• Journal of Chest Surgery
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• 제33권2호
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• pp.132-138
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• 2000

Background: Inhaled nitric oxide therapy causes selective pulmonary vasodilation in congenital heart diseases with pulmonary hypertension. However discontinuation of inhaled nitric oxide therapy may be complicated by abrupt life-threatening rebound pulmonary hypertension(RPH) The purpose of this study was to prevent by comparing group I(without RPH n=13) and group II(with RPH n=6) to determine the risk factors involved inthe development of the RPH. Material and Method: Between Januarty 6, 1998 and April 14, 1999. we studied 19 consecutive children who were treated with inhaled nitric oxide for clinically significant pulmonary hypertension after an open heart surgery for congenital heart disease. the ratio of males and females was 12:7 ranging in age from 10 days to 6040 days(16 years) To identify the effects of nitric oxide between two groups we measured heart rate mean and systolic pulmonary arterial pressure mean and systolic systemic arterial pressure central venous pressure pH paO2/FiO2 and O2 saturation before and after the initiation and just before the withdrawal of the inhaled nitric oxide. result: In 6 of 19 patients(32%) withdrawal of inhaled nitric oxide caused RPH. In the two groups inhaled nitrix oxide decreased in pulmonary arterial pressure(PAP) without decreasing the systemic arterial pressure(SAP) and increased PaO2/FiO2 Compared with patients who had no RPH(group I) patients who had RPH(group II) were older in age (1204$\pm$1688 versus 546$\pm$1654 days p<0.05) received less nitric oxide therapy(34$\pm$18 versus 67$\pm$46 hours p<0.05) has shorter weaning process(5$\pm$3 versus 15一13 hours p<0.05) and received lowerconcentration of initial nitric oxide supply(11$\pm$8 versus 17$\pm$8 ppm p>0.05) and lower concentration just before the withdrawal nitric oxide(4.2$\pm$2.6 versus 5.6$\pm$2.6 ppm, p>0.05) Conclusion : We speculate that older age shorter of nitric oxide therapy shorter weaning process are the risk factors of RPH.

• 한국콘텐츠학회논문지
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• 제9권7호
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• pp.211-217
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• 2009

본 연구에서는 알긴산올리고당의 일부 방사선 방어효과를 규명하기 위해 마우스에 3 Gy 선량의 방사선을 1회 전신 조사하여 방사선 유도 nitric oxide를 측정하였다. 측정결과 방사선조사 대조군에서 nitric oxide 생성이 하강된 반면 방사선조사 전 3일간 처치군 및 방사선조사 후 3일간 처치군에서 유의한 생성 증가를 보였고, 특히 방사선조사 전 3일간 처치군에서 가장 큰 차이를 보였다(P<0.001). 결론적으로, 항산화효과가 탁월한 알긴산올라고당은 nitric oxide의 생성 증가를 촉진시킴으로써 일부 방사선 방어작용을 수행한다는 사실을 규명하였고, 화학적 독성이 적은 자연산생물이 방사선방어제로 활용될 수 있음을 확인하였다.

• Toxicological Research
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• 제11권2호
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• pp.303-308
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• 1995

Nitric oxide, a physiological transmitter, is reported to mediate cellular injury in various tissues. Its reactivity to free radical is believed to be one of the reasons for its involvement in cytotoxicity. Menadione, a representative quinone, is cytotoxic to several cell systems including isolated hepatocyte, endothelial cell and red blood cells. Its toxic mechanism is related to oxidative stress, mediated by toxic free radicals. Our previous studies demonstrated that menadione induced cell lysis and increase of oxygen consumption in platelets. It has been reported that platelets have nitric oxide producing enzyme, nitric oxide synthase. Thus, we have investigated to manifest the role of nitric oxide.in menadione-induced cytotoxicity in rat platelets. Menadione induced cytotoxicity in platelets was unaffected by $N^G$-nitro-arginine methyl ester (L-NAME), selective and competitive inhibitor of nitric oxide synthase. We also invesitgated the role of extracellular nitric oxide in menadione-induced cytotoxicity of platelets by addition with sodium nitroprusside (SNP). SNP did not affect platelet cytotoxicity by menadione. These results suggested that nitric oxide which was generated endogeneously or exogeneously might have a negligible role in menadione-induced cytotoxicity in rat platelets.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1998년도 Proceedings of UNESCO-internetwork Cooperative Regional Seminar and Workshop on Bioassay Guided Isolation of Bioactive Substances from Natural Products and Microbial Products
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• pp.145-145
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• 1998

In the present study, we have demonstrated that taurine could stimulate the production of nitric oxide and the activity of ERK2 (extracellular signal regulated protein kinase or pp42 MAP kinase). Nitric oxide(NO), the product of inducible nitric oxide synthase(iNOS), is known to be implicated in the metabolism of bone. ERK cascade plays a key role in the gene expression of iNOS in osteoblastic cell. We investigated whether taurine (l-20mM) could stimulate ERK2 activity, nitric oxide production, and inducible nitric oxide synthase in osteoblast-like UMR-106 cells. Nitric oxide was measured spectophotometrically as nitrite and the activation of ERK2 and iNOS was studied using Western 145 blot analysis. Taurine increased the production of nitric oxide in a dose-dependent manner and the effect was reached to a maximum at 10 mM. The activation of iNOS were consistent with NO levels. The tyrosine phosphorylation of ERK2 was increased by taurine in a time-dependent manner. The these result suggest that taurine might stimulate the production of nitric oxide in osteoblast-like cells by the activation of ERK2 and could regulate the metabolism of bone via nitric oxide.

• 한국진공학회:학술대회논문집
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• 한국진공학회 2015년도 제49회 하계 정기학술대회 초록집
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• pp.158-158
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• 2015

Myoblast are myogenic precursors that proliferate, activate, and differentiate on muscle injury to sustain the regenerative capacity of skeletal muscle; The neuronal isoform of nitric oxide synthase (nNOS, termed also NOS-I) is expressed in normal adult skeletal muscle, suggesting important functions for Nitric oxide (NO) in muscle biology1,2,3. However, the expression and subcellular localization of NO in muscle development and myoblast differentiation are largely unknown. In this study, we examined effects of the nitric oxide generated by a microwave plasma torch, on proliferation/differentiation of rat myoblastic L6 cells. Experimental data pertaining to nitric oxide production are presented in terms of the oxygen input in units of cubic centimetres per minute. The various levels of nitric oxide are observed depending on the flow rate of nitrogen gas, the ratio of oxygen gas, and the microwave power4. In order to evaluate the potential of nitric oxide as an activator of cell differentiation, we applied nitric oxide generated from the microwave plasma torch to L6 skeletal muscles. Differentiation of L6 cells into myotubes was significantly enhanced the differentiation after nitric oxide treatment. Nitric oxide treatment also increase the expression of myogenesis marker proteins and mRNA level, such as myogenin and myosin heavy chain (MHC), as well as cyclic guanosine monophosphate (cGMP), However during the myotube differentiation we found that NO activate oxidative stress signaling erks expression. Therefore, these results establish a role of NO and cGMP in regulating myoblast differentiation and elucidate their mechanism of action, providing a direct link with oxidative stress signalling, which is a key player in myogenesis. Based on these findings, nitric oxide generated by plasma can be used as a possible activator of cell differentiation and tissue regeneration.

• BMB Reports
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• 제28권4호
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• pp.301-305
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• 1995

Considering the stimulatory effects of ginsenosides from Panax ginseng C. A. Meyer on the release of nitric oxide from bovine aortic endothelial cells in vitro and vasodilatation of rabbit pulmonary artery in vivo, the present study is designed to investigate the mechanism of nitric oxide release by ginsenosides in calf pulmonary artery endothelial cells, Nitric oxide release was determined in endothelial cells treated with ginsenosides and compared with those of the receptor-dependent agonists, bradykinin and ADP and the receptor-independent calcium ionophore $A_{23187}$. The results showed that total saponin and ginsenoside $Rg_1$, not $Rb_1$, stimulated nitric oxide release measured as conversion to L-citrulline. The nitric oxide releasing properties of total saponin and ginsenoside $Rg_1$ were different; total saponin stimulated only conversion to L-citrulline, like $A_{23187}$, while ginsenoside $Rg_1$ stimulated both L-arginine transport and conversion to L-citrulline, as bradykinin or ADP did.

• 한국자동차공학회논문집
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• 제6권1호
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• pp.27-35
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• 1998

This study describes the influence of combustion parameters on the nitric oxide emission, such as injection timing, air flow rate, injected amount of fuel, and compression ratio of engine. In order to determine the influence factors on the nitric oxide emission, the experiment were investigated with various parameters of engine cycle. According to the results of this study, the retardation of injection timing and the increases of airflow rate, and the decreases of fuel injection amount reduce the nitric oxide concentration in the exhaust emissions. Also, the increases of compression ration of engine increase in the concentration of nitric oxide formation in the combustion chamber. The results of this study give a guideline to decrease the nitric oxide formation by using the simulation program.

• 대한의생명과학회지
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• 제18권4호
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• pp.420-427
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• 2012

Sprague-Dawley (SD) rats were orally administered with NG-nitro-L-arginine methyl ester (L-NAME), which inhibits or blocks the production of nitric oxide from L-arginine in vascular endothelial cells and vessel tissue. We examined the effects of nitric oxide on some physiological changes such as blood pressure and heart rate, and confirms the apoptosis induced by the suppressed nitric oxide activity in the kidney. This study was performed to investigate correlation between the activities of nitric oxide and apoptosis by immunohistochemical changes of apoptotic control proteins with regulated chronic inhibition of nitric oxide. In the kidney from L-NAME-treated group, immunohistochemical reaction to the antigens of apoptosis inhibiting proteins such as bcl-2 and bcl-xL, exhibited a time-dependent reduction. The expression of apoptosis-inhibiting proteins such as bax and p53 increased expression in proportion to the duration of treatment. The most sensitive apoptosis regulating proteins to L-NAME were p53 in stimulation and bcl-2 in inhibition, respectively.

• 약학회지
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• 제42권5호
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• pp.540-543
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• 1998

The nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase is known to be responsible for the vasodilation and hypotension observed in septic shock. We have found that 8-epi-xanthatin from Xanthium strumarium L. inhibited the production of NO in LPS-activated RAW 264.7 cells ($IC_{50}$ value was 1.5 ${\mu}$M). This activity was resulted from the suppressing of inducible nitric oxide synthase enzyme expression.

• 대한치과의사협회지
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• 제39권11호통권390호
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• pp.936-946
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• 2001