• Korean Journal of Food Science and Technology
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• v.47 no.3
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• pp.380-387
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• 2015

The anti-amnesic effect of Artemisia argyi H against trimethyltin (TMT)-induced learning and memory impairment and its neuroprotective effect against $H_2O_2$-inducedoxidative stress were investigated. Cognitive behavior was examined by Y-maze and passive avoidance test for 4 weeks, which showed improved cognitive functions in mice treated with the extract. In vitro neuroprotective effects against $H_2O_2$-induced oxidative stress were examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromide and lactate dehydrogenase (LDH) assays. A. argyi H. extract showed protective effects against $H_2O_2$-induced neurotoxicity; moreover, LDH release into the medium was inhibited. Finally, high-performance liquid chromatography (HPLC) analysis showed that eupatilin and jaceosidin were the major phenolic compounds in A. argyi H. extract. These results suggest that A. argyi H. could be a good source of functional substances to prevent neurodegenerative diseases.

• Korean Journal of Agricultural and Forest Meteorology
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• v.17 no.1
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• pp.15-24
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• 2015

$CH_4$ is a trace gas and one of the key greenhouse gases, which requires continuous and systematic monitoring. The application of eddy covariance technique for $CH_4$ flux measurement requires a fast-response, laser-based spectroscopy. The eddy covariance measurements have been used to monitor $CO_2$ fluxes and their data processing procedures have been standardized and well documented. However, such processes for $CH_4$ fluxes are still lacking. In this note, we report the first measurement of $CH_4$ flux in a rice paddy by employing the eddy covariance technique with a recently commercialized wavelength modulation spectroscopy. $CH_4$ fluxes were measured for five consecutive days before and after the rice transplanting at the Gimje flux monitoring site in 2012. The commercially available $EddyPro^{TM}$ program was used to process these data, following the KoFlux protocol for data-processing. In this process, we quantified and documented the effects of three key corrections: (1) frequency response correction, (2) air density correction, and (3) spectroscopic correction. The effects of these corrections were different between daytime and nighttime, and their magnitudes were greater with larger $CH_4$ fluxes. Overall, the magnitude of $CH_4$ flux increased on average by 20-25% after the corrections. The National Center for AgroMeteorology (www.ncam.kr) will soon release an updated KoFlux program to public users, which includes the spectroscopic correction and the gap-filling of $CH_4$ flux.

• Korean Journal of Ecology and Environment
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• v.35 no.2 s.98
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• pp.92-102
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• 2002

This study was conducted to compare filtering abilities of three species of freshwater mussels (Cobicula fluminea, Corbicula leana and Unio douglasiae) and to evaluate their filter feeding effects on water quality change in experimental enclosure systems. Mussel feeding in both laboratory and enclosure resulted in decrease of particulate material, such as chlorophyll, total P, SS. In the treatment with 600 individuals of mussels, chllorophyll concentration and net primary productivity decreased from $87.3{\pm}4.5\;{\mu}g/L$ and $106.3{\pm}8.8\;{\mu}gC\;L^{-1}\;hr^{-1}$ to nearly the same level as the mussel-free enclosure ($25.0{\pm}0.5\;{\mu}g/L$ and $15.6{\pm}13.3\;{\mu}gC\;L^{-1}\;hr^{-1}$, respectively)(P< 0.05, n = 6, ANOVA). In concert with the decrease of chlorophyll concentration, not only was the transparency enhanced from 0.48 m to 1.2m but also the suspended solids and total phosphorus decreased from $22.0{\pm}1.0\;mg/L$ to $7.5{\pm}0.5\;mg/L$ and $133{\pm}0.8\;{\mu}g/L$ to $70{\pm}0.0\;{\mu}g/L$, respectively (P<0.001, $r^2$>0.71, n = 11). Although slight decrease of SRP concentration and the increase of inorganic nitrogen ($NH_3-N$ and $NO_2-N$) were observed in the mussel addition enclosure, there was no statistical difference between two enclosures. Based on the filtering rate on phytoplankton and nutrient release rate in forms of feces and pseudofeces, Corbicula leana appeared to be the most efficient filter-feeder among three mussel species. These results inidicate that Cobicula play an important role in controlling particulate sestons and thus it could be applied as a biocontroler for the water quality management in lakes and reservoirs with algal blooms.

• Journal of Life Science
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• v.26 no.1
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• pp.50-58
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• 2016

The root bark of Ulmus macrocarpa has been used in traditional medicine for the treatment of various diseases such as edema, infection and inflammation. Nevertheless, the biological activities and underlying mechanisms of the immunomodulatory effects remain unclear. In this study, as part of our ongoing screening program to evaluate the immunomodulatory potential of new compounds from traditional medicinal resources, we investigated the effects of U. macrocarpa water extract (UME) on immune modulation in a murine RAW 264.7 macrophage model. As immune response parameters, the productions of as nitric oxide (NO) and cytokines such tumor necrotic factor (TNF)-α, interleukin (IL)-1β and IL-10 were evaluated. Although the release of IL-1β remained unchanged in UME-treated RAW 264.7 macrophages, the productions of NO, TNF-α and IL-10 were significantly increased, along with the increased expression of inducible NO synthase, TNF-α and IL-10 expression at concentrations with no cytotoxicity. UME treatment also induced the nuclear translocation of nuclear factor κB (NF-κB), and phosphorylation of Akt and mitogen-activated protein kinases (MAPKs) indicating that UME activated macrophages through the activation of NF-κB, phosphoinositide-3-kinase (PI3K)/Akt and MAPKs signaling pathways in RAW 264.7 macrophages. Furthermore, pre-treatment with UME significantly attenuated the production of NO, but not TNF-α, IL-1β and IL-10, in lipopolysaccharide-stimulated RAW 264.7 cells suggesting that UME may be useful in preventing inflammatory diseases mediated by excessive production of NO. These findings suggest that the beneficial therapeutic effects of UME may be attributed partly to its ability to modulate immune functions in macrophages.

• Journal of Life Science
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• v.21 no.7
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• pp.953-960
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• 2011

Necrosis is characterized by the cell membrane rupture and release of the cellular contents, including high-mobility group box 1 protein (HMGB1), into the extracellular microenvironment. HMGB1 acts as a transcriptional regulator in nuclei, but exerts a pro-inflammatory and tumor-promoting cytokine activity when released into the extracellular space. Its overexpression is associated with tumor progression and chemoresistance. Thus, HMGB1 acts as a clinically important molecule in tumor biology. In this study, we examined whether HMGB1 affects cell death induced by anti-cancer drugs. Here we show that HMGB1 prevented cisplatin (alkylating agent)-induced apoptosis and switched the cell fate to necrosis in MCF-7, MDA-MB231, and MDA-MB361 cells. Similar apoptosis-to-necrosis switch effects of HMGB1 were observed in cells treated with 4-HC, another alkylating agent. In contrast, HMGB1 did not exert any significant effects on docetaxel (DOC)-induced apoptosis in MCF-7 cells. We also show that cisplatin-induced apoptosis was switched to necrosis in MCF-7 multicellular tumor spheroids (MTS) that were cultured for 8 days and had necrotic cores, but DOC-induced apoptosis was prevented without the apoptosis-to-necrosis switch. Finally, the levels of RAGE, a receptor of HMGB1, were increased with extended culture of MTS. These findings demonstrate that HMGB1 switches alkylating agent-induced apoptosis to necrosis, suggesting that the strategy to prevent necrosis occurring as an undesirable action of alkylating agent-based chemotherapy should be delineated to improve the efficacy of chemotherapy for cancer.

• Journal of Oral Medicine and Pain
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• v.34 no.3
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• pp.261-276
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• 2009

Lactacystin, a microbial natural product synthesized by Streptomyces, has been commonly used as a selective proteasome inhibitor in many studies. Proteasome inhibitors is known to be preventing the proliferation of cancer cells in vivo as well as in vitro. Furthermore, proteasome inhibitors, as single or combined with other anticancer agents, are suggested as a new class of potential anticancer agents. This study was undertaken to examine in vitro effects of cytotoxicity and growth inhibition, and the molecular mechanism underlying induction of apoptosis in SCC25 human tongue sqaumous cell carcinoma cell line treated with lactacystin. The viability of SCC25 cells, human normal keratinocytes (HaCaT cells) and human gingiva fibroblasts (HGF-1 cells), and the growth inhibition of SCC25 cells were assessed by MTT assay and clonogenic assay respectively. The hoechst staining, hemacolor staining and TUNEL staining were conducted to observe SCC25 cells undergoing apoptosis. SCC25 cells were treated with lactacystin, and Western blotting, immunocytochemistry, confocal microscopy, FAScan flow cytometry, MMP activity, and proteasome activity were performed. Lactacystin treatment of SCC25 cells resulted in a time- and does-dependent decrease of cell viability and a does-dependent inhibition of cell growth, and induced apoptotic cell death. Interestingly, lactacytin remarkably revealed cytotoxicity in SCC25 cells but not normal cells. And tested SCC25 cells showed several lines of apoptotic manifestation such as nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, the decrease of DNA contents, the release of cytochrome c into cytosol, the translocation of AIF and DFF40 (CAD) onto nuclei, the up-regulation of Bax, and the activation of caspase-7, caspase-3, PARP, lamin A/C and DFF45 (ICAD). Flow cytometric analysis revealed that lactacystin resulted in G1 arrest in cell cycle progression which was associated with up-regulation in the protein expression of CDK inhibitors, $p21^{WAF1/CIP1}$ and $p27^{KIP1}$. We presented data indicating that lactacystin induces G1 cell cycle arrest and apoptois via proteasome, mitochondria and caspase pathway in SCC25 cells. Therefore our data provide the possibility that lactacystin could be as a novel therapeutic strategy for human tongue squamous cell carcinoma.

• Sleep Medicine and Psychophysiology
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• v.2 no.2
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• pp.156-164
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• 1995

Objectives : Patients with obstructive sleep apnea syndrome(OSAS) often complain of nocturnal enuresis. There are a few reports that OSAS patients have altered renal function, and there are some evidences that the increased release of atrial natriuretic peptide(ANP) may be involved in the pathogenesis of nocturnal urinary symptoms of OSAS patients. In this study, we measured plasma ANP concentrations during waking and sleep in OSAS patients and normal controls to investigate whether there were differences of ANP concentrations between OSAS patients and normal subjects. Methods : 27 patients with OSAS and 10 normal subjects were studied. All subjects underwent a full-night polysomnographic study. Venous blood samples were separately drawn during waking and sleep. Plasma ANP concentrations were measured using radioimmunoassay. Results : In OSAS patients, ANP concentrations during sleep($122.9\;{\pm}\;29.9pg/ml$) were significantly higher than ANP concentrations during waking($60.2\;{\pm}\;5.8pg/ml$)(p < 0.05). However, in normal subjects, there was no significant difference between ANP concentrations during waking($59.2\;{\pm}\;5.7pg/ml$) and sleep($69.6\;{\pm}\;3.0pg/ml$)(p > 0.05). There was no significant difference of ANP concentrations during waking between OSAS patients($60.2\;{\pm}\;5.8pg/ml$) and normal controls($59.2\;{\pm}\;5.7pg/ml$)(p > 0.05), and also there was no significant difference during sleep between OSAS patients($122.9\;{\pm}\;29.9pg/ml$) and normal subjects($69.6\;{\pm}\;3.0pg/ml$)(p > 0.05). Plasma ANP concentrations during sleep showed significant positive correlations with apnea index(r = 0.3846, p < 0.05) and respiratory disturbance index(r = 0.3939, p < 0.05) in OSAS patients. Conclusion : These data suggest that, in OSAS patients, plasma ANP concentrations during sleep are significantly higher than plasma ANP concentrations during waking, and there is a positive correlation between the plasma ANP concentration during sleep and the severity of sleep apnea.

• Tuberculosis and Respiratory Diseases
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• v.46 no.1
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• pp.44-52
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• 1999

Background : Airway infiltration by inflammatory cells, particularly of eosinophils, is one of the characteristic features of asthma. Several mechanisms for the recruitment of eosinophil is focused on the CD4+ T lymphocyte for the preferential production of Th2-c1erived cytokines. Interleukin-10(IL-10) is identified cytokine with potent antiinflammatory activity. This molecule has been shown to inhibit the release of cytokine from inflammatory cells including Th2 cell, and also to inhibit eosinophil survival. We therefore attempted to determine whether decreased synthesis of IL-10 in the lung of bronchial asthma may contribute to inflammation that is characteristics of this dease. Method: Subjects were patients with bronchial asthma(n=23) and normal controls(n=11). IL-10 produced from peripheral mononuclear cell(PBMC) and in bronchoalveolar lavage(BAL) fluid was measured by ELISA method. Degree of bronchial inflammation was assessed by total cell counts and eosinophil percents in BAL fluid, eosinophil infiltration on bronchial biopsy tissue and $PC_{20}$ for methacholine. Results: The IL-10 level produced by PBMC and in BAL fluid from patient with bronchial asthma were not different with normal controls(respectively, $901.6\pm220.4$ pg/ml, $810.9\pm290.8$ pg/ml for PBMC, $24.5\pm9.5$ pg/mL $30.5\pm13.5$ pg/ml for BAL fluid p>0.05). There were significant negative correlation between IL-10 in BAL fluid and eosinophil percents in BAL fluid or degree of eosinophil infiltration in bronchial biopsy (respectively r=-0.522, r=-0.4486 p<0.05). However there was no difference of IL-10 level according to $PC_{20}$ for methacholine. There were no correlation between IL-10 production by PBMC and peripheral blood eosinophil counts or serum eosinophilic cationic protein levels(respectively r=0.1146, r=0.0769 p>0.05). Conclusion: These observation suggest that IL-10 may participate but not acts the crucial role in regulation of the airway inflammation in bronchial asthma.

• Tuberculosis and Respiratory Diseases
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• v.58 no.1
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• pp.43-53
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• 2005

Emphysema is characterized by air space enlargement and alveolar destruction. The mechanism responsible for the development of emphysema was thought to be protease/antiprotease imbalance and oxidative stress. A very recent study shows that alveolar cell apoptosis causes lung destruction and emphysematous changes. Thus, this study was performed to support the evidence for the role of apoptosis in the development of emphysema by characterizing cigarette smoke extract (CSE)-induced apoptosis in A549 (type II pneumocyte) lung epithelial cells. CSE induced apoptosis at low concentration (10% or less) and both apoptosis and necrosis at high concentration (20%). Apoptosis was demonstrated by DNA fragmentation using FACScan for subG1 fraction. Discrimination between apoptosis and necrosis was done by morphologic analysis using fluorescent microscopy with Hoecst 33342/propium iodide double staing and electron microscopy. Cytochrome c release was confirmed by using immunofluorescence with monoclonal anti-cytochrome c antibody. However, CSE-induced cell death did not show the activation of caspase 3 and was not blocked by caspase inhibitors. This suggests that CSE-induced apoptosis might be caspase-independent apoptosis. CSE-induced cell death was near completely blocked by N-acetylcystein and bcl-2 overexpression protected CSE-induced cell death. This results suggests that CSE might induce apoptosis through intracellular oxidative stress. CSE also activated p53 and functional knock-out of p53 using stable overexpression of HPV-E6 protein inhibited CSE-induced cell death. The characterization of CSE-induced cell death in lung epithelial cells could support the role of lung cell apoptosis in the pathogenesis of emphysema.

• Proceedings of the Ginseng society Conference
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• 1984.09a
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• pp.27-36
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• 1984

It was previously reported that red ginseng extract inhibited carcinogenesis by urethan, DMBA and aflatoxin $B_1E (Cancer Detection and Prevention, 6: 515-525, 1983). In an attempt to investigate the mechanism of the anticarcinogenic effect of ginseng, we assayed natural killer (N.K) activity in mice treated with urethan and benzo(a)pyrene. In our experiment newly born Swiss Webster mice, less than 24 hrs. old, were given a single subcutaneous injection of lmg of ure-than and 40ug of benzo(a)pyrene. The mice had been administered with ginseng since weaning, and sacrificed at various intervals. Major organs were examined both, with the naked eye and microscopically. N.K. activity of spleen cells was analyzed in a 12-hour $^{51}Cr^-release$ assay against YAC-1 cells. Administration of ginseng resulted in an increase of N.K. activity by $18\%$ at 4 weeks, $20\%$ (P < 0.05) at 6, $29\%$ (P < 0.05) at 12, and $13\%$ at 24 following a single injection of urethan. At the same time, significantly lower incidences of lung adenoma were noted at 6 weeks $(50\%)$ and 12 weeks $(27\%)$ following the administration of ginseng to urethan-injected mice. This result indicates that the enhancement of N.K. activity by ginseng makes a contribution to its anticarcinogenic effect. On the hand, N.K. activity was suppressed by benzo(a)pyrene during the time span of this experiment and it almost returned to the level of controls following the adminsitration of ginseng. However, the lung adenoma induced by benzo(a)pyrene began to occur at 48 weeks in which N.K. activity had naturally declined to a very low level in all experimental mice, and administration of ginseng did not decrease the incidence. In explanation of this result, we might propose that the recovery of the N.K. activity by ginseng had little effect on the incidence of lung adenoma because of the long latent period of carcinogenesis by benzo(a)pyrene. In conclusion, these results suggest that the anticarcinogenic effect of ginseng in urethan-treated mice may be related to the augmentation of N.K. activity.