• Title/Summary/Keyword: 산소투과

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Extending the Shelf-life of Yukwa Using Secondary Packaging (이차포장을 통한 유과의 저장성 연장)

  • Jung, Jun-Jae;Lee, Keun-Taik
    • Korean Journal of Food Science and Technology
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    • v.42 no.4
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    • pp.452-458
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    • 2010
  • This study aimed at improving the packaging technology of Yukwa to improve the quality and extend the shelflife using secondary packaging. After packaging the Yukwa using an OPP film, P2, P3, and P4 packaging materials were applied secondarily. Various films including (1) P1: OPP (oriented polypropylene), (2) P2: P1+OPP/LLDPE (linear low density polyethylene), (3) P3: P1+PET (polyethylene terephthalate)/NY (nylon)/CPP (cast polypropylene) and (4) P4: P1+PET/AL (aluminum)/NY/CPP (P4) were used for packaging Yukwa. The experiment was conducted at $25^{\circ}C$ for 12 weeks. P1 showed the highest acid value score (1.26 mg KOH/g), and P3 had the highest peroxide value score (32.91 meq/kg) among all packaging groups. Nevertheless, these values did not exceed the guideline values of 2.0 g KOH/g and 40 meq/kg specified in the Korean food code. The overall color difference showed a tendency for decreasing Hunter 'L' values and increasing 'a' and 'b' values; however, no noticeable difference in the outer appearance was observed in any of the packaging treatments except in the P1 for greater than 10 weeks of storage. Some texture defects were observed in the Yukwa when the moisture contents dropped below 5%. The P4 packaging treatment had the lowest moisture permeability and showed the least rheological deterioration change, followed by P3 and P2. In conclusion, the use of a secondary packaging with less gas and moisture permeability was more effective for maintaining the quality and extending the shelf-life of Yukwa than other types of packaging material.

The Effect of Surfactant Therapy for Acute Lung Injury Induced by Intratracheal Endotoxin Instillation in Rats (기관내 내독소 투여로 유발된 흰쥐의 급성폐손상에서 surfactant의 치료효과)

  • Kang, Yun-Jung;Park, Yong-Bum;Jee, Hyun-Suk;Choi, Jae-Chol;Kim, Jae-Yeol;Park, In-Won;Choi, Byoung-Whui
    • Tuberculosis and Respiratory Diseases
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    • v.48 no.4
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    • pp.487-499
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    • 2000
  • Background : Acute lung injury is an hypoxic respiratory failure resulting from damage to the alveolar-capillary membrane, which can be developed by a variety of systemic inflammatory diseases. In this study the therapeutic effects of intra-tracheal pulmonary surfactant instillation was evaluated in the intratracheal endotoxin induced acute lung injury model of a rat. Methods : Twenty Sprague-Dawley rats were divided into 4 groups, and normal saline (2 ml/kg, for group 1) or LPS (5 mg/kg, for group 2, 3, and 4) was instilled into the trachea respectively. Either normal saline (2 ml/kg, for group 1 & 2, 30 min later) or bovine surfactant (15 mg/kg, 30 min later for group 3, 5 hr later for group 5) was instilled into the trachea. The therapeutic effect of intratracheal surfactant therapy was evaluated with one chamber body plethysmography (respiratory frequency, tidal volume and enhanced pause), ABGA, BAL fluid analysis (cell count with differential, protein concentration) and pathologic examination of the lung. Results : Intratracheal endotoxin instillation increased the respiration rate decreased the tidal volume and int creased the Penh in all group of rats. Intratracheal instillation of surfactant decreased Penh, increased arterial oxygen tension, decreased protein concentration of BAL fluid and decreased lung inflammation at both times of administration (30 minute and 5 hour after endotoxin instillation). Conclusion : Intratracheal instillation of surfactant can be a beneficial therapeutic modality as discovered in the acute lung injury model of rats induced by intratracheal LPS intillation. It deserves to be evaluated for treatment of human acute lung injury.

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Microstructural property and catalytic activity of nano-sized MnOx-CeO2/TiO2 for NH3-SCR (선택적 촉매 환원법 재료로서 나노 사이즈 MnOx-CeO2/TiO2 촉매에 대한 미세 구조적 특성과 촉매활성 평가)

  • Hwang, Sungchul;Jo, Seung-hyeon;Shin, Min-Chul;Cha, Jinseon;Lee, Inwon;Park, Hyun;Lee, Heesoo
    • Journal of the Korean Crystal Growth and Crystal Technology
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    • v.26 no.3
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    • pp.115-120
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    • 2016
  • $CeO_2$ is used as a co-catalyst with $TiO_2$ to improve the catalytic activity of $MnO_x$ and characterization of nano-sized powder is identified with de-NOx efficiency. A comparison between $MnO_x-CeO_2/TiO_2$ and single $CeO_2$ was conducted in terms of microstructural analysis to observe the behavior of $CeO_2$ in the ternary catalyst. The $MnO_x-CeO_2/TiO_2$ catalyst was synthesized by sol-gel method and the average particle size of the single $CeO_2$ is about $285{\mu}m$ due to the low thermal stability, whereas the particle size $MnO_x-CeO_2/TiO_2$ is about 130 nm. The strong interaction between Ce and Ti was identified through the EDS mapping by transmission electron microscopy (TEM). The improvement about 20 % of $de-NO_x$ efficiency is observed in the low-temperature ($150^{\circ}C{\sim}250^{\circ}C$) and vigorous oxygen exchange by well-dispersed $CeO_2$ is the reason of catalytic activity improvement.

The Role of Tumor Necrosis Factor-$\alpha$ and Interleukin-$1{\beta}$ as Predictable Markers for Development of Adult Respiratory Distress Syndrome in Septic Syndrome (패혈증 증후군환자에서 성인성 호흡곤란 증후군 발생의 예측 지표서의 혈중 Tumor Necrosis Factor-$\alpha$와 Interleukin-$1{\beta}$에 관한 연구)

  • Koh, Youn-Suck;Jang, Yun-Hae;Kim, Woo-Sung;Lee, Jae-Dam;Oh, Soon-Hwan;Kim, Won-Dong
    • Tuberculosis and Respiratory Diseases
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    • v.41 no.5
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    • pp.452-461
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    • 1994
  • Background: Tumor necrosis factor(TNF)-$\alpha$ and Interleukin(lL)-$1{\beta}$ are thought to play a major role in the pathogenesis of the septic syndrome, which is frequently associated with adult respiratory distress syndrome(ARDS). In spite of many reports for the role of TNF-$\alpha$ in the pathogenesis of ARDS, including human studies, it has been reported that TNF-$\alpha$ is not sensitive and specific marker for impending ARDS. But there is a possibility that the results were affected by the diversity of pathogenetic mechanisms leading to the ARDS because of various underlying disorders of the study group in the previous reports. The purpose of the present study was to evaluate the roles of TNF-$\alpha$ and IL-$1{\beta}$ as a predictable marker for development of ARDS in the patients with septic syndrome, in which the pathogenesis is believed to be mainly cytokine-mediated. Methods: Thirty-six patients of the septic syndrome hospitalized in the intensive care units of the Asan Medical Center were studied. Sixteens suffered from ARDS, whereas the remaining 20 were at the risk of developing ARDS(acute hypoxemic respiratory failure, AHRF). In all patients venous blood samples were collected in heparin-coated tubes at the time of enrollment, at 24 and 72 h thereafter. TNF-$\alpha$ and IL-$1{\beta}$ was measured by an enzyme-linked immunosorbent assay (ELISA). All data are expressed as median with interquartile range. Results: 1) Plama TNF-$\alpha$ levels: Plasma TNF-$\beta$ levels were less than 10pg/mL, which is lowest detection value of the kit used in this study within the range of the $mean{\pm}2SD$, in all of the normal controls, 8 of 16 subjects of ARDS and in 8 in 20 subjects of AHRF. Plasma TNF-$\alpha$ levels from patients with ARDS were 10.26pg/mL(median; <10-16.99pg/mL, interquartile range) and not different from those of patients at AHRF(10.82, <10-20.38pg/mL). There was also no significant difference between pre-ARDS(<10, <10-15.32pg/mL) and ARDS(<10, <10-10.22pg/mL). TNF-$\alpha$ levels were significantly greater in the patients with shock than the patients without shock(12.53pg/mL vs. <10pg/mL) (p<0.01). There was no statistical significance between survivors(<10, <10-12.92pg/mL) and nonsurvivors(11.80, <10-20.8pg/mL) (P=0.28) in the plasma TNF-$\alpha$ levels. 2) Plasma IL-$1{\beta}$ levels: Plasma IL-$1{\beta}$ levels were less than 0.3ng/mL, which is the lowest detection value of the kit used in this study, in one of each patients group. There was no significant difference in IL-$1{\beta}$ levels of the ARDS(2.22, 1.37-8.01ng/mL) and of the AHRF(2.13, 0.83-5.29ng/mL). There was also no significant difference between pre-ARDS(2.53, <0.3-8.34ngfmL) and ARDS(5.35, 0.66-11.51ng/mL), and between patients with septic shock and patients without shock (2.51, 1.28-8.34 vs 1.46, 0.15-2.13ng/mL). Plasma IL-$1{\beta}$ levels were significantly different between survivors(1.37, 0.4-2.36ng/mL) and nonsurvivors(2.84, 1.46-8.34ng/mL). Conclusion: Plasma TNF-$\alpha$ and IL-$1{\beta}$ level are not a predictable marker for development of ARDS. But TNF-$\alpha$ is a marker for shock in septic syndrome. These result could not exclude a possibility of pathophysiologic roles of TNF-$\alpha$ and IL-$1{\beta}$ in acute lung injury because these cytokine could be locally produced and exert its effects within the lungs.

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Effect of Sanitation Treatment of Extending Shelf-life on Fresh Poultry Meats (계육(鷄肉)의 유통기간연장(流通期間延長)을 위(爲)한 위생처리방법(衛生處理方法)에 관(關)한 연구(硏究))

  • Cho, M.J.;Jang, P.H.;Park, K.B.;Lee, B.M.
    • Korean Journal of Food Science and Technology
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    • v.14 no.4
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    • pp.291-300
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    • 1982
  • In order to develop effective and simple sanitation method for the extention of shelf-life of fresh poultry meat, the effect of sanitizers, sanitation methods and packaging materials on the extention of shelf-life of poultry meats was observed at the $4^{\circ}C$ and room temp$(10{\sim}20^{\circ}C)$. The results are summarized as follows: 1. The autochonous skin microflora of poultry, before processing, were believed to be removed or killed during the scalding and plucking, and exposed dermal tissue was contaminated by microorganisms from the subsequent stages of processing. 2. In the final stage of poultry processing, total viable counts of microorganisms and coliforms were averaged to $3.5{\times}10^4/cm^2$ and $400/cm^2$, respectively. 3. The refrigerated shelf-life of fresh whole poultry carcasses at $3\;to\;4^{\circ}C$ was extended to 7 to 16 days compared to control with the various treatments of some sanitizers by dipping freshly chilled carcasses for 5 min or spraying 1 liter of sanitizers per carcasses. In the case of storage at $10\;to\;15^{\circ}C$, the shelf-life of poultry carcasses was extended to one to two days by the sanitation treatments compared to control. 4. Spraying sanitation was more effective than dipping sanitation, and 5 minutes dipping and one liter spraying per carcass were enough for effective sanitation of poultry carcasses in most sanitizers. 5. The packaging with an oxygen impermeable polyvinylidene chloride extended the shelf-life to 10 days and 5 days with polyethylene compared to control. When poultry carcasses were sanitized by continuous spraying with one liter of 30 ppm of chlorine and another one liter of 5% of potassium sorbate, packaged with polyvinylidene chlorlde were extended to about 30 days compared to control.

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Inflammatory Reponse of the Lung to Hypothermia and Fluid Therapy after Hemorrhagic Shock in Rats (흰쥐에서 출혈성 쇼크 후 회복 시 저체온법 및 수액 치료에 따른 폐장의 염증성 변화)

  • Jang, Won-Chae;Beom, Min-Sun;Jeong, In-Seok;Hong, Young-Ju;Oh, Bong-Suk
    • Journal of Chest Surgery
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    • v.39 no.12 s.269
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    • pp.879-890
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    • 2006
  • Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.