• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5391-5397
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• 2012

Background: Neuroblastoma (NB), like most human cancers, is characterized by genomic instability, manifested at the chromosomal level as allelic gain, loss or rearrangement. Genetics methods, as well as conventional and molecular cytogenetics may provide valuable clues for the identification of target loci and successful search for major genes in neuroblastoma. We aimed to investigate AURKA and MYCN gene rearrangements and the chromosomal aberrations (CAs) to determine the prognosis of neuroblastoma. Methods: We performed cytogenetic analysis by G-banding in 25 cases [11 girls (44%) and 14 boys (66%)] and in 25 controls. Fluorescence in situ hybridization (FISH) with AURKA and MYCN gene probes was also used on interphase nuclei to screen for alterations. Results: Some 18.4% of patient cells exhibited CAs., with a significant difference between patient and control groups in the frequencies (P<0.0001). Some 72% of the cells had structural aberrations, and only 28% had numerical chnages in patients. Structural aberrations consisted of deletions, translocations, breaks and fragility in various chromosomes, 84% and 52% of the patients having deletions and translocations, respectively. Among these expressed CAs, there was a higher frequency at 1q21, 1q32, 2q21, 2q31, 2p24, 4q31, 9q11, 9q22, 13q14, 14q11.2, 14q24, and 15q22 in patients. 32% of the patients had chromosome breaks, most frequently in chromosomes 1, 2, 3, 4, 5, 8, 9, 11, 12, 19 and X. The number of cells with breaks and the genomic damage frequencies were higher in patients (p<0.001). Aneuploidies in chromosomes X, 22, 3, 17 and 18 were most frequently observed. Numerical chromosome abnormalities were distinctive in 10.7% of sex chromosomes. Fragile sites were observed in 16% of our patients. Conclusion: Our data confirmed that there is a close correlation between amplification of the two genes, amplification of MYCN possibly contributing significantly to the oncogenic properties of AURKA. The high frequencies of chromosomal aberrations and amplifications of AURKA and MYCN genes indicate prognostic value in children with neuroblastomas and may point to contributing factors in their development.

• Journal of Korean Ophthalmic Optics Society
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• v.19 no.4
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• pp.487-492
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• 2014

Purpose: This study relates to the development of the 3X scope, whose objective part is configured with a doublet + a meniscus lens. Methods: By the initial condition of the objective part having a configuration of a doublet + a singlet, we could optimize the optical system of scope in order to minimize the finite ray aberrations of the objective part and the whole optical system of scope, and so we could develope a new type 3X scope. Results: On the condition of the objective part having a configuration of a doublet + a singlet, when the optical system of scope was optimized in order to minimize the finite ray aberrations, we could find that the singlet became the meniscus type lens having the concave shape to the direction of the doublet, and the longer the distance between the doublet and the meniscus lens is, the more the finite ray aberrations are minimized. Conclusions: In this study, we could develope a new type 3X scope of which finite ray aberrations can be reduced to 1/14 than the existing scope by adopting the objective part of the 3X scope having a configuration of three lenses composed of a doublet + a singlet. We could confirm that this reduction of aberrations can be a means to increase the effective aperture than the existing scope and to shorten the length of the optical system.

• The Korea Genome Conference
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• 2004.07a
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• pp.46.1-46.1
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• 2004

• Proceedings of the Optical Society of Korea Conference
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• 2002.11a
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• pp.208-209
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• 2002

• Proceedings of the Optical Society of Korea Conference
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• 2002.11a
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• pp.104-105
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• 2002

• Environmental Mutagens and Carcinogens
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• v.18 no.2
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• pp.89-92
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• 1998

The results of chromosome aberration test in mammalian cells in culture (Chinese hamster lung fibroblast cells) showed no induction of structural and numerical aberrations by YH1226, a cephalosporin antibiotic regardless of metabolic activation, while positive control group (mitomycin C and benzo(a)pyrene) showed structural chromosome aberrations of 25% and 10%, respectively. The in vivo induction of micronuclei was measured in polychromatic erythrocytes in bone marrow of male ddY mouse given YH1226 at 500, 250, 125 mg/kg by i.p. once. After 24 hours, animals were sacrificed and evaluated for the incidence of micronucleated polychromatic erythrocytes in whole erythrocytes. Although a positive response for induction of micronuclei in animals treated with mitomycin C demonstrated the sensitivity of the test system for detection of a chemical clastogen, YH1226 did not induce microunclei in bone marrow of ddY male mice.

• Toxicological Research
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• v.34 no.4
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• pp.311-324
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• 2018

Arsenic is one of the most toxic environmental toxicants. More than 150 million people worldwide are exposed to arsenic through ground water contamination. It is an exclusive human carcinogen. Although the hallmarks of arsenic toxicity are skin lesions and skin cancers, arsenic can also induce cancers in the lung, liver, kidney, urinary bladder, and other internal organs. Arsenic is a non-mutagenic compound but can induce significant cytogenetic damage as measured by chromosomal aberrations, sister chromatid exchanges, and micronuclei formation in human systems. These genotoxic end points are extensively used to predict genotoxic potentials of different environmental chemicals, drugs, pesticides, and insecticides. These cytogenetic end points are also used for evaluating cancer risk. Here, by critically reviewing and analyzing the existing literature, we conclude that inorganic arsenic is a genotoxic carcinogen.

• Journal of Food Hygiene and Safety
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• v.1 no.1
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• pp.13-21
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• 1986

Two short-term bioassays were employed to asses the mutagenic and clastogenic activities in browning reaction of pentose-creatine, pentose-glycine and pentose-creatine-glycine browning reaction model system. Methylene chloride extract of rhamnose-creatine-glycine browning reaction exhibited the strongest mutagenicity toward Salmonella typhimurium TA98 with S-9. Methylene chloride extract of pentose-creatine and pentose-glycine browning reaction solutions was also tested for mutagenicity, with positive responses. Methylene chloride extract of pentose-creatine-glycine browning reaction solutions induced significant increase in chromosome aberrations in the treated Chinese hamster ovary(CHO) cells. Each of pentose-creatine and pentose-glycine browning reaction solutions induced a relatively low frequency of chromosome aberrations in the treated cells.

• Korean Journal of Environmental Biology
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• v.21 no.4
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• pp.384-391
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• 2003

The induction of chromosome aberrations in Hordeum vulgare germs after irradiation is studied for the dose range of 10 to 1,000 mGy. The relationship between the frequency of aberrant cells and the absorbed dose is shown to be non -linear and has a dose-independent plateau within the range of 56-467 mGy where the level of cytogenetic damage is statistically significantly distinguished from the spontaneous level. The comparison of the goodness of the experimental data fitting with mathematical models of different complexities, using the most common quantitative criteria, demonstrates the benefit of the piecewise linear model over the linear and polynomial ones in approximating the cytogenetical disturbance frequency. The results of our study support the conclusion about indirect mechanism of chromosome aberrations induced by low doses or dose rates mutagenesis.

• Korean Journal of Optics and Photonics
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• v.9 no.3
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• pp.142-145
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• 1998

It is shown that the optical system with Gaussian pupil e, diffraction amplitude distribution is not affected by the presence of residual aberrations. The case of spherical aberration is treated, as an example, and the complex diffraction amplitude distribution at the neighbourhood of the image point is described analytically by using a recurrence formula.