• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2001.05a
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• pp.325-328
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• 2001

정상적인 뉴런의 활성전위는 외부에서 일정한 자극이 인가되었을 때 세포막을 기준으로 하여 각 이온간의 농도 차에 의해 발생한다. 최근에 관심이 되어지고 있는 쇼크에 의한 세포가 손상이 발생할 경우, 즉 신호를 받아들이고 전달하는 뉴런 중에서 축색에 이온채널이 이상증세를 발생하면 신경 전달 흐름을 흐트러지게 하여 이웃한 정상세포에게 커다란 영향을 미치게 된다. 이것은 병리학적인 중요한 역할을 하는 축색 내에 이상이 발생하였다고 가정을 하지만 이 가정을 뒷받침 해 주는 증거는 매우 적다고 보고되고 있다. 최근 연구에서 손상된 축색의 모델은 쇼크이후에 이온의 칼륨 채널에 blocking 현상이 발생하여 나트륨 이온이 다수 유입됨을 고려하고있다. 이에 본 연구에서는 쇼크나 충격에 의해 축색의 손상을 입을 경우 운동신경의 변형으로부터 병리학적인 중요한 이상결과를 일으킬 수 있는 상태를 고려하여 신경모델을 설계해 시뮬레이션 해 보았다.

• Environmental Analysis Health and Toxicology
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• v.19 no.3
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• pp.295-305
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• 2004

본 연구에서는 유전자 재조합 발광 박테리아를 이용하여 농약에 대한 박테리아의 스트레스 반응과 세포 독성을 분석하였다. 15종류의 농약에 대하여 유전자 손상, 생물막 손상, 산화적 손상 및 단백질 손상을 측정할 수 있는 발광 박테리아와 독성 유무로 인한 세포 독성을 측정할 수 있는 발광 박테리아, 5종을 이용하여 스트레스 반응을 분류하고 세포 독성 정토를 분석하였다. 그 결과, 농약의 화학적 구조가 박테리아의 스트레스 반응에 영향을 미치며, 산화과정이 진행 됨에 따라 독성의 작용 기작이 변하는 것을 확인 할 수 있었다. 이와 같은, 유전자 재조합 발광 박테리아를 이용한 생물체내의 독성 메커니즘에 대한 분석은 생태계 유해물질들에 의한 독성을 분석하고 예상하기 위해 적용될 수 있을 것이다.

• Clinical and Experimental Pediatrics
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• v.49 no.2
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• pp.198-202
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• 2006

Purpose : Fas is a cell surface receptor that transduces apoptotic death signals. Interaction of extracelluar domain of Fas with Fas ligand(FasL) triggers the apoptotic process in many diseases. We investigated the expression of Fas and FasL in the hippocampus of 7-day-old newborn rat brains following hypoxia-ischemia injury. Methods : The 7-days-old newborn rats were exposed to 8 percent oxygen for two hours after the ligation of right common carotid arteries. The newborn rats were killed and their brains were removed at 12, 14 and 48 hours after hypoxic-ischemic injury. The expressions of Fas and FasL of the right hippocampus were observed by western blotting and immunofluorescent staining. Results : Fas and FasL were strongly expressed in the right hippocampus ipsilateral to the ligation of the common carotid artery by western blotting at 12 hours following hypoxic-ischemic injury, and then slowly decreased. The immunofluorescent expressions of Fas and FasL strongly increased in the CA1 area of the right hippocampus at 12 and 24 hours following hypoxic-ischemic injury. The immunofluorescent expression of Fas decreased at 48 hours, but the expression of FasL persisted strongly at 48 hours following hypoxic-ischemic injury. Conclusion : The interaction of Fas with FasL on the cell surface may be involved in neuronal injury following hypoxic-ischemic injury in the developing brain.

• 한국체육학회지인문사회과학편
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• v.54 no.5
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• pp.769-780
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• 2015

This study investigated the changes in inflammatory mediators, immunocompetent cells and bone merrow progenitor cells by the magnitude of muscle damage and type of the muscle contraction in the elderly. Twenty older adults who had not been involved in a resistance-training program at least 6 months prior to the present study were assigned to eccentric exercise group (ECC, n=10) and concentric exercise group (CON, n=10). All subjects performed 10 sets of 6 maximal isokinetic eccentric (ECC 1) or concentric (CON) contractions with the non-dominant arm in a randomized, with 4 wk between bouts (ECC 2). Skeletal muscle damage index (ROM, VAS, Plasma CK), inflammation mediators (TNF-α, IL-1, IL-6), immunocomperent cells (CD3+, CD4+, CD8+, CD19+), bone merrow progenitor cell (CD34+) and leukocytes were measured before, immediately after, 2, 24, 48, 72, and 96 h after exercise. Changes in ROM and VAS were greater (P<.05) after ECC 1 than CON and ECC 2. Increases in TNF-α and IL-6 were greater (P<.05) 24, 48 and 72 h after ECC 1 than CON and ECC 2. Increases in neutrophils were greater (P<.05) 2 h after ECC 1 than CON and ECC 2. It was confirmed that muscle damage was greater following eccentric than concentric contractions as well as first bout than second bout in the elderly, and suggested that TNF-α, IL-6 and neutrophils should closely correlate with magnitude of muscle damage.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.43 no.4
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• pp.281-287
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• 2017

Stress in skin plays a significant role in both the direct/indirect regulation of cellular processes occurring in hair, which in turn affect the hair cycle. However, experimental data regarding the effects of stress-related corticotropin releasing factor (CRF) released by stress on the apoptotic process involved in hair is limited. Therefore, we investigated the acceleration of early-stage apoptosis induced by atopy-related stress using a 2,4-dinitrochlorobenzene NC/Nga mice model. Expression of CRF, its related proteins, annexin V, and mitochondrial dysfunction were measured by immunohistochemical analyses. Atopic stress strongly stimulated stress hormones response, such as CRF and adrenocorticotropic hormone, in outer epithelial sheath of the hair. Moreover, its stress induced mitochondrial damage and early-stage apoptosis of cells in hair root. These findings suggest that hair damage due to apoptosis in atopy model is accelerated in a high CRF environment. Importantly, the effect of stress-related CRF on apoptosis processes involved in atopy dermatitis-related hair loss, suggests that the CRF-regulating development or maintenance materials may provide effective therapeutic strategies for hair health.

• 대한방사선방어학회:학술대회논문집
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• 2011.04a
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• pp.74-75
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• 2011

• Korean Journal of Clinical Laboratory Science
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• v.51 no.2
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• pp.205-213
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• 2019

The protective effect of Agrimonia pilosa var. (AP) extract on potassium dichromate ($K_2Cr_2O_7$)-induced cytotoxicity in cultured NIH3T3 fibroblasts, was examined by performing an XTT assay for the cell viability and antioxidative effects, such as lactate dehydrogenase (LDH) activity and superoxide anion-radical (SAR) scavenging activity. In this study, $K_2Cr_2O_7$ decreased the cell viability significantly in a dose-dependent manner, and the $XTT_{50}$ value was determined to be $37.5{\mu}M$, which was highly-toxic according to the Borenfreund and Puerner' toxic criteria. The antioxidant, butylated hydroxytoluene (BHT), increased remarkably the cell viability damaged by $K_2Cr_2O_7$-induced cytotoxicity in these cultures. With regard to the protective effect of the AP extract on $K_2Cr_2O_7$-induced cytotoxicity, AP extract produced a significant increase in cell viability and antioxidative effects as the inhibitory ability LDH and SAR scavenging ability. These findings suggest that oxidative stress is involved in the cytotoxicity of $K_2Cr_2O_7$, and the AP extract effectively protected the cells from $K_2Cr_2O_7$-induced cytotoxicity by antioxidative effects. These results suggest that natural resources, such as AP extract, may be a putative therapeutic agent for the diminution or treatment of cytotoxicity induced by heavy metallic bases, such as $K_2Cr_2O_7$ correlated with oxidative stress.

• Journal of Applied Biological Chemistry
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• v.64 no.1
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• pp.69-74
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• 2021

Chronic alcohol is responsible for oxidative stress and neurodegenerative diseases such as dementia. In the present study, we investigated the antioxidant activity and protective effects of seed of Carthamus tinctorius L. on ethanol-induced C6 glial cells. Antioxidant effect of seed of C. tinctorius L. was measured by scavenging activity of 1,1-diphenyl-2-prcrylhydrazy (DPPH), hydroxyl radical (·OH), superoxide radical, and nitric oxide. The seed of C. tinctorius L. extract showed significant radical scavenging activities in a concentration-dependent manner. In particular, it revealed strong DPPH and ·OH scavenging activity, displaying more than 80% at 500 and 100 ㎍/mL, respectively. Treatment of 500 mM ethanol to C6 glial cell led to decline of cell viability and elevation of reactive oxygen species (ROS) generation. However, seed of C. tinctorius L.-treated groups significantly increased cell viability and decreased ROS levels, compared to ethanol-induced control group. These results suggest that seed of C. tinctorius L. would have protective effect against neuronal oxidative stress induced by alcohol.

• KSBB Journal
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• v.23 no.5
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• pp.381-386
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• 2008

Lipophilic ammonia is toxic gas and can easily diffuse across cell membranes. Excess ammonia is implicated in the pathogenesis of several metabolic disorders including hepatic encephalopathy and may result in the death. The purpose of this study was to clarify the inhibition effect of metronidazole on liver cell damage due to ammonia in human Hep G2 cell and rat hepatocytes. The effects of metronidazole were studied in ammonium chloride treated human Hep G2 cell (75 mM) and rat hepatocyte (100 mM) following $0.1{\mu}M$ metronidazole treatment. In MTZ+AC group, cell viabilities increased prominently and LDH activities decreased over 25% than AC group. Furthermore, ammonia level according to ammonium chloride treatment reduced over 30% and lipid peroxidation as an index of cell membrane damage decreased more than twice. By comparison with control, catalase activity showed more than 30% reduction in AC group while less than 10% reduction in MTZ+AC group, respectively. In addition, MTZ+AC group showed the similar cell structure as control in cell morphology study by using light microscope, and represented fluorescent intensity decrement compared with AC group in fluorescent microscopic study with avidin-TRITC fluorescent dye. And cleaved PARP expression due to ammonia reduced twofold or more in MTZ+AC group. As the results suggest, metronidazole may protect the liver cell by inhibiting cell damages due to ammonia and be used for an effective antagonist of ammonia in hyperammonemia.

• Journal of Chest Surgery
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• v.35 no.2
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• pp.87-93
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• 2002

Background: Predicting the important role of intercellular adhesion molecule-1 expression on the acute ischemia-reperfusion injury, we set out to demonstrate it by assessing the degree of expression of ICAM-1 after warm ischemia-reperfusion in canine unilateral lung ischemia model. Material and Method: Left unilateral lung ischemia was induced by clamping the left hilum for 100 minutes in seven adult mongrel dogs. After reperfusion, various hemodynamic pararmeters and blood gases were analyzed for 4 hours, while intermittently clamping the right hilum in order to allow observation of the injured Ieft lung function. The pulmonary venous blood was collected serially to measure TNF- and cICAM-1 level. After 4 hours of reperfusion, the lung tissue was biopsied to assess cICAM-1 expression, and to measure tissue malondialdehyde(MDA) and ATP level. Result: The parameters including arterial oxygen partial pressure, pulmonary vascular resistance and tissue MDA and ATP level suggested severe lung damage. Serum TNF-$\alpha$ level was 8.76$\pm$2.37 ng/ml at 60 minutes after reperfusion and decreased thereafter. The cICAM-1 level showed no change after the reperfusion during the experiment. The tissue cICAM-1 expression was confirmed in 5 dogs. Conclusion: The increase of TNF-$\alpha$ Ievel and expression of tissue ICAM-1 were demonstrated after ischemia reperfusion injury in canine lung model.