• 콘크리트학회논문집
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• 제18권1호
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• pp.125-132
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• 2006

최근 들어 툭별한 물리적 방법을 사용하지 않고 내구성능이 저하된 콘크리트의 성능을 회복시키는 방법의 일환으로서 콘크리트 표면보호재에 대한 관심이 높아지고 있다. 표면보호는 직접적인 의미로서는 콘크리트 구조물의 표면을 보호하는 것뿐만아니라 다양한 열화요인의 침투를 억제함으로서 내부의 콘크리트 및 철근의 열화를 억제하여 콘크리트 구조물을 보호하게 된다. 이와 같은 표면보호재 중 함침계 표면보호재는 콘크리트 표면층의 공극에 충전 혹은 생성물을 석출시켜 치밀한 층으로 하느 충전계와 콘크리트 표면층의 외부 및 내부표면의 성질을 개선하는 표면계로 분류하는 것이 가능하다. 따라서 본 연구는 규플르오르화염을 주성분으로 하는 표면형 함침계 표면보호제 도포에 의한 콘크리트 표면의 세공구조의 변화 및 중성화, 염해, 화학적 침식 등의 내구성 향상을 실험실증적으로 검토함으로서 콘크리트 구조물의 내구성향상 방안을 제시하고자 한다. 그 결과, 표면보호제를 도포함으로서 모든 물시멘트비에서 도포전과 비교하여 전세공용적이 감소하고 있으며, 특히 50nm이상의 비교적 큰 세공경인 모세관공극의 용적이 감소함으로서 물흡수성, 중성화 저항성, 내황산성, 염소이온침투 저항성 등의 내구성 향상에 기여하는 것으로 나타났으며, 그 효과는 물시멘트비가 클수록 높게 나타났다.

• 한국환경성돌연변이발암원학회지
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• 제17권2호
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• pp.97-108
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• 1997

The drugs or xenobiotics introduced to the body, are detoxified through the process of biotransformation in the body. In this process, most of the insoluble compounds become more polar, soluble and easily excretable. But, parts of introduced materials are metabolized to highly reactive electrophilic carcinogens through activation pathways. These metabolites are toxic and can react with DNA, RNA and proteins which are nucleophilic compounds. The objective of this study is to illustrate the aleactivation pathways of two highly reactive epoxide compounds, vinyl carbamate epoxide (VCO) and 2'-(4-nitrophenoxy)oxirane (NPO). They are the ultimate electrophilic carcinogens of ethyl carbamate(urethane) and 4-nitrophenyl vinyl ether, respectively. In this research, we studied the inhibition of the mutagenic activities of VCO or NPO by nuchieophiles [glutahione(GSH) and N-acetylcysteine(NAC)], detoxifying enzymes[epoxide hydrolase and glutathione-S-transferase(GST)] and intracellular organelles (microsomes and cytosol). In addition we also tested the suppression of DNA adducts formation by GSH and NAC. The results are summerized as follow. 1. The microsomes and cytosol which contain epoxide hydrolase and GST, respectively, decreased the mutagenicity of VCO (74% and 95%, respecfivel), and NPO (35% and 93%, respectively). The nucleophilic GSH and NAC decreased the mutagenicity by 86% (VCO) and 80% (NPO), 76% (VCO) and 40% (NPO), respectively. 2. The purified epoxide hydrolase decreased the mutagenicity of two epoxides in a dose-dependent manner, and GSH also decreased the mutagenicity in the presence of GST. 3. Formation of two DNA adducts, 7-(2'-oxoethyi)guanine (OEG) and N2,3-ethenoguanine(EG), were compared in the presence of calf thymus DNA and epoxide (VCO or NPO) in vitro system. The amounts of DNA adducts were decreased in the presence of GSH (25% and 29% in VCO, 32% and 29% in NPO), and NAC (14% and 16% in VCO, 21% and 11% in NPO), respectively. From these results, it is concluded that the ultimate carcinogenic metabolites, VCO and NPO, can be made in the body, but much of them may be inactivated and detoxified by the nucleophilic GSH, NAC and detoxifying enzymes (epoxide hydrolase and GST). Therefore, by these mechanism, the formation of DNA adducts and mutagenic activities of these two epoxides may be lowered in vivo.

• 대한약리학회지
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• 제25권1호
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• pp.67-74
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• 1989

배뇨반사수축에 미치는 ${\alpha}$-수용체 및 내인성 catecholamine의 영향을 검토하기 위하여 체중 $190{\sim}220g$의 암컷흰쥐를 사용하여 부신절제 및 6-OHDA, yohimbine, prazosin 그리고 hexamethoium 처치시의 guanabenz에 의한 배뇨반사 수축을 비교 관찰하였든 바 그 결과는 다음과 같다. Guanabenz 3, 10 및 $30\;{\mu}g/kg$를 정맥주사하였을 때 용량증가에 따라 배뇨 반사수축의 크기와 횟수가 감소되었으며 $100\;{\mu}g/kg$투여시에는 완전히 억제되었다. 국소적용시에는 약하였고, 측뇌 실내투여시에는 거의 나타나지 아니하였다. 그리고 phenylephrine은 배뇨반사수축에 아무런 영향을 주지 않았다. 6-OHDA를 처치시 방광최고내압과 수축크기가 유의성있게 증가 되었으나, 부신절제나 yohimbine, prazosin, hexamethonium 투여로는 방광수축에 거의 변화가 없었다. Guanabenz의 배뇨반사수측의 크기와 횟수의 억제에 대한 용량반응곡선이 hexamethonium, 부신절제, 6-OHDA-, yohimbine 처치시 오른쪽으로 이동하였다. Guanabenz에 의한 억제작용이 yohimbine 처치>6-OHDA>부신절제>hexamethonium순으로 약화되었으나 prazosin처치로는 약화되지 아니하였다. 이상과 같은 결과로 미루어 guanabenz에 의한 배뇨만사수축의 억제작용은 ${\alpha}_1$-수용체와는 관계없이 ${\alpha}_2$-수용체흥분작용에 기인되며, 이 억제작용은 부신수질 및 교감신경말단에서 유리되는 catecholamines이 관여된 것으로 사료된다.

• Molecules and Cells
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• 제43권10호
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• pp.889-897
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• 2020

K-RAS is frequently mutated in human lung adenocarcinomas (ADCs), and the p53 pathway plays a central role in cellular defense against oncogenic K-RAS mutation. However, in mouse lung cancer models, oncogenic K-Ras mutation alone can induce ADCs without p53 mutation, and loss of p53 does not have a significant impact on early K-Ras-induced lung tumorigenesis. These results raise the question of how K-Ras-activated cells evade oncogene surveillance mechanisms and develop into lung ADCs. RUNX3 plays a key role at the restriction (R)-point, which governs multiple tumor suppressor pathways including the p14^ARF-p53 pathway. In this study, we found that K-Ras activation in a very limited number of cells, alone or in combination with p53 inactivation, failed to induce any pathologic lesions for up to 1 year. By contrast, when Runx3 was inactivated and K-Ras was activated by the same targeting method, lung ADCs and other tumors were rapidly induced. In a urethane-induced mouse lung tumor model that recapitulates the features of K-RAS-driven human lung tumors, Runx3 was inactivated in both adenomas (ADs) and ADCs, whereas K-Ras was activated only in ADCs. Together, these results demonstrate that the R-point-associated oncogene surveillance mechanism is abrogated by Runx3 inactivation in AD cells and these cells cannot defend against K-Ras activation, resulting in the transition from AD to ADC. Therefore, K-Ras-activated lung epithelial cells do not evade oncogene surveillance mechanisms; instead, they are selected if they occur in AD cells in which Runx3 has been inactivated.

• Journal of Korean Neurosurgical Society
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• 제29권8호
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• pp.985-994
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• 2000

Objective : There are some advantages of trigeminal evoked potential(TEP) recording compared to other somatosensory evoked potential(SSEP) recordings. The trigeminal sensory pathway has a pure sensory nerve branch, a broader receptive field in cerebral cortex, and a shorter pathway. Despite these advantages, there is little agreement as to what constitutes a normal response and what wave forms truly characterize the intraoperative TEP. This study presents the normative data of TEP recorded on the epidural surface of the rat with a platinum ball electrode. Materials & Methods : Under general anesthesia with urethane, the adult Sprague-Dawley male rats(300-350g) were given electrical stimulation with two stainless steel electrodes which were inserted into the subcutaneous layer of the area around whiskers. A reference electrode was positioned in the temporalis muscle ipsilateral to the recording site. Results : TEPs were recorded in the Par I area of somatosensory cortex and recorded most apparently on the point of 2mm posterior from the bregma and 6mm lateral from the midline. The typical wave form consisted of 5 peaks (N1-P1-N2-P2-N3 according to emerging order, upward negativity). Each latency to corresponding peaks was not influenced by the different intensities of stimulation, especially from 1 to 5mA. Average latencies of 5 peaks were in the following order ; 7.7, 11.1, 15, 22.3, 29.4ms. There was also no significant difference between latencies before and after administration of muscle relaxant(pancuronium). For the electrophysiological localization of recorded waves, the action potential of a single unit was recorded with glass microelectrode(filled with 2M NaCl, $3-5M{\Omega}$) in the thalamus of rat. A sharp wave was recorded in the VPM nucleus, in which the latency was shorter than that of N1. This suggests that all 5 peaks were generated by neural activities in the suprathalamic pathway. Conclusion : In terms of recording near-field potentials, our data also suggests that TEP in the rat may be superior to other SSEPs. In overall, these results may afford normative data for the studies of supratentorial lesions such as hydrocephalus or cerebral ischemia which can have an influence on near-field potentials.

• Journal of Pharmaceutical Investigation
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• 제27권4호
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• pp.303-311
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• 1997

Proliposomal patch of clenbuterol, ${\beta}_2-agonist$ bronchodilator, was prepared and its feasibility as a novel transdermal drug delivery system was examined. Proliposomal granules containing clenbuterol was prepared by a standard method using sorbitol and lecithin with (Rx 2) or without cholesterol (Rx 1). The porous structure of sorbitol in the proliposomes was maintained allowing tree flowability of the granules. Following contact with water, the granules were converted probably to liposomes almost completely within several minutes. It indicates that proliposomes may be hydrated, when they are applied on the skin under occlusive condition in vivo, by the sweat to form liposomes. Clenbuterol release from Rx 1 and Rx 2 proliposomes to pH 7.4 isotonic phospate buffer (PBS) across cellulose membrane (mol. wt. cut-off of 12000-14000) was retarded significantly compared with that from the mixture of clenbuterol powder and blank proliposomes. Interestingly, proliposomes prepared with lecithin and cholesterol (i.e., Rx 2 proliposomes) showed much more retarded release of clenbuterol than proliposomes prepared only with lecithin (i.e.. Rx 1 proliposomes), indicating that clenbuterol release from proliposomes can be controlled by the addition of cholesterol to the proliposomes. Proliposomal patches were prepared using PVC film as an occlusive backing sheet, two sides adhesive tape (urethane, 1.45 mm thickness) as a reservoir for proliposome granules and Millipore MF-membrane (0.45 mm pore size) as a drug release-controlling membrane. Rx 1 or Rx 2 proliposomes containing 4.6 mg of clenbuterol were loaded into the reservoir of the patch. Clenbuterol release from the patches to pH 7.4 PBS was determined using USP paddle (50 rpm)-over-disc release method. Clenbuterol release from the proliposomal patches was much more retarded even than from a matrix type clenbuterol patch (Boehringer Ingelheim ltd). Being consistent with clenbuterol release from the proliposomal granules, the release from the patches was highly dependent on the presence of cholesterol in the proliposomes : Patches containing Rx 2 proliposomes showed several fold slower drug release than patches containing Rx 1 proliposomes. When the patch containing Rx 1 proliposomes was applied on to the back of a hair-removed rat, clenbuterol concentration in the rat blood was maintained during 6-72 hrs. Transdermal absorption of clenbuterol from the patch was accelerated when the patch was prehydrated with 50 ml of pH 7.4 PBS before topical application. Above results indicate that sustained transdermal delivery of clenbuterol is feasible using proliposomal patches if the cholesterol content and pore size of the release rate-controlling membrane of patches, for example, are appropriately controlled.

• 대한약리학회지
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• 제28권1호
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• pp.1-9
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• 1992

최근에 개발된 생체내 미세투석법을 이용하여 정상혈압 흰쥐(WKY)와 자연발생성 고혈압 흰쥐(SHR)의 후 시상하부에서 세포외액의 모노아민과 그 대사체들을 측정하였다. 뇌정위 고정장치에 의해서 미세투석관을 후 시상하부에 위치시킨후 링거액으로 관류하였다. 모노아민과 그 대사체들은 고속액체 크로마토그라피와 전기화학 검출기를 이용하여 정량하였다. 미세투석관의 시험관내 회수율 검사 결과, 관류액의 유속과 신경화학물질의 상대적 회수율 사이에는 역비례 관계가 있음이 확인되었다. 정상 혈압 흰쥐에서 후 사상하부의 관류액으로 부터 축정한 각종 신경화학물질의 세포외액 농도는 도파민 32nM, 노르에피네프린 50nM, 에피네프린 50nM, 세로토닌 73nM, 3.4-dihydroxyphenylacetic acid(DOPAC) 281 nM, homovanillic acid(HVA) 181 nM, 5-hydroxyindoleacetic acid(5HIAA) 3767nM이었다. 후 시상하부에서 측정된 신경전달물질의 기준치는 WHY와 SHR사이에 차이가 없었으나, DOPAC, HVA, 5HIAA의 기준치는 WKY에 비해서 SHR에서 유의하게 높게 나타났다. 본 연구는 중추 신경화학물질들의 생체내 측정에 미세투석법을 이용할 수 있음을 보여주었다.

• Journal of Yeungnam Medical Science
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• 제3권1호
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• pp.279-285
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• 1986

가토의 Ouabain유발 부정맥에 미치는 Carbamazepine의 영향을 검색한 결과 다음과 같은 결론을 얻었다. 1. Ouabain을 지속적으로 정맥 주사하여 64+$8.8{\mu}g/kg$이 투여되었을 때 부정맥이 발생 했으며, 이 양을 부정맥 유발 가능용량으로 정했다. 2. Ouabain $64{\mu}g/kg$을 단회 정맥 주사했을 때 발생한 부정맥은 약 7~9분간 지속된 후 모든 예에서 자연 소실되었고, 정상 심박동으로 회복된 지 20분 후 다시 동량의 Ouabain을 정맥 주사했을 때 모든 예에서 다시 나타났다. 3. 부정맥 유발 용량($64{\mu}g/kg$)의 Ouabain을 단회 정맥 주사한 후 부정맥이 나타난 것을 관찰 즉시 Carbamazepine을 투여한 결과 즉시 정상 신박동으로 환원되었으며 어느 정도 지속된 후 모든 예에서 부정맥이 발생했으나 즉시 동량의 Carbamazepine 투여로 다시 정상 심박동으로 환원되었다. 한편, Carbamazepine의 양이 증가되면서 항 부정백 작용의 기간은 길어졌으나 항 부정맥 작용없이 사망한 예가 많아졌다. 4. Carbamazepine을 단독 투여 해 본 결과 그 양이 증가함에 따라 심한 서맥, A-V block, 심방 세동 등이 나타나면서 심장이 정지함을 볼 수 있었다. 이상의 실험 결과로 미루어 Carbamazepine은 Ouabain의 독작용에 의한 심한 부정맥을 일시적으로 억제할 수 있으며, 보다 대량에서는 그 항 부정맥 작용이 보다 오래 지속할 수 있으나 Carbamazepine 자체의 심장에 대한 부작용이 발현될 위험이 존재한다고 생각된다.

• 보존과학회지
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• 제31권4호
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• pp.351-360
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• 2015

본 논문은 석조문화재 해체과정에서 발생할 수 있는 표면 손상부분 보강방안 마련을 위해 승화성 강화처리제인 시클로도데칸을 사용한 임시 강화처리제를 연구한 결과이다. 기존 발포성 우레탄 폼을 사용한 보강방법의 단점을 보완하기 위해 시클로도데칸을 용제에 희석하여 표면 및 박리 내부를 보강하여 부재를 해체한 후 $60^{\circ}C$ 내외의 열을 가해 승화시키는 처리방법에 관한 것이다. 이와 같은 방법은 시클로도데칸이 전량 승화되는 뛰어난 가역성과 손상된 표면의 보강과 강화에 필요한 강도를 담보할 수 있다는 장점이 있으나, 용제에 따라 효과가 다를 수 있으므로 본 연구에서는 석유에테르에 희석하는 방법 또는 중탕하여 적용하는 방법에 대한 연구를 진행하였다. 실험결과 현장에서의 작업여건을 고려하여 박리부분 주입 및 충전은 석유에테르 중탕 방법, 표면 도포는 석유에테르에 희석한 시클로도데칸으로 임시 강화처리하는 것이 가장 적합할 것으로 확인되었다.

• Journal of Microbiology and Biotechnology
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• 제20권9호
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• pp.1331-1338
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• 2010

This study was designed to investigate the potentially protective effects of Curcuma longa Linn. extract (CLE) on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity in rats. Male Sprague-Dawley rats were pretreated with 50 or 100mg/kg of CLE or 100mg/kg of butylated hydroxytoluene(BHT) for 14 days before $CCl_4$ administration. In addition, the CLE control group was pretreated with 100mg/kg CLE for only 14 days. Three hours after the final treatment, a single dose of $CCl_4$ (20mg/kg) was administrated intraperitoneally to each group. After the completion of this phase of the experiment, food and water were removed 12 h prior to the next step. The rats were then anesthetized by urethane and their blood and liver were collected. It was observed that the aspartate aminotransferase and alanine aminotransferase activities of the serum, and the hepatic malondialdehyde levels had significantly decreased in the CLE group when compared with the $CCl_4$-treated group. The antioxidant activities, such as superoxide dismutase, catalase, and glutathione peroxidase activities, in addition to glutathione content, had increased considerably in the CLE group compared with the $CCl_4$-treated group. Phase II detoxifying enzymes, such as glutathione S-transferase, were found to have significantly increased in the CLE group as opposed to the $CCl_4$-treated group. The content of Nrf2 was determined by Western blot analysis. Pretreated CLE increased the level of nuclear translocated Nrf2, and the Nrf2 then increased the activity of the antioxidant and phase II detoxifying enzymes. These results indicate that CLE has protective effects against $CCl_4$-induced hepatotoxicity in rats, via activities of antioxidant and phase II detoxifying enzymes, and through the activation of nuclear translocated Nrf2.