• 대한산업공학회지
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• 제31권1호
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• pp.1-9
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• 2005

This paper proposes the heuristic algorithm for the generalized GT problems to consider the restrictions which are given the number of machine cell and maximum number of machines in machine cell as well as minimum number of machines in machine cell. This approach is split into two phase. In the first phase, we use the similarity coefficient which proposes and calculates the similarity values about each pair of all machines and sort these values descending order. If we have a machine pair which has the largest similarity coefficient and adheres strictly to the constraint about birds of a different feather (BODF) in a machine cell, then we assign the machine to the machine cell. In the second phase, we assign parts into machine cell with the smallest number of exceptional elements. The results give a machine-part grouping. The proposed algorithm is compared to the Modified p-median model for machine-part grouping.

• Toxicological Research
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• 제17권
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• pp.205-210
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• 2001

One of the major focuses and perhaps the greatest challenges during the past decade in the discipline of immunotoxicology has been the elucidation of the molecular mechanisms responsible for immunotoxicity by specific agents. Much is currently understood about the basic underlying intracellular processes that control leukocyte effector function. This fundamental information in cell biology can now be applied toward developing systematic approaches, through the application of cell and molecular biology techniques, to identify the intracellular targets and processes disrupted by immunotoxicants. The objective of this paper is two fold. First to discuss fundamental principles of experimental design aimed at elucidation of cellular mechanisms in immunotoxicology; and second to discuss the application of molecular biology techniques in characterizing the mechanism of TCDD-induced B cell dysfunction as a working example.

• 대한전자공학회논문지
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• 제24권6호
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• pp.1074-1079
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• 1987

We present a fast, constructive algorithm for the automatic placement of standard cells, which consists of two steps. The first step is responsible for cell-row assignment of each cell, and converts the circuit connectivity into a multi-stage graph under to constraint that sum of the cell-widths in each stage of the multi-state graph does not exceed maximum cell-row width. Generatin of feed-through cells in the final layout was shown to be drastically reduced by this step. In the second step, the position of each cell within the row is determined one by one from left to right so that the cost function such as the local channel density is minimized. Our experimental result shows that this algorithm yields near optimal results in terms of the number of feed-through cells and the horizontal tracks, while running about 100 times faster than other iterative procedures such as pairwise interchange and generalized force directed relaxation method.

• 한국통신학회논문지
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• 제25권1B호
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• pp.48-55
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• 2000

본 논문에서는 전기장 프로브 교정용 비대칭형 TEM cell의 설계과정과 제작결과에 대해 나타내었다. 2cm$\times$2cm인 시험 공간(test space)에서 전자기장의 균일도가 $\pm$2 ㏈내를 유지하면서, 제1공진 주파수는 1.5GHz 이하에서 출현하도록 하고 제2공진 주파수는 약 GHz에서 출현할 수 있도록 제작하였다. 제작 결과 계산된 결과와 실험된 데이터가 일치함을 볼 수가 있었다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권22호
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• pp.9997-10001
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• 2014

Background: Curdione, one of the major components of Curcuma zedoaria, has been reported to possess various biological activities. It thus might be a candidate anti-flammatory and cancer chemopreventive agent. However, the precise molecular mechanisms of action of curdione on cancer cells are still unclear. In this study, we investigated the effect of curdione on breast cancer. Materials and Methods: Xenograft nude mice were used to detect the effect of curdione on breast cancer in vivo; we also tested the effect of curdione on breast cancer in vitro by MTT, Flow cytometry, JC-I assay, and western blot. Results: Firstly, we found that curdione significantly suppressed tumor growth in a xenograft nude mouse breast tumor model in a dose-dependent manner. In addition, curdione treatment inhibited cell proliferation and induced cell apoptosis. Moreover, after curdione treatment, increase of impaired mitochondrial membrane potential occurred in a concentration dependent manner. Furthermore, the expression of apoptosis-related proteins including cleaved caspase-3, caspase-9 and Bax was increased in curdione treatment groups, while the expression of the anti-apoptotic Bcl-2 was decreased. Inhibitors of caspase-3 were used to confirm that curdione induced apoptosis. Conclusions: Overall, our observations first suggested that curdione inhibited the proliferation of breast cancer cells by inducing apoptosis. These results might provide some molecular basis for the anti-cancer activity of curdione.

• The Korean Journal of Physiology and Pharmacology
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• 제26권6호
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• pp.519-530
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• 2022

Recent research indicates that lactate promotes the switching of vascular smooth muscle cells (VSMCs) to a synthetic phenotype, which has been implicated in various vascular diseases. This study aimed to investigate the effects of lactate on the VSMC phenotype switch and the underlying mechanism. The CCK-8 method was used to assess cell viability. The microRNAs and mRNAs levels were evaluated using quantitative PCR. Targets of microRNA were predicted using online tools and confirmed using a luciferase reporter assay. We found that lactate promoted the switch of VSMCs to a synthetic phenotype, as evidenced by an increase in VSMC proliferation, mitochondrial activity, migration, and synthesis but a decrease in VSMC apoptosis. Lactate inhibited miR-23b expression in VSMCs, and miR-23b inhibited VSMC's switch to the synthetic phenotype. Lactate modulated the VSMC phenotype through downregulation of miR-23b expression, suggesting that overexpression of miR-23b using a miR-23b mimic attenuated the effects of lactate on VSMC phenotype modulation. Moreover, we discovered that SMAD family member 3 (SMAD3) was the target of miR-23b in regulating VSMC phenotype. Further findings suggested that lactate promotes VSMC switch to synthetic phenotype by targeting SMAD3 and downregulating miR-23b. These findings suggest that correcting the dysregulation of miR-23b/SMAD3 or lactate metabolism is a potential treatment for vascular diseases.

• Tuberculosis and Respiratory Diseases
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• 제67권3호
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• pp.191-198
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• 2009

Background: Pemetrexed, a multi-targeted antifolate has been used as a second line treatment against non-small cell lung cancer (NSCLC). We aimed to clarify the efficacy and survival according to line of treatment, histologic type, and expression of thymidylate synthase (TS). Methods: Ninety-eight patients were treated with pemetrexed as a second line treatment (n=43) or as an additional course of treatment (n=55). TS expression was studied with immunohistochemistry and graded as 0 to 3 based on the extent of expression. Results: The response rate (RR) in 98 subjects was 10.2% and the disease control rate (DCR=PR+SD) was 30.6%. RR and DCR were 12.7% and 32.7% in non-squamous cell carcinoma (NSQC) compared to 7.0% and 27.9% in squamous cell carcinoma (SQC) (p>.05). No significant differences in RR and DCR were observed between a second line group (4.7%, 20.9%) and a further line group (14.5%, 38.2%). A similar trend was observed in the 88 response evaluable subjects. TS was expressed in 28.6% (grade 1), 24.5% (grade 2) and 7.1% (grade 3), respectively, and it was not expressed in 39.8% of subjects. TS expression rate was significantly higher in the SQC (72.1%) compared to NSQC (50.9%, p=0.033). However, the efficacy of pemetrexed was not significantly different by the extent of TS expression. Conclusion: Pemetrexed showed efficacy, not only in a second-line setting, but also in further lines of treatment for NSCLC. The efficacy of pemetrexed tended to be higher in patients with NSQC compared to SQC. TS expression rate was significantly higher in SQC compared to NSQC.

• Journal of Animal Science and Technology
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• 제48권1호
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• pp.39-48
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• 2006

본 연구는 1999년 1월부터 2004년 12월까지의 체세포점수의 검정일 자료를 이용하여 124,635개의 초산자료와 134,308개의 2산자료, 37,412개의 3산자료, 41787개의 4산자료, 37412개의 5산 자료를 이용하였다. 분석에 사용된 방법은 체세포 점수에 영향을 미치는 분만연도, 연령, 비유단계, 산차, 계절의 효과를 추정하기 위하여 GLM을 이용하여 최소자승법으로 분석하였으며, 검정일 모형을 이용한 분산성분 추정은 EM-REML 분석방법을 전산 프로그램한 REMLF90을 이용하였다. 각 산차별로 연령에 대한 효과는 연령이 낮은 군에서 체세포 점수가 낮게 나타났으며, 연령이 높은 군에서는 다소 높게 나타났다. 비유단계별 효과는 1산과 2산에서는 비유초기에서 체세포 점수가 낮게 나타났으며 비유말기에 3.151, 3.696로 높은 체세포 점수를 나타났으나, 3산, 4산, 5산에서는 비유중기에 높은 체세포 점수를 나타내었으며, 대체로 피크기에 체세포 점수가 높게 나타나는데 4산과 5산에서는 비유말기에 체세포 점수가 낮게 나타났다. 분만계절별 환경효과는 1산～5산 모두 대체로 9～11월에 체세포 점수가 낮게 나타났으며, 대체로 유량이 낮게 추정되는 6～8월 사이에는 체세포 점수가 대체로 높게 나타났다. 각 산차별 유전력은 1산에서 5산까지 각각 0.05, 0.09, 0.10, 0.05, 0.05를 나타냈으며, 유전분산값은 비유초기의 경우 2, 3, 5산에서 높게 나타났으며, 1산과 4산의 경우는 대체로 낮게 추정되었다.

• Molecules and Cells
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• 제40권3호
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• pp.202-210
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• 2017

The nonstructural protein 5A (NS5A) encoded by the human hepatitis C virus (HCV) RNA genome is a multifunctional phosphoprotein. To analyse the influence of NS5A on apoptosis, we established an Hep-NS5A cell line (HepG2 cells that stably express NS5A) and induced apoptosis using tumour necrosis factor $(TNF)-{\alpha}$. We utilised the MTT assay to detect cell viability, real-time quantitative polymerase chain reaction and Western blot to analyse gene and protein expression, and a luciferase reporter gene experiment to investigate the targeted regulatory relationship. Chromatin immunoprecipitation was used to identify the combination of $NF-{\kappa}B$ and miR-503. We found that overexpression of NS5A inhibited $TNF-{\alpha}$-induced hepatocellular apoptosis via regulating miR-503 expression. The cell viability of the $TNF-{\alpha}$ induced Hep-mock cells was significantly less than the viability of the $TNF-{\alpha}$ induced Hep-NS5A cells, which demonstrates that NS5A inhibited $TNF-{\alpha}$-induced HepG2 cell apoptosis. Under $TNF-{\alpha}$ treatment, miR-503 expression was decreased and cell viability and B-cell lymphoma 2 (bcl-2) expression were increased in the Hep-NS5A cells. Moreover, the luciferase reporter gene experiment verified that bcl-2 was a direct target of miR-503, NS5A inhibited $TNF{\alpha}$-induced $NF-{\kappa}B$ activation and $NF-{\kappa}B$ regulated miR-503 transcription by combining with the miR-503 promoter. After the Hep-NS5A cells were transfected with miR-503 mimics, the data indicated that the mimics could reverse $TNF-{\alpha}$-induced cell apoptosis and blc-2 expression. Collectively, our findings suggest a possible molecular mechanism that may contribute to HCV treatment in which NS5A inhibits $NF-{\kappa}B$ activation to decrease miR-503 expression and increase bcl-2 expression, which leads to a decrease in hepatocellular apoptosis.

• Asian Pacific Journal of Cancer Prevention
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• 제15권4호
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• pp.1699-1702
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• 2014

Objective: To evaluate clinical efficacy of a dose escalating schedule of paclitaxel concurrent with radiotherapy in treating patients with locally advanced non-small cell lung (NSCLC). Methods: Patients with locally advanced NSCLC were treated with conventional fractionated radiotherapy or three dimensional conformal radiotherapy (3 DCRT), concurrently with a dose escalating schedule of paclitaxel. All patients were divided into three groups, A with paclitaxel $30mg/m^2$, B with paclitaxel $60mg/m^2$ and C with paclitaxel $90mg/m^2$. Paclitaxel was repeated every week for a total of 4 or 6 weeks. Results: Among 109 patients, response rates were 68.8%, 71.1% and 71.8% (p>0.05) for group A (n=32), B (n=38), and C (n=39) respectively. Accordingly, disease control rates were 81.3%, 81.6% and 82.1% (p>0.05). Progression-free survival time was $8.0{\pm}5.0$ months, $11.6{\pm}6.1$ months, and $14.8{\pm}7.9$ months (p<0.05), respectively. Overall survival time was $15.4{\pm}7.6$ months, $18.2{\pm}8.0$ months, and $22.0{\pm}7.6$ months (p<0.05), one-year survival rates were 62.5%, 73.1% and 90.0% (p>0.05) and two-year survival rates were 31.3%, 38.5% and 50.0% (p<0.05). Main side-effects were bone marrow suppression, radiation related esophagitis and gastrointestinal reaction. Conclusion: In treating patients with NSCLC, concurrent chemoradiotherapy with paclitaxel improves early response compared with conventional fractionated radiotherapy or 3 DCRT. The survival rate was improved with the addition of paclitaxel, but there was an increase in adverse reactions when the dose of paclitaxel was increased.