• Proceedings of the Korea Water Resources Association Conference
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• 2010.05a
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• pp.1001-1005
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• 2010

본 연구는 식생지름에 따른 식생된 복단면 하천에서 수리특성에 관한 것이다. 또한 국외에서 개발된 모형들의 차이점과 적용가능성을 조사하는 것이다. 연구결과로써 주수로의 유속은 식생밀도 증가에 따라 증가하는 동안 경계면마찰계수는 감소하다가 어느 식생밀도 지점부터 일정하였다. 하상경사가 0.5 ‰와 식생직경이 12 mm일 경우 경계면마찰계수에 대한 Pasche 모형은 10.9 %, Bertram 모형은 12.4 %, Mertens 모형은 16.8 % 평균오차를 발생시켰다. 그러나 식생밀도가 증가할수록 Nuding 모형의 오차가 증가함을 볼 수 있으며, 평균오차가 60.5 % 발생되었다. 주수로의 실측된 유속에 대한 Pasche 모형의 평균오차는 2.8 %, Mertens 모형의 평균오차는 8.3 %, Bertram 모형의 평균오차는 14.7 %, Nuding 모형의 평균오차는 11.8 %이다. 그러므로 Pasche 모형은 실제 복단면 하천에 적용하기 위해 더 유용하다. Strickler 계수를 사용한 Bertram 모형은 다른 모형보다 계산이 복잡하지 않고 측정된 마찰계수 및 유속값과 잘 일치한다.

• Journal of Ginseng Research
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• v.37 no.3
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• pp.324-331
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• 2013

Channels formed by the co-assembly of the KCNQ1 subunit and the mink (KCNE1) subunit underline the slowly activating delayed rectifier $K^+$ channels ($I_{Ks}$) in the heart. This $K^+$ channel is one of the main pharmacological targets for the development of drugs against cardiovascular disease. Panax ginseng has been shown to exhibit beneficial cardiovascular effects. In a previous study, we showed that ginsenoside Rg3 activates human KCNQ1 $K^+$ channel currents through interactions with the K318 and V319 residues. However, little is known about the effects of ginsenoside metabolites on KCNQ1 $K^+$ alone or the KCNQ1 + KCNE1 $K^+$ ($I_{Ks}$) channels. In the present study, we examined the effect of protopanaxatriol (PPT) and compound K (CK) on KCNQ1 $K^+$ and $I_{Ks}$ channel activity expressed in Xenopus oocytes. PPT more strongly inhibited the $I_{Ks}$ channel currents than the currents of KCNQ1 $K^+$ alone in concentration- and voltage-dependent manners. The $IC_{50}$ values on $I_{Ks}$ and KCNQ1 alone currents for PPT were $5.18{\pm}0.13$ and $10.04{\pm}0.17{\mu}M$, respectively. PPT caused a leftward shift in the activation curve of $I_{Ks}$ channel activity, but minimally affected KCNQ1 alone. CK exhibited slight inhibition on $I_{Ks}$ and KCNQ1 alone $K^+$ channel currents. These results indicate that ginsenoside metabolites show limited effects on $I_{Ks}$ channel activity, depending on the structure of the ginsenoside metabolites.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.1
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• pp.21-28
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• 2010

Phenolic compounds affect intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) signaling. The study examined whether the simple phenolic compound octyl gallate affects ATP-induced $Ca^{2+}$ signaling in PC12 cells using fura-2-based digital $Ca^{2+}$ imaging and whole-cell patch clamping. Treatment with ATP ($100\;{\mu}M$) for 90 s induced increases in $[Ca^{2+}]_i$ in PC12 cells. Pretreatment with octyl gallate (100 nM to $20\;{\mu}M$) for 10 min inhibited the ATP-induced $[Ca^{2+}]_i$ response in a concentration-dependent manner ($IC_{50}=2.84\;{\mu}M$). Treatment with octyl gallate ($3\;{\mu}M$) for 10 min significantly inhibited the ATP-induced response following the removal of extracellular $Ca^{2+}$ with nominally $Ca^{2+}$-free HEPES HBSS or depletion of intracellular $Ca^{2+}$ stores with thapsigargin ($1\;{\mu}M$). Treatment for 10 min with the L-type $Ca^{2+}$ channel antagonist nimodipine ($1\;{\mu}M$) significantly inhibited the ATP-induced $[Ca^{2+}]_i$ increase, and treatment with octyl gallate further inhibited the ATP-induced response. Treatment with octyl gallate significantly inhibited the $[Ca^{2+}]_i$ increase induced by 50 mM KCI. Pretreatment with protein kinase C inhibitors staurosporin (100 nM) and GF109203X (300 nM), or the tyrosine kinase inhibitor genistein ($50\;{\mu}M$) did not significantly affect the inhibitory effects of octyl gallate on the ATP-induced response. Treatment with octyl gallate markedly inhibited the ATP-induced currents. Therefore, we conclude that octyl gallate inhibits ATP-induced $[Ca^{2+}]_i$ increase in PC12 cells by inhibiting both non-selective P2X receptor-mediated influx of $Ca^{2+}$ from extracellular space and P2Y receptor-induced release of $Ca^{2+}$ from intracellular stores in protein kinase-independent manner. In addition, octyl gallate inhibits the ATP-induced $Ca^{2+}$ responses by inhibiting the secondary activation of voltage-gated $Ca^{2+}$ channels.

• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.17 no.5
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• pp.61-69
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• 2017

The study on interference channel is very important information theoretically and many studies have been done on it. However, even in the simplest case, even in the case of two user interfering channels, the channel capacity is not yet known except in special cases. Recently, research on the multiplexing gain that shows the tendency of the transmission rate in the high signal to noise ratio (SNR) band has been actively carried out, instead of accurately grasping the channel capacity. Obtaining optimal multiplexing gain can reveal trends in channel capacity at high signal-to-noise ratio bands. In an interfering channel with two users, the best multiplexing gain can be obtained by eliminating the interference. However, recent research shows that when the number of users is more than three, the optimal multiplexing gain can not be obtained only by zero forcing and a new technique called interference sorting is needed. There are two types of interference sorting techniques. Beamforming A method of effectively separating signals and interference by properly selecting matrices and constructing structured codes using rational numbers and irrational numbers. The interference alignment technique can achieve optimal multiplexing gain in various environments such as interference channel, X channel, compound broadcast channel, and multi hop network for multi source multi destination. In recent years, it has also been applied to distributed storage. Lee et al., "Lattice Code Interference Alignment in Cooperative Multipoint Transmission (COMP) for Interference Channels of Three Users", Journal of the Institute of Electronics Engineers, vol.49-TC,no.6,2012. In this paper, the DoF of delayed channel information is obtained.

• Journal of Ginseng Research
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• v.41 no.1
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• pp.103-112
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• 2017

Background: 20(S)-Protopanaxadiol 20-O-D-glucopyranoside, also called compound K (CK), exerts antidiabetic effects that are mediated by insulin secretion through adenosine triphosphate (ATP)-sensitive potassium ($K_{ATP}$) channels in pancreatic ${\beta}$-cells. However, the antidiabetic effects of CK may be limited because of its low bioavailability. Methods: In this study, we aimed to enhance the antidiabetic activity and lower the toxicity of CK by including it with ${\beta}$-cyclodextrin (CD) (CD-CK), and to determine whether the CD-CK compound enhanced pancreatic islet recovery, compared to CK alone, in an alloxan-induced diabetic zebrafish model. Furthermore, we confirmed the toxicity of CD-CK relative to CK alone by morphological changes, mitochondrial damage, and TdT-UTP nick end labeling (TUNEL) assays, and determined the ratio between the toxic and therapeutic dose for both compounds to verify the relative safety of CK and CD-CK. Results: The CD-CK conjugate ($EC_{50}=2.158{\mu}M$) enhanced the recovery of pancreatic islets, compared to CK alone ($EC_{50}=7.221{\mu}M$), as assessed in alloxan-induced diabetic zebrafish larvae. In addition, CD-CK ($LC_{50} =20.68{\mu}M$) was less toxic than CK alone ($LC_{50}=14.24{\mu}M$). The therapeutic index of CK and CD-CK was 1.98 and 9.58, respectively. Conclusion: The CD-CK inclusion complex enhanced the recovery of damaged pancreatic islets in diabetic zebrafish. The CD-CK inclusion complex has potential as an effective antidiabetic efficacy with lower toxicity.

• KSCE Journal of Civil and Environmental Engineering Research
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• v.30 no.6B
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• pp.607-615
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• 2010

Vegetation drag tends to raise water level by retarding the flow. Previous studies have focussed on either the vertical structure modeling or the one-dimensional modeling, which can hardly be used to simulate the vegetative streams in practical engineering. Therefore, this paper presents a two-dimensional numerical model based on the depth-averaged flow equations. Vegetation drags are reflected in the flow equations, assuming non-flexible rigid cylinders. For validations, flow properties measured in both rectangular and compound channels are compared with simulated data, showing good agreement. Then, the model is applied to a reach in the Han River and the impact of floodplain vegetation on the flow is investigated.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.23-30
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• 1989

Buprenorphine, one of the mixed agonist-antagonist opioid drugs was used to inverstigate the opioid receptor on frog sciatic nerve A fibers. Action potentials were recorded for 4 hrs by a sucrose gap apparatus which were separated by four rubber membranes. To examine the one of the mechanism of action of buprenorphine, meperidine or naloxone was added after or before the treatment of buprenorphine. The results of this experiment were as follows: 1. Buprenorphine suppressed significantly the compound action potentials of frog sciatic nerve, and the maximal effects were shown both at $10^{-4}\;M$ and at $10^{-8}\;M$. 2. The dose-response relationship of buprenorphine on the depressant effect in frog sciatic nerve was biphasic and inverted U-shaped. 3. Buprenorphine blocked the effect of Meperidine $(10^{-3}\;M)$ on this preparation. 4. The depressant effcct of Buprenorphine on frog sciatic nerve was blocked by $10^{-8}\;M$ naloxone. From the above results, buprenorphine acts as one of agoinist-antagonistic effect on frog sciatic nerve, and the opioid receptor on this preparation is located on or near the intracellular opening of the sodium channels, which are sensitive to naloxone.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.1
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• pp.1-9
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• 2010

AMP-activated protein kinase (AMPK) protects various tissues and cells from ischemic insults and is activated by many stimuli including mechanical stretch. Therefore, this study investigated if the activation of AMPK is involved in stretch-induced cardioprotection (SIC). Intraventricular balloon and aorto-caval shunt (ACS) were used to stretch rat hearts ex vivo and in vivo, respectively. Stretch preconditioning reduced myocardial infarct induced by ischemia-reperfusion (I/R) and improved post-ischemic functional recovery. Phosphorylation of AMPK and its downstream substrate, acetyl-CoA carboxylase (ACC) were increased by mechanical stretch and ACC phosphorylation was completely blocked by the AMPK inhibitor, Compound C. AMPK activator (AICAR) mimicked SIC. Gadolinium, a blocker of stretch-activated ion channels (SACs), inhibited the stretch-induced phosphorylation of AMPK and ACC, whereas diltiazem, a specific L-type calcium channel blocker, did not affect AMPK activation. Furthermore, SIC was abrogated by Compound C and gadolinium. The in vivo stretch induced by ACS increased AMPK activation and reduced myocardial infarct. These findings indicate that stretch preconditioning can induce the cardioprotection against I/R injury, and activation of AMPK plays an important role in SIC, which might be mediated by SACs.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.57-63
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• 2004

Fluoxetine, a widely used anti-depressant compound, has several additional effects, including blockade of voltage-gated ion channels. We examined whether fluoxetine affects ATP-induced calcium signaling in PC12 cells by using fura-2-based digital calcium imaging and assay for $[^3H]-inositol$ phosphates (IPs). Treatment with ATP $(100\;{\mu}M)$ for 2 min induced $[Ca^{2+}]_i$ increases. The ATP-induced $[Ca^{2+}]_i$ increases were significantly decreased by removal of extracellular $Ca^{2+}$ and treatment with the inhibitor of endoplasmic reticulum $Ca^{2+}$ ATPase thapsigargin $(1\;{\mu}M)$. Treatment with fluoxetine for 5 min blocked the ATP-induced $[Ca^{2+}]_i$ increase concentration-dependently. Treatment with fluoxetine $(30\;{\mu}M)$ for 5 min blocked the ATP-induced $[Ca^{2+}]_i$ increase following removal of extracellular $Ca^{2+}$ and depletion of intracellular $Ca^{2+}$ stores. While treatment with the L-type $Ca^{2+}$ channel antagonist nimodipine for 10 min inhibited the ATP-induced $[Ca^{2+}]_i$ increases significantly, treatment with fluoxetine alone blocked the ATP-induced responses. Treatment with fluoxetine also inhibited the 50 mM $K^+-induced$ $[Ca^{2+}]_i$ increases completely. However, treatment with fluoxetine did not inhibit the ATP-induced $[^3H]-IPs$ formation. Collectively, we conclude that fluoxetine inhibits ATP-indueed $[Ca^{2+}]_i$ increases in PC12 cells by inhibiting both an influx of extracellular $Ca^{2+}$ and a release of $Ca^{2+}$ from intracellular stores without affecting IPs formation.

• Journal of Mechanical Science and Technology
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• v.20 no.9
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• pp.1483-1491
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• 2006

The pumping performance of molecular drag pumps (MDP) has been investigated experimentally. The exporimented MDPs are a disk-type drag pump (DTDP), helical-type drag pump(HTDP) and compound drag pump (CDP), respectively In the case of the DTDP, spiral channels of a rotor are cut on both upper surface and lower surface of a rotating disk, and the corresponding stator is a planar disk. In the case of the HTDP, the rotor has six rectangular grooves. The CDP consists with the DTDP, at lower part, and with the HTDP, at upper part. The experiments are performed in the outlet pressure range of $0.2{\sim}533Pa$. The inlet pressure and compression ratio are measured under the various conditions of outlet pressure and throughputs, and nitrogen is used for the test gas. At the outlet pressure of 0.2Pa, the ultimate pressure has been reached to $1.0{\times}10^{-2}Pa$ for the HTDP, $1.3{\times}10^{-4}Pa$ for the DTDP, and $3.6{\times}10^{-5}Pa$ for the CDP. The maximum compression ratio of the CDP is much higher than those of the DTDP or HTDP. Consequently, the ultimate pressure of the CDP is the lowest one.