• The Journal of Korean Institute of Communications and Information Sciences
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• v.19 no.6
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• pp.1095-1106
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• 1994

This paper presents a method for determining optimal grayscale function processing(FP) morphological filters under the least square (LMS) error criterion. The optimal erosion and dilation filters with a grayscale structuring element(GSE) are determined by minimizing the mean square error (MSE) between the desired signal and the filter output. It is shown that convergence of the erosion and dilation filters can be achieved by a proper choice of the step size parameter of the LMS algorithm. In an attempt to determine optimal closing and opening filters, a matrix representation of both opening and closing with a basis matrix is proposed. With this representation, opening and closing are accomplished by a local matrix operation rather than cascade operations. The LMS and back-propagation algorithm are utilzed for obtaining the optimal basis matrix for closing and opening. Some results of optimal morphological filters applied to 2-D images are presented.

• Journal of Environmental Health Sciences
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• v.31 no.4 s.85
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• pp.316-321
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• 2005

4개 업종(축전지제조업, 광명단 제조업, 2차 제련업, 라디에타 제조업)에서 근무하는 총 100명의 근로자를 대상으로 8단계다단충돌기(eight stages personal cascade imparter)에 의한 입자 크기 별 납농도를 측정하였다 크기 별 납 농도는 총납(PbA), 흡입성납(IPM-PbA), 흉곽성납(TPM-PbA), 호흡성납(RPM-PbA), $1{\mu}m$ 미만의 납$(Pb_{1\mu})$ 그리고 $1{\mu}m$ 이상의 소화성납$(Pb_{ing})$이었다. 동일한 근로자(100명)를 대상으로 혈액에서 납농도를 측정하였다. 혈액 중 납은 원자흡광광도계(atomic absorption spectrometry)의 Zeeman effect graphite furnace를 이용하여 분석하였다. 총 납의 노출농도는 노출기준$(50\;ug/m^3)$을 크게 초과하였다. 평균 호흡성 납 노출농도$(115.7\;ug/m^3)$ 총 납의 노출기준을 훨씬 초과하였다. $1{\mu}m$미만의 납$(Pb_{1\mu})$ 노출농도의 범위는 0.7에서 $(492.2\;ug/m^3)$이나 되었다. 근로자의 $46\%$가 혈액 중 납 농도 40 ug/dL을 초과하였다. 60 ug/dL을 초과한 경우도 $13\%$나 되었다. 입자 크기가 큰 납인 총납, 흡입성 납 그리고 호흡성 납 농도는 혈액 중 납 농도와 유의한 상관을 보였다(p<0.0001). 그러나 가장 높은 상관은 $1{\mu}m$미만의 납$(Pb_{1\mu})$ 혈액 중 납과의 관계였다. T-test에서 $50ug/m^3$이상의 호흡성 납을 나타낸 근로자 그룹과 $50ug/m^3$ 이하의 근로자 그룹간에의 혈액 중 납 농도는 유의한 차이가 있는 것으로 나타났다(p=0.000). 이러한 연구결과는 입자크기 구분이 없는 현재의 총납에 의한 노출기준과 측정방법은 미세 납 먼지에 노출되는 근로자의 납흡수를 보호하는데 한계점이 있다는 것을 의미한다. 향후 납 입자크기는 물론 근로자의 개인적인 위생과 작업내용 등을 변수로 납 흡수에 영향을 미치는 종합적인 요인을 찾아내는 연구를 진행할 필요가 있다.

• Journal of Korean Society for Atmospheric Environment
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• v.14 no.1
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• pp.11-23
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• 1998

The purpose of this study was to survey chemical distribution of inorganic elements and ions in the submicron particles, to characterize qualitatively emitting sources by factor analysis, and finally to reveal existing patterns in terms of chemical compounds by a stepwise multiple regression analysis. Total of 141 samples were collected by a cascade impactor from 1989 to1996. Fifteen chemical species (Al, Ba, Cd, K, Pb, Cu, Fe, Ni, $Cl^-, NO_3^-, SO_4^{2-}, K^+, Mg^{2+}, Ca^{2+}, and Na^+$) were characterized by AAS and IC. The study showed that average seasonal levels of submicron particulate matters $(d_p<0.43 \mum)$ were 18.7 $\mug/m^3$ in spring, 15.5 $\mug/m^3$ in summer, 15.7 $\mug/m^3$ in fall, and 24.5 $\mug/m^3$ in winter, respectively. All of the anion concentrations in the particle were highest in the winter season. By applying a factor analysis, 5 source patterns were qualitatively obtained, such as sulfate related source, nitrate related source, oil burning source, calcium related source, and coal combustion source. Finally, when applying a stepwise multiple regression analysis, the results clearly showed that $Na^+ and Ca^{2+}, K^+ and Ca^{2+}, NO_3^-$ and relative humidity, $Cl^-$ and ambient temperature, $Ca^{2+} and Cl^-, Mg^{2+} and SO_4^{2-}, Na^+ and NO_3^-, and Ca^{2+} and NO_3^-$, respectively, are negatively contributed to each other. As a result of those statistical analysis, we could suggest that some chemical compounds in the submicron particles such as$NaNO_3, MgSO_4, Ca(NO_3)_2, and CaCl_2$ may not exist on the filter as final composing products; however, other compounds may possibly exist in the form of $Mg(NO_3)_2, CaSO_4, Na_2SO_4, K_2SO_4, MgCl_2, NaCl, and KCl$. Thus, it must be necessary to identify differences between the results of above statistical analysis and of the real world by laboratory experiments.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.2
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• pp.143-155
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• 2023

Percutaneous coronary intervention and acute coronary syndrome are both closely tied to the frequently occurring complication of coronary microembolization (CME). Resveratrol (RES) has been shown to have a substantial cardioprotective influence in a variety of cardiac diseases, though its function and potential mechanistic involvement in CME are still unclear. The forty Sprague-Dawley rats were divided into four groups randomly: CME, CME + RES (25 mg/kg), CME + RES (50 mg/kg), and sham (10 rats per group). The CME model was developed. Echocardiography, levels of myocardial injury markers in the serum, and histopathology of the myocardium were used to assess the function of the cardiac muscle. For the detection of the signaling of TLR4/MyD88/NF-κB along with the expression of pyroptosis-related molecules, ELISA, qRT-PCR, immunofluorescence, and Western blotting were used, among other techniques. The findings revealed that myocardial injury and pyroptosis occurred in the myocardium following CME, with a decreased function of cardiac, increased levels of serum myocardial injury markers, increased area of microinfarct, as well as a rise in the expression levels of pyroptosis-related molecules. In addition to this, pretreatment with resveratrol reduced the severity of myocardial injury after CME by improving cardiac dysfunction, decreasing serum myocardial injury markers, decreasing microinfarct area, and decreasing cardiomyocyte pyroptosis, primarily by blocking the signaling of TLR4/MyD88/NF-κB and also reducing the NLRP3 inflammasome activation. Resveratrol may be able to alleviate CME-induced myocardial pyroptosis and cardiac dysfunction by impeding the activation of NLRP3 inflammasome and the signaling pathway of TLR4/MyD88/NF-κB.

• Molecules and Cells
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• v.28 no.4
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• pp.321-329
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• 2009

Rapid production of nitric oxide (NO) and reactive oxygen species (ROS) has been implicated in the regulation of innate immunity in plants. A potato calcium-dependent protein kinase (StCDPK5) activates an NADPH oxidase StRBOHA to D by direct phosphorylation of N-terminal regions, and heterologous expression of StCDPK5 and StRBOHs in Nicotiana benthamiana results in oxidative burst. The transgenic potato plants that carry a constitutively active StCDPK5 driven by a pathogen-inducible promoter of the potato showed high resistance to late blight pathogen Phytophthora infestans accompanied by HR-like cell death and $H_2O_2$ accumulation in the attacked cells. In contrast, these plants showed high susceptibility to early blight necrotrophic pathogen Alternaria solani, suggesting that oxidative burst confers high resistance to biotrophic pathogen, but high susceptibility to necrotrophic pathogen. NO and ROS synergistically function in defense responses. Two MAPK cascades, MEK2-SIPK and cytokinesis-related MEK1-NTF6, are involved in the induction of NbRBOHB gene in N. benthamiana. On the other hand, NO burst is regulated by the MEK2-SIPK cascade. Conditional activation of SIPK in potato plants induces oxidative and NO bursts, and confers resistance to both biotrophic and necrotrophic pathogens, indicating the plants may have obtained during evolution the signaling pathway which regulates both NO and ROS production to adapt to wide-spectrum pathogens.

• Proceedings of the Microbiological Society of Korea Conference
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• 2007.05a
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• pp.120-122
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• 2007

All living organisms use numerous signal-transduction pathways to sense and respond to their environments and thereby survive and proliferate in a range of biological niches. Molecular dissection of these signalling networks has increased our understanding of these communication processes and provides a platform for therapeutic intervention when these pathways malfunction in disease states, including infection. Owing to the expanding availability of sequenced genomes, a wealth of genetic and molecular tools and the conservation of signalling networks, members of the fungal kingdom serve as excellent model systems for more complex, multicellular organisms. Here, we employed Cryptococcus neoformans as a model system to understand how fungal-signalling circuits operate at the molecular level to sense and respond to a plethora of environmental stresses, including osmoticshock, UV, high temperature, oxidative stress and toxic drugs/metabolites. The stress-activated p38/Hog1 MAPK pathway is structurally conserved in many organisms as diverse as yeast and mammals, but its regulation is uniquely specialized in a majority of clinical Cryptococcus neoformans serotype A and D strains to control differentiation and virulence factor regulation. C. neoformans Hog1 MAPK is controlled by Pbs2 MAPK kinase (MAPKK). The Pbs2-Hog1 MAPK cascade is controlled by the fungal "two-component" system that is composed of a response regulator, Ssk1, and multiple sensor kinases, including two-component.like (Tco) 1 and Tco2. Tco1 and Tco2 play shared and distinct roles in stress responses and drug sensitivity through the Hog1 MAPK system. Furthermore, each sensor kinase mediates unique cellular functions for virulence and morphological differentiation. We also identified and characterized the Ssk2 MAPKKK upstream of the MAPKK Pbs2 and the MAPK Hog1 in C. neoformans. The SSK2 gene was identified as a potential component responsible for differential Hog1 regulation between the serotype D sibling f1 strains B3501 and B3502 through comparative analysis of their meiotic map with the meiotic segregation of Hog1-dependent sensitivity to the fungicide fludioxonil. Ssk2 is the only polymorphic component in the Hog1 MAPK module, including two coding sequence changes between the SSK2 alleles in B3501 and B3502 strains. To further support this finding, the SSK2 allele exchange completely swapped Hog1-related phenotypes between B3501 and B3502 strains. In the serotype A strain H99, disruption of the SSK2 gene dramatically enhanced capsule biosynthesis and mating efficiency, similar to pbs2 and hog1 mutations. Furthermore, ssk2, pbs2, and hog1 mutants are all hypersensitive to a variety of stresses and completely resistant to fludioxonil. Taken together, these findings indicate that Ssk2 is the critical interface protein connecting the two-component system and the Pbs2-Hog1 pathway in C. neoformans.

• International Journal of Oral Biology
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• v.43 no.2
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• pp.61-68
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• 2018

Codium fragile (Suringar) Hariot is an edible green seaweed that belong to the Codiaceae family and has been used in Oriental medicine for the treatment of enterobiasis, dropsy, and dysuria. Methanol extract of codium fragile has anti-oxidant, anti-inflammatory and anti-cancer properties, although the anti-cancer effect on oral cancer has not yet been reported. In this study, we investigated the anti-cancer activity and the mechanism of cell death by methanol extracts of Codium fragile (MeCF) on human FaDu hypopharyngeal squamous carcinoma cells. Our data showed that MeCF inhibits cell viability in a dose-dependent manner, and markedly induced apoptosis, as determined by the MTT assay, Live/Dead assay, and DAPI stain. In addition, MeCF induced the proteolytic cleavage of procaspase -3, -7, -9 and poly(ADP-ribose) polymerase(PARP), and upregulated or downregulated the expression of mitochondrial-apoptosis factor, Bax(pro-apoptotic factor), and Bcl-2(anti-apoptotic factor). Futhermore, MeCF induced a cell cycle arrest at the G1/S phase through suppressing the expression of the cell cycle cascade proteins, p21, CDK4, CyclinD1, and phospho-Rb. Taken together, these results indicated that MeCF inhibits cell growth, and this inhibition is mediated by caspase- and mitochondrial-dependent apoptotic pathways through cell cycle arrest at the G1/S phase in human FaDu hypopharyngeal squamous carcinoma cells. Therefore, methanol extracts of Codium fragile can be provided as a novel chemotherapeutic drug due to its growth inhibition effects and induction of apoptosis in human oral cancer cells.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8177-8186
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• 2016

The present study was aimed at determining the effects of alkylating and oxidative stress inducing agents on a newly identified variant of DNA polymerase beta ($pol{\beta}{\Delta}_{208-304}$) specific for ovarian cancer. $Pol{\beta}{\Delta}_{208-304}$ has a deletion of exons 11-13 which lie in the catalytic part of enzyme. We compared the effect of these chemicals on HeLa cells and HeLa cells stably transfected with this variant cloned into in pcDNAI/neo vector by MTT, colony forming and apoptosis assays. $Pol{\beta}{\Delta}_{208-304}$ cells exhibited greater sensitivity to an alkylating agent and less sensitivity towards $H_2O_2$ and UV when compared with HeLa cells alone. It has been shown that cell death in $Pol{\beta}{\Delta}_{208-304}$ transfected HeLa cells is mediated by the caspase 9 cascade. Exon 11 has nucleotidyl selection activity, while exons 12 and 13 have dNTP selection activity. Hence deletion of this part may affect polymerizing activity although single strand binding and double strand binding activity may remain same. The lack of this part may adversely affect catalytic activity of DNA polymerase beta so that the variant may act as a dominant negative mutant. This would represent clinical significance if translated into a clinical setting because resistance to radiation or chemotherapy during the relapse of the disease could be potentially overcome by this approach.

• Journal of Radiation Protection and Research
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• v.41 no.2
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• pp.123-131
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• 2016

Background: With the increase in the number of particle accelerator facilities under either operation or construction, the accurate calculation using Monte Carlo codes become more important in the shielding design and radiation safety evaluation of accelerator facilities. Materials and Methods: The calculations with different physics models were applied in both of cases: using only physics model and using the mix and match method of MCNPX code. The issued conditions were the interactions of 600 MeV proton and $290MeV{\cdot}n^{-1}$ oxygen with a carbon target. Both of cross-section libraries, JENDL High Energy File 2007 (JENDL/HE-2007) and LA150, were tested in this calculation. In the case of oxygen ion interactions, the calculation results using LAQGSM physics model and JENDL/HE-2007 library were compared with D. Satoh's experimental data. Other Monte Carlo calculations using PHITS and FLUKA codes were also carried out for further benchmarking study. Results and Discussion: It was clearly found that the physics models, especially intra-nuclear cascade model, gave a great effect to determine proton-induced secondary neutron spectrum in MCNPX code. The variety of physics models related to heavy ion interactions did not make big difference on the secondary particle productions. Conclusion: The variations of secondary neutron spectra and particle transports depending on various physics models in MCNPX code were studied and the result of this study can be used for the shielding design and radiation safety evaluation.

• Molecules and Cells
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• v.27 no.2
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• pp.251-255
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• 2009

Sepsis is the leading cause of death in critically ill patients. Today, around 60% of all cases of sepsis are caused by Gram-negative bacteria. The cell wall component lipopolysaccharide (LPS) is the main initiator of the cascade of cellular reactions in Gram-negative infections. The core receptors for LPS are toll-like receptor 4 (TLR4), MD-2 and CD14. Attempts have been made to antagonize the toxic effect of endotoxin using monoclonal antibodies against CD14 and synthetic lipopolysaccharides but there is as yet no effective treatment for septic syndrome. Here, we describe an inhibitory effect of a phosphatidylethanolamine derivative, PE-DTPA (phosphatidylethanolamine diethylenetriaminepentaacetate) on LPS recognition. PE-DTPA bound strongly to CD14 ($K_d$, $9.52{\times}10^{-8}M$). It dose dependently inhibited LPS-mediated activation of human myeloid cells, mouse macrophage cells and human whole blood as measured by the production of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and nitric oxide, whereas other phospho-lipids including phosphatidylserine and phosphatidylethanolamine had little effect. PE-DTPA also inhibited transcription dependent on $NF-{\kappa}B$ activation when it was added together with LPS, and it rescued LPS-primed mice from septic death. These results suggest that PE-DTPA is a potent antagonist of LPS, and that it acts by competing for binding to CD14.