• Tuberculosis and Respiratory Diseases
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• v.54 no.5
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• pp.532-541
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• 2003

Background : Phospholipase $A_2$ ($PLA_2$) has been known to be involved in the pathogenesis of acute lung injury (ALI) including ARDS. Since doxycycline has the property of inhibiting secretory group II $PLA_2$, the therapeutic effect of doxycycline hyclate was investigated for gut ischemia/reperfusion (I/R)-induced ALI in Sprague-Dawley rats. Methods : ALI was induced in Sprague-Dawley rats by clamping of the superior mesenteric artery for 60 min, followed by 120 min of reperfusion. To confirm the pathogenetic mechanisms of this ALI associated with neutrophilic oxidative stress, we measured bronchoalveolar lavage (BAL) protein content and lung MPO, and performed cyto-chemical electron microscopy for detection of free radicals, assay of $PLA_2$ activity and cytochrome-c reduction assay. Results : In gut I/R-induced ALI rats, protein leakage, pulmonary neutrophil accumulation, free radical production and lung $PLA_2$ activity were all increased. These effects were reversed by doxycycline hyclate. Conclusion : Doxycycline appears to be effective in ameliorating the gut I/R-induced ALI by inhibiting $PLA_2$, thereby decreasing the production of free radicals from neutrophils.

• Advances in materials Research
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• v.7 no.2
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• pp.149-162
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• 2018

Following our previous work, we have conducted further systematic studies to investigate the effects of reactive blending on the thermal and mechanical properties of blends of poly(lactic acid) (PLA) and a liquid rubber, polybutadiene (LPB). The toughened PLAs were prepared by melt-blending the PLA with various contents (0-9 wt.%) of the LPB in the absence or presence of dicumyl peroxide (DCP), a radical initiator. It was found that the rubber domains were homogeneously dispersed at the nanoscale in the PLA matrix up to 9 wt.% of LPB thanks to the reactive blending in the presence of DCP. Owing to the compatibilization of PLA with LPB through reactive blending, the elongation and toughness of PLA was enhanced, while the hydrolytic degradation of PLA was reduced.

• Biomolecules & Therapeutics
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• v.9 no.4
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• pp.263-269
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• 2001

In this study, we tried to investigate whether poly-L-arginine (PLA) (MW 10,800) significantly affect mucin release from cultured hamster airway goblet cells and the mucosubstances of hypersecretory air-way goblet cells of rats. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled with $^3$H-glucosamine for 24 hr and chased for 30 min in the presence of varying concentrations of PLA to assess the effects on $^3$H-mucin release. Possible cytotoxicities of PLA were assessed by measuring both Lactate Dehydrogenate (LDH) release and by checking the possible changes on the morphology of HTSE cells during treatment. For in vivo experiment, hyperplasia of rat airway goblet cells and increase in intraepithelial mucosubstances were induced by exposing rats to SO$_2$ for 3 weeks and varying concentrations of PLA were administered inhalationally to assess the effects on the mucosubstances of airway goblet cells of rats. The results were as follows : (1) PLA significantly inhibited mucin release from cultured HTSE cells in a dose-dependent manner; (2) there was no significant release of LDH and no significant change on the morphology of cultured HTSE cells during treatment; (3) PLA also affected the intraepithelial mucosubstances of hypersecretory rats and restored them to the levels of control animals. We conclude that PLA inhibit mucin release from airway goblet cells without significant cytotoxicity and possibly normalize the hypersecretion of airway mucosubstances in vivo. This finding suggests that PLA might function as an airway mucoregulative agent.

• KOREAN JOURNAL OF PACKAGING SCIENCE & TECHNOLOGY
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• v.29 no.2
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• pp.103-110
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• 2023

The study aimed to enhance the properties of polylactic acid (PLA), a biodegradable and biocompatible substitute for fossil-based plastics. Since the applicability of PLA has been limited because of its toughness and brittleness, microfibrillated cellulose (MFC) and propolis were introduced into PLA. As a result, the PLA film with MFC/propolis showed significant improvements in mechanical strength, elongation, and storage modulus, while also experiencing a decrease in the glass transition temperature. Additionally, the presence of polyphenols in propolis led to a reduction in light transmittance in the UV wavelength range. These enhancements are attributed to MFC tightly bonding with PLA polymers, and propolis acting as a plasticizer and mediator between MFC and PLA, preventing agglomeration. These reinforced PLA films have the potential to be used in flexible packaging for light-sensitive products.

• Journal of Microbiology and Biotechnology
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• v.27 no.2
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• pp.342-349
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• 2017

Polylactic acid (PLA) has been highlighted as an alternative renewable polymer for the replacement of petroleum-based plastic materials, and is considered to be biodegradable. On the other hand, the biodegradation of PLA by terminal degraders, such as microorganisms, requires a lengthy period in the natural environment, and its mechanism is not completely understood. PLA biodegradation studies have been conducted using mainly undefined mixed cultures, but only a few bacterial strains have been isolated and examined. For further characterization of PLA biodegradation, in this study, the PLA-degrading bacteria from digester sludge were isolated and identified using a polymer film-based screening method. The enrichment of sludge on PLA granules was conducted with the serial transference of a subculture into fresh media for 40 days, and the attached biofilm was inoculated on a PLA film on an agar plate. 3D optical microscopy showed that the isolates physically degraded the PLA film due to bacterial degradation. 16S rRNA gene sequencing identified the microbial colonies to be Pseudomonas sp. MYK1 and Bacillus sp. MYK2. The two isolates exhibited significantly higher specific gas production rates from PLA biodegradation compared with that of the initial sludge inoculum.

• Proceedings of the Korean Society of Dyers and Finishers Conference
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• 2011.11a
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• pp.52-52
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• 2011

PLA 섬유는 폴리머의 주성분이 옥수수에서 추출한 모노머를 중합한 화학섬유가 아닌 인체친화적인 식물성 소재이며 생분해성이 좋은 친환경 소재로 최근 주목받고 있는 섬유소재이다. 본 연구에서는 아토피완화용 여러 섬유 구조체 개발에서 사용되는 섬유소재중 PLA 원사에 항균성 물질을 혼입하여 PLA 항균사 제조를 위한 연구를 수행하였다. PLA Grade의 점도가 낮아질수록 Grade별 용융 지수값은 차이를 나타내지만 방사온도 $230^{\circ}C$를 변곡점으로 하여 용융점도가 급격히 변하였으며, 특히 방사온도 $240^{\circ}C$의 경우 용융지수가 100을 넘어가고 폴리머의 색깔이 황갈색을 띄어 폴리머의 열분해가 많이 일어났을 것으로 판단되었다. PLA의 적정 방사온도 구간은 $210{\sim}225^{\circ}C$ 구간이 최적이며 그 이상에서는 Color 변화 및 물성 저하가 나타나는 것으로 판단되었다. 항균성 PLA 섬유를 제조하기 위하여 피톤치드계 유기항균제를 이용하였으며, 피톤치드에 기능성 엘라스토머를 사용하여 Capsulation을 진행하였다. 이러한 유기항균제 Powder의 경우 비중이 낮아 표면적로 인하여 마스터배치 칩을 만드는 공정에서 잘 혼합되지 않는 문제점이 발생하였으나, 피톤치드의 함량을 조절하여 PLA와의 마스터배치 칩 제조를 시험하였다. 압출온도와 토출량, Screw 조건(Mixing, Zone)을 시험하여 적정 조건을 설정하였다. 항균사 PLA 섬유는 Sheath/Core 복합방사 형태와 단독사 형태의 2가지 Type을 제조하였다. Sheath/Core 복합방사 폴리머 구성은 Sheath부에 PLA항균사, Core부에 PLA 또는 저융점 PET를 사용하였다. Core부의 폴리머는 제사성에 큰 영향을 미치지 않았으나, 항균 마스터배치의 함량이 증가할수록 Pack압 상승이 급격히 일어나는 단점이 나타났다. 항균제 5% 정도가 혼입되어 있는 경우에 2.1 이상의 정균활성치와 99.8% 정도의 정균감소율 성능을 나타내었다. PLA 단독사의 경우, 항균제 최적 함량은 3% 이상으로 정균활성치 5.5 이상, 정균감소율 99.9%의 우수한 항균특성을 나타내었다.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.5
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• pp.401-408
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• 2009

$K^+$-$Cl^-$-cotransport (KCC) has been reported to have various cellular functions, including proliferation and apoptosis of human cancer cells. However, the signal transduction pathways that control the activity of KCC are currently not well understood. In this study we investigated the possible role of phospholipase $A_2$ ($PLA_2$)-arachidonic acid (AA) signal in the regulatory mechanism of KCC activity. Exogenous application of AA significantly induced $K^+$ efflux in a dose-dependent manner, which was completely blocked by R-(+)-[2-n-butyl-6,7 -dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1Hinden-5-yl]oxy]acetic acid (DIOA), a specific KCC inhibitor. N-Ethylmaleimide (NEM), a KCC activatorinduced $K^+$ efflux was significantly suppressed by bromoenol lactone (BEL), an inhibitor of the calciumindependent $PLA_2$ ($iPLA_2$), whereas it was not significantly altered by arachidonyl trifluoromethylketone ($AACOCF_3$) and p-bromophenacyl bromide (BPB), inhibitors of the calcium-dependent cytosolic $PLA_2$ ($cPLA_2$) and the secretory $PLA_2$ ($sPLA_2$), respectively. NEM increased AA liberation in a doseand time-dependent manner, which was markedly prevented only by BEL. In addition, the NEM-induced ROS generation was significantly reduced by DPI and BEL, whereas $AACOCF_3$ and BPB did not have an influence. The NEM-induced KCC activation and ROS production was not significantly affected by treatment with indomethacin (Indo) and nordihydroguaiaretic acid (NDGA), selective inhibitors of cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Treatment with 5,8,11,14-eicosatetraynoic acid (ETYA), a non-metabolizable analogue of AA, markedly produced ROS and activated the KCC. Collectively, these results suggest that $iPLA_2$-AA signal may be essentially involved in the mechanism of ROS-mediated KCC activation in HepG2 cells.

• Journal of Yeungnam Medical Science
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• v.21 no.2
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• pp.177-190
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• 2004

Background: Secretory phospholipase $A_2$ ($sPLA_2$) are a group of extracellular enzymes that release fatty acids at the sn-2 position of phospholipids. Group IIA $sPLA_2$ ($sPLA_2$-IIA) has been detected in the inflammatory fluids, and its plasma level increases in the inflammatory disease. This study examined the effect of $sPLA_2$-IIA on mouse macropahges in order to investigate the potential mechanism of $sPLA_2$-induced inflammation. Materials and Methods: Wild type $PLA_2$ and mutant H48Q $PLA_2$ were purified from HEK293 cells transfected with the corresponding plasmids, and the $PLA_2$ activities were measured using 1-palmitoyl-2-[1-$^{14}C$]linoleoyl-3-phosphatidylethanolamine as substrates. The TNF-${\alpha}$ and IL-6 released in the supernatants were determined by ELISA. In addition, the TNF-${\alpha}$ and IL-6 mRNA were analyzed by RT-PCR. Results: $sPLA_2$-IIA stimulated the production of TNF-${\alpha}$ and IL-6 in a dose- and time-dependent manner. In addition, the effect of $sPLA_2$-IIA on cytokine production from the macrophage was found to be associated with the accumulation of their specific mRNA. The mRNA levels of TNF-${\alpha}$ and IL-6 peaked at 2 and 6 hours in a time-dependent manner, respectively. Conclusion: In conclusion, the production of proinflammatory cytokine might be mediated by the binding of $sPLA_2$-IIA to the receptors.

• Tuberculosis and Respiratory Diseases
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• v.48 no.2
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• pp.246-259
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• 2000

Background: As one of the etiologies of acute respiratory distress syndrome(ARDS), sepsis is one of the morbid causes of this cryptogenic malady. Even though many documents on the role of endotoxin(ETX) in the pathogenesis of ARDS have been issued, still the underlying mechanism associated with oxidative stress and activation of $PLA_2$ has been controversial. In the present study, the role of phospholipase $A_2(PLA_2)$ in the neutrophilic respiratory burst, which is presumed to cause acute lung injury during sepsis, was probed. Method: In glutathione-depleted Sprague-Dawley rats, lung leak, infiltration of neutrophils, $PLA_2$ activity and lipid peroxidation in the lung were measured after intratracheal instillation of endotoxin(delete). In addition, gamma glutamyl transferase(GGT) activity and the amount of pulmonary surfactant were measured. Morphologically, the changes in ultrastructure and cytochemical demonstration of oxidants were presented to confirm the neutrophilic oxidative stress and to elucidate the effects of $PLA_2$ activation on(delete) oxidative stress. Results: Instillation of ETX to glutathione-depleted rats intensified lung leak and lipid peroxidation when compared with non-glutathione depleted rats treated with the endotoxin. Moreover, oxidative stress was confirmed by the assay of GGT and malondialdehyde. Functionally, the depletion of glutathione altered the secretion of pulmonary surfactant from alveolar type II cells. Ultrastructurally and cytochemicaliy, oxidative stress was also confirmed after treatment of with ETX and diethylmaleate(DEM). Conclusion: The endotoxin-induced acute lung injury was mediated by oxidative stress, which in turn was provoked by the neutrophilic respiratory burst. The activation of $PLA_2$ in the lung seems to playa pivotal role in the oxidative stress of the lung.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.503-516
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• 2001

Background : The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. Method : In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung. Results : In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils. Conclusion : A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.