• Korean Journal of Pharmacognosy
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• v.44 no.3
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• pp.269-274
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• 2013

In this study, we investigated the anticancer effect of rice bran extract in HL-60 human promyelocytic leukemia cells. The extract of rice bran inhibited the proliferation of HL-60 cells. When treated with the rice bran extract, we could observe the apoptotic characteristics such as apoptotic bodies and the increase of sub-G1 hypodiploid cell population, increase of Bax level, decrease of Bcl-2 expression, cleavage of procaspase-3, cleavage of procaspase-9 and cleavage of poly(ADP-ribose) polymerase(PARP) in HL-60 cells. Furthermore, the apoptosis induction of HL-60 cells treated with the rice bran extract was also accompanied by the inactivation of mitogen-activated protein kinases (MAPK) such as ERK1/2 MAPK and p38 MAPK. In addition, the rice bran extract induced the down-regulation of c-myc. These data suggested that the rice bran extract could induce the apoptosis via the inactivation of ERK1/2 MAPK and p38 MAPK, and the down-regulation of c-myc in HL-60 acute pomyelocytic leukemia cells. The results support that the rice bran extract might have potential for the treatment of acute promyelocytic leukemia.

• Korean Journal of Breeding Science
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• v.43 no.1
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• pp.1-13
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• 2011

Low temperature stress is one of the major negative factors affecting vegetative and reproductive growth of rice. To better understand responses of rice plants to low temperature we analyzed transcriptome expression patterns in glumous flower of cold-tolerant japonica rice variety, Stejaree45, and cold-susceptible variety, HR19621-AC6 at booting stage under cold water irrigation. A total of 2,411 probes were differentially expressed by low temperature in glumous flowers of the two varieties. Some important genes involved in hormone biosynthesis showed variety-specific regulation. Expression of GA20ox3 and GA2ox, among the genes involved in GA biosynthesis, was regulated differentially in the two varieties. Among the genes involved in IAA biosynthesis, YUCCA1 and TAA1:1 showed variety-specific regulation. Among the genes involved in cytokinin biosynthsis and signaling, expression of LOG, HK1 and HK3 was significantly down-regulated only in the cold-susceptible variety. Among the genes involved in ABA biosynthesis, NSY and AAO3 were down-regulated only in the cold-tolerant variety. In general, genes involved in GA, IAA and cytokinin biosynthesis responded to cold temperature in such a way that capacity of those bioactive hormones is maintained at relatively higher levels under cold temperature in the cold-tolerant variety, which can help minimize cold stress imposed to developing reproductive organs in the cold-tolerant variety.

• Biomedical Science Letters
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• v.26 no.4
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• pp.288-295
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• 2020

Infection of Helicobacter pylori on gastric mucosa is associated with various gastric diseases. According to the WHO, H. pylori causes gastric cancer and has been classified as a class I carcinogen. Riboflavin is an essential vitamin which presents in a wide variety of foods. Previous studies have shown that riboflavin/UVA was effective against the growth inhibition of Staphylococcus aureus, S. epidermidis and multidrug-resistant Pseudomonas aeruginosa and had the potential for antimicrobial properties. Thus, we hypothesized that riboflavin has a potential role in the growth inhibition of H. pylori. To demonstrate inhibitory concentration of riboflavin against H. pylori, we performed agar and broth dilution methods. As a result, we found that riboflavin inhibited the growth of H. pylori. The MIC was 1 mM in agar and broth dilution test. Furthermore, to explain the inhibitory mechanism, we investigated whether riboflavin has an influence on the replication-associated molecules of the bacteria using RT-PCR to detect mRNA expression level in H. pylori. Riboflavin treatment of H. pylori led to down-regulation of polA and dnaB mRNA expression levels in a dose dependent manner. After then, we also confirmed whether riboflavin has cytotoxicity to human cells. We used AGS, a gastric cancer cell line, and treated with riboflavin did not show statistically significant decrease of cell viability. Thus, these results indicate that riboflavin can suppress the replication machinery of H. pylori. Taken together, these findings demonstrate that riboflavin inhibits growth of H. pylori by inhibiting replication of the bacteria.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.540-545
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• 2022

Betulin is a triterpenoid natural product contained in several medicinal plants including Betulae Cortex. These medicinal plants have been used for controlling diverse inflammatory diseases in folk medicine and betulin showed anti-inflammatory, antioxidative, and anticancer activities. In this study, we tried to examine whether betulin exerts a regulative effect on the gene expression of MUC5AC mucin under the status simulating a pulmonary inflammation, in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with betulin for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h or the indicated periods. The MUC5AC mucin mRNA expression and mucin glycoprotein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. To elucidate the action mechanism of betulin, effect of betulin on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated by western blot analysis. The results were as follows: 1) Betulin significantly suppressed the production of MUC5AC mucin glycoprotein and down-regulated MUC5AC mRNA expression induced by PMA in NCI-H292 cells. 2) Betulin inhibited NF-κB activation stimulated by PMA. Suppression of inhibitory kappa B kinase (IKK) by betulin led to the inhibition of the phosphorylation and degradation of inhibitory kappa B alpha (IκBα), and the nuclear translocation of NF-κB p65. This, in turn, led to the down-regulation of MUC5AC glycoprotein production in NCI-H292 cells. These results suggest betulin inhibits the gene expression of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

• The Korean Journal of Air & Space Law and Policy
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• v.32 no.2
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• pp.3-31
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• 2017

On 12 October 2017, the English Royal Courts of Justice delivered its decision about air carrier's compensation liability for the flight delay. In the cases the passengers suffered delays at a connecting point and, consequently, on arrival at their final destination. They claimed compensation under Regulation 261/2004 (the "Regulation"), as applied by the Court of Justice of the European Union (the "CJEU") in Sturgeon v. Condor [2009]. The principal issues were whether delays suffered by the passengers during the second leg of their respective journeys were compensable under the Regulation, whether there was jurisdiction under the Regulation and whether the right to compensation under the Regulation is, insofar as non-Community air carriers are concerned, excluded by virtue of the exclusive liability regime established under the Montreal Convention 1999. The passengers, the plaintiff, argued that the relevant delay was not that on flight 1 but that suffered at the "final destination". They maintained that there was no exercise by the EU of extraterritorial jurisdiction as the delay on flight 2 was merely relevant to the calculation of the amount of compensation due under the Regulation. The air carrier, the defendant, however argued that the only relevant flights for the purpose of calculating any delay were the first flights (flights 1) out of EU airspace, as only these flights fell within the scope of the Regulation; the connecting flights (flights 2) were not relevant since they were performed entirely outside of the EU by a non-Community carrier. Regarding the issue of what counts as a delay under the Regulation, the CJEU held previously on another precedents that the operating carrier's liability to pay compensation depends on the passenger's delay in arriving at the "final destination". It held that where the air carrier provides a passenger with more than one directly connecting flight to enable him to arrive at their destination, the flights should be taken together for the purpose of assessing whether there has been three hours' or more delay on arrival; and that in case of directly connecting flights, the final destination is the place at which the passenger is scheduled to arrive at the end of the last component flight. In addition, the Court confirmed that the Regulation applied to flights operated by non-Community carriers out of EU airspace even if flight 1 or flight 2 lands outside the EU, since the Regulation does not require that a flight must land in the EU. Accordingly, the passengers' appeal from the lower Court was allowed, while that of air carrier was dismissed. The Court has come down firmly on the side of the passengers in this legal debate. However, this result is not a great surprise considering the recent trends of EU member states' court decisions in the fields of air transport and consumer protection. The main goal of this article is to review the Court's decision and to search historical trend of air consumer protection especially in EU area.

• The Journal of Internal Korean Medicine
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• v.30 no.4
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• pp.674-684
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• 2009

Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. This study was undertaken to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO). Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO. Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of a rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.1-9
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• 2017

Intestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.2
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• pp.155-161
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• 2014

Overexpression of amyloid precursor protein with the Swedish mutation causes abnormal hyperphosphorylation of the microtubule-associated protein tau. Hyperphosphorylated isoforms of tau are major components of neurofibrillary tangles, which are histopathological hallmarks of Alzheimer's disease. Protein phosphatase 2A (PP2A), a major tau protein phosphatase, consists of a structural A subunit, catalytic C subunit, and a variety of regulatory B subunits. The B subunits have been reported to modulate function of the PP2A holoenzyme by regulating substrate binding, enzyme activity, and subcellular localization. In the current study, we characterized regulatory B subunit-specific regulation of tau protein phosphorylation. We showed that the PP2A B subunit PPP2R2A mediated dephosphorylation of tau protein at Ser-199, Ser-202/Thr-205, Thr-231, Ser-262, and Ser-422. Down-regulation of PPP2R5D expression decreased tau phosphorylation at Ser-202/Thr-205, Thr-231, and Ser-422, which indicates activation of the tau kinase glycogen synthase kinase 3 beta ($GSK3{\beta}$) by PP2A with PPP2R5D subunit. The level of activating phosphorylation of the $GSK3{\beta}$ kinase Akt at Thr-308 and Ser-473 were both increased by PPP2R5D knockdown. We also characterized B subunit-specific phosphorylation sites in tau using mass spectrometric analysis. Liquid chromatography-mass spectrometry revealed that the phosphorylation status of the tau protein may be affected by PP2A, depending on the specific B subunits. These studies further our understanding of the function of various B subunits in mediating site-specific regulation of tau protein phosphorylation.

• Explosives and Blasting
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• v.20 no.4
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• pp.5-15
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• 2002

For the noise reduction measures in a construction field where noise sources such as blasting and pile driving works exist, the construction of the sound barrier near the noise source or receiver is often the most economic measure in order to exclude the propagated sound. The dimension of the barrier is decided by the noise and construction design, and the constructive quality of a soundproof panel shall be secured in accordance with KS F4770 to guarantee the safety of sound barriers. In this paper the problems included in the KS F4770-1 that is the regulation for the metallic sound barrier of the absorption type are identified and it is suggested what to be corrected or improved. Through a series of the analyses, conclusion were reached that it is required to improve test methods in KS F4770-1 as well as to break down loads for building more cost-effective sound barrier. In addition, KS F4770-1 was compared with ZTV-Lsw 88 which is the german regulation for sound barrier design. As a result, it was found that the Korean regulation is more conservative than that of Germany.

• Natural Product Sciences
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• v.24 no.1
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• pp.13-20
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• 2018

Estragole is a naturally occurring phenylpropanoid obtained from essential oils found in a broad diversity of plants. Although the phenylpropanoids show many biological activities, clear regulation of the inflammatory signaling pathways has not yet been determined. Here, we scrutinized the anti-inflammatory effect of estragole. The anti-inflammatory effect of estragole was determined through the inhibitory mechanisms of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), nuclear factor kappa B ($NF-{\kappa}B$), and mitogen-activated protein kinases (MAPK) pathways and the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2)/heme oxygenase (HO)-1 pathways in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Estragole significantly inhibited NO production, iNOS and COX-2 expression as well as LPS-induced $NF-{\kappa}B$ and MAPK activation. Furthermore, estragole suppressed LPS-induced intracellular ROS production but up-regulated the stress response gene HO-1 via the activation of transcription factor Nrf-2. These findings demonstrate that estragole inhibits the LPS-induced expression of inflammatory mediators via the down-regulation of iNOS, COX-2, $NF-{\kappa}B$, and MAPK pathways, as well as the up-regulation of the Nrf-2/HO-1 pathway, indicating that this phenylpropanoid has potential therapeutic and preventive applications in various inflammatory diseases.