• 한국구조물진단유지관리공학회 논문집
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• 제19권3호
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• pp.92-103
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• 2015

최근 들어 FRP 판을 영구 거푸집 및 주요 인장보강재로 활용하기 위한 새로운 콘크리트 교량 바닥판 시스템 개발에 대한 연구가 활발히 진행되고 있다. 영구거푸집과 인장 보강재로의 병행이용은 기존의 콘크리트 바닥판 보다 공사비와 공사기간을 절감 할 수 있다. 본연구에서는 영구거푸집 및 주요인장재로 활용한 FRP 판의 종류에 따른 현장타설 콘크리트와 부착응력에 대해 실험을 수행하였다. 부착성능 평가를 실시하였고, 부착특성을 나타내는 중요한 변수중에 하나로서 부착 강도 및 부착면의 파괴 매커니즘 특성을 알 수 있는 계면 파괴에너지를 나타내었다. 일반콘크리트에서 계면 파괴에너지는 GF11의 경우 0.24kN/m이고, GF21의 경우에는 0.43kN/m, GF31과 CF11의 경우에는 각각 0.46kN/m와 0.44kN/m로 나타났고, RFCON에서는 GF12의 경우 0.52kN/m, GF22와 CF12에서는 각각 0.36kN/m와 0.51kN/m로 나타났다.

• Genomics & Informatics
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• 제6권4호
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• pp.210-222
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• 2008

Due to the polygenic nature of cancer, it is believed that breast cancer is caused by the perturbation of multiple genes and their complex interactions, which contribute to the wide aspects of disease phenotypes. A systems biology approach for the identification of subnetworks of interconnected genes as functional modules is required to understand the complex nature of diseases such as breast cancer. In this study, we apply a 3-step strategy for the interpretation of microarray data, focusing on identifying significantly perturbed metabolic pathways rather than analyzing a large amount of overexpressed and underexpressed individual genes. The selected pathways are considered to be dysregulated functional modules that putatively contribute to the progression of disease. The subnetwork of protein-protein interactions for these dysregulated pathways are constructed for further detailed analysis. We evaluated the method by analyzing microarray datasets of breast cancer tissues; i.e., normal and invasive breast cancer tissues. Using the strategy of microarray analysis, we selected several significantly perturbed pathways that are implicated in the regulation of progression of breast cancers, including the extracellular matrix-receptor interaction pathway and the focal adhesion pathway. Moreover, these selected pathways include several known breast cancer-related genes. It is concluded from this study that the present strategy is capable of selecting interesting perturbed pathways that putatively play a role in the progression of breast cancer and provides an improved interpretability of networks of protein-protein interactions.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제18권3호
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• pp.411-427
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• 1996

The purpose of this study was to observe the healing process and the distribution of fibronectin in injured condylar cartilage and bone by using LM and SEM. In order to perform this study, 40 male rat, weighing about 250g were selected. Under general anesthesia with Pentobarbital sodium, condylar cartilage and neck bone were resected. Then, the wound was irrigated with saline and closed with 5-0 chromic catgut and 4-0 silk by layer-to-layer suturing. The experimental rats were sacrificed by perfusion with 3% paraformaldehyde at 1st and 4th week after operation. The condylar process and surrounding tissues were cut, demineralized, dehydrated and embedded in paraffin. The histological observation of the specimens in LM level was performed after H-E stain and Azan stain. For localization of fibronectin, immunostaining was achieved by the avidin-biotin complex method. To study the change on condylar surface, the specimens were dehydrated, dried, gold coated and were observed with a scanning electron microscope(Hitachi S-2300). The results were as follows ; 1. The cartilage group and the bone group were repaired with epiphyseal cartilage layer on the cut surface as the normal control group. 2. The cut surface was repaired more quickly in the cartilage group than in the bone group. 3. Chondrocytes, diferentiated during healing, were stained strongly to anti-fibronectin, and fibronectin was supposed to participatein chondrocyte differentiation and cartilagenous matrix formation. 4. Fibronectin was distributed more in the new bone than in the old bone, and the osteoblasts surrounding it were also stained strongly. Fibronectin was supposed to participate in new bone matrix formation. 5. Fibronectin is supposed to be associated with the differentiation, migration and adhesion of chondrocyte and osteoblast and to participate in endochondral bone formation.

• Genomics & Informatics
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• 제10권1호
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• pp.16-22
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• 2012

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the $PKD1$ and $PKD2$ genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of $PKD1$ and $PKD2$ demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that $PKD1$ and $PKD2$ probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by $PKD1$ and $PKD2$ mutations are not fully understood. To address this question, we presently created $Pkd2$ knockout and $PKD2$ transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the $PKD2$ or knockout of the $Pkd2$. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different $PKD2$ expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in $PKD2$-related mechanisms of ADPKD pathogenesis.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제27권4호
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• pp.308-313
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• 2001

The purpose of this study is to validate the potential etiologic factors for temporomandibular disorder(TMD). TMJ arthroscopic examination was performed in upper joint compartment of 32 joints from 20 patients with mandibular fractures. Synovial fluid was collected from the upper joint space during pumping manipulation with normal saline. Cytologic smearing and histomorphologic exam of synovial fluid were performed in 15 joints. Prostaglandin $E_2(PGE_2)$ concentration was measured in 11 joints. Leukotriene $B_4(LTB_4)$ concentration was measured in 8 joints. There were several arthroscopic variables such as ecchymosis, fibrillation, and adhesion. Histomorphologic exam showed a variety of findings such as bloody smears, cellular cluster, degenerated cells and cartilage, undifferentiated crystal. Mean $PGE_2$ concentrations were 316.5 pg/ml. Mean LTB4 concentrations were 45.9pg/ml. This study demonstrated a variety of findings on inflammatory and degenerative changes of TMJ. Because acute trauma such as mandibular fracture is a major etiologic factor in cartilage degradation and biochemical and intraarticular pathology, clinicians must identify and address TMJ signs and symptoms during follow-up periods in the long term.

• Nutrition Research and Practice
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• 제9권4호
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• pp.343-349
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• 2015

BACKGROUND/OBJECTIVES: Fermentation of dietary fiber results in production of various short chain fatty acids in the colon. In particular, butyrate is reported to regulate the physical and functional integrity of the normal colonic mucosa by altering mucin gene expression or the number of goblet cells. The objective of this study was to investigate whether butyrate modulates mucin secretion in LS174T human colorectal cells, thereby influencing the adhesion of probiotics such as Lactobacillus and Bifidobacterium strains and subsequently inhibiting pathogenic bacteria such as E. coli. In addition, possible signaling pathways involved in mucin gene regulation induced by butyrate treatment were also investigated. MATERIALS/METHODS: Mucin protein content assay and periodic acid-Schiff (PAS) staining were performed in LS174T cells treated with butyrate at various concentrations. Effects of butyrate on the ability of probiotics to adhere to LS174T cells and their competition with E. coli strains were examined. Real time polymerase chain reaction for mucin gene expression and Taqman array 96-well fast plate-based pathway analysis were performed on butyrate-treated LS174T cells. RESULTS: Treatment with butyrate resulted in a dose-dependent increase in mucin protein contents in LS174T cells with peak effects at 6 or 9 mM, which was further confirmed by PAS staining. Increase in mucin protein contents resulted in elevated adherence of probiotics, which subsequently reduced the adherent ability of E. coli. Treatment with butyrate also increased transcriptional levels of MUC3, MUC4, and MUC12, which was accompanied by higher gene expressions of signaling kinases and transcription factors involved in mitogen-activated protein kinase (MAPK) signaling pathways. CONCLUSIONS: Based on our results, butyrate is an effective regulator of modulation of mucin protein production at the transcriptional and translational levels, resulting in changes in the adherence of gut microflora. Butyrate potentially stimulates the MAPK signaling pathway in intestinal cells, which is positively correlated with gut defense.

• 콘크리트학회지
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• 제9권4호
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• pp.197-205
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• 1997

폴리머 콘크리트를 오버레이 콘크리트로서 기존 시멘트 콘크리트 위에 타설할 경우 폴리머 콘크리트의 경화수축으로 말미암아 전단응력, 수직응력 및 축응력이 발생되며 이러한 응력은 폴리머 콘크리트와 기존 시멘트 콘크리트 사이의 접착성능에 영향을 미쳐 결국 역학적 성질 및 내구성이 저하될 수 있다. 오버레이 콘크리트의 수축응력은 본 실험에서 실시한 구속된 오버레이 콘크리트의 구속해제에 의한 수축변형량과 탄성계수로서 구할 수 있다. 본 연구에서는 폴리머 종류, 오버레이 콘크리트 두께, 양생시간과 온도에 따른 폴리머 콘크리트 및 폴리머 시멘트 콘크리트의 수축에 의한 축응력을 측정하여 폴리머 콘크리트를 각종 교량등의 오버레이 콘크리트로 사용하멩 있어서 기초적 자료를 제공하고자 하였다. 연구결과, 폴리머 콘크리트의 경화수축응력은 폴리머의 종류, 양생온도, 재령 및 두께에 의해 영향을 크게 받는 것으로 나타났다.

• Molecular & Cellular Toxicology
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• 제2권4호
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• pp.273-278
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• 2006

95 squamous cell lung carcinoma samples (normal tissue: 40 samples, tumor: 55 samples) were analyzed with 8 K cDNA microarray. 1-way ANOVA test was employed to select differentially expressed genes in tumor with FDR<0.01. Among the selected 1,655 genes, final 212 genes were chosen according to the expression fold change and used for following analysis. The expression of up-regulated 64 genes was verified with Reverse Transcription PCR and 10 genes were identified as candidates for SCC markers. In our opinion, those candidates can be exploited as diagnostic or therapeutic purposes. Gene Ontology (GO) based analysis was performed using those 212 genes, and following categories were revealed as significant biological processes: Immune response (GO: 0006955), antigen processing (GO: 0030333), inflammatory response (GO: 0006954), Cell adhesion (GO: 0007155), and Epidermis differentiation (GO: 0008544). Gene set enrichment analysis (GSEA) also carried out on overall gene expression profile with 522 functional gene sets. Glycolysis, cell cycle, K-ras and amino acid biosynthesis related gene sets were most distinguished. These results are consistent with the known characteristics of SCC and may be interconnected to rapid cell proliferation. However, the unexpected results from ERK activation in squamous cell carcinoma gripped our attention, and further studies are under progress.

• 대한두경부종양학회지
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• 제3권1호
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• pp.37-54
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• 1987

The aim of surgery for all parotid masses is directed toward total removal of the tumor with adequate safe margins of adjacent normal tissue and preservation of the facial nerve whenever possible. Reconstructive procedures following parotidectomy for benign or low grade malignant lesions are most commonly necessary if soft tissue deficits appear at the angle of the mandible below the earlobe as a major cosmetic deformity. This is a report of Z4 cases with a diagnosis of parotid tumor who were treated using various surgical procedures at Department of Plastic and Reconstructive Surgery, Hanyang University Hospital over the period of 4 years from January, 1983 to December, 1986. Among 24 cases, 11 cases were reconstructed by Sternocleidomastoid muscle flap at the same time that extirpative surgery is outlined. The advantage of Sternocleidomastoid muscle flap is the coverage of the facial nerve, so adhesion between the facial nerve and skin was prevented. Absorption and loss of bulk was not found such as dermofat graft. It was a simple method. Neither donor site defect nor sternocleidomastoid muscle deformity was developed. Sternocleidomastoid muscle flap have been found satisfactory in maintaining filled-out soft tissue hollows with good result cosmetically and functionally.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2002년도 창립10주년기념 및 국립독성연구원 의약품동등성평가부서 신설기념 국재학술대회:생물학적 동등성과 의약품 개발 전략을 위한 국제심포지움
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• pp.89-96
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• 2002

The importance of apoptosis in normal development and pathogenesis has been well recognized, and explosive progress towards dissecting its commitment step has been made during the past decade. Mitochondria, Apaf-1, caspase, and bcl-2 family members play central roles in the commitment step. However, it is still unclear how upstream cell survival pathways regulate apoptosis. It is also unknown whether the bcl-2 family members have any effect on the upstream survival pathways. We have demonstrated that the anti-apoptotic gene product bcl-2 greatly induces expression of the tissue inhibitor of metalloproteinase-1 (TIMP-1) in human breast epithelial cells. Surprisingly, we found that TIMP-1, like bcl-2, is a potent inhibitor of apoptosis induced by a variety of stimuli. Functional studies indicate that TIMP-1 inhibits a classical apoptotic pathway mediated by caspases, and that focal adhesion kinase (FAK)/Pl 3-kinase and mitogen activated protein kinase (MAPK) are critical for TIMP- 1 -mediated cell survival. We also showed specific association of TIMP-1 with the cell surface. Consistently, a 150-H)a surface protein was identified in MCF10A cells that specifically binds TIMP-1. Taken together, we hypothesize that TIMP-I binding on the cell surface induces a cell survival pathway that regulates the common apoptosis commitment step. The results of these studies will address a new paradigm in the regulation of apoptosis by an extracellular molecule TIMP-1, and also greatly enhance our understanding of TIMP-1's pleiotropic activity in many physiological and pathological processes. This information may also be useful in designing more rational therapeutic interventions aimed at modulating the anti-apoptotic activity of TIMP-1 .