• 한국가구학회지
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• 제18권2호
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• pp.91-99
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• 2007

Modernity which is superficial phenomenon set off the mass scale for mass consumption and provide uniformly artificial environment. But natural destruction, environment pollution, resources exhaustion and so on has been caused by this and now ecology is threatened by destruction and damage beyond the limitation and human beings survival is even threatened. Accordingly furniture development for environment preservation considered environment problem is the urgent real situation. Recent paradigm is the concept of Eco-design which is the green design possible to live together in symbiosis, and new types of alternative furniture are needed in Korea as well. 'Furniture for disassembly' is presented as new method for alternative furniture. Furniture for disassembly can be presented by mainly two directions. The first main characteristic is what is assembled by the use of woodworking joints technique as an assembly structure system without any hardware. The second is what is presented as the structure possible to be assembled by simple manual tools with hardware without any glue. The advantages of furniture for disassembly are environment preservation, space application, transportation efficiency and shapeliness. In manufacture method which is different from present furniture, the application of traditional truss technique which uses various types of custom-made and connection technique in case of assemble structure system without hardware is the typical differences. This assembly method expects not only interest induction about assembly and disassembly of diagram per sub materials but also the development of emotion, the improvement of collaboration, space perception ability and shape sense, the improvement of solid body structure insight and so on, when it use in the furniture for children with the application to many kinds of structure with BANGDOOSANJ (Wedged), JUMUGJANGBU (Dovetail) or NABIEUNJANG (Dovetail Keys) and so on.

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2001년도 춘계학술발표대회
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• pp.59-59
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• 2001

Interleukin-10 (IL-10) is known as a regulator of inflammation and pathogenesis in mammalian organs, but its precise role is little known in the mammary gland. Our initial experiment showed that IL-10 expression levels in mice decreased at the lactation stage otherwise increased at the involution stage. To reveal the effects of IL-10 on the involution of mammary gland, expression profiles of the apoptosis-related genes were examined in transgenic mice expressing human IL-10 as well as in knock-out mice (IL-10-/-). Mild inflammatory legions by lymphocytes were observed in the mammary glands of transgenic lines at the lactation stage. The expression of TRAIL (Tumor necrosis factor-Related Apoptosis-Inducing Ligand) among the apoptosis-related genes was highly elevated in the transgenic mice while others were not significantly changed. Furthermore, TRAIL was down regulated by four fold in the IL-10-/- mice at the involution stage. The expression of DR4 was elevated at the involution stage of normal mice. DR4 was detected in the milk of transgenic mice but absent in that of normal mice. Our results proposed that the elevated IL-10 at the involution stage recruit lymphocytes and induce TRAIL and DR4 genes, therefore, lead to enter involution stage of mammary glands.

• The Korean Journal of Physiology and Pharmacology
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• 제13권3호
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• pp.251-256
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• 2009

Previous observations suggest that Bis, a Bcl-2-binding protein, may playa role the neuronal and glial differentiation in vivo. To examine this further, we investigated Bis expression during the in vitro differentiation of P19 embryonic carcinoma cells induced by retinoic acid (RA). Western blotting and RT-PCR assays showed that Bis expression was temporarily decreased during the free floating stage and then began to increase on day 6 after the induction of differentiation. Double immunostaining indicated that Bis-expressing cells do not express several markers of differentiation, including NeuN, MAP-2 and Tuj-1. However, some of the Bis-expressing cells also were stained with GFAP-antibodies, indicating that Bis is involved glial differentiation. Using an shRNA strategy, we developed bis-knock down P19 cells and compared them with control P19 cells for the expression of NeuroD, Mash-1 and GFAP during RA-induced differentiation. Among these, only GFAP induction was significantly attenuated in Pl9-dnbis cells and the population showing GFAP immunoreactivity was also decreased. It is noteworthy that distribution of mature neurons and migrating neurons was disorganized, and the close association of migrating neuroblasts with astrocytes was not observed in P19-dnbis cells. These results suggest that Bis is involved in the migration-inducing activity of glial cells.

• The Korean Journal of Physiology and Pharmacology
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• 제20권6호
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• pp.649-655
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• 2016

TonEBP belongs to the Rel family of transcription factors and plays important roles in inflammation as well as kidney homeostasis. Recent studies suggest that TonEBP expression is also involved in differentiation of several cell types such as myocytes, chondrocytes, and osteocytes. In this study, we investigated the roles of TonEBP during adipocyte differentiation in 3T3-L1 cells. TonEBP mRNA and protein expression was dramatically reduced during adipocyte differentiation. Sustained expression of TonEBP using an adenovirus suppressed the formation of lipid droplets as well as the expression of FABP4, a marker of differentiated adipocytes. TonEBP also inhibited the expression of $PPAR{\gamma}$, a known master regulator of adipocytes. RNAi-mediated knock down of TonEBP promoted adipocyte differentiation. However, overexpression of TonEBP did not affect adipogenesis after the initiation of differentiation. Furthermore, TonEBP expression suppressed mitotic clonal expansion and insulin signaling, which are required early for adipocyte differentiation of 3T3-L1 cells. These results suggest that TonEBP may be an important regulatory factor in the early phase of adipocyte differentiation.

• Asian Pacific Journal of Cancer Prevention
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• 제15권6호
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• pp.2777-2783
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• 2014

The purpose of this study was to explore the expression of ATAD2 in ovarian tumor tissue as well as its relationship with degree of malignancy. Tumor tissue from 110 cases of ovarian cancer was collected in accordance with the Declaration of Helsinki for evaluation of ATAD2 expression iimmunohistochemistry, quantitative PCR (qPCR) and Western blotting. The correlation between the ATAD2 expression and and the prognosis of ovarian cancer was evaluated by Cox regression model. In addition, HO-8910 and OVCAR-3 cells were transfected with two siRNAs targeting ATAD2. Cell viability was evaluated with MTT assay, and cell migration by transwell migration assay. ATAD2 was shown to be highly expressed in 65.5% (72/110) of ovarian cancer cases, both at transcriptional and protein levels. Moreover, highly expression was positively correlated with degree of malignancy. Knock-down of ATAD2 in HO-8910 and OVCAR-3 cells was found to reduce cell migration. In addition, follow-up visits of the patients demonstrated that the 5-year survival rate was lower in patients with high expression of ATAD2. Our study suggested that ovarian tumor tissue may have highly expressed ATAD2, which is associated with tumor stage, omentum-metastasis, ascites and CA-125. Increased ATAD2 may play important roles in tumor proliferation and migration. ATAD2 could serve in particular as a prognostic marker and a therapeutic target for ovarian cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제16권7호
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• pp.3061-3065
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• 2015

Background: Rac3, a member of the Rac family of small guanosine triphosphatases (GTPases), regulates a variety of cell functions, including the organization of the cytoskeleton, cell migration, and invasion. Overexpression of Rac3 has been reported in several human cancers. However, the role of Rac3 in lung cancer (LC) has not been determined in detail. The purpose of this study was to investigate the effect of silencing of Rac3 expression in human LC cells and the consequences for cell survival. Materials and Methods: Lentivirus small hairpin RNA (shRNA) interference techniques were utilized to knock down the Rac3 gene. Gene and protein expression was quantified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. LC cell apoptosis was examined by annexin V-APC /propidium iodide staining. Results: Efficient silencing of Rac3 strongly inhibited A549 cell proliferation and colony formation ability, and significantly decreased tumor growth. Moreover, flow cytometry analysis showed that knockdown of Rac3 led to G2/M phase cell cycle arrest as well as an excess accumulation of cells in the G1 and S phase. Conclusions: Thus, functional analysis using shRNAs revealed a critical role for Rac3 in the tumor growth of LC cells. shRNA silencing of Rac3 could provide an effective strategy to treat LC.

• 대한토목학회논문집
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• 제13권4호
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• pp.15-25
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• 1993

복합재료를 효과적으로 사용하기 위하여 복합재료 구조물의 설계기준 개발을 위한 연구가 진행되고 있다. 금속 셀의 좌굴에 대한 설계시에는 초기 결함의 영향과 탄성임계좌굴응력을 근거로 한 녹다운계수(Knock-down factor)를 정의하는 것이 중요한 과정이나 복합재료 쉘의 좌굴에 대한 설계시에는 초기 결함에 대한 민감도가 거의 연구되어 있지 않은 실정이다. 복합재료 쉘의 좌굴거동에 영향을 주는 설계변수는 많기 때문에, 쉘의 설계시 이 변수들로 인한 초기 결함 민감도를 분석하기 위하여 많은 실험을 필요로 하고 있으며 실험 이외의 다른 방법으로서는 이미 검증된 수치모델을 사용하는 것이다. 본 논문에서는 복합재료 쉘요소를 개발하는데 사용된 이론을 요약, 정리 하였으며 수치예제를 통하여 본 연구에서 제안한 쉘요소의 정확성을 검증하였다. 그리고 축방향으로 압축을 받는 GFRP 곡선형 판넬의 설계시 고려해야 하는 각 변수들을 다양하게 변화시키면서 좌굴거동에 미치는 영향을 유한요소 모델링에 의해 고찰하였다. 방법으로서 초기 결합 및 두께의 진폭을 고려한 비선형 해석과 고유치 해석을 수행하였으며 이 결과를 이용하여 녹다운 계수를 산출하였다.

• BMB Reports
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• 제51권2호
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• pp.85-91
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• 2018

Pluripotent stem cell (PSC) variations can cause significant differences in the efficiency of cardiac differentiation. This process is unpredictable, as there is not an adequate indicator at the undifferentiated stage of the PSCs. We compared global gene expression profiles of two PSCs showing significant differences in cardiac differentiation potential. We identified 12 up-regulated genes related to heart development, and we found that 4 genes interacted with multiple genes. Among these genes, Gata6 is the only gene that was significantly induced at the early stage of differentiation of PSCs to cardiomyocytes. Gata6 knock-down in PSCs decreased the efficiency of cardiomyocyte production. In addition, we analyzed 6 mESC lines and 3 iPSC lines and confirmed that a positive correlation exists between Gata6 levels and efficiency of differentiation into cardiomyocytes. In conclusion, Gata6 could be utilized as a biomarker to select the best PSC lines to produce PSC-derived cardiomyocytes for therapeutic purposes.

• Asian Pacific Journal of Cancer Prevention
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• 제13권7호
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• pp.3233-3238
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• 2012

Esophageal carcinoma (EC) is one of the most aggressive cancers with a poor prognosis. Understanding the molecular mechanisms underlying esophageal cancer progression is a high priority for improved EC diagnosis and prognosis. Recently, MSP58 was shown to behave as an oncogene in colorectal carcinomas and gliomas. However, little is known about its function in esophageal carcinomas. We therefore examined the effects of MSP58 knockdown on the growth of esophageal squamous cell carcinoma (ESCC) cells in vitro and in vivo in order to gain a better understanding of its potential as a tumor therapeutic target. We employed lentiviral-mediated small hairpin RNA (shRNA) to knock down the expression of MSP58 in the ESCC cell lines Eca-109 and EC9706 and demonstrated inhibition of ESCC cell proliferation and colony formation in vitro. Furthermore, flow cytometry and western blot analyses revealed that MSP58 depletion induced cell cycle arrest by regulating the expression of P21, CDK4 and cyclin D1. Notably, the downregulation of MSP58 significantly inhibited the growth of ESCC xenografts in nude mice. Our results suggest that MSP58 may play an important role in ESCC progression.

• BMB Reports
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• 제44권5호
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• pp.352-357
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• 2011

The effect of human MutY homolog (hMYH) on the activation of checkpoint proteins in response to hydroxyurea (HU) and ultraviolet (UV) treatment was investigated in hMYH-disrupted HEK293 cells. hMYH-disrupted cells decreased the phosphorylation of Chk1 upon HU or UV treatment and increased the phosphorylation of Cdk2 and the amount of Cdc25A, but not Cdc25C. In siMYH-transfected cells, the increased rate of phosphorylated Chk1 upon HU or UV treatment was lower than that in siGFP-transfected cells, meaning that hMYH was involved in the activation mechanism of Chk1 upon DNA damage. The phosphorylation of ataxia telangiectasia and Rad3-related protein (ATR) upon HU or UV treatment was decreased in hMYH-disrupted HEK293 and HaCaT cells. Co-immunoprecipitation experiments showed that hMYH was immunoprecipitated by anti-ATR. These results suggest that hMYH may interact with ATR and function as a mediator of Chk1 phosphorylation in response to DNA damage.