• Applied Chemistry for Engineering
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• v.16 no.3
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• pp.312-316
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• 2005

Adsorption characteristics of $CO_2$ on activated carbons were evaluated using dynamic adsorption method in a fixed bed with acid treatment, LiOH impregnation and water vapor supply. Physical and chemical properties of the activated carbons were measured using SEM, EDS, nitrogen adsorption, FTIR and XRD. Nitric acid treatment led to the decrease in BET surface area and the increase in oxygen content of virgin activated carbon, and it produced a new functional group that included nitrogen. For the reduction of BET surface area by LiOH impregnation, the nitric acid treated activated carbon (NAC) was less than the virgin activated carbon (AC). Large particles of LiOH were present on the carbon surface when the content of LiOH was over 2 wt%. The adsorbed amount of $CO_2$ on activated carbon in a fixed bed increased with the acid treatment, LiOH impregnation and water vapor supply. The XRD results indicated that LiOH was converted to $Li_2CO_3$ after the adsorption of $CO_2$ on LiOH precursor.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.6
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• pp.2219-2225
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• 2015

SHP1 negatively regulates the Janus kinase 2/signal transducer and activator of transcription (JAK2/STAT) signaling pathway, which is constitutively activated in myeloproliferative neoplasms (MPNs) and leukemia. Promoter hypermethylation resulting in epigenetic inactivation of SHP1 has been reported in myelomas, leukemias and other cancers. However, whether SHP1 hypermethylation occurs in MPNs, especially in Chinese patients, has remained unclear. Here, we report that aberrant hypermethylation of SHP1 was observed in several leukemic cell lines and bone marrow mononuclear cells from MPN patients. About 51 of 118 (43.2%) MPN patients including 23 of 50 (46%) polycythaemia vera patients, 20 of 50 (40%) essential thrombocythaemia and 8 of 18 (44.4%) idiopathic myelofibrosis showed hypermethylation by methylation-specific polymerase chain reaction. However, SHP1 methylation was not measured in 20 healthy volunteers. Hypermethylation of SHP1 was found in MPN patients with both positive (34/81, 42%) and negative (17/37, 45.9%) JAK2V617F mutation. The levels of SHP1 mRNA were significantly lower in hypermethylated samples than unmethylated samples, suggesting SHP1 may be epigenetically inactivated in MPN patients. Furthermore, treatment with 5-aza-2'-deoxycytidine (AZA) in K562 cells showing hypermethylation of SHP1 led to progressive demethylation of SHP1, with consequently increased reexpression of SHP1. Meanwhile, phosphorylated JAK2 and STAT3 were progressively reduced. Finally, AZA increased the expression of SHP1 in primary MPN cells with hypermethylation of SHP1. Therefore, our data suggest that epigenetic inactivation of SHP1 contributes to the constitutive activation of JAK2/STAT signaling. Restoration of SHP1 expression by AZA may contribute to clinical treatment for MPN patients.

• Journal of the Korean Applied Science and Technology
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• v.36 no.4
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• pp.1259-1267
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• 2019

Anti-inflammatory and anti-oxidative activities were examined on the extract of Dendranthema indicum (D. indicum) flowers. The flowers were extracted two times for 24 h each with 70% ethanol. Upon the biological activities screening, the ethanol extract exhibited potent free radical scavenging activities and inhibited the production of nitric oxide on LPS-induced RAW264.7 macrophages effectively without causing cell toxicity. Further purification by medium pressure liquid hromatography (MPLC) and identification of the isolates led to identification of cynaroside (1) and apigetrin (2). The chemical structures of the isolated compounds were elucidated based on spectroscopic data including nuclear magnetic resonance (NMR) spectra, as well as comparison of the data to the literature values. Also, the quantitative analysis of the compounds was perfromed by high-performance liquid chromatography (HPLC). The isolates 1 and 2 were determined to inhibite the nitric oxide (NO) production dose-dependently. Based on these results, it was suggested that D. indicum extract could be useful as anti-inflammatory agents in cosmetics applications.

• Journal of Ginseng Research
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• v.42 no.2
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• pp.165-174
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• 2018

Background: Extended endoplasmic reticulum (ER) stress may initiate apoptotic pathways in cancer cells, and ER stress has been reported to possibly increase tumor death in cancer therapy. We previously reported that caspase-8 played an important role in compound K-induced apoptosis via activation of caspase-3 directly or indirectly through Bid cleavage, cytochrome c release, and caspase-9 activation in HL-60 human leukemia cells. The mechanisms leading to apoptosis in A549 and SK-MES-1 human lung cancer cells and the role of ER stress have not yet been understood. Methods: The apoptotic effects of compound K were analyzed using flow cytometry, and the changes in protein levels were determined using Western blot analysis. The intracellular calcium levels were monitored by staining with Fura-2/AM and Fluo-3/AM. Results: Compound K-induced ER stress was confirmed through increased phosphorylation of $eIF2{\alpha}$ and protein levels of GRP78/BiP, XBP-1S, and $IRE1{\alpha}$ in human lung cancer cells. Moreover, compound-K led to the accumulation of intracellular calcium and an increase in m-calpain activities that were both significantly inhibited by pretreatment either with BAPTA-AM (an intracellular $Ca^{2+}$ chelator) or dantrolene (an RyR channel antagonist). These results were correlated with the outcome that compound K induced ER stress-related apoptosis through caspase-12, as z-ATAD-fmk (a specific inhibitor of caspase-12) partially ameliorated this effect. Interestingly, 4-PBA (ER stress inhibitor) dramatically improved the compound K-induced apoptosis. Conclusion: Cell survival and intracellular $Ca^{2+}$ homeostasis during ER stress in human lung cancer cells are important factors in the induction of the compound K-induced apoptotic pathway.

• Macromolecular Research
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• v.17 no.12
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• pp.963-968
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• 2009

Liquid crystal (LC; E7 and/or ML-0249)-embedded, poly(vinylidenefluoride-co-hexafluoropropylene) (PVdF-co-HFP)-based, polymer electrolytes were prepared for use in dye-sensitized solar cells (DSSCs). The electrolytes contained 1-methyl-3-propylimidazolium iodide (PMII), tetrabutylammonium iodide (TBAI), and iodine ($I_2$), which participate in the $I_3^-/I^-$ redox couple. The incorporation of photochemically stable PVdF-co-HFP in the DSSCs created a stable polymer electrolyte that resisted leakage and volatilization. DSSCs, with liquid crystal(LC)-embedded PVdF-co-HFP-based polymer electrolytes between the amphiphilic ruthenium dye N719 absorbed to the nanocrystalline $TiO_2$ photoanode and the Pt counter electrode, were fabricated. These DSSCs displayed enhanced redox couple reduction and reduced charge recombination in comparison to that fabricated from the conventional PVdF-co-HFP-based polymer electrolyte. The behavior of the polymer electrolyte was improved by the addition of optimized amounts of plasticizers, such as ethylene carbonate (EC) and propylene carbonate (PC). The significantly increased short-circuit current density ($J_{sc}$, $14.60\;mA/cm^2$) and open-circuit voltage ($V_{oc}$, 0.68 V) of these DSSCs led to a high power conversion efficiency (PCE) of 6.42% and a fill factor of 0.65 under a standard light intensity of $100\;mW/cm^2$ irradiation of AM 1.5 sunlight. A DSSC fabricated by using E7-embedded PVdF-co-HFP-based polymer electrolyte exhibited a maximum incident photon-to-current conversion efficiency (IPCE) of 50%.

• Korean Journal of Veterinary Research
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• v.16 no.1
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• pp.77-96
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• 1976

In order to investigate the effects and acting mechanism on ovaries, thyroid glands and hypophyses of rabbits in short term administration of sulfadimethoxine (SDM) as medical dose, a total of 90 virgin albino rabbits (mean body weight, 1,362g) were selected at random and alloted to two groups. Rabbits in one group served as controls and the others were administered SDM of 50 mg/kg/day for 5 weeks, and then reared without medication for 4 weeks. Pathological changes of the three organs were observed each week for 9 weeks and the results obtained were summarized as follows: 1. Mean body weights of both groups manifested slow increasing tendency but mean hypophysis weights fluctuated throughout the experimental term. Mean ovary weights of experiments were decreased significantly from the 3rd to 6th week but mean thyroid weights of experiments were increased significantly from the 1st to 6th week compared with those of controls. 2. Many ovarian follicles of each developing stage showed follicular atresia accompanying atrophy or necrosis of oocytes and of disintegrated follicular cells. Theca interna cells and sudanophilic interstitial cells showed atrophy and diminished sudanophilic granules and also liquor folliculi were diminished. These changes icreased from the 1st week, remaining so for 5 weeks and returned to normal status in the 8th or 9th week. 3. The thyroid gland showed a typical hyperplastic goiter. Hypertrophic and hyperplastic epithelia follicular manifested cuboidal or columnar form showing tiny or small vacuoles in cytoplasm. The follicles showed atrophy and decreasing colloidal materials. Necrotic and regenerative changes were also present. The interfollicular vessels showed congestion and hemorrhage. These changes increased from the 1st week, remaining so for 5 weeks and returned to normal status in the 9th week. 4. The rates of differential cell counts of hypophyses revealed increase of basophils (gonadotrophs and thyrotrophs) and decrease of chromophobes. Basophils which had diminished granules stainable with HE, PAS and AF revealed hypertrophy, hyperplasia, and increasing of tiny or small vacuoles in cytoplasm. These changes increased from the 1st week, remaining so for 5 weeks and returned to normal status in the 8th or 9th week. As summarized above histologically, administration of SDM led thyrotrophs and gonadotrophs of pituitary glands to hyperactivity but revealed retrogressive and compensatory changes with functional disturbance in ovaries and thyroid glands. These changes were transitional and attributed to direct actions of the drugs on the ovaries and thyroid glands.

• Tuberculosis and Respiratory Diseases
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• v.75 no.2
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• pp.59-66
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• 2013

Background: This study was conducted in order to elucidate the effects of docetaxel on the growth of peroxiredoxin 1 (Prx1) knockdown A549 xenograft tumors and further tested the role of Prx1 as a predictor for how a patient would respond to docetaxel treatment. Methods: Effects of docetaxel on the growth of scrambled- and shPrx1-infected A549 xenograft tumors in nude mice were measured. Moreover, immunohistochemical expression of Prx1 was evaluated in paraffin-embedded tissues from 24 non-small cell lung cancer patients who had received docetaxel-cisplatin regimens as a first-line treatment. Results: Docetaxel treatment in Prx1 knockdown xenograft tumor resulted in reduced tumors growth compared with other groups. Prx1 knockdown increased the production of cleaved caspases-8 and -9 in the control itself compared to scramble tumors. Moreover, docetaxel treatment in Prx1 knockdown tissue led to an increased protein band. Phosphorylated Akt was found in Prx1 scramble tissues. Phosphorylated FOXO1 was detected in the docetaxel treatment group. On the other hand, Prx1 knockdown completely suppressed the Akt-FOXO1 axis. The median progression-free survival (PFS) of patients with low Prx1 expression was 7 months (95% confidence interval [CI], 6.0-7.7), whereas the median progression-free survival of patients with high Prx1 expression was 4 months (95% CI, 4.0-5.0). However, high Prx1 expression was not associated with decreased PFS (p=0.114). Conclusion: Our findings suggest that elevated Prx1 provides resistance to docetaxel treatment through suppression of FOXO1-induced apoptosis in A549 xenograft tumors, but may not be related with the predictive significance for response to docetaxel treatment.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.247-254
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• 2017

Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.

• The Journal of the Convergence on Culture Technology
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• v.2 no.4
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• pp.31-40
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• 2016

The hardware of the human body is given the life force by the sentence which is the physiological software that the program for cell activation by the electrical signal enters. The aim of this study is to create a better therapeutic environment for the human body that groaned with errors in the physiological and cognitive systems that are transmitted to neurons and neurons. The sentence program of the rated sijo, which is the software of the human body which has the function as a conductor to connect the emotions of joy, anger, sadness, and enthusiasm to the human mental system, can be connected to the neuron system of the human body, we tried to identify the principle of operating the motherboard of mind in humanities. Once these principles are identified, we can figure out how to minimize side effects and lead the body to a therapeutic program. The research found that there is a strong energy source that can operate the motherboard of the heart very quickly in the rated Sijo. This is because it is confirmed that new coding and re-coding of a number of rated sijo, or a new syllable of one syllable followed by the original syllable of the original syllable, are formed quickly and therapeutically.This has led to the possibility of literary therapy for mankind to upgrade the human psychic system in abundance through the function of the interaction between the sentence as a conductor that is synaptically connected to the human body and the mainboard of the mind attached to the human body without side effects in the future.

• Proceedings of the Korean Society for Bioinformatics Conference
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• 2001.10a
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• pp.61-86
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• 2001

All cancers are caused by abnormalities in DNA sequence. Throughout life, the DNA in human cells is exposed to mutagens and suffers mistakes in replication, resulting in progressive, subtle changes in the DNA sequence in each cell. Since the development of conventional and molecular cytogenetic methods to the analysis of chromosomal aberrations in cancers, more than 1,800 recurring chromosomal breakpoints have been identified. These breakpoints and regions of nonrandom copy number changes typically point to the location of genes involved in cancer initiation and progression. With the introduction of molecular cytogenetic methodologies based on fluorescence in situ hybridization (FISH), namely, comparative genomic hybridization (CGH) and multicolor FISH (m-FISH) in carcinomas become susceptible to analysis. Conventional CGH has been widely applied for the detection of genomic imbalances in tumor cells, and used normal metaphase chromosomes as targets for the mapping of copy number changes. However, this limits the mapping of such imbalances to the resolution limit of metaphase chromosomes (usually 10 to 20 Mb). Efforts to increase this resolution have led to the "new"concept of genomic DNA chip (1 to 2 Mb), whereby the chromosomal target is replaced with cloned DNA immobilized on such as glass slides. The resulting resolution then depends on the size of the immobilized DNA fragments. We have completed the first draft of its Korean Genome Project. The project proceeded by end sequencing inserts from a library of 96,768 bacterial artificial chromosomes (BACs) containing genomic DNA fragments from Korean ethnicity. The sequenced BAC ends were then compared to the Human Genome Project′s publicly available sequence database and aligned according to known cancer gene sequences. These BAC clones were biotinylated by nick translation, hybridized to cytogenetic preparations of metaphase cells, and detected with fluorescein-conjugated avidin. Only locations of unique or low-copy Portions of the clone are identified, because high-copy interspersed repetitive sequences in the probe were suppressed by the addition of unlabelled Cotl DNA. Banding patterns were produced using DAPI. By this means, every BAC fragment has been matched to its appropriate chromosomal location. We have placed 86 (156 BAC clones) cytogenetically defined landmarks to help with the characterization of known cancer genes. Microarray techniques would be applied in CGH by replacement of metaphase chromosome to arrayed BAC confirming in oncogene and tumor suppressor gene: and an array BAC clones from the collection is used to perform a genome-wide scan for segmental aneuploidy by array-CGH. Therefore, the genomic DNA chip (arrayed BAC) will be undoubtedly provide accurate diagnosis of deletions, duplication, insertions and rearrangements of genomic material related to various human phenotypes, including neoplasias. And our tumor markers based on genetic abnormalities of cancer would be identified and contribute to the screening of the stage of cancers and/or hereditary diseases