• Radiation Oncology Journal
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• v.22 no.3
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• pp.217-224
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• 2004

Purpose: It is well known that the radiosensitivity of tumor cells can be significantly reduced under hypoxic conditions. Hypoxia-inducible factor-1 $\alpha$ (HIF-1 $\alpha$) plays a pivotal role in the essential adaptive responses to hypoxia. Therefore this study investigated the relationship between HIF-1 $\alpha$ expression and radiosensitivity. M Mouse hepatoma cell line hepafcic7 and HIF-1 $\beta$-deficient mutant cell line hepa1C4 were used to analyze the role of HIF-1 a. on radiosensitivity. These cells were exposed for 6 h to desferrioxamine (DFX) before radiation. HIF-1$\alpha$. expression was examined by Western blot. Apoptosis was assessed by DNA fragmentation, propidium iodide staining, and apoptotic cell death detection ELISA kit. Radiation sensitivity was determined using MTT assay. The radiobioiogical parameters, surviving fractions at 2 Gy and 8 Gy, and mean inactivation dose (MID) from the linear-quadratic model were used to assess radiation sensitivity in the statistical analyses. Results: The expression of HIF-1 $\alpha$. was Increased, whereas apoptosis was decreased, by radiation In the presence of DFX In hepal cl c7, but not In hepal C4. The radlosensitivity of hepal C4 cells was not significantly affected by DFX treatment. The radiosensitivlty of hepal cl c7 cells was significantly decreased in the presence of DFX Conclusion: The expression of HIF-1 w by hypoxia-mimic agent DFX reduced apoptosls and radiosensitlvity in mouse hepatoma cell line hepafclc7. These results suggested that HIF-1 u could be Induced by irradiation in hypoxic ceils of tumor masses, and that this mlght Increase radioresistance in hypoxic cells.

• Neonatal Medicine
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• v.17 no.1
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• pp.44-52
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• 2010

Purpose : The aim of this study was to develop a model for necrotizing enterocolitis (NEC) in the neonatal rat using endotoxin and hypoxia, a plausible insult in a neonatal intensive care and to investigate the role of apoptosis as the underlying mechanism. Methods : Newborn rats were given oral endotoxin and intermittent 8% hypoxia$\pm$caspase inhibitor. The intestinal histology was evaluated using hematoxylin-eosin staining. Apoptosis was analyzed with TUNEL staining and by measuring the caspase 3 activity in the intestinal lysates. IEC-6 cells were assessed for apoptosis and the expression of Bax, Bcl-2, Fas and FasL was measured after treatment with endotoxin and hypoxia. Results : Oral endotoxin (5 mg/kg) and exposure to 8% hypoxia of 60-min duration twice induced human NEC-like lesions in the rat intestine. Intestinal tissue revealed increased apoptosis and caspase-3 activity. After caspase inhibitor treatment, the grades of both apoptosis and NEC were significantly reduced. IEC-6 cells exhibited increased apoptosis and caspase 3 activity after endotoxin and hypoxia treatment and significantly increased Bax/Bcl- 2 ratio compared to control cells. Conclusion : This neonatal rat model of NEC which was induced by oral endotoxin and intermittent hypoxia showed increased apoptosis of intestinal epithelial cells that was mediated by caspase 3 activation. Our model has a advantage in the study of NEC because the use of much more clinically plausible insults may provide a suitable model for the investigation of its pathophysiology and therapeutic trials.

• Journal of Life Science
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• v.23 no.10
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• pp.1223-1229
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• 2013

Ursolic acid (UA) a bio-active ingredient found in a variety of fruits and vegetables, and it has potent antioxidant activity. However, the role of UA in mouse embryonic stem (ES) cells is poorly understood. This study investigated the functional role of UA in regulating the development of mouse ES cells under hypoxia. Hypoxia did not exert a significant effect on the undifferentiated state of mouse ES cells. However, it induced reactive oxygen species (ROS) generation and increased the level of lactate dehydrogenase (LDH) production at 48 h of hypoxic exposure. Conversely, oxidative stress induced by hypoxia was significantly inhibited by UA ($30{\mu}M$) pretreatment. Hypoxia significantly decreased cell survival and the level of [$^3H$] thymidine incorporation, both of which recovered following pretreatment of UA. In addition, UA decreased the apoptotic effect of hypoxia by attenuating caspase-3 cleavage or by recovering cellular inhibition of the apoptotic protein (cIAP)-2 and Bcl-2 expression. We further found that UA decreased senescence-associated beta-galactosidase activity. We suggest that UA is a natural antioxidant and one of the functional modulators of hypoxia-induced survival, apoptosis, proliferation, and aging in mouse ES cells.

• Horticultural Science & Technology
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• v.28 no.6
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• pp.980-984
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• 2010

Research regarding respiration rate, off-flavor related material and freshness maintenance effect of active MA mini-packaging on perilla leaves has been carried in this study. Respiration rate was highly maintained at high oxygen treatments ($CO_2:O_2:N_2$=0:30:70 and 0:50:50), higher than non-treatment and low oxygen treatments (6:2:92, 0:10:90) during the storage period, and ethylene production was relatively higher. However, off-flavor related materials, acetaldehyde and ethanol production was noticeably low. Weight losses of non-treatment and low-oxygen treatment were about 1.8 and 1.4%, respectively. At the fifth day of storage there was no weight loss. Ascorbic acid content was 13.3 mg/100 g F.W. at the first day of storage. At the third day of storage non-treatment showed the lowest value of ascorbic acid, 8.8 mg/100 g F.W. Ascorbic acid content of active MA treatment gradually decreased without a striking difference as the storage day extended. Chlorophyll content was the lowest at the fifth day of storage with non-treatment, 47.5 (SPAD-502 unit) while the active MA treatment maintained high level of chlorophyll content, 53.0. Sensory evaluation (vision) showed that marketability gradually decreased but was maintained in high oxygen treatments (0:30:70 and 0:50:50), even at the fifth day of storage. Occurrence of off-flavor in non-treatment at the fifth day of storage was extremely low, 2.6; whereas high in high oxygen treatment, 3.4. Active MA packaging maintained freshness two more days at room temperature (about $27^{\circ}C$).

• Journal of Life Science
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• v.20 no.7
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• pp.991-998
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• 2010

Hypoxia is an indicative of pro-apoptotic and anti-apoptotic biphasic effects, which appear to be dependent upon the cell type and the condition of the cells. The hypoxia-mimetic agent, cobalt chloride ($CoCl_2$), has been shown to induce apoptosis in a variety of cell types, but the mechanism by which this occurs has yet to be thoroughly elucidated. Puromycin-sensitive aminopeptidase (PSA) gene was decreasingly expressed in response to $CoCl_2$. In this report, puromycin pretreatment applied to PC-3 cells resulted in apoptosis. To determine whether PSA is involved in apoptosis, we examined the apoptotic properties of the PC-3 cells after siRNA knockdown of PSA. PSA siRNA-induced PSA silencing revealed that endogenous PSA may be involved in apoptosis of the PC-3 cells. These results indicated that PSA may perform a vital function in cell survival of the PC-3 cells.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.289-289
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• 1994

흰쥐 적출 대동맥을 이용하여 혈관근의 $Na^{+}$/$Ca^{2+}$ 교환계의 기능과 성질을 구명코자 $Na^{+}$/$Ca^{2+}$ 교환계를 통한 수축 반응을 관찰하고 이때의 조직내 $Ca^{2+}$ 농도, cGMP 농도 및 이 수축에 대한 차단제와 저산소 처리의 영향을 조사하였다. 흰쥐 적출 대동맥은 $Na^{+}$ free 영양액하에서 수축반응을 일으켰고 이 수축 반응 ($Na^{+}$ free 수축반응)은 KCl 농도 증가에 비례하여 증가하였다. KCI 21.6mM 하의 $Na^{+}$ free유발 수축반응은 amiloride전처리하에서 용량-의존성으로 억제되었고 특히 tonic 수축반응이 예민하게 소실되었으며, benzamil과 verapamil 전처리하에서도 유의하게 억제되었다.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1172-1175
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• 2007

We observed that exogenously applied ethanol changed the activities of aldehyde oxidases (AO) in the primary roots of maize (Zea mays). The stimulatory effect of ethanol on the aldehyde oxidase activities was concentration dependent; the AO activities were slightly weaker with 0.2 - 0.4% ethanol and stronger with 0.8 - 1.0% ethanol than the level of control. The promotion of AO activities was not explained by the increased transcription of two AO genes in maize. In contrast, ethanol strongly increased the amount of AO proteins, indicating that ethanol enhanced AO activities by promoting the translation. Among three alcohols including ethanol, methanol and isopropanol, only ethanol promoted AO activities. These results suggested that enhancement of AO activities was specific to ethanol, whose level could be naturally increased when the plant roots drove fermentation to overcome low oxygen stresses.

• Tuberculosis and Respiratory Diseases
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• v.57 no.1
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• pp.37-46
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• 2004

Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$ $CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.

• Journal of Life Science
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• v.14 no.2
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• pp.291-295
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• 2004

Rooibos (Aspalathus linearis) (RB) is a leguminous shrub native to the mountainous areas of the northwestern Cape Province in South Africa. RB tea infusions are the fermentation products of its leaves and fine sterns, and known to have a high antioxidative activity due to the presence of flavonoids and phenolic acids. We investigated the effects of RB tea on the alleviation of oxidative stress on cultured rat cortical neurons in a hypoxic model. Measurement of lactate dehydrogenase (LDH) released into culture media revealed that RB increased cell viabilities in both normoxia (6-18%) and hypoxia (2-24%) dose-dependently (10-100 $\mu\textrm{g}$/ml) on 16 days in vitro (3 days after treatment). Visualization of cell morphology by expression of GFP-Hsc70 fusion protein showed that RB (50 $\mu\textrm{g}$/ml) reduced the average vacuolated soma from 55.4$\pm$4.59% (no RB addition) to 40.9$\pm$6.3% (RB addition) on 5 days after hypoxia. Our results proves efficacy of RB in the neuroprotection of hypoxic neurons and extend application for RB into the prevention and/or treatment of neuronal damages.

• Korean Journal of Heritage: History & Science
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• v.48 no.3
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• pp.138-153
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• 2015

For preventing the biological damage domestically, insect damage control method using chemical medicine has been applied. However, it is trend to avoid existing chemical medicine such as Methyl bromide because of the problem of being harmful to human body and environment. Therefore, the research for new medicine to replace this has been done and the interest to the physical treatment such as temperature(high & low) treatment, hypoxic treatment, carbon dioxide treatment, and radiation treatment has increased. However the systematic application standard and way has not been established. Therefore, in this research, we are going to organize present condition of domestic cultural asset preventing biological damage after the 1980's. It will also consider the direction through the characteristic of technology, limit, and replacement medicine by examining the past research.