is devoted to proposing a new approach for damage detection of structures. In this technique, the biconjugate gradient method (BCG) is employed. To remedy the noise effects, a new preconditioning algorithm is applied. The proposed preconditioner matrix significantly reduces the condition number of the system. Moreover, based on the characteristics of the damage vector, a new direct search algorithm is employed to increase the efficiency of the suggested damage detection scheme by reducing the number of unknowns. To corroborate the high efficiency and capability of the presented strategy, it is applied for estimating the severity and location of damage in the well-known 31-member and 52-member trusses. For damage detection of these trusses, the time history responses are measured by a limited number of sensors. The results of numerical examples reveal high accuracy and robustness of the proposed method.

• 한국전산유체공학회:학술대회논문집
• /
• 한국전산유체공학회 2003년도 The Fifth Asian Computational Fluid Dynamics Conference
• /
• pp.299-300
• /
• 2003

• 한국전산유체공학회:학술대회논문집
• /
• 한국전산유체공학회 2006년도 PARALLEL CFD 2006
• /
• pp.83-84
• /
• 2006

• 한국생명과학회:학술대회논문집
• /
• 한국생명과학회 2006년도 제47회 학술심포지움 및 추계국제학술대회
• /
• pp.73.1-73.1
• /
• 2006

• 대한자기공명의과학회:학술대회논문집
• /
• 대한자기공명의과학회 1999년도 제4차 추계학술대회 초록집
• /
• pp.57-58
• /
• 1999

• The Korean Journal of Physiology and Pharmacology
• /
• 제8권2호
• /
• pp.95-100
• /
• 2004

Ischemic preconditioning (IPC) has been accepted as a heart protection phenomenon against ischemia and reperfusion (I/R) injury. The activation of ATP-sensitive potassium $(K_{ATP})$ channels and the release of myocardial nitric oxide (NO) induced by IPC were demonstrated as the triggers or mediators of IPC. A common action mechanism of NO is a direct or indirect increase in tissue cGMP content. Furthermore, cGMP has also been shown to contribute cardiac protective effect to reduce heart I/R-induced infarction. The present investigation tested the hypothesis that $K_{ATP}$ channels attenuate DNA strand breaks and oxidative damage in an in vitro model of I/R utilizing rat ventricular myocytes. We estimated DNA strand breaks and oxidative damage by mean of single cell gel electrophoresis with endonuclease III cutting sites (comet assay). In the I/R model, the level of DNA damage increased massively. Preconditioning with a single 5-min anoxia, diazoxide $(100\;{\mu}M)$, SNAP $(300\;{\mu}M)$ and 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate (8-pCPT-cGMP) $(100\;{\mu}M)$ followed by 15 min reoxygenation reduced DNA damage level against subsequent 30 min anoxia and 60 min reoxygenation. These protective effects were blocked by the concomitant presence of glibenclamide $(50\;{\mu}M)$, 5-hydroxydecanoate (5-HD) $(100\;{\mu}M)$ and 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate, Rp-isomer (Rp-8-pCPT-cGMP) $(100\;{\mu}M)$. These results suggest that NO-cGMP-protein kinase G (PKG) pathway contributes to cardioprotective effect of $K_{ATP}$ channels in rat ventricular myocytes.

• Biomolecules & Therapeutics
• /
• 제24권5호
• /
• pp.495-500
• /
• 2016

This study aimed to explore the neuroprotection and mechanism of isoflurane on rats with spinal cord ischemic injury. Total 40 adult male Sprague-Dawley rats were divided into the four groups (n=10). Group A was sham-operation group; group B was ischemia group; group C was isoflurane preconditioning group; group D was isoflurane preconditioning followed by ischemia treatment group. Then the expressions of TWIK-related $K^+$ channel 1 (TREK1) in the four groups were detected by immunofluorescent assay, real time-polymerase chain reactions (RT-PCR) and western blot. The primary neurons of rats were isolated and cultured under normal and hypoxic conditions. Besides, the neurons under two conditions were transfected with green fluorescent protein (GFP)-TREK1 and lentivirual to overexpress and silence TREK1. Additionally, the neurons were treated with isoflurane or not. Then caspase-3 activity and cell cycle of neurons under normal and hypoxic conditions were detected. Furthermore, nicotinamide adenine dinucleotide hydrate (NADH) was detected using NAD+/NADH quantification colorimetric kit. Results showed that the mRNA and protein expressions of TREK1 increased significantly in group C and D. In neurons, when TREK1 silenced, isoflurane treatment improved the caspase-3 activity. In hypoxic condition, the caspase-3 activity and sub-G1 cell percentage significantly increased, however, when TREK1 overexpressed the caspase-3 activity and sub-G1 cell percentage decreased significantly. Furthermore, both isoflurane treatment and overexpression of TREK1 significantly decreased NADH. In conclusion, isoflurane-induced neuroprotection in spinal cord ischemic injury may be associated with the up-regulation of TREK1.

• The Korean Journal of Physiology and Pharmacology
• /
• 제22권5호
• /
• pp.467-479
• /
• 2018

The aging process induces a plethora of changes in the body including alterations in hormonal regulation and metabolism in various organs including the heart. Aging is associated with marked increase in the vulnerability of the heart to ischemia-reperfusion injury. Furthermore, it significantly hampers the development of adaptive response to various forms of conditioning stimuli (pre/post/remote conditioning). Aging significantly impairs the activation of signaling pathways that mediate preconditioning-induced cardioprotection. It possibly impairs the uptake and release of adenosine, decreases the number of adenosine transporter sites and down-regulates the transcription of adenosine receptors in the myocardium to attenuate adenosine-mediated cardioprotection. Furthermore, aging decreases the expression of peroxisome proliferator-activated receptor gamma co-activator 1-alpha ($PGC-1{\alpha}$) and subsequent transcription of catalase enzyme which subsequently increases the oxidative stress and decreases the responsiveness to preconditioning stimuli in the senescent diabetic hearts. In addition, in the aged rat hearts, the conditioning stimulus fails to phosphorylate Akt kinase that is required for mediating cardioprotective signaling in the heart. Moreover, aging increases the concentration of $Na^+$ and $K^+$, connexin expression and caveolin abundance in the myocardium and increases the susceptibility to ischemia-reperfusion injury. In addition, aging also reduces the responsiveness to conditioning stimuli possibly due to reduced kinase signaling and reduced STAT-3 phosphorylation. However, aging is associated with an increase in MKP-1 phosphorylation, which dephosphorylates (deactivates) mitogen activated protein kinase that is involved in cardioprotective signaling. The present review describes aging as one of the major confounding factors in attenuating remote ischemic preconditioning-induced cardioprotection along with the possible mechanisms.