• Journal of Nutrition and Health
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• v.48 no.2
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• pp.180-191
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• 2015

Purpose: There is a lack of data on the energy cost of children's everyday activities, adult values are often used as surrogates. In addition, the influence of body weight on the energy cost of activity when expressed as metabolic equivalents (METs) has not been vigorously explored. Methods: In this study 20 elementary school students 9~12 years of age completed 18 various physical activities while energy expenditure was measured continuously using a portable telemetry gas exchange system ($K_4b^2$, Cosmed, Rome, Italy). Results: The average age was 10.4 years and the average height and weight was 145.1 cm and 43.6 kg, respectively. Oxygen consumption ($VO_2$), energy expenditure and METs at the time of resting of the subjects were 5.41 mL/kg/min, 1.44 kcal/kg/h, and 1.5 METs, respectively. METs values by 18 physical activities were as follows: Homework and reading books (1.6 METs), playing game with a mobile phone or video while sitting (1.6 METs), watching TV while sitting on a comfortable chair (1.7 METs), playing video game or mobile phone game while standing (1.9 METs), sweeping a room with a broom (2.7 METs) and playing a board game (2.8 METs) belong to light intensity physical activities. By contrary, speedy walking and running were 6.6 and 6.7 METs, respectively, which belong to high intensity physical activities over 6.0 METs. When the effect of body weight on physical activity energy expenditure was determined, $R^2$ values increased with 0.116 (playing a game at sitting), 0.176 (climbing up and down stairs), 0.246 (slow walking), and 0.455 (running), which showed that higher activity intensity increased explanation power of body weight on METs value. Conclusion: This study is important for direct evaluation of energy expenditure by physical activities of children, and it could be used directly for revising and complementing the existing activity classification table to fit for children.

• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.451-463
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• 2006

Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.

• Korean Journal of Soil Science and Fertilizer
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• v.16 no.1
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• pp.20-27
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• 1983

A series of laboratory experiment was conducted to find out the chemical composition, characterization of humic substances by physical and chemical methods and reaction of Na-pyrophosphate, $Ca(OH)_2$ and rice straw with albumin on the degradation of soil organic matter in the volcanic ask soils of the Jeju Island. Results obtained were summarized as follows: 1. The contents of organic matter, available silicon, active iron and aluminum concentration in volcanic ash the soils were remarkably higher but available phosphorous was comparatively lower than the mineral soils. In volcanic ash soil, the contents of potassium, calcium and magnessium were higher in upland soil than that of forest soil. The ratios of active $Al^{{+}{+}{+}}/Fe^{{+}{+}}$, C/P and $K/Ca^+$ Mg were apparently high in volcanic ash soils while that of $SiO_2$/O.M. was high in mineral soil. 2. The carbon/nitrogen ratio in humin, humic acid content in organic matter, and carbon contents of humin in total carbon of soil organic matter were apparently higher in the volcanic ash soils than in the mineral soils, The total nitrogen and fractions of acid or alkali soluble nitrogen were remarkably high in volcanic ash soils while mineralizable nitrogen ($NH_4$-N and $NO_3$) contents were high in mineral soils. 3. The values of K600, RF and log K were also higher in volcanic ash soils than those in mineral soils, and the absorbance in the visible range were high and color was dark in the soil of which humification was progressed Extracted humic acid from volcanic ash soil was less reactive to the oxidizing chemical reagent and was persistance to the acid or alkali hydrolysises. 4. The major oxygen-containing functional groups in humic substances of volcanic ash soils were phenolic-OH alcoholic-OH and carboxyl groups while those in mineral soil were methoxyl and carbonyl groups. 5. Absorption spectra of alkaline solution of humic acid ranged from 200 nm to maxima 500 nm. Visible spectra peaks of from humic substances in the visible region were recognized at 350, 420, 450 and 480 nm. Only one single absorbance peak was observed in the visible region at 362 nm for Heugag series and two absorbance Peak were also at 360 nm and 390 nm for Yeungrag series. 6. Evolution of carbon as $Co_2$ was increased with addition of Na-pyrophosphate in Namweon and Heugag series, and "priming effects" took place on the soil organic matter decomposition by addition of rice straw with albumin in Ido series.

• Economic and Environmental Geology
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• v.50 no.4
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• pp.287-302
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• 2017

The carbonate rocks of the Daegi Formation are composed of the limestone at the upper and lower zones, and the dolomite at the middle zone, in which the upper zone has higher CaO content than others. The colors of carbonate rock in the Daegi Formation can be divided into five types; white, light brown, light gray, gray, and dark gray. The white to light gray colored rocks correspond to the high purity limestone with 53.15 ~ 55.64 wt. % CaO, and the light brown colored rocks contain 20.71 ~ 21.67 wt. % MgO. The bleaching of carbonate rocks are not related to CaO composition of the rocks, as light gray rocks tend to be higher in CaO content than those of the white rocks at the lower zone. The pelitic components are also occasionally increased in white limestone than light grey one. $Al_2O_3$ is one of the most difficult content to remove during hydrothermal processes, so the interpretation that the limestone is purified together with hydrothemral bleaching, has little merit. The wide range (over 16 ‰) of ${\delta}^{18}O_{SMOW}$, smaller variation (within 2 ‰) of ${\delta}^{13}C_{PDB}$ are apparent in both the upper and lower zones, which indicate the Daegi Formation had been affected overall by hydrothermal fluids. The K-Ar isotopic age of hydrothermal alteration in the GMI limestone mine is $85.1{\pm}1.7Ma$. Gradual change from grey through light grey to white limestone is accompaned by lower oxygen stable isotope values, which is major evidence that the hydrothermal effect is the main process of the bleaching. Although the Daegi Formation has suffered from hydrothermal activity and increase in whiteness, there is no clear evidence demonstrating the relationship between bleaching and high purity of limestone. The purification of limestone has nothing to do with the hydrothermal activity in this area. Instead, it should be considered that the change of sedimentary environment related to see-level fluctuation which can prevent deposition of pelitic components especially $Al_2O_3$ contrbuted to the formation of the high purity limestone in the upper zone of the Daegi Formation. Considering the evidences such as increase in CaO content of limestone by depth, gradual change from calcite to dolomite at the lower zones, and occurring the high purity limestone at the upper zone, the interpretation of sequence stratigraphic aspect to the formation of the high purity Daegi limestone appears to be more suitable than that of hydrothermal alteration origin.

• 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.

• Clinical and Experimental Pediatrics
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• v.45 no.5
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• pp.596-602
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• 2002

Purpose : The purpose of this study was to analyze the association of peripheral neutrophil count with the development of respiratory failure in preterm infants. Methods : A retrospective study was conducted from January 1993 to December 1999 on 44 preterm infants, who were admitted to the neonatal intensive care unit of St. Francisco hospital. Preterm infants(birth weight 500 to 1,350 gm) who had a complete blood count obtained within 2 hours after delivery. Patients in the lowest of neutrophil count(early neutropenia, < $1.0{\times}10^9/L$) were compared with patients in the remaining group. Results : Low neutrophil count were transient in early neutropenia group. The concentration the circulating neutrophil count rose from $0.85{\pm}0.11{\times}10^9/L$ at average of 2 hours after delivery to $5.3{\pm}2.7{\times}10^9/L$ at 24 hours after delivery in the early neutropenia group and from $3.6{\pm}1.6{\times}10^9/L$ to $5.8{\pm}3.2{\times}10^9/L$ in the non-neutropenia group during the same time period. Compare to the non-neutropenia group, the neutropenia group had a lower birth weight($1,046.50{\pm}180.76gm$ Vs $1,156.70{\pm}124.99gm$), a lower Apgar score(1 min : $3.41{\pm}1.18$ Vs $4.30{\pm}1.46$, 5 min : $5.41{\pm}0.87$ Vs $6.15{\pm}0.95$), and a higher incidence of bronchopulmonary dysplasia(27.27% Vs 7.0%). Patients who had early neutropenia were more likely to require mechanical ventilation, supplemental oxygen and hospital stay. Also, main effect factors for the two groups were birth weight(Odds ratio=5.457, 95% CI=1.551-27.525), initial peripheral blood white cells(odds ratio=8.308, 95% CI=2.054-52.699), and bronchopulmonary dysplasia(odds ratio=0.099, 95% CI=0.017-0.397). Conclusion : A low count of neutrophil in the systemic circulation of premature infants within 2 hours of birth is associated with more severe respiratory distress.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.231-238
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• 1994

Backgroud: Since the demonstration of the fact that vascular relaxation by acetylcholine(Ach) results from the release of relaxing factor from the endothelium, the identity and physiology of this endothelium-derived relaxing factor(EDRF) has been the target for many researches. EDRF has been identified as nitric oxide(NO). With the recent evidences that EDRF is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the role of EDRF in modulating the pulmonary circulation is not compeletely clarified. To investigate the endothelium-dependent pulmonary vasodilation and the role of EDRF during hypoxic pulmonary vasoconstriction, we studied the effects of $N^G$-monomethyl-L-arginine(L-NMMA) and L-arginine on the precontracted pulmonary arterial rings of the rat in normoxia and hypoxia. Mothods: The pulmonary arteries of male Sprague Dawley(300~350g) were dissected free of surrounding tissue, and cut into rings. Rings were mounted over fine rigid wires, in organ chambers filled with 20ml of Krebs solution bubbled with 95 percent oxygen and 5 percent carbon dioxide and maintained at $37^{\circ}C$. Changes in isometric tension were recorded with a force transducer(FT.03 Grass, Quincy, USA) Results: 1) Precontraction of rat pulmonry artery with intact endothelium by phenylephrine(PE, $10^{-6}M$) was relaxed completely by acetylcholine(Ach, $10^{-9}-10^{-5}M$) and sodium nitroprusside(SN, $10^{-9}-10^{-5}M$), but relaxing response by Ach in rat pulmonary artery with denuded endothelium was significantly decreased. 2) L-NMMA($10^{-4}M$) pretreatment inhibited Ach($10^{-9}-10^{-5}M$)-induced relaxation, but L-NMMA ($10^{-4}M$) had no effect on relaxation induced by SN($10^{-9}-10^{-5}M$). 3) Pretreatment of the L-arginine($10^{-4}M$) significantly reversed the inhibition of the Ach ($10^{-9}-10^{-5}M$)-induced relaxation caused by L-NMMA($10^{-4}M$) 4) Pulmonary arterial contraction by PE($10^{-6}M$) was stronger in hypoxia than normoxia but relaxing response by Ach($10^{-9}-10^{-5}M$) was decreased, 5) With pretreatment of L-arginine($10^{-4}M$), pulmonary arterial relaxation by Ach($10^{-9}-10^{-5}M$) in hypoxia was reversed to the level of relaxation in normoxia. Conclusion: It is concluded that rat pulmonary arterial relaxation by Ach is dependent on the intact endothelium and is largely mediated by NO. Acute hypoxic pulmonary vasoconstriction is related to the suppression on NO formation in the vascular endothelium.

• 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.