• Carbon letters
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• v.7 no.1
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• pp.34-41
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• 2006

The objective of this paper is to compare the variation of surface properties by hydrochloric acid pre-treatment and of metallic potassium and their salts loading effect for activated carbon after surfaces transformation by acid. From the results of nitrogen adsorption, each isotherm shows a distinct knee band, which is closely related to the characteristic of microporous carbons with capillary condensation in micropores. In order to present the causes of the differences in surface properties and $S_{BET}$ after the samples were treated with hydrochloric acid, pore structure and surface morphology are investigated by adsorption analysis. X-ray diffraction (XRD) patterns indicate that activated carbons show better performance for metallic potassium and potassium salts by pre-treatment with hydrochloric acid. Scanning electron microscopy (SEM) pictures of potassium/activated carbon particles provide information about the homogeneous distribution of metal or metal complex on the surface. For the chemical composition microanalysis for potassium treatment of the activated carbon pre-treated with hydrochloric acid, samples were analyzed by energy disperse X-ray (EDX). Finally, the type and quality of oxygen groups are determined from the method proposed by Boehm. A positive influence of the acidic groups on the carbon surface by acid treatment is also demonstrated by an increase in the contents of potassium salts with increasing of acidic groups calculated from Boehm titration.

• IMMUNE NETWORK
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• v.1 no.3
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• pp.221-229
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• 2001

Background: Inactivation of tumor suppressor genes is believed to be important in the development of many human malignancies. Recently, several lines of evidence have indicated that the wild type p53 gene located at 17p13.3, may function as a tumor suppressor gene and that a mutant p53 gene could promote transformation by inactivating normal p53 function in a dominant negative fashion. These broad spectrum of p53 mutation in human cancers provide that mutant p53 and their protein may be potential targets of tumor diagnostic and therapeutic interventions. Method: Colony formation was performed to investigate growth suppressional ability. p53 expression pattern was examined by western blot and p53-mediated transactivation ability was assessed by CAT activity. SNU C2A cells were observed in apoptotic aspects induced by etoposide and $H_2O_2$ treatment, detecting sensitivity on agent, DNA fragmentation through agarose gel, chromatin condensation by fluorescence microscope, and cell cycle distribution by FACS. Result: 1) p53 mutant his179arg ($histidine{\rightarrow}arginine$) detected in SNU C2A cells lost transcriptional activity and growth suppression ability, showing dominant negative effect on its wild type p53. 2) Etoposide-treated SNU C2A cells induced apoptosis, exhibiting dramatic reduction of cell growth, DNA fragmentation, nuclear condensation formation of apoptotic body and increment of sub-G1 cell fraction. 3) Etoposide and $H_2O_2$-treated SNU C2A cells have no high increase of p53 expression and overexpressed p53 protein changed localization, from cytoplasm to nucleus. Also, p53-mediated transcriptional activity was increased by agents-treatment. Conclusion: SNU C2A cells coexpress wild-type and mutant p53 protein induced apoptosis in the condition on DNA damage, through localizational shift from cytoplasm to nucleus of p53 protein rather than the induction of p53 protein. SNU C2A cells derived mutant p53 his179arg abrogated both the growth supression ability and transactivational activity, showing inhibition effect on transcriptional activity of wild type p53, but did not repress the activity of wild type p53 in SNU C2A cells owing to dominant activity of wild type. These cell condition may provide new gene therapeutic implications leading effective antiproliferation of cell when mutant and wild-type p53 protein were co-expressed in cell.

• Biomolecules & Therapeutics
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• v.17 no.4
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• pp.438-445
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• 2009

We investigated global gene expression from both mouse liver and mouse hepatic cell lines treated with acetaminophen (APAP) in order to compare in vivo and in vitro profiles and to assess the feasibility of the two systems. During our analyses of gene expression profiles, we picked up several down-regulated genes, such as the cytochrome P450 family 51 (Cyp51), sulfotransferase family cytosolic 1C member 2 (Sult1c2), 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1 (Hmgcs1), and several genes that were up-regulated by APAP, such as growth arrest and DNA-damage-inducible 45 alpha (Gadd45a), transformation related protein 53 inducible nuclear protein 1 (Trp53inp1) and zinc finger protein 688 (Zfp688). For validation of gene function, synthesized short interfering RNAs (siRNAs) for these genes were transfected in a mouse hepatic cell line, BNL CL.2, for investigation of cell viability and mRNA expression level. We found that siRNA transfection of these genes induced down-regulation of respective mRNA expression and decreased cell viability. siRNA transfection for Cyp51 and others induced morphological alterations, such as membrane thickening and nuclear condensation. Taken together, siRNA transfection of these six genes decreased cell viability and induced alteration in cellular morphology, along with effective inhibition of respective mRNA, suggesting that these genes could be associated with APAP-induced toxicity. Furthermore, these genes may be used in the investigation of hepatotoxicity, for better understanding of its mechanism.

• Molecular & Cellular Toxicology
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• v.1 no.2
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• pp.73-77
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• 2005

Nickel is the one of potent environmental, the occupational pollutants and the classified human carcinogens. It is a serious hazard to human health, when the metal exposure. To prevent human diseases from the heavy metals, it is seemingly important that understanding of how nickel exerts their toxicity and carcinogenic effect at a molecular and a genomic level. The process of nickel absorption has been demonstrated as phagocytosis, iron channel and diffusion. Uptaked nickel has been suggested to induce carcinogenesis via two pathways, a direct DNA damaging pathway and an indirect DNA damaging pathway. The former was originated from the ability of metal to generate Reactive Oxygen Species (ROS) and the reactive intermediates to interact with DNA directly. Ni-generated ROS or Nickel itself, interacts with DNAs and histones to cause DNA damage and chromosomal abnormality. The latter was originated from an indirect DNA damage via inhibition of DNA repair, or condensation and methylation of DNA. Cells have ability to protect from the genotoxic stresses by changing gene expression. Microarray analysis of the cells treated with nickel or nickel compounds, show the specific altered gene expression profile. For example, HIF-I (Hypoxia-Inducible Factor I) and p53 were well known as transcription factors, which are upregulated in response to stress and activated by both soluble and insoluble nickel compounds. The induction of these important transcription factors exert potent selective pressure and leading to cell transformation. Genes of metallothionein and family of heat shock proteins which have been known to play role in protection and damage control, were also induced by nickel treatment. These gene expressions may give us a clue to understand of the carcinogenesis mechanism of nickel. Further discussions on molecular and genomic, are need in order to understand the specific mechanism of nickel toxicity and carcinogenicity.

• Transactions of the Korean hydrogen and new energy society
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• v.28 no.3
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• pp.238-245
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• 2017

Mg-Ni nanoparticles were synthesized by a physical vapor condensation method (DC arc-discharge) in a mixture of argon and hydrogen atmosphere, using compressed mixture of micro powders as the raw materials. The crystal phases, morphology, and microstructures of nanoparticles were analyzed by means of X-ray diffraction (XRD) and high-resolution transmission electron microscopy (HRTEM). It was found that the intermetallic compounds of $Mg_2Ni$ and $Mg_2Ni$ formed with existence of phases of Mg, Ni, and MgO in Mg-Ni nanoparticles. After one cycle of hydrogen absorption/desorption process (activation treatment), Mg-Ni nanoparticles exhibited excellent hydrogen absorption properties. $Mg_2Ni$ phase became the main phase by aphase transformation during the hydrogen treatments. The phenomenon of refinement of grain size in the nanoparticle was also observed after the hydrogen absorption/desorption processes, which was attributed to the effect of volume expansion/shrinkage and subsequent break of nanoparticles. Maximum hydrogen absorption contents are 1.75, 2.21 and 2.77 wt.% at 523, 573 and 623 K, respectively.

• Korean Chemical Engineering Research
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• v.48 no.1
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• pp.20-26
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• 2010

Water soluble organic and inorganic species are important components in atmospheric aerosol particles and may act as cloud condensation nuclei to indirectly affect the climate. To characterize organic and elemental carbon(OC and EC), water-soluble organic carbon(WSOC) and inorganic ionic species contents, daily $PM_{2.5}$ measurements were made during the wintertime at an urban site of Gwangju. Average concentrations of WSOC, $NO_3^-$, $SO_4^{2-}$ and $NH_4^+$, which are major components in the water-soluble fraction in PM2.5, are 2.11, 5.73, 3.51 and $3.31{\mu}g/m^3$, respectively, representing 12.0(2.9~23.9%), 21.0(12.9~37.6%), 11.6(2.5~25.9%) and 11.7%(3.8~18.6%) of the $PM_{2.5}$, respectively. Abundance of water soluble organic compounds ranged from 5.4 to 35.9% of total water soluble organic and inorganic components with a mean of 17.6%. Even though the sampling was performed during the winter, the average contributions of secondary OC and WSOC, as deduced from primary OC/EC(or WSOC/EC) ratio, were relatively high, accounting for 17.9%(0~44.4%) of the total OC and 11.2%(0.0~51.4%) of the total WSOC, respectively. During the sampling period, low $SO_4^{2-}/(SO_4^{2-}+SO_2$) ratio of 0.14(0.03~0.32) and relative humidity condition in the winter time suggest an possibility of impact of long-range transport and/or aqueous transformation processes such as metal catalyzed oxidation of sulfur, in-cloud processes, etc.

• Journal of Radiation Protection and Research
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• v.32 no.4
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• pp.140-156
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• 2007

This research was performed to investigate the morphological changes of folliculus ovary according to the radiation dose. The whole body radiation of 200 cGy, 400 cGy, and 600 cGy was given to the each groups of 5 months-aged female mouse. Various staining methods used in this research are: Hematosylin-Eosin method, and immunohistochemistrical methods using BrdU, TUNEL, p53, p21, PCNA and inhibin. The minute structural changes of folliculus ovary were observed through an electron microscope with high magnification. The morphological changes of growing folliculus ovary became distinct as the dose of X-rays increased. Especially, the nuclei of granular cells showed manifest condensation and the changes of the transparent zone were distinct. As a result of histochemical reaction according to Masson's trichrome method and reticular fiber method, the changed granular cells, the deformed basilar membrane of folliculus ovary and the abnormal arrangement of the reticular fiber were observed. In the reaction of BrdU, the granular cells of normal folliculus ovary with positive reaction rapidly decreased according to the increase of the dose of X-rays. In TUNEL study, granular cells showing positive reaction in retarded folliculus ovary were expanded to growing folliculus ovary and primordial folliculus ovary according to the increase of the dose of X-rays. In case of 600 cGy of X-rays, oocyte underwent apoptosis. In p53 immunohistochemistry, p53 manifested to be stronger as the dose of X-rays increased. p53 reactivity was manifested distinctively in all cells comprising folliculus ovary following irradiation of 600 cGy. p21 was manifested in granular cells of folliculus ovary and showed very positive reaction around follicular antrum according to the increase of the dose of X-rays. In PCNA, positive reaction was manifested in growing folliculus ovary, mature folliculus ovary and primordial folliculus ovary, but the extent of the reaction decreased as the dose of the X-rays decreased. The finding that the reaction of granular cells around folliculus ovary was stronger than that near follicular membrane indicates that what was damaged first by X-ray was the cells near folliculus ovary and follicular antrum. The reactivity of $inhibin-{\alpha}$ showed difference according to the growing stage of folliculus ovary: $inhibin-{\alpha}$ showed the most strong reaction in mature folliculus ovary with follicular antrum. There was strong reaction in granular cells around follicular membrane but $inhibin-{\alpha}$ did not occur at all in theca cells comprising follicular membrane. $Inhibin-{\alpha}$ in ovary tissue exposed to 400 cGy of X-rays was manifested more strongly than in ovary tissue exposed to 600 cGy of X-rays, which was related to the phenomenon that granular cells of mature folliculus ovary underwent necrosis or apoptosis increasingly due to X-rays. In an electron microscope with high magnification, nuclei and protoplasm of granular cells in growing folliculus ovary abruptly underwent minute structural changes according to the increase of dose of X-rays. Cell residue, by-product of cell decease, neutrophil and macrophage around follicular antrum were observed. The minute structural changes in granular cells showed typical characteristics of apoptosis: the increase of electronic density due to nuclear condensation, fragmentation of nuclei and atrophy of protoplasm. Necrosis of cells was identified but it was not so remarkable. Macrophage with apoptotic bodies was scattered. Proportional to the radiation dose, we found that the generation of heterogeneous substance of normal ovary texture's follicular fluid, the emergence of dyeing characteristic in the basilar membrane of folicle, the generation of apoptosis, and the transformation of macrophages, etc. From this results, we can infer the possible radiation hazard on the ovary of cervix cancer patient with radiation therapy.