25 research outputs found

    Hox Genes are Differentially Expressed during Mouse Placentation

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    The placenta is an extraembryonic tissue that is formed between mother and fetus and mediates delivery of nutrients and oxygen from the mother to the fetus. Because of its essential role in sustaining the growth of the fetus during gestation, defects in its development and function frequently result in fetal growth retardation or intrauterine death, depending on its severity. Vertebrate Hox genes are well known transcription factors that are essential for the proper organization of the body plan during embryogenesis. However, certain Hox genes have been known to be expressed in placenta, implying that Hox genes not only play a crucial role during embryonic patterning but also play an important role in placental development. So far, there has been no report that shows the expression pattern of the whole Hox genes during placentation. In this study, therefore, we investigated the Hox gene expression pattern in mouse placenta, from day 10.5 to 18.5 of gestation using real-time RT-PCR method. In general, the 5" posterior Hox genes were expressed more in the developing placenta compared to the 3" Hox genes. Statistical analysis revealed that the expression of 15 Hox genes (Hoxa9, -a11, -a13/ -b8, -b9/ -c6, -c9, -c13/ -d1, -d3, -d8, -d9, -d10, -d11, -d12) were significantly changed in the course of gestation. The majority of these genes showed highest expression at gestational day 10.5, suggesting their possible role in the early stage during placental development.ope

    ๊ทผ์œ„์ถ•์„ฑ ์ธก์‚ญ ๊ฒฝํ™”์ฆ ์ƒ์ฅ๋ชจ๋ธ์— lentiviral vector ์ด์šฉ GDNF ๋ฐœํ˜„ ์ธ๊ฐ„ ์‹ ๊ฒฝ์ค„๊ธฐ์„ธ

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    Dept. of Medical Science/์„์‚ฌ[ํ•œ๊ธ€]๊ทผ์œ„์ถ•์„ฑ ์ธก์‚ญ ๊ฒฝํ™”์ฆ(ALS)์€ ์ ์ง„์ ์ธ ์šด๋™์‹ ๊ฒฝ์›์„ธํฌ์˜ ์†Œ์‹ค๋กœ ์ธํ•˜์—ฌ ์‚ฌ๋ง์— ์ด๋ฅด๋Š” ๋Œ€ํ‘œ์ ์ธ ์‹ ๊ฒฝํ‡ดํ–‰์„ฑ ์งˆํ™˜์ด๋‹ค. 2~3% ์ •๋„์˜ ALS๊ฐ€ SOD1 ์œ ์ „์ž์˜ ๋Œ์—ฐ๋ณ€์ด์— ์˜ํ•ด์„œ ๋ฐœ์ƒํ•˜๋Š”๋ฐ, SOD1 ํ˜•์งˆ์ „ํ™˜ ์ฅ๊ฐ€ ๋Œ€ํ‘œ์ ์ธ ALS ๋™๋ฌผ๋ชจ๋ธ์ด๋‹ค. ์ด ๋™๋ฌผ๋ชจ๋ธ์„ ์ด์šฉํ•ด์„œ ๋งŽ์€ ๋ณ‘๋ฆฌํ•™ ์—ฐ๊ตฌ ๋ฐ ์น˜๋ฃŒ๋ฒ• ์—ฐ๊ตฌ๊ฐ€ ์ง„ํ–‰๋˜๊ณ  ์žˆ์œผ๋‚˜ ์•„์ง๊นŒ์ง€ ํŠน๋ณ„ํ•œ ์น˜๋ฃŒ๋ฐฉ๋ฒ•์€ ์—†๋Š” ์ƒํ™ฉ์ด๋‹ค. ์‹ ๊ฒฝ์ค„๊ธฐ์„ธํฌ๋Š” ๊ฐ„ํŽธํ•˜๊ฒŒ ์‹ ๊ฒฝ๊ณ„ ์ด์‹์ด ๊ฐ€๋Šฅํ•˜๊ณ , ์ด์ฃผ ๋ฐ ์ƒ์ฐฉ ๋Šฅ๋ ฅ์„ ๊ฐ€์ง€๋ฉฐ, ์†์ƒ๋œ ์กฐ์ง์—์„œ ์—ผ์ฆ๋ฐ˜์‘์„ ๊ฐ์†Œ์‹œํ‚ฌ ๋ฟ๋งŒ ์•„๋‹ˆ๋ผ ๊ฐ์ข… ์‹ ๊ฒฝ์˜์–‘์ธ์ž๋ฅผ ๋ถ„๋น„ํ•˜๋„๋ก ํ•  ์ˆ˜ ์žˆ๋‹ค. ๊ทธ๋ฆฌ๊ณ  GDNF๋Š” ๋Œ€ํ‘œ์ ์ธ ์šด๋™์‹ ๊ฒฝ์›์„ธํฌ์˜ ์‹ ๊ฒฝ์˜์–‘์ธ์ž์ด๋‹ค. ๋ณธ ์—ฐ๊ตฌ์—์„œ๋Š” GDNF๋ฅผ ๋ฐœํ˜„ํ•˜๋Š” lentivirus๋ฅผ ๋งŒ๋“ค์–ด ์ธ๊ฐ„ ์‹ ๊ฒฝ์ค„๊ธฐ์„ธํฌ์— ์ด์‹ํ•œ ํ›„, ์ด์‹ํ•œ ์„ธํฌ์˜ ๋ถ„ํ™” ๋ฐฉ์‹์„ ๊ด€์ฐฐํ•˜๊ณ , ํ–‰๋™ ๊ฒ€์‚ฌ์™€ ์ƒ์กด ๋ถ„์„์„ ์‹ค์‹œํ•˜์—ฌ ์งˆ๋ณ‘์— ๋ฏธ์น˜๋Š” ์˜ํ–ฅ์„ ๋ถ„์„ํ•˜์˜€๋‹ค. GDNF๋ฅผ ๋ฐœํ˜„ํ•˜๋Š” ์ธ๊ฐ„ ์‹ ๊ฒฝ์ค„๊ธฐ์„ธํฌ๋Š” ๋‡Œ ๋ฐ ์ฒ™์ˆ˜์— ๊ฑธ์ณ ๊ด‘๋ฒ”์œ„ํ•œ ์ด์ฃผ ๋Šฅ๋ ฅ์„ ๋ณด์—ฌ ์ฃผ์—ˆ์œผ๋ฉฐ, ์ƒ๋‹น๋ถ€๋ถ„ ์ฒ™์ˆ˜์—์„œ excitatory amino acid transporter 2 (EAAT2)๋ฅผ ๋ฐœํ˜„ํ•˜๋Š” ์„ฑ์ƒ์„ธํฌ๋กœ ๋ถ„ํ™”ํ•˜์˜€๋‹ค. ์ด๋Š” GDNF์™€ ํ•จ๊ป˜ ๊ณต๋™์ž‘์šฉ์„ ํ•˜์—ฌ ์ƒ์ฒด๋‚ด์˜ ์šด๋™์‹ ๊ฒฝ์›์„ธํฌ์˜ ํฌ๊ธฐ๋ฅผ ์ฆ๊ฐ€์‹œ์ผฐ๋‹ค. ํ•˜์ง€๋งŒ, ์ „์ฒด์ ์œผ๋กœ ์šด๋™๋Šฅ๋ ฅ์˜ ์ฆ๊ฐ€๋Š” ์—†์—ˆ์œผ๋ฉฐ, ์ƒ์กด์ผ์ˆ˜๋Š” ์˜คํžˆ๋ ค ๊ฐ์†Œํ•˜์˜€๋‹ค. ์ƒ์กด์ผ์ˆ˜์˜ ๊ฐ์†Œ๋Š” ํ˜„์ €ํžˆ ์•…ํ™”๋œ ์•”์ปท ์ฅ์˜ ์ƒ์กด์ผ์ˆ˜ ๋•Œ๋ฌธ์ด์—ˆ๋‹ค. ์‹ ๊ฒฝ์˜์–‘์ธ์ž์˜ ์ค‘์ถ”์‹ ๊ฒฝ๊ณ„๋กœ์˜ ์žฅ๊ธฐ๋ฐœํ˜„์ด ์ข‹์ง€ ์•Š์€ ์—ญํ• ์„ ํ•œ ๊ฒƒ์œผ๋กœ ๋ณด์ด๋ฉฐ, ํŠนํžˆ GDNF๋Š” ์•”์ปท ์ฅ์—์„œ ๊ณผ๋„ํ•œ ๋ฐœํ˜„์ด ์ผ์–ด๋‚˜ ๋ถ€์ž‘์šฉ์„ ์ผ์œผํ‚จ ๊ฒƒ์œผ๋กœ ๋ณด์ธ๋‹ค. ์ด๋ฒˆ ์‹คํ—˜์„ ํ†ตํ•ด์„œ ์ ์ ํ•œ ์ˆ˜์ค€์˜ ์‹ ๊ฒฝ์˜์–‘์ธ์ž์˜ ๋ฐœํ˜„๊ณผ ์˜ฌ๋ฐ”๋ฅธ ์œ„์น˜๋กœ์˜ ์‹ ๊ฒฝ์˜์–‘์ธ์ž ์ „๋‹ฌ์ด ์ค‘์š”ํ•œ ์š”์†Œ์ž„์„ ์•Œ ์ˆ˜ ์žˆ์—ˆ๋‹ค. ์ด์™€ ๋”๋ถˆ์–ด ALS ๋™๋ฌผ ๋ชจ๋ธ์˜ ์„ฑ์ ์ดํ˜•์ด ์งˆ๋ณ‘ ์—ฐ๊ตฌ์— ํฐ ์˜ํ–ฅ์„ ๋ฏธ์น  ์ˆ˜ ์žˆ์Œ์„ ์•Œ ์ˆ˜ ์žˆ์—ˆ๋‹ค. [์˜๋ฌธ]Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive and lethal motor neuronal death. About 2-3% of ALS is caused by mutation in the Cu/Zn superoxide dismutase 1 (SOD1) gene. The mutant SOD1 transgenic rodent is a major model of the disease. Even though there are several discrepancies in human cases, many pathological and clinical investigations were conducted using this model. Neural stem cells have migration, integration, and differentiation capacity. They also have anti-inflammatory effects and could deliver several trophic factors into injured central nervous system (CNS) tissues. Glial cell line-derived neurotrophic factor (GDNF) is a potent trophic factor for motor neurons. In this study, we investigated the effects of intrathecal and/or intraventricular transplantation of human neural stem cells (hNSCs) on the neurobehavior and survival of ALS mice. The hNSCs were engineered to express GDNF by lentiviral vector before transplantation. Donor cells showed engraftment and migration into the injured brain and spinal cord parenchyma. The transplanted GDNF-expressing hNSCs showed trophic effects on motor neurons of the spinal cord. The host motor neurons displayed larger cell bodies and longer cellular processes than those in the vehicle-injected control group. Donor cells also differentiated into GDNF- and excitatory amino acid transporter 2 (EAAT2)-expressing astrocytes. Transplantation of GDNF-expressing hNSCs showed motor neuronal trophic effects. However, improvement of motor performance in ALS mice was not observed on the whole, except initial short-term improvement after transplantation of hNSCs. Moreover, survival of hNSCs-transplanted ALS mice worsened compared to vehicle-injected mice. This result was largely due to the decreased survival period in female ALS mice in the cell treatment group. The results imply that long-term trophic factor delivery could be harmful, and there is a sexual dimorphism in the rodent ALS model. The inappropriate delivery of trophic factors in the CNS of ALS mice could be another possibility for the low treatment efficacy of hNSCs transplantation. Therefore, investigation of the pathogenetic mechanisms of ALS and appropriate hNSCs transplantation techniques should be developed in the future.ope

    ็‡Ÿๆฅญ่ฎ“ๆธก(Sell-off)์˜ ๆฑบๅฎš่ฆๅ› ์— ๊ด€ํ•œ ์‹ค์ฆ์  ์—ฐ๊ตฌ

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    ํ•™์œ„๋…ผ๋ฌธ(์„์‚ฌ)--์„œ์šธ๋Œ€ํ•™๊ต ๋Œ€ํ•™์› :๊ฒฝ์˜ํ•™๊ณผ ๊ฒฝ์˜ํ•™์ „๊ณต,1999.Maste

    Study on design and fabrication processes of high-power klystron amplifier tubes

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    ํ•™์œ„๋…ผ๋ฌธ(๋ฐ•์‚ฌ)--์„œ์šธ๋Œ€ํ•™๊ต ๋Œ€ํ•™์› :์›์žํ•ต๊ณตํ•™๊ณผ ํ•ต์œตํ•ฉ์ „๊ณต,2000.Docto

    A Study on the Surge Protection of Shipboard Electrical and Electronic Devices

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    The surge on the shipboard is generated by an insulation breakdown, a short circuit and a switch operation, and is propagated via power, signal and communication, control cables and hull. The surge may lead to serious damage to electrical and electronic devices on shipboard. With this background, this thesis analyzed the power system of ships and carried out an experimental study on the surge protective method and device. Parallel type surge protective devices(SPD) with the 220[V] and the 440[V] rated voltage, and a series type SPD with the 220[V] rated voltage for electrical sensitive devices are designed and fabricated. A surge generator specified in IEC 61000-4-5 which can produce 8/20[us] current up to 15[kA] was fabricated to evaluate the proposed SPDs. The performance of the SPDs were evaluated by an un-powered test which applies the 8/20[us] surge current up to 10[kA] and by a powered test which superimpose a surge on the 220[V] and 60[Hz]. The maximum residual voltage of the parallel type SPD for the un-powered and the powered test were 1290[V] and 891[V], and of the series type SPD were 875[V] and 656[V], respectively. The experimental results showed that the series type SPD is more effective to protect electrical sensitive devices such as signal and communication devices since the series type SPD suppresses surge lower residual voltage than the parallel one. Also, insulation voltage of the shipboard electrical and electronic devices were compared to the residual voltage of the SPDs. The residual voltages of the SPDs were lower than the demanded insulation voltage level for the mains of the 220[V] and the 440[V]. Therefore, it was confirmed that the proposed SPDs have a sufficient performance to protect the shipboard electrical and electronic devices from surge voltages.๋ชฉ ์ฐจ ๋ชฉ ์ฐจ โ…ฐ ๊ทธ๋ฆผ ๋ฐ ํ‘œ ๋ชฉ์ฐจ โ…ฒ Abstract โ…ด ์ œ 1 ์žฅ ์„œ ๋ก  1 1.1 ์—ฐ๊ตฌ๋ฐฐ๊ฒฝ 1 1.2 ์—ฐ๊ตฌ๋ชฉ์  ๋ฐ ๋‚ด์šฉ 2 ์ œ 2 ์žฅ ์ด ๋ก  3 2.1 ์„œ์ง€์˜ ๋ฐœ์ƒ๊ณผ ์ „ํŒŒ 3 2.2 ์‹œํ—˜ ๊ทœ์ • 5 2.3 ์„œ์ง€๋ฐฉํ˜ธ์†Œ์ž 11 2.4 ์„ ๋ฐ•์ „๋ ฅ๊ณ„ํ†ต 17 ์ œ 3 ์žฅ ์„ค๊ณ„ ๋ฐ ์ œ์ž‘ 20 3.1 ์„œ์ง€๋ฐฉํ˜ธ์žฅ์น˜ 20 3.2 ์„œ์ง€๋ฐœ์ƒ์žฅ์น˜ 26 ์ œ 4 ์žฅ ํ‰๊ฐ€ ๋ฐ ๋ถ„์„ 31 4.1 ๋ณ‘๋ ฌํ˜• ์„œ์ง€๋ฐฉํ˜ธ์žฅ์น˜ 31 4.2 ์ง๋ ฌํ˜• ์„œ์ง€๋ฐฉํ˜ธ์žฅ์น˜ 37 ์ œ 5 ์žฅ ๊ฒฐ ๋ก  42 ์ฐธ ๊ณ  ๋ฌธ ํ—Œ 4

    (The) effect of prenatal administration of dexamethasone on mouse placenta development

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    ์˜๊ณผํ•™๊ณผ/์„์‚ฌํƒœ๋ฐ˜์€ ์ž„์‹  ์ค‘์— ํƒœ์•„์˜ ์„ฑ์žฅ์— ํ•„์ˆ˜์ ์ธ ๊ธฐ๊ด€์ด๋‹ค. ์ด ๊ธฐ๊ด€์€ ๋‚ด๋ถ„๋น„ ๊ธฐ๊ด€์œผ๋กœ ์ž‘์šฉํ•˜๋ฉฐ ์ด ์™ธ์—๋„ ํ˜ธํก์— ํ•„์š”ํ•œ ๊ฐ€์Šค์™€ ์˜์–‘๋ถ„์˜ ๊ตํ™˜, ๋ฉด์—ญ ์žฅ๋ฒฝ์œผ๋กœ์„œ์˜ ์—ญํ•  ๋“ฑ ๋‹ค์–‘ํ•œ ๊ธฐ๋Šฅ์„ ์ˆ˜ํ–‰ํ•œ๋‹ค. ๋”ฐ๋ผ์„œ ํƒœ๋ฐ˜์˜ ์ ์ ˆํ•œ ๋ฐœ๋‹ฌ์€ ๋ฐฐ์•„์™€ ํƒœ์•„์˜ ์ƒ์กด ๋ฐ ์ ์ ˆํ•œ ์„ฑ์žฅ๊ณผ ์„ฑ์ˆ™์— ๊ฒฐ์ •์ ์ธ ์—ญํ• ์„ ํ•˜๋ฉฐ, ํƒœ๋ฐ˜์˜ ์œ ์ „์  ํ‘œํ˜„ํ˜•์  ํŠน์„ฑ์— ์˜ํ•ด ํƒœ์•„์˜ ์šด๋ช…์ด ๊ฒฐ์ •๋œ๋‹ค๊ณ  ๋ณผ ์ˆ˜ ์žˆ๋‹ค. ์ž„์‹  ์ค‘ ํƒœ๋ฐ˜์— ๋ฌธ์ œ๊ฐ€ ๋ฐœ์ƒํ–ˆ์„ ์‹œ ํƒœ์•„์˜ ์„ฑ์žฅ์ด ์ง€์—ฐ๋˜์–ด ๋ฏธ์ˆ™์•„๋กœ ์ถœ์ƒํ•˜๊ฒŒ ๋˜๊ฑฐ๋‚˜, ์‹ฌํ•œ ๊ฒฝ์šฐ ํƒœ์•„์˜ ์‚ฌ๋ง๋„ ๊ฐ€๋Šฅํ•˜๋‹ค. ์ด๋Ÿฐ ์ ์ ˆํ•˜์ง€ ๋ชปํ•œ ํƒœ๋ฐ˜์˜ ๋ฐœ์ƒ์„ ์ผ์œผํ‚ค๋Š” ์š”์ธ์œผ๋กœ์จ, ์ž„์‹  ๊ธฐ๊ฐ„ ์ค‘์˜ ๋ชจ์ฒด๋กœ๋ถ€ํ„ฐ ์œ ๋ž˜๋œ ์ŠคํŠธ๋ ˆ์Šค๊ฐ€ ์žˆ๋‹ค. ์ŠคํŠธ๋ ˆ์Šค๋กœ ์ธํ•œ ๊ธฐ์ „์€ ์ŠคํŠธ๋ ˆ์Šค์— ๋Œ€ํ•œ ์ •๋ณด๊ฐ€ ์‹œ์ƒํ•˜๋ถ€์˜ paraventricular nuclei (PVN)์— ์ž…๋ ฅ๋˜๊ฒŒ ๋˜๋ฉด corticotrophin releasing hormone (CRH)๊ณผ arginine vasopressin (AVP)์ด ๋ถ„๋น„๊ฐ€ ๋˜๊ณ , ์ด๋Š” ๋‡Œํ•˜์ˆ˜์ฒด ์ „์—ฝ์—์„œ์˜ adrenocorticotrophin (ACTH)์˜ ๋ถ„๋น„๋ฅผ ์ž๊ทนํ•œ๋‹ค. ์ด๋Š” ๊ณง์ด์–ด ๋ถ€์‹  ํ”ผ์งˆ์„ ์ž๊ทนํ•˜์—ฌ glucocorticoid ์˜ ๋ถ„๋น„๋ฅผ ์ด‰์ง„ํ•œ๋‹ค.Glucocorticoid๋Š” ํƒœ๋ฐ˜์— ์กด์žฌํ•˜๋Š”11ฮฒ hydroxysteroid dehydrogenase Type II (11ฮฒ-HSD2) ๋ผ๋Š” ํšจ์†Œ๊ฐ€ glucocorticoid๋ฅผ ๋ถˆํ™œ์„ฑ ํ˜•ํƒœ๋กœ ์ „ํ™˜์‹œํ‚ค๋ฏ€๋กœ ํ•ด์„œ ๋ชจ์ฒด์—์„œ ์œ ๋„๋œglucocorticoid๋กœ ๋ถ€ํ„ฐ ํƒœ์•„๋ฅผ ๋ณดํ˜ธํ•œ๋‹ค. ๊ทธ๋Ÿฌ๋‚˜ ๋ณธ ์‹คํ—˜์—์„œ ์‚ฌ์šฉํ•˜๋Š” ํ•ฉ์„ฑ glucocorticoid์˜ ์ผ์ข…์ธ dexamethasone์€ ์ด๋ ‡๊ฒŒ ํƒœ๋ฐ˜ ๋‚ด ์กด์žฌํ•˜๋Š” 11ฮฒ-HSD2์˜ ๋ณดํ˜ธ ์—†์ด glucocorticoid receptor ๋กœ์˜ ์ง์ ‘์ ์ธ ์ž‘์šฉ์ด ๊ฐ€๋Šฅํ•˜๊ฒŒ ํ•˜์—ฌ, ๋ฐ”๋กœ ํƒœ์•„์— ์˜ํ–ฅ์„ ๋ผ์น  ์ˆ˜๊ฐ€ ์žˆ๋‹ค.์ด๋Ÿฌํ•œ ํ•ฉ์„ฑ glucocorticoid์˜ ์ŠคํŠธ๋ ˆ์Šค ์œ ๋„ํšจ๊ณผ๋กœ HPA (Hypothalamic-Pituitary-Adrenal) axis์˜ ๋ฐœ๋‹ฌ๊ณผ ๊ธฐ๋Šฅ์„ ๋ถ•๊ดด์‹œํ‚ค๊ณ , ๊ทธ๋กœ ์ธํ•ด ํƒœ์•„์˜ ์„ฑ์žฅ์„ ๋ฐฉํ•ดํ•˜์—ฌ ์ถœ์ƒ ์ดํ›„์—๋„ ๋‹ค์–‘ํ•œ ์งˆํ™˜์— ์ทจ์•ฝํ•˜๊ฒŒ ํ•œ๋‹ค. ์ƒ์ฅ์—์„œ๋Š” ์ž„์‹  15,16,17์ผ์— ํ•ฉ์„ฑ glucocorticoid์˜ ์ผ์ข…์ธ dexamethasone์„ ์ฒ˜๋ฆฌํ•œ ํ›„์— ํฌ์ƒ์‹œ์ผœ ํƒœ๋ฐ˜์˜ ํ˜•ํƒœ๋ฅผ ๊ด€์ฐฐํ•˜๊ณ  ์œ ์ „์ž ๋ฐœํ˜„์˜ ๋ณ€ํ™”๋ฅผ ๋ถ„์„ํ•œ ๊ฒฐ๊ณผ์— ๋”ฐ๋ฅด๋ฉด, ํƒœ๋ฐ˜๊ณผ ํƒœ์•„์˜ ์ฒด์ค‘ ๊ฐ์†Œ๊ฐ€ ๊ด€์ฐฐ๋˜์—ˆ๋‹ค. ๋˜ํ•œ ์ถœ์ƒ ์ „์— dexamethasone์„ ์ฒ˜๋ฆฌํ•œ ๋‹ค๋ฅธ ์‹คํ—˜์—์„œ๋„ ํƒœ์•„์˜ ๋ผˆ ์„ฑ์žฅ์„ ์–ต์ œํ•˜๋Š” ๊ฒƒ์ด ๋ณด๊ณ ๋œ ๋ฐ” ์žˆ๋‹ค. ์ด๋Ÿฌํ•œ ๋ณด๊ณ ๋“ค์€ ํ•ฉ์„ฑ glucocorticoid๊ฐ€ ํƒœ์•„์—๊ฒŒ ์ง์ ‘์ ์ธ ์ŠคํŠธ๋ ˆ์Šค๋ฅผ ์ฃผ๋Š” ๊ฒƒ์„ ์˜๋ฏธํ•˜๋ฉฐ, ๋” ๋‚˜์•„๊ฐ€ ์ถœ์ƒ ์ „์— ๋ชจ์ฒด์—์„œ ์œ ๋„๋œ ์ŠคํŠธ๋ ˆ์Šค๊ฐ€ ํƒœ์•„์— ๋ฏธ์น˜๋Š” ์˜ํ–ฅ์˜ ์ค‘์š”์„ฑ์„ ์ƒ๊ฐํ•˜๊ฒŒ ํ•œ๋‹ค. ๋ณธ ์—ฐ๊ตฌ์—์„œ๋Š” ์ƒ์ฅ์˜ ์ž„์‹ ๊ธฐ๊ฐ„ ์ค‘ ๋ณดํ˜ธ๋ง‰ ์—ญํ• ์„ ํ•˜๋Š” ํƒœ๋ฐ˜์ด ๋ชจ๊ณ„ ์ชฝ์œผ๋กœ๋ถ€ํ„ฐ ์˜จ ์ŠคํŠธ๋ ˆ์Šค๋กœ ์ธํ•ด ๋ฐ›๋Š” ์˜ํ–ฅ์„ ํƒœ๋ฐ˜์˜ ํ˜•ํƒœ์ , ์œ ์ „์ ์œผ๋กœ ์–ด๋– ํ•œ ์˜ํ–ฅ์„ ๋ฐ›๋Š”์ง€๋ฅผ ์•Œ์•„ ๋ณด์•˜๋‹ค.ope

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