• Journal of the Korean Electrochemical Society
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• v.16 no.2
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• pp.65-69
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• 2013

In order to improve capacitance of activated carbon for electric double layer capacitors, peptide bond was induced on the surface of the activated carbon by urea. Urea induced activated carbon has been stabilized through carbonization. Electrochemical characteristics was observed by cyclic voltammetry for specific capacitance, electrochemical impedance spectroscope for measuring resistance and charge-discharge for testing the cyclic ability. In the result, specific capacitance is increased about 22.9% than the activated carbon. And it shows excellent cycle performance and decreasing resistance with the introduction of nitrogen functional groups.

• Applied Chemistry for Engineering
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• v.5 no.1
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• pp.37-43
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• 1994

Mononitrotoluenes were reduced to aminotoluenes using porphyrin as a catalyst in the presence of several types of reductants including hydrogen sulfide and 1, 4-dithiothreitol(DTT). Intermediates and final products of porphyrin-catalyzed reduction of mononitrotoluenes were identified and a pathway for the reduction of the nitro group to the corresponding amino group was proposed. The optimum pH for the reduction was determined. The catalytic activity of the porphyrin was confirmed by UV/VIS absorption spectra and basic kinetics of porphyrin-catalyzed reduction were studied. Of several types of reductants tested, DTT sodium hydrosulfite, and hydrogen sulfide were seen to give significant reduction of nitrobodies. When hydrogen sulfide was used as a reductant hydrogen sulfide and nitrotoluenes were removed simultaneously.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.5
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• pp.435-440
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• 2013

While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 ${\mu}g/kg/day$) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynucleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.

• Journal of Yeungnam Medical Science
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• v.16 no.2
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• pp.181-192
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• 1999

Background: Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells, accounts for the biological activity of endothelium derived relaxing factor. Previous studies demonstrated that nitric oxide inhibitor, $N^{\omega}$-Nitro-L-Arginine(NNA) diminished the hyperdynamic splanchnic and systemic circulation in portal hypertensive rats The present study was done to determine the role of nitric oxide in the development of hyperdynamic circulations in the prehepatic portal hypertensive rat model produced by partial portal vein ligation. Methods: The portal hypertensive rats were divided into water ingestion group and NNA ingestion group. After partial portal vein ligation, NNA ingestion group and water ingestion group received NNA 1mg/kg/day and plain water through the mouth for 14 days, respectively. Cardiac output, mean arterial pressure, organ blood flow and porto-systemic shunting were measured by radioisotope labeled microsphere methods. Vascular resistances were calculated by standard equation. Results: There were significant decreases in mean arterial pressure, increases in cardiac output and cardiac index, and decreases in total systemic and splanchnic vascular resistance in portal hypertensive rats compared to normal control group (p<0.01). Compared to the water ingestion group, significantly increased mean arterial pressure with decreased cardiac output and cardiac index were developed in the NNA ingestion group. Total systemic and splanchnic vascular resistance were significantly increased in the NNA ingestion group compared to water ingestion group (p<0.05). But, there was no significant difference in portal pressure between the two groups. Conclusion: The hemodynamic results of this study indicate that hyperdynamic circulation in prehepatic portal hypertensive rat mode1 was attenuated by ingestion of NNA. Nitric oxide may play an important role in the development of hyperdynamic circulation with splanchnic vasodilation in chronic portal hypertension.

• Korean Journal of Weed Science
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• v.14 no.2
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• pp.81-93
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• 1994

This study was conducted to characterize herbicidal activity of the new type diphenylether compounds inducing bleaching(whitening) in relation to their chemical structures and to find out the herbicidal action mechanism. Bleaching was highly appeared in the compounds which have short chain alkyl or allyl group of cabamoyl type in meta position of A ring and nitro group in para position of B ring, and KC6361 showed the highest efficacy among these derivatives. Rice was tolerant to KC6361 at 2.0kg/ha. The applications of this compound at 0.25~1.0kg/ha provided acceptable control of the various weeds including large crabgrass, barnyardgrass, pigweed and so on. In the dark condition, KC6361 decreased carotenoid contents but increased chlorophyll in etiolated cucumber cotyledon. By the increase of light intensity, the carotenoid biosynthesis was more inhibited than the chlorophyll biosynthesis. The incorporation of $C^{14}$-acetate into lipid was slightly inhibited. Both KC6361 and norflurazon stimulated growth of dwarf rice(cv. Daneunbanju). These results suggest that both KC6361 and norflurazon may have the same action sites. To confirm this hypothesis, the changes of carotenoid intermediates in cucumber cotyledon and barnyardgrass leaf treated with KC6361 were investigated. Phytoene and phytofluene were increased but ${\beta}$-carotene was decreased, indicating that KC6361 inhibited phytoene and/or phytofluene dehydrogenase like norflurazon.

• Biomedical Science Letters
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• v.11 no.3
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• pp.355-363
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• 2005

This study aimed to investigate the cerebroprotective effect of vascular endothelial growth factor (VEGF) on permanent focal cerebral ischemia in Sprague-Dawley rats. Right middle cerebral artery (MCA) was occluded for 6 and 24 hours by an intraluminal monofilament technique. An open cranial window was made on the right parietal bone for determination of continuous changes in regional cerebral blood flow (rCBF) by laser-Doppler flowmetry. The infarct size was morphometrically determined using the 2,3,5-triphenyltetrazolium chloride technique. Brain edema was determined by measuring brain water content. In normal rats, rCBF was significantly increased by intravenous infusion of VEGF for 10 minutes. The VEGF-induced increase in rCBF was significantly inhibited by pretreatment with suramin, a heparin-binding growth factor inhibitor as well as $N^{\omega}-nitro-L-arginine$, a nitric oxide synthase inhibitor. In focal cerebral ischemic rats, the amplitude of decrease in rCBF during ischemic period was significantly less in VEGF-treated group, compared with that in vehicle-treated group. The cerebral infarct size was reduced by VEGF in a dose-dependent manner. The brain edema formation was dose-dependently reduced by VEGF in 24-hour MCA occlusion group but not in 6-hour MCA occlusion group. It is suggested that VEGF not only improves the rCBF during cerebral ischemic period but also reduces the brain edema formation, and thereby exert a protective effect on focal cerebral ischemia in rats.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.345-351
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• 1998

The role of nitric oxide (NO) in the hemorrhagic hypotension was examined using a NO synthase inhibitor, $N^{\omega}-nitro-L-arginine$ methyl ester (L-NAME), in conscious rats. The rats were bled at a constant rate (2 ml/kg/min) through a femoral arterial catheter until the mean arterial pressure (MAP) was reduced by 50 mmHg. We studied the responses to hemorrhage under normal condition (Control) and after the pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6, NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME produced a sustained increase in MAP and decrease in heart rate (HR). During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated groups than in Control group, but the control group showed same response to NOX1.6. HR greatly increased in NOX groups. The recovery from hemorrhagic hypotension was slowed in the control group, which was not treated with L-NAME. In comparison with the control group, NOX8 and NOX1.6-treated groups registered a significant recovery in MAP during the 15 min recovery period, but NOX40 brought about only a slight increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced significant bradycardic responses before and after hemorrhage and significant depressor response only after hemorrhagic hypotension regardless of pretreatment with L-NAME. These data suggest that the role of NO in blood pressure regulation is greater after hemorrhagic hypotension than basal condition, but the effect of NO can be detrimental to the recovery from hemorrhagic hypotension. In addition, the bradycardic response of L-arginine provides indirect evidence that NO may inhibit sympathetic activity, especially after hemorrhagic hypotension.

• Journal of Nutrition and Health
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• v.26 no.7
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• pp.829-838
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• 1993

This study was designed to compare the effect of different dietary fats on the incidence of colorectal tumor, the level of plasma thromboxane B2(TXB2) and fatty acid profiles of platelet and colonic mucosal lipids in N - methyl - N - nitro - N - nitrosoguanidine(MNNG) - treated rats. Male Sprague Dawley rats, at 8 weeks old, were divided into 2 groups and infused intrarectally with saline(control group) or with 2mg MNNG(carcinogen-treated group) twice a week for 3 weeks. Each group was again divided into 4 groups and fed one of four diets(BT, CO, PO, FO) containing dietary fat at 9%(w/w) level for 37 weeks, Dietary fats were beef tallow(7.2%)+corn oil(1.8%) for BT, corn oil(9.0%) for CO, perilla oil(9.0%) for PO, fish oil (6.5%)+corn oil (2.5%) for FO diets. MNNG-treated rats had colonic tumor, while no tumors(adenocarcinoma and adenoma) than others. Tumor sizes in BT-MNNG rats ranged from 2mm papillary form to 15mm of polypoid. However, the size of tumors in PO-MNNG or FO-MNNG rats could not be measured by gross examination. BT-MNNG and CO-MNNG groups were higher in the level of plasma TXB2 and the ratio of c20 : 4/c20 :5 platelet. PO-MNNG groups were lower in the ratio of c20 : 4/c20 : 5(p<0.05) in fatty acid of colonic mucosal lipids suggesting that perilla oil and fish oil could reduce the level of PGE2 and TXB2 by modifying its precursor content and restrain tumor promotion in colon. Effect of perilla oil rich in $\alpha$-linolenic acid on colon carcinogenesis was similar to that of fish oil and thus perilla oil could have a protective effect against colon cancer possibly by inhibiting the production of arachidonic acid metabolite.

• Korean Journal of Microbiology
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• v.20 no.2
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• pp.53-66
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• 1982

1. When Chong Ju and Chung Ju soils possessing different physicochemical properties were treated with 500 ppm of TOK and incubated in flooded anaerobic condition for 2, 4, and 6 months, respectively, they produced 4-Chloro-4'-amino diphenyl ether, 2,4-Dichloro-4'-amino diphenyl ether(amin-TOK), N-[4'-(4-Chlorophenoxy)] phenyl acetamide, and N-[4'-(4-Chlorophenoxy)] phenyl formamide as the metabolities. This result indicates that TOK undergose the reduction of its $NO_2\;to\;NH_2$ group, dechlorination, acetylation, and formylation under this condition. The cleavage of ether linkage does not occur. In addition, TOK degrades more readily in Chung Ju soil which is characterized by pH 6.43 and higher contents of $Ca^{++}$ and C.E.C. than in Chong Ju soil which is lower in pH, $Ca^{++}$, and C.E.C. 2. In the aerobic incubation of TOK of 25ppm in Chung Ju soil suspension for 21 days, the ratio of the resulting metabolites, TOK : amino-TOK : 4-Chloro-4'-amino diphenyl ether was 100 : 130 : 76. Meanwhile, in the 42 day incubation, the ratio was 100 : 19 : 5, which indicates that TOK in aerobic condition dose not necessrily degrade as a function of the incubation period. 3. The citrate buffer extract of Chung Ju soil has the capability of degrading TOK, which was verified to be due to the action of the microorganisms involved. 4. Twelye strains of soil bacteria were isolated from the TOK-treated soils. In the incubation of TOK in pure cultures of the respective isolates, the strain T-1-1 isolated from Chong Ju soil had almost no degradability whereas the strain T-2-3 was the most potent. The degradation of TOK by the isolates constituted mostly the reduction of the nitro group to amino group. 5. In a test for the degradability of TOK by some selected microorganisms, Pseudomonas species were more potent than fungi. Yet, Isolate B which had been isolated from Chung Ju soil suspension was the most potent.

• Tuberculosis and Respiratory Diseases
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• v.43 no.3
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• pp.420-433
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• 1996

Background : There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitirc oxide synthase(NOS) activity in the neurogenic inflammation of airways. Method : To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, $N^{\omega}$-nitro-L-arginine (L-NNA) on plasma extravastion were evaluated in four groups of Sprague-Dawley rats ; sham operation group(sham NANC group), electrical vagal stimulation group(NANC2 group), intravenous pretreatment groups with FK224 (1mg/kg ; FK224 group), and L-NNA(1mg/kg ; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells(iNOS), brain(bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results : The results are that plasma extravsation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment(P<0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224(P<0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea(p<0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion : These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.