• Journal of the korean academy of Pediatric Dentistry
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• v.32 no.3
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• pp.416-426
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• 2005

Intravenous sedation have many advantages of rapid onset and recovery, ability of control sedation levels and duration through titration. Midazolam is most commonly used intravenous medication for sedation in pediatrics, endoscopy, oncologic procedures and so on. But in dentistry, midazolam intravenous sedation is usually for adult, and there are few reports for children. Todays, children who need sedation become more and older, intravenous sedation technique is going a matter of concern in pediatric dentistry. The purpose of this paper is to evaluate the efficacy of sedation and clinical success for different initial dosage of midazolam in intravenous sedation for pediatric dental patients. 16 healthy children (male 10, female 6), mean age $54.7{\pm}10.7$ months, who needed at least two separate treatment visits requiring local anesthesia were chosen for this study. Every children were taken 0.3mg/kg, maximum 5mg of midazolam by intramuscular route, and then 30~50% $N_2O-O_2$ for 10 minutes was given. On every visits, one of the following 2 different initial dosage was given by intravenous route : (1) Group I : 0.1mg/kg Midazolam (2) Group II : 0.2mg/kg Midazolam. Additional dosage was half of the first dose. Physiologic parameters (oxygen saturation, heart rate, respiratory rate, end-tidal carbon dioxide pressure) was recorded by ten procedure steps. Behavior was videotaped and rated using Ohio State University Behavioral Rating Scale and Automated Counting System by one investigator, blind to administered dosage. After the treatment, operator evaluated the clinical success. Physiologic parameters were stable and within normal range during treatment in both groups. The analyzed sedative effect, in behavioral evaluation, ratio of favorable Quiet was higher in group II, and clinical success rate of group II was better than group I. Induction time was rapid in group II, and recovery time was rapid in group I. And there was no statistically difference between two groups in every results.

• Food Science and Preservation
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• v.19 no.6
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• pp.799-806
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• 2012

This experiment was conducted to establish the optimum conditions for high $CO_2$ gas treatment in combination with a proper gas-permeable packaging film to maintain the quality of fig fruit (Ficus carica L). Among the fig fruits with different high $CO_2$ treatments, the quality change was most effectively controlled during storage in the 70%-$CO_2$-treated fig fruit. Harvested fig fruit was packaged using microperforated oriented polypropylene (MP) film to maintain the optimum gas concentrations in the headspace of packaging for the modified-atmosphere system. MP film had an oxygen transmission rate of about $10,295cm^3/m^2$/day/atm at $25^{\circ}C$. The weight loss, firmness, soluble-solid content (SSC), acidity (pH), skin color (Hunter L, a, b), and decay ratio of the fig fruits were monitored during storage at 5 and $25^{\circ}C$. The results of this study showed that the OPP film, OPP film + 70% $CO_2$, and MP film+70% $CO_2$ were highly effective in reducing the loss rate, firmness and decay occurrence rate of fig fruits that were packaged with them during storage. In the case of using treatments with packages of OPP film and OPP film+70% $CO_2$, however, adverse effects like package bursting or physiological injury of the fig may occur due to the gas pressure or long exposure to $CO_2$. Therefore, the results indicated that MP film containing 70% $CO_2$ can be used as an effective treatment to extend the freshness of fig fruits for storage at a proper low temperature.

• 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.

• The Korean Journal of Physiology
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• v.20 no.1
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• pp.53-63
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• 1986

Carbon monoxide(CO) poisoning has been one of the major environmental problems because of the tissue hypoxia, especially brain tissue hypoxia, due to the great affinity of CO with hemoglobin. Inhalation of the pure oxygen$(0_2)$ under the high atmospheric pressure has been considered as the best treatment of CO poisoning by the supply of $0_2$ to hypoxic tissues with dissolved from in plasma and also by the rapid elimination of CO from the carboxyhemoglobin(HbCO). Hydrogen peroxide $(H_2O_2)$ was rapidly decomposed to water and $0_2$ under the presence of catalase in the blood, but the intravenous administration of $H_2O_2$ is hazardous because of the formation of methemoglobin and air embolism. However, it was reported that the enema of $H_2O_2$ solution below 0.75% could be continuously supplied $0_2$ to hypoxic tissues without the hazards mentioned above. This study was performed to evaluate the effect of $H_2O_2$ enema on the elimination of CO from the HbCO in the recovery of the acute CO poisoning. Rabbits weighting about 2.0 kg were exposed to If CO gas mixture with room air for 30 minutes. After the acute CO poisoning, 30 rabbits were divided into three groups relating to the recovery period. The first group T·as exposed to the room air and the second group w·as inhalated with 100% $0_2$ under 1 atmospheric pressure. The third group was administered 10 ml of 0.5H $H_2O_2$ solution per kg weight by enema immediately after CO poisoning and exposed to the room air during the recovery period. The arterial blood was sampled before and after CO poisoning ana in 15, 30, 60 and 90 minutes of the recovery period. The blood pH, $Pco_2\;and\;Po_2$ were measured anaerobically with a Blood Gas Analyzer and the saturation percentage of HbCO was measured by the Spectrophotometric method. The effect of $H_2O_2$ enema on the recovery from the acute CO poisoning was observed and compared with the room air group and the 100% $0_2$ inhalation group. The results obtained from the experiment are as follows: The pH of arterial blood was significantly decreased after CO poisoning and until the first 15 minutes of the recovery period in all groups. Thereafter, it was slowly increased to the level of the before CO poisoning, but the recovery of pH of the $H_2O_2$ enema group was more delayed than that of the other groups during the recovery period. $Paco_2$ was significantly decreased after CO poisoning in all groups. Boring the recovery Period, $Paco_2$ of the room air group was completely recovered to the level of the before CO Poisoning, but that of the 100% $O_2$ inhalation group and the $H_2O_2$ enema group was not recovered until the 90 minutes of the recovery period. $Paco_2$ was slightly decreased after CO poisoning. During the recovery Period, it was markedly increased in the first 15 minutes and maintained the level above that before CO Poisoning in all groups. Furthermore $Paco_2$ of the $H_2O_2$ enema group was 102 to 107 mmHg and it was about 10 mmHg higher than that of the room air group during the recovery period. The saturation percentage of HbCO was increased up to the range of 54 to 72 percents after CO poisoning and in general it was generally diminished during the recovery period. However in the $H_2O_2$ enema group the diminution of the saturation percentage of HbCO was generally faster than that of the 100% $O_2$ inhalation group and the room air group, and its diminution in the 100% $O_2$ inhalation group was also slightly faster than that of the room air group at the relatively later time of the recovery period. In conclusion, the enema of 0.5% $H_2O_2$ solution is seems to facilitate the elimination of CO from the HbCO in the blood and increase $Paco_2$ simultaneously during the recovery period of the acute CO poisoning.

• 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.