• 한국의학물리학회:학술대회논문집
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• 한국의학물리학회 2006년도 제33회 추계학술대회 발표논문집
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• pp.142-142
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• 2006

• 식품기술
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• 제24권4호
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• pp.640-646
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• 2011

• Journal of Radiation Protection and Research
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• 제11권1호
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• pp.51-56
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• 1986

방사선(放射線)의 의학적(醫學的) 진단치료(診斷治療) 이용률(利用率)이 증가(增加)함에 따라 의료인(醫療人)과 환자(患者)들에 대한 방사선(放射線) 피폭확률(被曝確率)이 비예적(比例的)으로 증가(增加)되어 정량적(定量的)인 분석(分析)과 피폭관리(被曝管理)의 필요성(必要性)이 요구(要求)되고 있다. 연세(延世) 암센터는 암치료(癌治療)를 위하여 설치사용(設置使用)되고 있는 의료용(醫療用) 고(高)에너지 선형가속기(線型加速器)에 대한 누출(漏出) 및 산난선(散亂線)의 방어벽(防禦壁)과 방어계획(防禦計劃)이 이미 준비(準備)되어 있다. 그러나 장치(裝置)의 사용빈도(使用頻度)가 증가(增加)됨에 따라 치료실내(治療室內)의 공간(空間) 선량분포(線量分布)와 광핵반응(光核反應)으로 인한 유도방사능(誘導放射能)의 위험성(危險性)을 인식(認識)하고 이들에 대한 노출량(露出量)을 전리함(電離函), 열형광측정기(熱螢光測程器) 및 에너지 분석기등(分析器等)을 이용(利用)하여 측정(測定)하였다. 18 MeV 전자선(電子線)에 의한 실중선량(室中線量)은 1 m 지점(地點)에서 종양선량(腫瘍線量)의 0.02%였고 X-선(線)에 의한 실중선량(室中線量)은 약(約) 0.12%였다. 선형가속기(線型加速器)에서 10 MV X-선(線)을 30 Gy 조사(照射)한 직후 광핵반응(光核反應)에 의한 유도방사능(誘導放射能)을 측정(測定)한 결과(結果) 0.65 mR/hr 였으며 광핵반응(光核反應)에 의한 중성자(中性子) 방사화(放射化)는 주로 Cu-64, W-185, Mo-94, Ta-182등(等)의 원소(元宵)로 추정(推定)할 수 있었다.

• Nuclear Engineering and Technology
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• 제2권2호
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• pp.73-84
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• 1970

Solanum andigena의 괴경생성형상과 스테톨의 관계를 구명하기 위하여 방사성 매바론산을 이용하여 대사를 연구하였다. 괴경생성에 단일광조성수도를 요하는 단일식물과 괴경을 생성치 않는 장일식물을 접목 시켰을때 장일식물이 괴경생성 홀몬을 받아 괴경을 생성하는 현상을 스테로이드와 결부시켜 구명할려고한것이다. 이 연구에서 각종 방사성 스테톨이 특수장치한 까스 크로마토 그라피로서 분리 측정되었다. 여기서 분리된 각종 스테톨이 직정 괴경생성홀몬이라는 근거는 찾을 수 없으며, 이들이 괴경의 포대성장에 필요한 인자로서 관여하고 있는 것으로 논의되었다.

• 대한미생물학회지
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• 제35권3호
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• pp.203-214
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• 2000

Porphyromonas gingivalis has been implicated in periodontal diseases. Accumulating evidence suggests that cardiovascular disease is the most prevalent medical problem in patients with periodontal diseases. In order to check the possibility that P. gingivalis is involved in coronary heart disease, the present study was performed to observe P. gingivalis adherence and invasion of human coronary artery endothelial cells (HCAEC) and production of cytokines and growth factors by HCAEC upon P. gingivalis infection. $^3H$-labeled P. gingivalis 381 was incubated with HCAEC for 90 min. The radioactivity of the washed HCAEC was a measure of the absorbed (adhering and invading) P. gingivalis. The absorption radioactivity of the HCAEC infected by P. gingivalis was determined to be 59.58% of the input bacterial cells. In contrast, the absorption radioactivity of the cells infected by S. gordonii Challis which was employed as a control was negligible (0.59%). DPG3, a P. gingivalis mutant defective of fimbriae, appeared to be impaired to some extent in capability of adherence/invasion as compared to that of the parental strain 381, showing 43.04% of the absorption radioactivity. The absorption radioactivity of the HCAEC infected by P. gingivalis 381 in the presence of excessive fimbriae at the concentrations of $50\;{\mu}g$ and $100\;{\mu}g/ml$ was 57.27 and 45.44%, respectively. Invasion of HCAEC by P. gingivalis 381 was observed by an antibiotic (metronidazole) protection assay and transmission electron microscopy (TEM). In the antibiotic protection assay, invasion by the bacterium was measured to be 0.73, 1.09, and 1.51% of the input bacterial cells after incubation for 30, 60, and 90 min, respectively. Invasion by DPG3 was shown to be 0.16% after 90-min incubation. In comparison of invasion efficiency at 90 min of the incubation, the invasion efficiency of DPG3 was 0.37% while that of its parental strain 381 was 2.54%. The immunoblot analysis revealed fimbriae of P. gingivalis did not interact with the surface of HCAEC. These results suggest that fimbriae are not the major contribution to the adherence of P. gingivalis to HCAEC but may be important in the invasion of HCAEC by the bacterium. The presence of cytochalasin D ($1\;{\mu}g/ml$) and staurosporine ($1\;{\mu}M$) reduced the invasion of HCAEC by P. gingivalis 381 by 78.86 and 53.76%, respectively, indicating that cytoskeletal rearrangement and protein kinase of HCAEC are essential for the invasion. Infection of P. gingivalis induced HCAEC to increase the production of TNF-${\alpha}$. by 60.6%. At 90 min of the incubation, the HCAEC infected with P. gingivalis cells was apparently atypical in the shape, showing loss of the nuclear membrane and subcellular organelles. The overall results suggest that P. gingivalis may cause coronary heart disease by adhering to and invading endothelial cells, and subsequently damaging the cells.

• Journal of Radiation Protection and Research
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• 제14권2호
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• pp.45-50
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• 1989

원자력병원 싸이클로트른 중성자선(中性子線) 치료실의 방사선 준위(準位)를 측정함으로써 방사선 안전도를 검토하여 보았다. 중성자선 치료실내 방사선 노출은 주로 isocentric gantry에 내장된 중성자선 표적(標的)과 조사야(照射野)를 결정하는 collimator의 방사화(放射化)로 인한 잔류방사능(殘留放射能) (remanent radioactivity)에 의해 결정 된다. 측정결과 선량율(線量率)은 과다하지 않았고 개인 집적선량(集積線量)도 허용치 이내였다. 방사선 작업종사자로서의 의료기사는 환자치료 시 매 조사(照射) 완료 직후부터 5분간 멸살(滅殺)시간을 갖도록 조치하였다.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2003년도 추계학술대회
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• pp.1180-1185
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• 2003

One of the main degradation of steam generator tubes is stress corrosion cracking induced by residual stress. The resulting damages can cause tube bursting or leakage of the primary water which contained radioactivity. Primary water stress corrosion crack occurs at the location of tube/tubesheet hard rolled transition zone. In order to investigate the effect of shot peening on stress corrosion cracking, stress intensity factors are calculated for the crack which is located in the induced residual stress field.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.219-219
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• 1996

Mucin release from hamster tracheal surface epithelial(HTSE) cells can be stimulated by extracellular ATP via activation of P$_2$ purinoceptors located on the cell surface which appears to be coupled to phospholipase C via G proteins. However, our preliminary data indicate that the ATP-induced mucin release involves, in part, activation of PKC, but not an increase in the intracellular Ca++ level, suggesting the presence of another pathway which is separate from the PLC-PKC pathway, In this study, we intended to confirm the previous observation and subsequently identify an additional mechanism. Confluent HTSE cells were metabolically labeled with either $^3$H-glucosamine or $^3$H-arachidonic acid(AA), and release of either $^3$H-mucin or $^3$H-AA was quantified following various treatments. $^3$H-mucin was assayed using the sepharose CL-4B gel-filtration method, whereas $^3$H-AA liberation was measured by counting $^3$H-radioactivity in the chase medium. We found that: (1)Desensitization of PKC by pretreatment with PMA completely abolished the mucin releasing effect of PMA but partially inhibited the ATP-induced mucin release; (2) ATP increases release of $^3$H-AA in a dose-dependent fashion; (3) mepacrine, an inhibitor of PLA$_2$, attenuates ATP-induced mucin release in a dose-dependent fashion. These results confirm our previous notion that the PLC-PKC pathway is responsible, in part, for ATP-induced mucin release. Furthermore, activation of PLA$_2$ appears to be an additional pathway which is involved in ATP-induced mucin release.

• Archives of Pharmacal Research
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• 제22권5호
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• pp.474-478
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• 1999

Modulation of unscheduled DNA synthesis by dehydroepiandrosterone (DHEA) after exposure to various chemical carcinogens was investigated in the primary rat hepatocytes. Unscheduled DNA synthesis was induced by treatment of such direct acting carcinogens as methly methanesulfonate (MMS) and ethyl methanesulfonate (EMS) or procarcinogens including benzo(a)pyrene (BaP) and 7, 12-dimethylbenz(a)anthracene (DMBA). Unscheduled DNA synthesis was determined by measuring [methyl-3H]thymidine radioactivity incorporated into nuclear DNA of hepatocytes treated with carcinogens in the presence or absence of DHEA. Hydroxyurea $(5{\times}10^{-3} M)$was added to growth medium to selectively suppress normal replication. DHEA at concentrations ranging from $(1{\times}10^{-6} M)$ to$(5{\times}10^{-4} M)$ did not significantly inhibit unscheduled DNA synthesis induced by either MMS $(1{\times}10^{-4} M)$ or EMS $(1{\times}10^{-2} M)$. In contrast, DHEA-significantly inhibited unscheduled DNA synthesis induced by BaP $(6.5{\times}10^{-5} M)$ and DMBA.$(2{\times}10^{-5} M)$. DHEA-induced hepatotoxicity in rats was examined using lactate dehydrogenase (LDH) release as an indicator of cytotoxicity. DHEA exhibit no significant increase in LDH release compared with the control at 18 h. These data suggest that nontoxic concentration of DHEA does not affect the DNA excision repair process, but it probably influence the enzymatic system responsible for the metabolic activation of procarcinogens and thereby decreases the amount of the effective DNA adducts formed by the ultimate reactive carcinogenic species.

• 대한핵의학회지
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• 제18권1호
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• pp.45-53
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• 1984

The purpose of this study is to observe the changes of pulmonary capillary permeability and various hemodynamic parameters before and after Positive End-Expiratory Pressure(PEEP) in Adult Respiratory Distress Syndrome (ARDS). Using a canine oleic acid induced ARDS model, we measured the pulmonary capillary permeability with a slope of lung: heart radioactivity ratio, hemodynamic parameters with Swan-Ganz catheter and blood gas tensions. 1) In normal and ARDS dogs, the PEEP didn't significantly influence the slope of lung: heart radioactivity ratio. But in ARDS group the slope index was increased compaired with that of control group (p<0.05). 2) Also in ARDS group, $PaO_2$ was significantly decreased, and $PaCO_2,\;PvCO_2$, MPAP, $AaDO_2$, Qs/Qt were significantly increased compared with those of control group (p<0.05). 3) In normal dogs, the PEEP didn't influence blood pH or gas tension, $AaDO_2$, Qs/Qt, or hemodynamics. 4) In ARDS dogs, however, the PEEP significantly increased $PaO_2$ and decreased $AaDO_2$, Qs/Qt (p<0.05).