• Tuberculosis and Respiratory Diseases
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• v.58 no.1
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• pp.31-42
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• 2005

Background : Peroxiredoxins (Prxs) are a relatively newly recognized, novel family of peroxidases that reduce $H_2O_2$ and alkylhydroperoxide into water and alcohol, respectively. There are 6 known isoforms of Prxs present in human cells. Normally, Prxs exist in a head-to-tail homodimeric state in a reduced form. However, in the presence of excess $H_2O_2$, it can be oxidized on its catalytically active cysteine site into inactive oxidized forms. This study surveyed the types of the Prx isoforms present in the pulmonary epithelial, macrophage, endothelial, and other cell lines and observed their response to oxidative stress. Methods : This study examined the effect of exogenous, excess $H_2O_2$ on the Prxs of established cell lines originating from the pulmonary epithelium, macrophages, and other cell lines, which are known to be exposed to high oxygen partial pressures or are believed to be subject to frequent oxidative stress, using non-reducing SDS polyacrylamide electrophoresis (PAGE) and 2 dimensional electrophoresis. Result : The addition of excess $H_2O_2$ to the culture media of the various cell-lines caused the immediate inactivation of Prxs, as evidenced by their inability to form dimers by a disulfide cross linkage. This was detected as a subsequent shift to its monomeric forms on the non-reducing SDS PAGE. These findings were further confirmed by 2 dimensional electrophoresis and immunoblot analysis by a shift toward a more acidic isoelectric point (pI). However, the subsequent reappearance of the dimeric Prxs with a comparable, corresponding decrease in the monomeric bands was noted on the non-reducing SDS PAGE as early as 30 minutes after the $H_2O_2$ treatment suggesting regeneration after oxidation. The regenerated dimers can again be converted to the inactivated form by a repeated $H_2O_2$ treatment, indicating that the protein is still catalytically active. The recovery of Prxs to the original dimeric state was not inhibited by a pre-treatment with cycloheximide, nor by a pretreatment with inhibitors of protein synthesis, which suggests that the reappearance of dimers occurs via a regeneration process rather than via the de novo synthesis of the active protein. Conclusion : The cells, in general, appeared to be equipped with an established system for regenerating inactivated Prxs, and this system may function as a molecular "on-off switch" in various oxidative signal transduction processes. The same mechanisms might applicable other proteins associated with signal transduction where the active catalytic site cysteines exist.

• Tuberculosis and Respiratory Diseases
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• v.55 no.3
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• pp.250-256
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• 2003

Background : Anthracofibrosis, a descriptive term for multiple black pigmentation with fibrosis on bronchoscopic examination, has a close relationship with active tuberculosis (TB). However, TB activity is determined in the later stage by the TB culture results in some cases of anthracofibrosis. Therefore, it is necessary to identify early markers of TB activity in anthracofibrosis. There have been several reports investigating the serum levels of IL-2 $sR{\alpha}$, IFN-${\gamma}$ and TBGL antibody for the evaluation of TB activity. In the present study, we tried to measure the above mentioned serologic markers for the evaluation of TB activity in patients with anthracofibrosis. Methods : Anthracofibrosis was defined when there was deep pigmentation (in more than two lobar bronchi) and fibrotic stenosis of the bronchi on bronchoscopic examination. The serum of patients with anthracofibrosis was collected and stored under refrigeration before the start of anti-TB medication. The serum of healthy volunteers (N=16), patients with active TB prior to (N=22), and after (N=13), 6 month-medication was also collected and stored. Serum IL-2 $sR{\alpha}$, IFN-${\gamma}$ were measured with ELISA kit (R&D system, USA) and serum TBGL antibody was measured with TBGL EIA kit (Kyowa Inc, Japan). Results : Serum levels of IL-2 $sR{\alpha}$ in healthy volunteers, active TB patients before and after medication, and patients with anthracofibrosis were $640{\pm}174$, $1,611{\pm}2,423$, $953{\pm}562$, and $863{\pm}401$ pg/ml, respectively. The Serum IFN-${\gamma}$ levels were 0, $8.16{\pm}17.34$, $0.70{\pm}2.53$, and $2.33{\pm}6.67$ pg/ml, and TBGL antibody levels were $0.83{\pm}0.80$, $5.91{\pm}6.71$, $6.86{\pm}6.85$, and $3.22{\pm}2.59$ U/ml, respectively. The serum level of TBGL antibody was lower than of other groups (p<0.05). There was no significant difference of serum IL-2 $sR{\alpha}$ and IFN-${\gamma}$ levels among the four groups. Conclusion : The serum levels of IL-2 $sR{\alpha}$, IFN-${\gamma}$ and TBGL antibody were not useful in the evaluation of TB activity in patients with anthracofibrosis. More useful ways need to be developed for the differentiation of active TB in patients with anthracofibrosis.

• Journal of Life Science
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• v.17 no.6 s.86
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• pp.791-797
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• 2007

We studied the inhibitory effect of solvent fractions from doenjang on mutagenicity using Salmonella typhimurium TA100 in Ames test. We also investigated the effect of solvent fractions from doenjang on the growth of tumor cells and the production of interleukin-2 (IL-2). The treatment of dichlorormethane and ethylacetate fractions (2.5 mg/assay) from doenjang to Ames test system inhibited aflatoxin B$_1$ (AFB$_1$) induced mutagenicity by 96% and 97%, respectively, and showed a higher antimutagenic effect than other solvent fractions. In case of N-methyl-N'-nitro-N-nitrosoguamidine (MNNG) induced mutagenicity, the ethylacetate fraction showed the highest inhibitory effect (by 75%) among the other sol-vent fractions, although the inhibitory effect was not stronger compared to AFB$_1$ induced mutagenicity. The treatment of dichloromethane and ethylacetate fractions markedly inhibited the growth of Yac-1 (by 80% and 94%, respectively) and sacroma-180 cancer cells (by 60% and 96%, respectively) after 4 days of incubation at 37${\circ}$C. To elucidate the immunological mechanism of antitumor activity of doenjang, spleen cells of Balb/c mouse were exposed to the dichloromethane and ethyl-acetate fractions for 24 hours at 37${\circ}$C . The culture supernatants following the treatment of djchloromethane and ethylacetate factions to spleen cells increased the production of IL-2. These results indicated that the anticarcinogenic effect of doenjang was mediated by the production of IL-2.

• Journal of the Korean Institute of Traditional Landscape Architecture
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• v.37 no.1
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• pp.56-67
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• 2019

In order to investigate the issue with the proper name of eshel(Tamarix aphylla) mentioned in the Bible, analysis of morphological taxonomy features of plants, studies on the symbolism of the Tamarix genus, analysis of examples in Korean classics and Chinese classics, and studies on the problems found in translations of Korean, Chinese and Japanese Bibles. The results are as follows. According to plant taxonomy, similar species of the Tamarix genus are differentiated by the leaf and flower, and because the size is very small about 2-4mm, it is difficult to differentiate by the naked eye. However, T. aphylla found in the plains of Israel and T. chinensis of China and Korea have distinctive differences in terms of the shape of the branch that droops and its blooming period. The Tamarix genus is a very precious tree that was planted in royal courtyards of ancient Mesopotamia and the Han(漢) Dynasty of China, and in ancient Egypt, it was said to be a tree that gave life to the dead. In the Bible, it was used as a sign of the covenant that God was with Abraham, and it also symbolized the prophet Samuel and the court of Samuel. When examining the example in Korean classics, the Tamarix genus was used as a common term in the Joseon Dynasty and it was often used as the medical term '$Ch{\bar{e}}ngli{\check{u}}$(檉柳)'. Meanwhile, the term 'wiseonglyu(渭城柳)' was used as a literary term. Upon researching the period and name of literature related to $Ch{\bar{e}}ngli{\check{u}}$(檉柳) among Chinese medicinal herb books, a total of 16 terms were used and among these terms, the term Chuísīliǔ(垂絲柳) used in the Chinese Bible cannot be found. There was no word called 'wiseonglyu(渭城柳)' that originated from the poem by Wang Wei(699-759) of Tang(唐) Dynasty and in fact, the word 'halyu(河柳)' that was related to Zhou(周) China. But when investigating the academic terms of China currently used, the words Chuísīliǔ(垂絲柳) and $Ch{\bar{e}}ngli{\check{u}}$(檉柳) are used equally, and therefore, it appears that the translation of eshel in the Chinese Bible as either Chuísīliǔ (垂絲柳) or $Ch{\bar{e}}ngli{\check{u}}$(檉柳) both appear to be of no issue. There were errors translating tamarix into 'やなぎ(willow)' in the Meiji Testaments(舊新約全書 1887), and translated correctly 'ぎょりゅう(檉柳)' since the Colloquial Japanese Bible(口語譯 聖書 1955). However, there are claims that 'gyoryu(ぎょりゅう 檉柳)' is not an indigenous species but an exotics species in the Edo Period, so it is necessary to reconsider the terminology. As apparent in the Korean classics examples analysis, there is high possibility that Korea's T. chinensis were grown in the Korean Peninsula for medicinal and gardening purposes. Therefore, the use of the medicinal term $Ch{\bar{e}}ngli{\check{u}}$(檉柳) or literary term 'wiseonglyu' in the Korean Bible may not be a big issue. However, the term 'wiseonglyu' is used very rarely even in China and as this may be connected to the admiration of China and Chinese things by literary persons of the Joseon Dynasty, so the use of this term should be reviewed carefully. Therefore, rather than using terms that may be of issue in the Bible, it is more feasible to transliterate the Hebrew word and call it eshel.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.