• The Journal of Internal Korean Medicine
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• v.34 no.4
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• pp.384-404
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• 2013

Objectives : Effects of Bogijetong-tang (BJT) on peripheral nerve regeneration have been reported in a previous study on BJT but additional study on a damaged peripheral neuropathy where its damage level is physically and chemically more severe was needed. Plus, this study was conducted because there haven't been any studies for BJT on central nerve regeneration. Methods : In order to check the effect on central nerve regeneration, the study on cerebellum cells was started and the sciatic nerve was used to observe the effects on a peripheral nerve which was severely damaged both physically and chemically. Nerve recovery effects were observed by analyzing target proteins such as phospho-extracellular signal-regulated kinase, ${\beta}1$ integrin, neurofilament 200, growth-associated protein-43, cyclin-dependent kinase 1, phospho-vimentin, phospho-Smad, and caspase 3. Results : The significant changes of target protein in cerebellum neurons have been observed. The changes of index protein on the axon regeneration and the nerve recovery in the sciatic nerve have been observed and the effects on cell protection were observed, as well. Conclusions : This study confirmed that BJT made a significant influence on nerve protection and recovery of a damaged peripheral neuropathy and it also made a possibility of its regeneration in a damaged central nerve injury.

• Toxicological Research
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• v.20 no.3
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• pp.179-185
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• 2004

Helicobacter pylori (H. pylori) infects more than half of the people in the world as a major microbe to cause most of gastric diseases. Recently, cytotoxin associated-antigen A (CagA) is believed as one of the most important virulence factors of H. pylori. Molecular toxicological pathway of CagA is necessary to investigate for understanding the pathological and toxicological aspects of H. pylori, since this virulence protein harasses intercellular processes of host cells to get profit for the survival of H. pylori. CagA is coded from cag pathogenicity island (cag PAI) and translocated into host cells by Type 4 secretion system (TFSS). Tyrosine phosphorylation of CagA targets Src homology 2-containing phosphotyrosine phosphatase (SHP-2) to form a CagA-SHP-2 complex. This complex depends on the similarity of sequence between EPIYA motif and Src homology 2 domain (SH2 domain) of CagA. The generation of growth factors is an essential role of CagA in protecting and healing gastric mucosa for the survival of H. pylori. On the other hand, the activation of IL-8 by CagA induces neutrophils generating inflammation and free radicals. Indeed, free radicals are well known carcinogen to induce DNA damage. In addition, the transduction of mitogen-activation signal by CagA is one of the interesting features to understand how to cause cancer. The relationship between cancer and inflammation with CagA was mainly discussed in this review.

• Biomolecules & Therapeutics
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• v.25 no.4
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• pp.427-433
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• 2017

Previously, we demonstrated that galangin (3,5,7-trihydroxyflavone) protects human keratinocytes against ultraviolet B (UVB)-induced oxidative damage. In this study, we investigated the effect of galangin on induction of antioxidant enzymes involved in synthesis of reduced glutathione (GSH), and investigated the associated upstream signaling cascades. By activating nuclear factor-erythroid 2-related factor (Nrf2), galangin treatment significantly increased expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS). This activation of Nrf2 depended on extracellular signal-regulated kinases (ERKs) and protein kinase B (AKT) signaling. Inhibition of GSH in galangin-treated cells attenuated the protective effect of galangin against the deleterious effects of UVB. Our results reveal that galangin protects human keratinocytes by activating ERK/AKT-Nrf2, leading to elevated expression of GSH-synthesizing enzymes.

• The Journal of the Acoustical Society of Korea
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• v.16 no.6
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• pp.76-84
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• 1997

Loose parts monitoring system(LPMS), which is used to detect metallic loose parts in the nuclear power plant, plays an important role in safe and reliable operation of the plant. To prevent from the damage due to the loose parts, most domestic nuclear power plants are using, or planning to use LPMS. However, these LPMS's, which are all invented from overseas and thereby depend on the oversea technologies, are very expensive, and are known to be inefficient to diagnose loose parts due to the lack of fundamental know-how of LPMS. Therefore, the main purpose of this paper is to propose and to realize a new loose parts localization algorithm which is simple and efficient enough even for the inexperienced operators to diagnose loose parts accurately and promptly. Considering practical nuclear power plant circumstances, some simulations for estimating the loose parts location have been done. The results show that the proposed method, called a modified circle intersection method, performs high resolved loose parts localization with 3.4% of error.

• Journal of the Korean Society for Nondestructive Testing
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• v.21 no.3
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• pp.251-260
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• 2001

Damage Profess of CFRP laminates under monotonic tensile test was characterized by the correlation between Acoustic Emission(AE) and Ultrasonic Test(UT). The amplitude distribution of AE signal from a specimens is an aid to the determination of the extent of the different fracture mechanism such as matrix crack, debonding, fiber pullout and fiber fracture as load is increased. In addtion, the characteristics of ultrasonic amplitude attenuation are useful lot analysis of the different type of fracture mechanism. Different orientation of carbon fiber reinforced plastic specimens were used to investigate the AE amplitude range and ultrasonic amplitude attenuation. Finally, loading-unloading tests were carried out to check Felicity effect. During the tests, ultrasonic amplitude attenuation was investigated at the same time and compared with AE parameters. The result showed that two parameters of both AE and UT could be effectively used for analysis of fracture mechanism in CFRP laminates.

• Transactions of the Korean Society of Mechanical Engineers A
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• v.40 no.8
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• pp.721-724
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• 2016

Because of the inherent uncertainties caused by the manufacturing process variations, future loading conditions, and incomplete damage models, the lifetimes of mechanical structures under field conditions are significantly different from the results obtained in the laboratories. In this study, a dual sensor was developed to prognosticate the fatigue failure of structures under these uncertain conditions, and its effectiveness was demonstrated on a rectangular columnar structure under repeated uni-axial loading. The dual sensor is a slightly weaker structure embedded in the target structure, so that failure occurs in the sensor earlier than in the target structure. From the signal differences in the strain gauges in the embedded dual sensor, it is possible to differentiate between the normal status and warning status, even under variable loads.

• The Journal of Korean Medicine
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• v.22 no.4
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• pp.58-68
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• 2001

Objectives : This study was designed to investigate the protective mechanisms of Samul-tang (SMT) on $H_2O_2$-induced toxicity in H9c2 cardiomyoblast cells. Methods : The cultured cells were pretreated with SMT and exposed to $H_2O_2$. The cell damage was assessed by using MTT assay. Also, we used Hoechst staining, Western blotting analysis. Results : SMT significantly reduced both $H_2O_2$-induced cell death and chromatin fragmentation. The decrease of Bcl2 expression by $H_2O_2$ was inhibited by SMT. In addition, the increase of Bax expression was also inhibited by SMT. In particular, Fas expression, which is generally recognized as cell death inducing signal by Fas/FasL interaction, was markedly decreased by $H_2O_2$ in a time-dependent manner, whereas this decrease was completely prevented by SMT. The cotreatment of SMT and $H_2O_2$ in H9c2 cells also induced the phosphorylation of ERK in a time-dependent manner. Moreover, PD098059, a specific inhibitor of ERKl/2, attenuated the protective effect of SMT on $H_2O_2$-induced toxicity in H9c2 cardiomyoblast cells. Furthermore, the protective effect of SMT was significantly blocked by treatment of SB203580, a specific inhibitor of p38. Conclusions : Taken together, this study suggests that the protective effects of the water extract of SMT against oxidative damages may be mediated by the modulation of Bel2 and Bax expression via the regulation of ERK and p38 signaling pathway.

• Smart Media Journal
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• v.5 no.4
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• pp.131-137
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• 2016

Since the phenomenon that the consumers slip important calls since they do not know the receiving information of the smart phone in spaces which smart phones can not be carried, the development of technology to solve this problem is urgent and the cases of burglary and losses of smart phones during hobby and recreation life are increasing and especially since burglary behaviors are occurring much in places such as bathing resort, swimming pool, Korean dry sauna, sauna and spa etc, the schemes to protect smart phones during hobbies and recreation life is needed. Since the smart watch, the conventional wearable device are high price machines and due to the burden about A/S costs for the damage or failure of the machine during exercise, hobbies and recreation activities, the burden about the use is high, development of products which can reduce such burden and emphasize the usefulness is urgent and in order to solve this problem, the added value and psychological repercussion effect will be very high in areas of smart phone users and utilizing them by developing the system which can know if the smart phone has received calls at least in places where smart phones can not be carried.

• Molecules and Cells
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• v.39 no.12
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• pp.869-876
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• 2016

Cantharidin (CTD) is an active compound isolated from the traditional Chinese medicine blister beetle and displayed anticancer properties against various types of cancer cells. However, little is known about its effect on human chronic myeloid leukemia (CML) cells, including imatinib-resistant CML cells. The objective of this study was to investigate whether CTD could overcome imatinib resistance in imatinib-resistant CML cells and to explore the possible underlying mechanisms associated with the effect. Our results showed that CTD strongly inhibited the growth of both imatinib-sensitive and imatinib-resistant CML cells. CTD induced cell cycle arrest at mitotic phase and triggered DNA damage in CML cells. The ATM/ATR inhibitor CGK733 abrogated CTD-induced mitotic arrest but promoted the cytotoxic effects of CTD. In addition, we demonstrated that CTD downregulated the expression of the BCR-ABL protein and suppressed its downstream signal transduction. Real-time quantitative PCR revealed that CTD inhibited BCR-ABL at transcriptional level. Knockdown of BCR-ABL increased the cell-killing effects of CTD in K562 cells. These findings indicated that CTD overcomes imatinib resistance through depletion of BCR-ABL. Taken together, CTD is an important new candidate agent for CML therapy.

• Toxicological Research
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• v.17 no.3
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• pp.215-223
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• 2001

Cadmium is an ubiquitous toxic metal and chronic exposure to cadmium results in the accumulation of cadmium in the liver and kidneys. In contrast, acute exposure leads to damage mainly in the liver. Apoptosis induced by cadmium has been shown in many tissues in vivo and in cultured cells in vitro. However, the molecular mechanism of cadmium-induced apoptosis is not clear in hepatocyte. To investigate the induction of apoptosis in the hepatocyte, we used mouse hepatoma cell line, Hepalclc7 cells, and analysed the molecules that involved in cadmium-induced apoptosis. Cadmium induced the genomic DNA fragmentation, PARP cleavage, and activation of caspase-3 like protease. Caspase-9 cysteine protease was activated in a time-dependent manner but caspase-8 cysteine protease was not significantly activated in cadmium-treated Hepalclc7 cells. Cadmium also induced mitochondrial dysfunction including cytochrome c release from mitochondria, change oj mitochondrial membrane potential tranition, and tranlocation of Bax Protein into mitochondria. These results strong1y indicated that the signal Pathway of apoptotic death in cadmium-treated Hepalclc7 cells is modulated by caspase cascade via mitochondria.