• 한국산학기술학회논문지
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• 제10권2호
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• pp.256-263
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• 2009

한국철도공사에서는 기존선의 신호시스템을 지상의 ATS 시스템에 의한 신호 현시에 따라 운전자가 제한속도 이내로 열차를 운전하던 방식에서 지상의 발리스로부터 이동권한을 전송받아 차상신호시스템(ATP)에서 Speed Profile을 생성하여 운전하는 Bombardier Transport사의 ATP 시스템으로 개량하고 있다. 한국철도기술연구원에서는 기존선의 속도 향상을 위해 틸팅열차를 개발하여 10만 km 주행시험 중이며, 중앙선에 투입이 가시화되고 있다. 이러한 틸팅열차를 ATP 시스템에 의해 운전할 때 곡선구간에서 현재 제한되어지고 있는 곡선부 통과 속도를 증속하는 것이 쉽지 않은 형편이다. 따라서 향후 ATP 시스템의 국산화 개발이 이루어질 것을 대비하여 선행적으로 ATP 시스템의 핵심 기술인 선행열차에 따른 후행열차의 안전제동모델 및 열차간격제어 기술을 연구 개발할 필요성이 있다. 본 논문에서는 이를 위하여 발리스를 이용하는 ATP 시스템의 안전제동모델 및 열차간격제어 기술을 개발하고 그 성능을 시뮬레이션 하였다.

• 자연과학논문집
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• 제5권2호
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• pp.3-11
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• 1992

ADP 농도를 증가시킴에 따라 미토콘드리아에 의한 Phosphocreatine의 생성속도는 포화 경향을 보이면서 증진되었다. 이 조건에서 Phosphocreatne 생성 속도를 측정하여 가해준 ADP에 대한 Km값을 구해본 결과 0. 0185 mM 임을 알았고, 이 Km값은 미토콘드리아의 Oxidative Phosphoryla-tion게와 연계되지 않은 (추출한) 미토콘드리아 Creatine Kinase의 ATP에 대한 Km 값인 0. 21mM보다 훨씬 낮음을 알 수 있었다. 이 외에도 ADP 존재하에 Oxidative Phosphorylation에 의한 ATP 생성에 대한 Creatine Kinase의 활성의 영향을 살펴본 결과 이 조건에서 Phosphocreatine은 반응시간에 정비례하게 생성 되었으나, 생성된 ATP는 반응시간에 무관함을 보였다. 또한 Oxidative Phosphorylation에 의해 미토콘드리아 외부 Respiration 용액 내에 이 ATP가 축적되는 속도도 미토콘드리아 Creatine Kinase의 Phosphocreatine 생성과 무관함을 알수 있었다. 이상의 결과들은 Mitochondrial Creatine Kinase가 Oxidative Phosphorylation계와 기능적으로 밀접하게 연계되어 ATP가 아닌 Phophocreatine이 에너지 전달 물질로 직접 이용될 가능성을 시사해준다.

• Biomolecules & Therapeutics
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• 제12권1호
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• pp.25-33
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• 2004

In this study we investigated whether ATP loss was involved in the potentiated death of immunostimulated rat primary astrocytes in glucose-deprived condition. Rat primary astrocytes immunostimulated with LPS plus IFN-${\gamma}$ for 48 h underwent death upon glucose deprivation, which dependent on the production of peroxynitrite. Intracellular ATP level synergistically decreased by glucose deprivation in immunostimulated astrocytes but not in control cells, and the loss of ATP occurred well ahead of the LDH release. The synergistic cell death and ATP loss by immunostimulation and glucose deprivation were inhibited by iNOS inhibitor (L-NAME and L-NNA) or peroxynitrite decomposition catalyst (also a superoxide anion scavenger), Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP). Exogenous addition of peroxynitrite generator, SIN-l timedependently induced ATP loss and cell death in the glucose-deprived astrocytes. Depletion of intracellular glutathione (GSH) and dis겨ption of mitochondrial transmembrane potential (MTP) were also observed under same conditions. Supply cellular ATP by the addition of exogenous adenosine or ATP during glucose deprivation inhibited ATP depletion, GSH depletion, MTP disruption and cell death in SIN-l treated or immunostimulated astrocytes. This study showed that perturbation in the regulation of intracellular ATP level in immunostimulated astrocytes might make them more vulnerable to energy challenging stimuli.

• The Korean Journal of Physiology and Pharmacology
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• 제3권5호
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• pp.507-512
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• 1999

Contribution of prostaglandins $D_2,\;E_2\;and\;I_2\;(PGD_2,\;PGE_2\;and\;PGI_2)$ on the regulation of ATP-sensitive $K^+$ channel $(K_{ATP}\;channel)$ was investigated in isolated single rat ventricular cardiac myocytes using the patch clamp technique. $PGD_2,\;PGE_2\;and\; PGI_2$ did not affect $K_{ATP}$ channel activity in the inside-out patch, but increased channel activity in a dose-dependent manner when the channel activities were attenuated by the administration of 100 ${\mu}M$ ATP to the internal solution in the inside-out patch. Channel activations by the prostaglandins were abolished by 50 ${\mu}M$ glibenclamide, a $K_{ATP}$ channel blocker. Dose-response curves of relative channel activity against the ATP concentrations of internal solution in the inside-out patch were shifted to the right in the presence of those three prostaglandins. The rank order of the channel stimulatory potencies $(as\;IC_{50}\;for\;ATP)$ calculated from the dose-response curves were $PGI_2\;>\;PGD_2\;>\;PGE_2.$ Conductance of the channel was not changed by those three prostaglandins. In conclusion, we suggest that prostaglandins $D_2,\;E_2\;and\;I_2$ are involved in the regulation of $K_{ATP}$ channel activity in certain circumstances, and that those three prostaglandins may cause myocardial relaxation by opening $K_{ATP}$ channels, thus protecting the heart from ischema.

• The Korean Journal of Physiology and Pharmacology
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• 제3권3호
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• pp.293-303
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• 1999

The influences of specific protein phosphatase and protein kinase inhibitors on the ATP-sensitive $K^+\;(K_{ATP})$ channel-opening effect of pinacidil were investigated in single rat ventricular myocytes using patch clamp technique. In cell-attached patches, pinacidil $(100\;{\mu}M)$ induced the opening of the $K_{ATP}$ channel, which was blocked by the pretreatment with H-7 $(100\;{\mu}M)$ whereas enhanced by the pretreatment with genistein $(30\;{\mu}M)$ or tyrphostin A23 $(10\;{\mu}M)$. In inside-out patches, pinacidil $(10\;{\mu}M)$ activated the $K_{ATP}$ channels in the presence of ATP (0.3 mM) or AMP-PNP (0.3 mM) and in a partial rundown state. The effect of pinacidil $(10\;{\mu}M)$ was not affected by the pretreatment with protein tyrosine phosphatase 1B $(PTP1B,\;10\;{\mu}g\;ml^{-1}),$ but blocked by the pretreatment of protein phosphatase 2A $(PP2A,\;1\;U\;ml^{-1})$. In addition, pinacidil $(10\;{\mu}M)$ could not induce the opening of the reactivated $K_{ATP}$ channels in the presence of H-7 $(100\;{\mu}M)$ but enhanced it in the presence of ATP (1 mM) and genistein $(30\;{\mu}M).$ These results indicate that the $K_{ATP}$ channel-opening effect of pinacidil is not mediated via phosphorylation of $K_{ATP}$ channel protein or associated protein, although it still requires the phosphorylation of serine/threonine residues as a prerequisite condition.

• 대한전기학회:학술대회논문집
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• 대한전기학회 1999년도 하계학술대회 논문집 C
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• pp.1227-1229
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• 1999

The ATP Draw is a graphical mouse-driven preprocessor to ATP on the Windows Platform. User can build a graphical picture of the electric circuit by selecting components from menus. In this paper, ATP Draw is used to analyze power transformer transient characteristics and lightning overvoltage phenomenon in underground transmission cables. The results obtained by simulations will be used to identify the response of the digital protection algorithms in power system equipment

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1997년도 학술발표회
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• pp.11-12
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• 1997

A concept that extracellular ATP plays a role as a neurotransmitter is now widely accepted. ATP released from nerve terminals transmits both excitatory and inhibitory signals to postsynaptic neurons, muscle cells, and non-excitable cells. ATP-activated channels are effectors that convert the binding of ATP into the opening of ion channel pores in postsynaptic membrane.(omitted)

• 한국산학기술학회논문지
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• 제11권10호
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• pp.3911-3916
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• 2010

본 논문에서는 틸팅열차의 안전성 확보 및 운행효율 향상을 위해 "한국형 틸팅열차 신뢰성 평가 및 운용기술개발" 연구과제의 한 분야로 추진된 ATP 차상장치의 시운전시험에 대한 내용 및 결과를 제시하고 있다. 기존선의 속도 향상과 KTX 비수혜지역의 여객 서비스 향상을 위해 틸팅열차를 개발하였으며 개발된 틸팅열차의 신뢰성 평가를 위해 기존에 사용되고 있는 ATS 장치에 의한 12만 km 주행 시운전 시험을 진행하였다. KTX가 운행되지 않는 지역인 중앙선 및 충북선을 비롯한 6개 기존 노선을 200km/h 이상으로 고속화하기로 하였으며, 이에 따라 열차제어시스템은 기존의 ATS 장치에서 ATP 장치로 개량하여야 한다. 따라서 틸팅열차에도 ATP 차상장치를 설치하여 운행 적합성을 확인하여야 하기 때문에 경부선 및 호남선 ATP 구축사업에 사용된 것과 동일한 ATP 차상장치를 틸팅열차에 설치하여 시운전 시험을 수행하였으며 설치된 ATP 차상장치의 기능 및 성능이 틸팅열차의 운행에 적합함을 확인하였다.

• Archives of Pharmacal Research
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• 제29권11호
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• pp.1032-1041
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• 2006

Extracellular adenosine 5'-triphosphate (ATP) affects the function of many tissues and cells. To confirm the biological activity of ATP on human myeloid leukemic cells, F-36P and HL-60, cells were treated with a variety of concentrations of ATP. The stimulation with extracellular ATP induced the arrest of cell proliferation and cell death. from the analysis of Annexin-V staining and caspase activity by flow cytometry. The Annexin-V positive cells in both cell lines were dramatically increased following ATP stimulation. The expression of P2 purinergic receptor genes was confirmed, such as P2X1, P2X4, P2X5, P2X7 and P2Y1, P2Y2, P2Y4, P2Y5, P2Y6, P2Y11 in both leukemic cell lines. Interestingly, ATP induced intracellular calcium flux in HL-60 cells but not in F-36P cells, as determined by Fluo-3 AM staining. Cell cycle analysis revealed that ATP treatment arrested both F-36P and HL-60 cells at G1/G0. Taken together, these data showed that extracellular ATP via P2 receptor genes was involved in the cell proliferation and survival in human myeloid leukemic cells, HL-60 and F-36P cells by the induction of apoptosis and control of cell cycle. Our data suggest that treatment with extracellular nucleotides may be a novel and powerful therapeutic avenue for myeloid leukemic disease.

• Molecules and Cells
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• 제38권7호
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• pp.616-623
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• 2015

P2 receptors are membrane-bound receptors for extracellular nucleotides such as ATP and UTP. P2 receptors have been classified as ligand-gated ion channels or P2X receptors and G protein-coupled P2Y receptors. Recently, purinergic signaling has begun to attract attention as a potential therapeutic target for a variety of diseases especially associated with gastroenterology. This study determined the ATP and UTP-induced receptor signaling mechanism in feline esophageal contraction. Contraction of dispersed feline esophageal smooth muscle cells was measured by scanning micrometry. Phosphorylation of $MLC_{20}$ was determined by western blot analysis. ATP and UTP elicited maximum esophageal contraction at 30 s and $10{\mu}M$ concentration. Contraction of dispersed cells treated with $10{\mu}M$ ATP was inhibited by nifedipine. However, contraction induced by $0.1{\mu}M$ ATP, $0.1{\mu}M$ UTP and $10{\mu}M$ UTP was decreased by U73122, chelerythrine, ML-9, PTX and $GDP{\beta}S$. Contraction induced by $0.1{\mu}M$ ATP and UTP was inhibited by $G{\alpha}i_3$ or $G{\alpha}q$ antibodies and by $PLC{\beta}_1$ or $PLC{\beta}_3$ antibodies. Phosphorylated $MLC_{20}$ was increased by ATP and UTP treatment. In conclusion, esophageal contraction induced by ATP and UTP was preferentially mediated by P2Y receptors coupled to $G{\alpha}i_3$ and $G{\alpha}q$ proteins, which activate $PLC{\beta}_1$ and $PLC{\beta}_3$. Subsequently, increased intracellular $Ca^{2+}$ and activated PKC triggered stimulation of MLC kinase and inhibition of MLC phosphatase. Finally, increased $pMLC_{20}$ generated esophageal contraction.