• Applied Chemistry for Engineering
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• v.27 no.2
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• pp.205-209
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• 2016

The influence of titania nanorods with an average diameter of 10 nm and an average length of 30 nm on the electrohydrodynamic instability of block copolymer (polystyrene-b-poly(2-vinylpyridine)) thin film was investigated in this article. The presence of titania nanorods increased the dielectric constant of the film, which resulted in a systematic reduction in the wavelength of the surface instability. Cross-sectional transmission electron microscopy analysis indicated that the migration/aggregation of titania nanorods did not occur as a result of the applied electric field. This work can provide a simple route to the pattern formation using electrohydrodynamic instability with an aid of nanoparticles.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.406-414
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• 2005

The genetic instability of cancer cells may be related to inappropriately activated DNA repair pathways. In present study, the modulated expression of DNA-dependent protein kinase (DNA-PK), a major DNA repair protein, in human cancer metastatic cells was tested. The expressions of Ku70/80, regulatory subunit of DNA-PK, and the Ku DNA-binding activity in various highly metastatic cell lines were higher than those in each parental cell line. Also, the expression of DNA-PKcs, catalytic subunit of DNA-PK, and the kinase activity of the whole DNA-PK complex in highly metastatic cells were significantly increased as compared to those of parental cells, suggesting that the enhanced DNA repair capacity of metastatic cells could be associated with aberrant use of DNA repair, which may mediate tumor progression and metastatic potential. Increased EGFR (epidermal growth factor receptor) signaling has been associated with tumor invasion and metastasis, and the linkage between EGFR-mediated signaling and DNA-PK has been suggested. This study showed that PKI166, the new EGFR tyrosine kinase inhibitor, modulated the expressions of Ku70/80 and DNA-PKcs and also revealed the chemosensitization effect of PKI166 against metastatic cells may be in part due to inhibition of Ku70/80. These results suggest that interference in EGFR signaling by EGFR inhibitor resulted in the impairment of DNA repair activity, and thus DNA-PK could be possible molecular targets for therapy against metastatic cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.49 no.4
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• pp.453-465
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• 2000

Background : Lung carcinogenesis is a multistage process involving alterations in multiple genes and diverse pathway. Mutational activation of oncogenes and inactivation of tumor suppressor genes, and subsequent increased genetic instability are the major genetic events. The p53 gene and FHIT gene as tumor suppressor genes contribute to the pathogenesis of lung cancer, evidenced by mutation, microsatellite instability(MI) and loss of heterozygosity(LOH). Methods : We analysed genetic mutations of p53 and FHIT gene in 29 surgical specimens of nonsmall cell lung cancer using PCR-single strand conformation polymorphism, DNA sequencing and RT-PCR. MI and LOH were analyzed in loci of D3S1285, D9S171, and TP53. Results : In 2 cases, point mutation of p53 gene was observed on exon 5. MI of 3 times and LOH of 14 times were observed in at least one locus. In terms of the location of microsatellite, D3S1285 as a marker of FH1T was observed in 5 cases out of 26 specimens; D9S171 as a marker of p16 in 5 out of 17; and TP53 as a marker of p53 in 7 out of 27. In view of histologic type, squamous cell carcinoma presented higher frequency of microsatellite alteration, compared to others. Mutation of FHIT gene was observed in 11 cases and 6 cases of those were point mutation as a silent substitution on exon 8. FHIT mRNA expression exhibited deletion on exon 6 to 9 in 4 cases among 15 specimens, presenting beta-actin normally. Conclusion : Our results show comparable frequency of genetic alteration in nonsmall cell lung cancer to previous studies of Western countries. Microsatellite analysis might have a role as a tumor marker especially in squamous cell carcinoma. Understanding molecular abnormalities involved in the pathogenesis could potentially lead to prevention, earlier diagnosis and the development of novel investigational approaches to the treatment of lung cancer.

• Journal of the Korean Institute of Intelligent Systems
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• v.17 no.5
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• pp.640-647
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• 2007

This paper presents a joint controller for a humanoid robot based on genetic algorithm. h humanoid robot has basically instability during walking because it isn't fixed on the ground. Moreover nonlinearities of the joints increase its instability. If one of them isn't satisfied, the robot may fall down at the ground during walking. To attack one of those problems, joint controller is proposed. It can perform tracking control preciously and reduce the effect of nonlinearities by gear, limitation of the input voltage, coulomb friction and so on. This controller is based on fuzzy-sliding mode controller (FSMC) and compensator and control gains are searched by a proposed genetic algorithm. It can reduce the effect by nonlinearities. Also, to improve the tracking performance, the proposed controller has motion controller. From the given controller, a humanoid robot can moved more preciously. Here, all the processes are investigated through simulations and it is verified experimentally in a real joint system for a humanoid robot.

• Journal of Life Science
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• v.17 no.6 s.86
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• pp.741-747
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• 2007

In the azoospermic patients, there are many of undiagnosed factors related to genetic bases. Among them, Klinefelter's syndrome (47,XXY; KS) and Y-chromosomal microdeletion with normal karyotype(46,XY; YMNK) are the most frequent causes of male infertility. This research focused on the comparative analysis of YMNK (n = 66) and K5 (n = 30) patients suffered from male infertility in Korean population. We used the polymerase chain reaction (PCR) approach including 19 pairs of sequence-tagged site (STS) primers for detecting the Y-chromosomal microdeletion on AZFa, b, c regions, indicating that Y chromosomal microdeletions were almost evenly occurred in AZF all regions in Korean population. Comparative analysis indicated that 34.9% YMNK and 73.4% KS patients harbored the microdeleted Y-chromosome. It seems to be high instability of Y-chromosome in KS patients than that of YMNK infertility patients. Taken together, genome instability containing microdeletion could bring male infertility with the disturbance of normal spermatogenesis.

• Journal of Life Science
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• v.29 no.9
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• pp.1047-1054
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• 2019

Transposable elements (TEs) occupy approximately 45% of the human genome and can enter functional genes randomly. During evolutionary radiation, multiple copies of TEs are produced by duplication events. Those elements contribute to biodiversity and phylogenomics. Most of them are controlled by epigenetic regulation, such as methylation or acetylation. Every species contains their own specific mobile elements, and they are divided into DNA transposons and retrotransposons. Retrotransposons can be divided by the presence of a long terminal repeat (LTR). They show various biological functions, such as promoter, enhancer, exonization, rearrangement, and alternative splicing. Also, they are strongly implicated to genomic instability, causing various diseases. Therefore, they could be used as biomarkers for the diagnosis and prognosis of diseases such as cancers. Recently, it was found that TEs could produce miRNAs, which play roles in gene inhibition through mRNA cleavage or translational repression, binding seed regions of target genes. Studies of TE-derived miRNAs offer a potential for the expression of functional genes. Comparative analyses of different types of miRNAs in various species and tissues could be of interest in the fields of evolution and phylogeny. Those events allow us to understand the importance of TEs in relation to biological roles and various diseases.

• The Journal of the Korean bone and joint tumor society
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• v.8 no.3
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• pp.69-75
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• 2002

Werner's syndrome is a rare autosomal recessive disorder manifesting as premature aging. It is also known to be characterized by a high frequency of malignant tumors, especially sarcomas. However, Werner's syndrome may be not only a premature aging disease but also a cancer syndrome, because the malignant tumors in these patients are different from those of normal population with respect to involved site, histological type, and age of onset. Recent studies found Werner's syndrome was caused by a mutation of Werner helicase suggesting that WRN helicase may participate in metabolism and repair of DNA. And a dysfunction of WRN helicase may induce the genomic instability causing somatic mutations. Further studies of Werner's syndrome associated with sarcoma might give much informations about the normal aging process and the pathogenesis of sarcomas.

• Journal of Korea Society of Industrial Information Systems
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• v.18 no.6
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• pp.25-30
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• 2013

In nanoscale MOSFET technology, aging effects such as Negative Bias Temperature Instability(NBTI), Hot carrier Injection(HCI), Time Dependent Dielectric Breakdown (TDDB) and so on which affect circuit reliability can lead to severe degradation of digital circuit performance. Therefore, this paper has proposed the adaptive compensation circuit to overcome the aging effects of digital circuits. The proposed circuit deploys a power gating structure with variable power switch width and variable forward body-biasing voltage in order to adaptively compensate for aging induced performance degradation, and has been designed in 45nm technology.

• Journal of Life Science
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• v.30 no.11
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• pp.1012-1020
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• 2020

Remicade is a therapeutic biosimilar natural antibody in which the mouse variable domain has been linked to the human constant domain. It is a chimeric monoclonal antibody specific to tumor necrosis factor-alpha (TNF-α) and has been developed for the treatment of rheumatoid arthritis. To investigate the biological activity of the Remicade antibody, we carried out a bioinformatics study using a protein data bank to characterize the TNF-α antigen binding mechanism of the Remicade natural antibody. Because the production of the Remicade antibody is often limited by genetic instability of the natural antibody-producing cell, we generated a Remicade single-chain variable domain fragment antibody (Remicade) in which a heavy chain variable domain (VH) is joined with a light chain variable domain (VL) by a polypeptide linker. Furthermore, Remicade was fused to a leucine zipper (RemicadeScZip) for higher production and higher antigen-binding activity than Remicade. The Remicade and Remicade ScZip were expressed in Escherichia coli and purified by a Ni⁺-NTA-agarose column. As expected, the purified proteins had migrated as 28.80 kDa and 33.96 kDa in sodium dodecyl sulfate-polyacrylamide electrophoresis. The TNF-α antigen binding activity of Remicade was not observed by ELISA and western blot. In contrast, RemicadeScZip showed antigen-binding activity. Additional bio-layer interferometry analysis confirmed the antigen-binding activity of RemicadeScZip, suggesting that the leucine zipper stabilized the folding of RemicadeScZip in a denatured condition and improved the TNF-α antigenbinding activity.

• Journal of Genetic Medicine
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• v.6 no.2
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• pp.175-178
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• 2009

The 22q11.2 duplication syndrome is an extremely variable disorder with a phenotype ranging from normal to congenital defects and learning disabilities. Recently, the detection rate of 22q11.2 duplication has been increased by molecular techniques, such as array CGH. In this study, we report a familial case of 22q11.2 duplication detected prenatally. Her first pregnancy was terminated because of 22q11.2 duplication detected incidentally by BAC array CGH. The case was referred due to second pregnancy with same 22q11.2 duplication. We perfomed repeat amniocentesis for karyotype and FISH analysis. Karyotype analysis from amniocytes and parental lymphocytes were normal, while FISH analysis of interphase cells presented a duplication of 22q11.2 in the fetus and phenotypically normal mother. The fetal ultrasound showed grossly normal finding. After genetic counseling about variable phenotype with intrafamilial variability with 50% recurrence rate, the couple decided to continue the pregnancy. The newborn had no apparent congenital abnormalities until 2 weeks after birth. We recommend that family members of patients with a 22q11.2 duplication be tested by the interphase FISH analysis. Also, we point out the importance of genetic counseling and an evaluation of the clinical relevance of diagnostic test results.