• Journal of Korean Society of Environmental Engineers
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• v.30 no.3
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• pp.323-330
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• 2008

The study presents the results of 1,4-dioxane degradation using zero valent (Fe$^0$) or Fe$^{2+}$ ions with and without UV. During the reaction, the change of [Fe$^{2+}$] and [Fe$^{2+}$]/[Fe(t)], the concentration ratio of ferrous ion to total iron ion in solution was measured. Less than 10% degradation of 1,4-dioxane was observed by UV-only, Fe$^0$-only, and Fe$^{2+}$-only conditions, and also the changes of [Fe$^{2+}$] and [Fe$^{2+}$]/[Fe(t)] were minimal in each reaction. However, the oxidation of Fe$^0$ was enhanced with the irradiation of UV by approximately 25% and the improvement of 1,4-dioxane degradation was observed. Fenton reaction ($Fe^{2+}+H_2O_2$) showed higher degradation efficiency of 1,4-dioxane until 90 min, which of the degradation was stopped after that time. In the reaction of Fe$^{2+}$ and UV, the ratio of [Fe$^{2+}$]/[Fe(t)] decreased then slowly increased after a certain time indicating the reduction of Fe3+ to Fe$^{2+}$. In case of Fe$^0$ in the presence of UV, the first-order rate constant was found to be 1.84$\times$10$^{-3}$ min$^{-1}$ until 90 min, and then changed to 9.33$\times$10$^{-3}$ min$^{-1}$ when the oxidation of Fe$^{2+}$ mainly occurred. In this case [Fe$^{2+}$]/[Fe(t)] kept decreasing for the reaction. However, the addition of perchlortae (ClO$_4^-$) in the reaction of Fe$^0$ and UV induced the continuous increase of [Fe$^{2+}$]/[Fe(t)] ratio. The results mean the primary degradation factor of 1,4-dioxane is the oxidation by the radicals generated from the redox reaction between Fe$^{2+}$ and Fe$^{3+}$. Also, both UV and ClO$_4^-$ played the role inducing the reduction of Fe$^{3+}$, which is important to degrade 1,4-dioxane by enhancing the generation of radicals.

• Radiation Oncology Journal
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• v.17 no.3
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• pp.238-248
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• 1999

Purpose : To assess the histomorphologic changes in the rat lung injury induced by radiation, to determine whether captopril reduces the rat lung injury and to evaluate change in TNF-${\alpha}$ and TGF-${\beta}$ in rat lung damage by radiation and captopril Methods and material : Right lungs in male Sprague-Dawley rats were divided irradiation alone (10, 20, 30 Gy) or radiation (same dose with radiation alone group) with captopril (500 mg/L). Radiation alone group were sacrificed at twelve hours and eleven weeks after radiation and radiation with captopril group (captopril group) were sacrificed at eleven weeks after radiation with captopril. We examined the light microscope and electron microscopic features in the groups. Results : In radiation alone group, there were patch parenchymal collapse and consolidation at twelve hours after radiation. The increase of radiation dose shows more prominent the severity and broader the affected areas. Eleven weeks after radiation, the severity and areas of fibrosis had increased in proportion to radiation dose given in the radiation alone group. There was notable decrease of lung fibrosis in captopril group than in radiation alone group. The number of mast cells rapidly increased with increase of radiation dose in radiation alone group and the degree of increase of mast cell number and severity of collagen accumulation more decreased in captopril group than in radiation alone group. In radiation alone group, expression of TNF-${\alpha}$ and TGF-${\beta}$ increased according to increase of radiation dose at twelve hours after radiation in both group. At eleven weeks after radiation, expression of TGF-${\beta}$ increased according to increase of radiation dose in radiation group but somewhat decreased in captopril group. In the captopril group the collagen deposition increased but less dense than those of radiation alone group. The severity of perivascular thickening, capillary change, the number and degranulation of mast cells more decreased in the captopril group than in the radiation alone group. Conclusion : It is concluded that the effect of captopril in the rat lungs after radiation was considered to be due to its effect on inhibition of mast cells and reduction of collagen deposition, and captopril may be protect in lung damage after radiation. We observed expression of TNF-${\alpha}$ and TGF-${\beta}$ increased at the early phase after radiation and expression of TGF-${\beta}$ increased in proportion to increase of radiation dose at the chronic phase after radiation. This results will contribute to future investigation in reduction mechanism of captopril in lung damage after radiation.

• Korean Journal of Veterinary Research
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• v.32 no.1
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• pp.15-24
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• 1992

The effects of CC the ovulatory response, oocyte normality, ovarian steroidogenesis and subsequent embryo developmental potential were examined in PMSG-treated rats. On Days of 25~27 of age, immature female Sprague Dawley rats were treated with three different doses(0.05, 0.1 or 1.0mg /day) of clomiphene citrate or vehicle. The females subsequently received 4IU PMSG on Day 28 and/or 10IU hCG on Day 30, and were killed on Day 31. Some females given 0.1mg CC or vehicle with 4IU PMSG were then mated and killed on Days 2, 3, 4 and 5 of pregnancy. Compared to vehicle(control) group, by increasing the doses of CC, there were a significant decrease in the ovulatory response as judged by both the proportion of rats ovulating and the mean number of oocytes per rat and a marked reduction of ovarian weight. The increasing doses of CC substantially promoted the degeneration(%) of oocytes ovulating in a dose-dependent manner. The CC-mediated inhibitions of the ovulatory response and ovarian weight were oompletely overcome by a subsequent treatment of hCG. Increasing doses of CC resulted in a siginificant elevation of serum estradiol with the decreased levels of progesterone and androgens. The additive treatment with hCG was effective to reduce the elevation of estradiol and to increase the reduction of progesterone produced by high dose(1.0mg) of CC. The preimplantation embryos recovered from 0.1mg CC-treated pregnant rats demonstrated a progressive early loss from Day 3 of pregnancy with a significant increase in the percentage of degeneration during all periods examined, compared to controls. The rate of progressive embryo cleavage in the CC-treated rats were slower than that in controls from Day 3 of pregnancy. Additionally, the percentage of the cleaved embryos recovered from the CC-treated rats remained significantly lower consistently from Day 2 of pregnancy, compared to control regimen. These results demonstrate a possible mechanism of CC-mediated inhibition of ovulatory response in the rats which may include the attenuation or blockade of the endogenous secretion of gonadotropins and also suggest that its detrimental effects observed on oocyte normality and embryonic development may be caused by abnormal follicular steroidogenesis( especially elevated estradiol) preceding fertilization.

• Journal of Life Science
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• v.32 no.1
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• pp.11-22
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• 2022

N-methyl-D-aspartate (NMDA) receptors have received considerable attention regarding their involvement in glutamate-induced neuronal excitotoxicity. Resveratrol has been shown to exhibit neuroprotective effects against this kind of overactivation, but the underlying cellular mechanisms are not yet clearly understood. In this study, HT-22 neuronal cells were treated with NMDA in Mg²⁺-free buffer and subsequently used as an experimental model of glutamate excitotoxicity to elucidate the mechanisms of resveratrol-induced neuroprotection. We found that NMDA treatment causes a drop in MTT reduction ability, disrupts inside-negative transmembrane potential of mitochondria, depletes cellular ATP levels, and stimulates intracellular ROS production. Double fluorescence imaging studies demonstrated an increased formation of mitochondrial permeability transition (MPT) pores accompanied by apoptotic cell death, while cobalt protoporphyrin and bilirubin showed protective effects against NMDA-induced mitochondrial injury. On the other hand, zinc protoporphyrin IX significantly attenuated the protective effects of resveratrol which was itself shown to enhance heme oxygenase-1 (HO-1) mRNA and protein expression levels. In cells transfected with HO-1 small interfering RNA, resveratrol failed to suppress the NMDA-induced effects on MTT reduction ability and MPT pore formation. The present study suggests that resveratrol may prevent mitochondrial injury in NMDA- treated HT-22 cells and that enhanced expression of HO-1 is involved in the underlying cellular mechanism.

• Tuberculosis and Respiratory Diseases
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• v.56 no.5
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• pp.465-484
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• 2004

Background : Insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) inhibits the proliferation of non-small cell lung cancer (NSCLC) cells by inducing apoptosis. Methods : In this study, we investigated whether hypermethylation of IGFBP-3 promoter play an important role in the loss of IGFBP-3 expression in NSCLC. We also studied the mechanisms that mediate the silencing of IGFBP-3 expression in the cell lines which have hypermethylated IGFBP-3 promoter. Results : The IGFBP-3 promoter has hypermethylation in 7 of 15 (46.7%) NSCLC cell lines and 16 (69.7%) of 23, 7 (77.8%) of 9, 4 (80%) of 5, 4 (66.7 %) of 6, and 6 (100%) of 6 tumor specimens from patients with stage I, II, IIIA, IIIB, and IV NSCLC, respectively. The methylation status correlated with the level of protein and mRNA in NSCLC cell lines. Expression of IGFBP-3 was restored by the demethylating agent 5'-aza-2'-deoxycytidine (5'-aza-dC) in a subset of NSCLC cell lines. The Sp-1/ Sp-3 binding element in the IGFBP-3 promoter, important for promoter activity, was methylated in the NSCLC cell lines which have reduced IGFBP-3 expression and the methylation of this element suppressed the binding of the Sp-1 transcription factor. A ChIP assay showed that the methylation status of the IGFBP-3 promoter influenced the binding of Sp-1, methyl-CpG binding protein-2 (MeCP2), and histone deacetylase (HDAC) to Sp-1/Sp-3 binding element, which were reversed by by 5'-aza-dC. In vitro methylation of the IGFBP-3 promoter containing the Sp-1/Sp-3 binding element significantly reduced promoter activity, which was further suppressed by the overexpression of MeCP2. This reduction in activity was rescued by 5'-aza-dC. Conclusion : These findings indicate that hypermethylation of the IGFBP-3 promoter is one mechanism by which IGFBP-3 expression is silenced and MeCP2, with recruitment of HDAC, may play a role in silencing of IGFBP-3 expression. The frequency of this abnormality is also associated with advanced stages among the patients with NSCLC, suggesting that IGFBP-3 plays an important role in lung carcinogenesis/progression and that the promoter methylation status of IGFBP-3 may be a marker for early molecular detection and/or for monitoring chemoprevention efforts.

• Journal of Intelligence and Information Systems
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• v.26 no.3
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• pp.71-90
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• 2020

Recently, the global insurance industry is rapidly developing digital transformation through the use of artificial intelligence technologies such as machine learning, natural language processing, and deep learning. As a result, more and more foreign insurers have achieved the success of artificial intelligence technology-based InsurTech and platform business, and Ping An Insurance Group Ltd., China's largest private company, is leading China's global fourth industrial revolution with remarkable achievements in InsurTech and Digital Platform as a result of its constant innovation, using 'finance and technology' and 'finance and ecosystem' as keywords for companies. In response, this study analyzed the InsurTech and platform business activities of Ping An Insurance Group Ltd. through the ser-M analysis model to provide strategic implications for revitalizing AI technology-based businesses of domestic insurers. The ser-M analysis model has been studied so that the vision and leadership of the CEO, the historical environment of the enterprise, the utilization of various resources, and the unique mechanism relationships can be interpreted in an integrated manner as a frame that can be interpreted in terms of the subject, environment, resource and mechanism. As a result of the case analysis, Ping An Insurance Group Ltd. has achieved cost reduction and customer service development by digitally innovating its entire business area such as sales, underwriting, claims, and loan service by utilizing core artificial intelligence technologies such as facial, voice, and facial expression recognition. In addition, "online data in China" and "the vast offline data and insights accumulated by the company" were combined with new technologies such as artificial intelligence and big data analysis to build a digital platform that integrates financial services and digital service businesses. Ping An Insurance Group Ltd. challenged constant innovation, and as of 2019, sales reached $155 billion, ranking seventh among all companies in the Global 2000 rankings selected by Forbes Magazine. Analyzing the background of the success of Ping An Insurance Group Ltd. from the perspective of ser-M, founder Mammingz quickly captured the development of digital technology, market competition and changes in population structure in the era of the fourth industrial revolution, and established a new vision and displayed an agile leadership of digital technology-focused. Based on the strong leadership led by the founder in response to environmental changes, the company has successfully led InsurTech and Platform Business through innovation of internal resources such as investment in artificial intelligence technology, securing excellent professionals, and strengthening big data capabilities, combining external absorption capabilities, and strategic alliances among various industries. Through this success story analysis of Ping An Insurance Group Ltd., the following implications can be given to domestic insurance companies that are preparing for digital transformation. First, CEOs of domestic companies also need to recognize the paradigm shift in industry due to the change in digital technology and quickly arm themselves with digital technology-oriented leadership to spearhead the digital transformation of enterprises. Second, the Korean government should urgently overhaul related laws and systems to further promote the use of data between different industries and provide drastic support such as deregulation, tax benefits and platform provision to help the domestic insurance industry secure global competitiveness. Third, Korean companies also need to make bolder investments in the development of artificial intelligence technology so that systematic securing of internal and external data, training of technical personnel, and patent applications can be expanded, and digital platforms should be quickly established so that diverse customer experiences can be integrated through learned artificial intelligence technology. Finally, since there may be limitations to generalization through a single case of an overseas insurance company, I hope that in the future, more extensive research will be conducted on various management strategies related to artificial intelligence technology by analyzing cases of multiple industries or multiple companies or conducting empirical research.

• Journal of Life Science
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• v.19 no.4
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• pp.423-428
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• 2009

Selenium was investigated using human origin preadipocytes to see whether it possesses preventive or therapeutic effects for obesity. Unveiling the potential of selenium in the reduction of adipogenesis can help predict the therapeutic capabilities of selenium in obesity. In the present study, the molecular mechanism of the inhibition of adipogenesis by selenium was explored to unravel the involvement of the AMP-activated protein kinase. There is emerging evidence that AMPK, a sensor of cellular energy status, is a possible molecular target of controlling adipocyte differentiation on the basis of discovery that AMPK is responsible for the major metabolic responses to exercise, and integration of nutritional and hormonal signals to modulate feeding behavior or energy expenditure in the hypothalamus. Treatment of selenium resulted in inhibition of the adipocyte differentiation process and induction of mature apoptosis in 3T3-L1 adipocytes. We hypothesized that selenium may exert anti-adipogenic potential though modulating AMPK. We have found that selenium significantly activated AMPK and phosphorylated its substrate acetyl-CoA carboxylase ($ACC-serine^{79}$) during the inhibitory process of adipocytes. Also, the inhibition process of adipocyte differentiation by selenium was comparable to either reveratrol or a synthetic AMPK activator, AICAR (5-aminoimidazole-4-carboxamide-1-${\beta}$-D-ribofuranoside). To evaluate the involvement of AMPK in anti-lipogensis, we applied AICAR and Compound C, an AMPK inhibitor, to 3T3-L1-adipocytes and found that AMPK is required for the adipocyte differentiation blocking process. These results suggest that selenium has a potential to control adipogenesis and that this effect is mediated by AMPK, an essential kinase for both inhibition of adipocyte differentiation and apoptosis of mature adipocytes.

• IMMUNE NETWORK
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• v.8 no.1
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• pp.21-28
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• 2008

Background: A co-inhibitory molecule, B7-H4, is believed to negatively regulate T cell immunity by suppressing T cell proliferation and inhibiting cytokine production. However, the mechanism behind B7-H4-mediated tolerance remains unclear. Methods: Balb/c $(H-2^d)$ mice were fed with dendritic cell line, DC2.4 $(H-2^d)$ every day for 10 days. Meantime, mice were hydrodynamically injected with recombinant plasmid expressing B7-H4 fusion protein (B7-H4.hFc) or hFc via tail vein. One day after last feeding, mice were immunized with allogeneic B6 spleen cells. 14 days following immunization, mice were challenged with B6 spleen cells to ear back and the ear swelling was determined the next day. Subsequently, a mixed lymphocyte reaction (MLR) was also performed and cytokines profiles from the reaction were examined by sandwich ELISA. Frequency of immunosuppressive cell population was assayed with flow cytometry and mRNA for FoxP3 was determined by RT-PCR. Results: Tolerant mice given plasmid expressing B7-H4.hFc showed a significant reduction in ear swelling compared to control mice. In addition, T cells from mice given B7-H4.hFc plasmid revealed a significant hyporesponsiveness of T cells against allogeneic spleen cells and showed a significant decrease in Th1 and Th2 cytokines such as IFN-${\gamma}$, IL-5, and TNF-${\alpha}$. Interestingly, flow cytometric analysis showed that the frequency of CD4+CD25+FoxP3+ Tregs in spleen was increased in tolerant mice given recombinant B7-H4.hFc plasmid compared to control group. Conclusion: Our results demonstrate that B7-H4 synergistically potentiates oral tolerance induced by allogeneic cells by increasing the frequency of FoxP3+ CD4+CD25+ Treg and reducing Th1 and Th2 cytokine production.

• Journal of Life Science
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• v.28 no.8
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• pp.945-954
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• 2018

Omega-3 polyunsaturated fatty acids (${\omega}3$-fatty acid) have been found to possess anticancer properties in a variety of cancer cell lines and animal models, but their effects in human tongue squamous cell carcinomas (SCCs) remain unclear. This study was designed to examine the effect of ${\omega}3$-fatty acid desaturase (fat-1) gene expression on invasion and tumorigenicity in human tongue SCC cells and the molecular mechanism of its action. Docosahexaenoic acid (DHA) treatment inhibited in vitro invasion in a dose-dependent manner. In zymography, matrix metalloproteinase-9 (MMP-9) and Matrix metallopeptidase-2 (MMP-2) activities were reduced, and MMP-9 and MMP-2 promoter activities were inhibited by the DHA treatment. In addition, cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) promoter reporter activities were inhibited in SCC-4 and SCC-9 cells after the DHA treatment. To investigate the effect of a high level of endogenous ${\omega}3$ fatty acids, a stable SCC-9 cell line expressing the ${\omega}3$-desaturase gene (fSCC-9sc) was generated. The growth rate and colony-forming capacity of fSCC-9sc were remarkably decreased as compared with those of fSCC-9cc. Likewise, the tumor size and volume of fSCC-9sc implanted into nude mice were significantly inhibited, with increases in the cell death index. Furthermore, a transwell chamber invasion assay showed a reduction in cell invasion of the fSCC-9sc lines when compared with that of the fSCC-9cc line. These findings suggested that fat-1 gene expression inhibited tumorigenicity, as well as invasion in human tongue SCC cells. Thus, utilization of ${\omega}3$ fatty acids may represent a promising therapeutic approach for chemoprevention and the treatment of human tongue SCCs.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.1-11
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• 1989

In this study, it was aimed to investigate the role of serotonergic neurotransmission in nucleus tractus solitarius (NTS) for the central regulation of blood pressure and heart rate and its involvement in baroreceptor reflex activation in rats. A microinjection of 5-hydroxytryptamine (5-HT) into the NTS produced decreases in blood pressure and heart rate. Maximal decreases were $34.4{\pm}1.6$ mmHg and $41.7{\pm}10.2$ beats per min by 300 pmol of 5-HT. Microinjections of ${\alpha}-methylnor-adrenaline$ $({\alpha}-MNE)$ and clonidine manifested similar decreases in blood pressure and heart rate. The hypotensive and bradycardial effects of 5-HT were blocked by previous applications of 5-HT antagonists, ritanserin, methysergide and ketanserin into the NTS, respectively. By pretreatment with reserpine and 6-hydroxydopamine (6-OHDA, i.c.v.), both hypotensive and bradycardial effects of 5-HT were significantly attenuated. Pretreatment with 5, 7-dihydroxytryptamine (5,7-DHT, i.c.v.) enhanced the hypotensive and bradycardial effects of 5-HT. Similarly, following pretreatment with 6-OHDA, the effects of clonidine were increased. Pretreatment either with 5,7-DHT or 6-OHDA significantly attenuated the sensitivity of baroreflex produced either by phenylephrine or by sodium nitroprusside. When either 5,7-DHT or 6-OHDA was injected into the NTS $(5,7-DHT;\;8{\mu}g\;6-OHDA;\;10{\mu}g)$, both of the baroreflex sensitivities were impaired. In the immunohistochemical study, the injection of 6-OHDA into the the NTS led to reduction of axon terminal varicosity, however, the injection did not reduce the numbers of catecholaminergic cell bodies. Likewise, when 5,7-DHT was injected into the NTS, the varicosity of serotonergic axon terminals was markedly reduced. Based on these results, it is suggested that (1) stimulation of serotonergic receptors in the NTS leads to decreases in blood pressure and heart rate as observed with the stimulation of catecholaminergic system, (2) both serotonergic and catecholaminergic receptors may be located postsynaptically, and (3) the serotonergic neurons as well as catecholaminergic neurons may have a close relevance for the activation of baroreflex.