• 대한전기학회:학술대회논문집
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• 대한전기학회 1993년도 하계학술대회 논문집 B
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• pp.605-608
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• 1993

Breakdown characteristics of a small rod-to-rod microairgap has been studied for obtain an optimum breakdown voltage and an airgap spacing to be used as an emission control means by the electrical arc-burning unburnt carbon particulates exhausted from a power station burner. It is found that the breakdown voltage at the rod-to-rod airgap spacing in the rang of $1{\sim}100{\mu}m$ decreased with decrease in the rod-to-rod airgap spacing. And there were no minimum breakdown voltage on a $V_b$-Pd characteristics which is known as the minimum voltage in Paschen's law in air atmosphere. Breakdown voltages of the airgap at the constant airgap spacing were $V_{b-dc}>V_{b-ac}>V_{b-pulse}$, and it was lowest for the pulse voltage applied. As a result, it is found that a pulse power was one of effective power compared with dc or ac to be used as such an unburnt carbon particulate emission control means and the airgap spacing became to several tens ${\mu}m$, then the breakdown voltages were down to several handreds voltages.

• The Korean Journal of Physiology and Pharmacology
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• 제26권1호
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• pp.25-36
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• 2022

To identify the effect and mechanism of carbon monoxide (CO) on delayed rectifier K⁺ currents (I_K) of human cardiac fibroblasts (HCFs), we used the wholecell mode patch-clamp technique. Application of CO delivered by carbon monoxidereleasing molecule-3 (CORM3) increased the amplitude of outward K⁺ currents, and diphenyl phosphine oxide-1 (a specific I_K blocker) inhibited the currents. CORM3-induced augmentation was blocked by pretreatment with nitric oxide synthase blockers (L-NG-monomethyl arginine citrate and L-NG-nitro arginine methyl ester). Pretreatment with KT5823 (a protein kinas G blocker), 1H-[1,-2,-4] oxadiazolo-[4,-3-a] quinoxalin-1-on (ODQ, a soluble guanylate cyclase blocker), KT5720 (a protein kinase A blocker), and SQ22536 (an adenylate cyclase blocker) blocked the CORM3 stimulating effect on I_K. In addition, pretreatment with SB239063 (a p38 mitogen-activated protein kinase [MAPK] blocker) and PD98059 (a p44/42 MAPK blocker) also blocked the CORM3's effect on the currents. When testing the involvement of S-nitrosylation, pretreatment of N-ethylmaleimide (a thiol-alkylating reagent) blocked CO-induced I_K activation and DL-dithiothreitol (a reducing agent) reversed this effect. Pretreatment with 5,10,15,20-tetrakis(1-methylpyridinium-4-yl)-21H,23H porphyrin manganese (III) pentachloride and manganese (III) tetrakis (4-benzoic acid) porphyrin chloride (superoxide dismutase mimetics), diphenyleneiodonium chloride (an NADPH oxidase blocker), or allopurinol (a xanthine oxidase blocker) also inhibited CO-induced I_K activation. These results suggest that CO enhances I_K in HCFs through the nitric oxide, phosphorylation by protein kinase G, protein kinase A, and MAPK, S-nitrosylation and reduction/oxidation (redox) signaling pathways.

• 한국자원식물학회지
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• 제19권2호
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• pp.331-335
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• 2006

해양심층수의 처리에서 처리농도가 높아짐에 따라 대조구보다 작물의 생육이 떨어짐으로 과실의 생육과 수량은 감소한다. 평균 생체중은 전체적으로 양액 내 해양심층수의 농도가 높을수록 감소하는 경향이었다. 특히 1화방에 비하여 2화방의 생계중이 처리농도가 높아질수록 현저히 감소하였다. 과실의 고형물 함량은 심층수의 농도가 높을수록 증가하는 경향이었다. 제 1화방의 경우 10mM과 20mM 처리구에서 가장 많이 증가하였으나, 제 2화방의 경우 30mM과 40mM 처리구가 가장 많이 증가하였다. 토마토 과실을 구성하는 당은 glucose와 fructose가 대부분이었고 sucrose는 미량만 검출되었다. 과실 내 fructose와 glucose의 함량이 처리농도가 높을수록 줄어드는 이유는 심층수에 의해 생긴 염 스트레스에 의해 잎의 생육이 저하된 것에 기인한 것으로 보인다. 이 실험에서는 20mM 처리구의 라이코펜 함량이 가장 많은 것으로 나타났으며 무처리구와 나머지 처리구의 함량은 크게 차이가 없는 것으로 나타났다. 심층수 처리는 염 스트레스로 작용하여 에틸렌 형성을 유도 및 촉진시켜 과실의 성숙이 빨라진 것으로 생각되었다. 해양심층수의 처리는 가용성 고형물 함량과 lycopene 함량을 높임으로써 토마토 과실의 품질에 효과가 있으나 생체중의 감소로 인한 생산량 감소가 생긴다. 이에 적정처리 농도인 20mM로 처리하였을 때 고품질의 과실 생산이 가능함과 동시에 생산량 감소를 최소화할 수 있을 것으로 생각된다. 전체 ginsenosides 중 Re의 농도가 전 처리구에서 모두 가장 높은 함량을 차지하였으며, ginsenosides의 총함량은 EC 8 처리구를 제외한 전 처리구에서 대조구 보다 높게 나타났다. PT/PD의 값은 EC 8 처리구가 1.31로 가장 낮았고, EC 6 처리구가 2.52로 가장 높았으며, 나머지 처리구는 큰 차이가 없었다.

• 동아시아식생활학회지
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• 제24권3호
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• pp.335-350
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• 2014

Compared to the large numbers of studies on the diabetes, hyperlipidemia and cancer therpeutic effects of ginseng, the anti-obese effect and mechanisms of ginsengs have not been studied as much. To determine the effects of ginseng on obesity, 14 keywords (ginseng, ginsenoside, obesity, weight, fat, diet, overeat, appetite, lipid, 3T3-L1, adipocyte, food intake, adipogenesis and lipolysis) were combined in searching a database. Fifty-six articles published from 1983 to 2012 as well as 656 patents registered until Aug $17^{th}$, 2012, were screened for anti-obese effects of ginseng. In the classification of experimental methods, 16 papers on 3T3-L1 cells, 38 papers on animals and three papers on human were reviewed. In terms of obese mechanisms of action, the most commonly used biomarkers were in order of lipid profiles > weight change > blood glucose > adipocytokine. Most ginseng studies on obesity focused on AMPK, $PPAR{\gamma}$, GLUT-4, PI3K and SREBP-1. Korean white ginseng extracts and Re repressed the lipogenesis genes such as PPARc2, SREBP-1c, LPL, FAS and DGAT1. However, ginseng or ginsenosides, PD (Rb1) and PT (Re), showed different or contradictory results. Water and ethanol extraction of ginseng showed contradictory effects on the secretion of inflammatory cytokines, wheras IL-6 was repressed by ethanol extracts and TNF-${\alpha}$ repressed by Re in vitro. Based on the literature, further studies on anti-obese mechanisms of ginseng, such as the inflammation-related obesity or cross signals between the adipocytes and the environments, are needed, instead of more studies on its hypolipidemic and hypoglycemic effects.

• 대한한방내과학회지
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• 제30권2호
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• pp.388-398
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• 2009

Background and Objective: Luffae Fructus Retinervus (LFR) is used for investigating symptoms of inflammation. We have evaluated the anti-inflammatory effect of LFR by analyzing the expression of pro-inflammatory cytokines. Materials and Methods : We differentiated THP-l cells into macrophage-like cells by treatment with PMA. Inflammation was induced by treatment with LPS and PMA. We determined the safe concentration of LFR by using the MTS and MTT assays and using PD 98059 as a negative control for comparison of the anti-inflammatory effect of LFR. Results : The MTS and MTT analysis showed that the cell survival rate was >80% within the LFR concentration range of 10-100 ng/ml and began to decrease to >80% at 1 ${\mu}g/ml$. By RT-PCR analysis, the gene expression of TNF-${\alpha}$, IL-8, TGF-${\beta}$, IL-6, IL-${\beta}$1, and IL-10 levels were down-regulated when monocyte-derived macrophages were treated with concentrations of LFR between 10 ng/mL and 100 ng/mL. Conclusion : We conclude that LFR exerts an anti-inflammatory effect by inhibiting the expression of pro-inflammatory activity. The results suggest a promising way to treat general inflammatory diseases.

• Archives of Pharmacal Research
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• 제28권10호
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• pp.1190-1195
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• 2005

The objective of this study was to develop an assay for mequitazine (MQZ) for the study of the bioavailability of the drug in human subjects. Using one mL of human plasma, the pH of the sample was adjusted and MQZ in the aqueous phase extracted with hexane; the organic layer was then evaporated to dryness, reconstituted and an aliquot introduced to a gas chromatograph/mass spectrometer (GC/MS) system with ion-trap detector. Inter- and intra-day precision of the assay were less than 15.1 and $17.7{\%}$, respectively; Inter- and intra-day accuracy were less than 8.91 and $18.6{\%}$, respectively. The limit of quantification for the current assay was set at 1 ng/mL. To determine whether the current assay is applicable in a pharmacokinetic study for MQZ in human, oral formulation containing 10 mg MQZ was administered to healthy male subjects and blood samples collected. The current assay was able to quantify MQZ levels in most of the samples. The maximum concentration ($C_{max}$ was 8.5 ng/mL, which was obtained at 10.1 h, with mean half-life of approximately 45.5 h. Under the current sampling protocol, the ratio of $AUC_{t{\rightarrow}last}$ to $AUC_{t{\rightarrow}{\infty}}$ was $934{\%}$, indicating that the blood collection time of 216 h is reasonable for MQZ. Therefore, these observations indicate that an assay for MQZ in human plasma is developed by using GC/MS with ion-trap detector and validated for the study of pharmacokinetics of single oral dose of 10 mg MQZ, and that the current study design for the bioavailability study is adequate for the drug.

• The Korean Journal of Physiology and Pharmacology
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• 제20권1호
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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.

• 대한핵의학회지
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• 제39권1호
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• pp.9-14
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• 2005

목적 : 좌각차단이나 우심실조율박동과 같은 부정맥을 가진 환자들에서 심근관류는 의미있게 변화한다는 것이 알려져 있다. 비정상적인 심근관류는 심실조기흥분에 의해서도 야기될 수 있다고 알려져 있지만, 그 위치 범위 강도와 부전도로와의 관계는 아직 정립되어 있지 않았다. 이에 WPW 증후군 환자에서 부전도로의 위치와 SPECT상에서 관류양상의 관계에 대해 알아보고자 하였다. 대상 및 방법 : WPW 증후군 환자 11명에 대해 Adenosine 99m-Tc MIBI 또는 Tl-201 심근관류 SPECT를 시행하였다, 관류결손은 Fitzpatrick's algorithm을 기초로 한 심전도 또는 전기생리학적검사 및 전극도자 절제술을 이용한 부전도로의 위치와 비교하였다. 결과: 11명의 환자들의 평균 나이는 $39.9{\pm}8.6$세 였고, 비특이적인 흉통을 호소하거나, 증상이 없었다. 11명 모두 관삳동맥의 위험도에 관한 계산도표를 이용하여 관상동맥질환의 확률을 예측했으나 0.1 이하로 위험도가 낮았고 이중 4명은 관상동맥조영술을 시행한 결과 3명은 정상이었고 1명은 관동맥 협착 (50%) 부위의 심근혈류가 정상이었다. 4명의 환자에서 전기생리학적검사 및 전극도자 절제술을 시행하였다. 9명의 가역적 그리고 1명의 비가역적 관류결손이 관찰되었고. 범위는 소에서 대까지 강도는 경도에서 중등도까지 나왔다. 부전도로의 위치가 우외측인 1명은 관류결손이 없었으나, 그 외의 환자들은 다양한 양상을 보였다. 부전도로의 위치가 좌외측인 환자중 1명에 대해 전극도자 절제술을 시행하였고 6주후에 SPECT를 한 결과 시술 전에 있던 관류결손의 범위가 현저하게 감소하였다. 결론: WPW환자에서 심근관류결손은 다양한 범위, 강도 및 위치를 가진다. 거의 대부분의 환자에서 비정상적인 관류결손이 나타났으나, SPECT 소견으로 부전도로의 위치를 특이적으로 예측하기는 어려웠다. 그러므로 WPW증후군 환자에서 심근관류 SPECT의 결과를 주의 깊게 해석해야 한다.

• Asian Pacific Journal of Cancer Prevention
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• 제14권3호
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• pp.1965-1967
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• 2013

Background: To obtain the maximum additional information about the prognosis of gastric cancer, we compared CA-50 with other previously defined markers. Materials and Methods: This hospital based study was carried out in the Department of Biochemistry of Nepalese Army Institute of Health Sciences between $1^{st}$ July 2012 and $31^{st}$ December 2012. The variables collected were age, gender, AFP, CEA, CA19-9, and CA50, assayed with ELISA reader for all cases. The cut off values for serum AFP, CEA, CA19-9, and CA-50 were 10 ${\mu}g/l$, 10 ${\mu}g/l$, 37 U/ml, and 20 U/ml, respectively according to the manufacturer's instructions. Approval for the study was obtained from the institutional research ethical committee. Results: Of the 40 examined patients, 13 patients had tumors located in the upper third of the stomach, 6 patients had tumors in the middle third, 16 patients had tumors in the lower third, and 5 patients had tumors occupying two-thirds of the stomach or more. The distribution of lymph node staging of the patients was as follows: 7 patients belonged to N0, 9 patients to N1 stage, 10 patients to N2 stage, and 14 patients to N3 stage. The statistical method of Cox proportional hazards using multivariate analysis also illustrated that tumor markers including CEA (2.802), CA19-9 (2.690), CA50 (2.101), were independent prognostic factors, as tumor size (1.603), and lymph node stage (1.614). Conclusions: The tumour markers now available, like CEA, CA 19-9 and CA 50, chiefly perceive advanced gastric cancer. The preoperative rise in those tumour marker level have a prognostic significance and may be clinically helpful in choosing patients for adjuvant management.

• Parasites, Hosts and Diseases
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• 제62권1호
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• pp.30-41
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• 2024

The dense granule protein of Toxoplasma gondii, inhibitor of signal transducer and activator of transcription 1 (IST) is an inhibitor of signal transducer and activator of transcription 1 (STAT1) transcriptional activity that binds to STAT1 and regulates the expression of inflammatory molecules in host cells. A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-γ and TNF-α, is activated without infection. In relation to inflammatory liver injury, we hypothesized that Toxoplasma gondii inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1/IRF-1 mechanism in liver inflammation. This study used IFN-γ and TNF-α as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1/IRF-1 axis. In stable cells transfected with TgIST, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-κB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9/10/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3/8/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-γ/TNF-α stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.