Heterotrophic bacteria are a major member of the microbial loop in the marine ecosystem and play an important role in the biogeochemical cycle decomposing organic matter. Therefore study of bacterial variation is important to understand the material cycle and energy flow of marine ecosystems. We investigated the monthly variations of bacteria and environmental factors in the Youngsan River estuary, and the correlation between bacteria and phytoplankton biomass (chlorophyll-a) including size-structure. As a result, bacteria of the Youngsan River estuary were higher in the surface than in the bottom layer, and higher in the summer than in winter. And the closer to the dike, the abundance increased, and it increased to the peaks in August, September, and June 2019 at the station closest to the dike. The chlorophyll-a also increases at the stations and time when the bacterial abundance was high and they correlates positively displaying no difference between size fractions. The results indicate that organic matter derived from phytoplankton has an effect on bacterial variation but no size-dependent effects. In addition, the seasonal pattern of bacteria increasing in proportion to the water temperature suggests the effect of water temperature on the growth of bacteria. No association of bacterial abundance variation with nutrient supply due to freshwater input was observed. In this study, dissolved oxygen was depleted and hypoxia was observed for a short time when a strong stratification was not developed. This may be resulted from the supply of organic matter from phytoplankton and the consumption of oxygen due to bacterial decomposition.
KSCE Journal of Civil and Environmental Engineering Research
/
v.1
no.1
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pp.53-68
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1981
Most clays under sustained load exhibit time-dependent deformation because of creep movement of soil particles and many investigators have attempted to relate their findings to the creep behavior of natural ground and to the long-term stability of slopes. Since the creep behavior of clays may assume a variety of forms depending on such factors as soil plasticity, activity and water content, it is difficult and complicated to analyse the creep behavior of clays. Rheological models composed of linear springs in combination with linear or nonlinear dashpots and sliders, are generally used for the mathematical description of the time-dependent behavior of soils. Most rheological models, however, have been proposed to simulate the behavior of secondary compression for saturated clays and few definitive data exist that can evaluate the behavior of non-saturated clays under the action of sustained stress. The clays change gradually from a solid state through plastic state to a liquid state with increasing water content, therefore, the rheological models also change. On the other hand, creep is time-dependent, and also the effect of thixotropy is time-function. Consequently, there may be certain correlations between creep behavior and the effects of thixotropy in compacted clays. In addition, the states of clay depend on water content and hence the height of the specimen under drained conditions. Futhermore, based on present and past studies, because immediate elastic deformation occurs instantly after the pressure increment without time-delayed behavior, the factor representing immediate elastic deformations in the rheological model is necessary. The investigation described in this paper, based on rheological model, is designed to identify the immediate elastic deformations and the effects of thixotropy and height of clay specimens with varing water content and stress level on creep deformations. For these purposes, the uniaxial drain-type creep tests were performed. Test results and data for three compacted clays have shown that a linear top spring is needed to account for immediate elastic deformations in the rheological model, and at lower water content below the visco-plastic limit, the effects of thixotropy and height of clay specimens can be represented by the proposed rheological model not considering the effects. Therefore, the rheological model does not necessitate the other factors representing these effects. On the other hand, at water content higher than the visco-plastic limit, although the state behavior of clays is visco-plastic or viscous flow at the beginning of the test, the state behavior, in the case of the lower height sample, does not represent the same behavior during the process of the test, because of rapid drainage. In these cases, the rheological model does not coincide with the model in the case of the higher specimens.
The present study was designed to examine effects of polyphenolic compounds isolated from red wine (PCRW) on the release of catecholamines (CA) from the isolated perfused model of the rat adrenal medulla, and to clarify its mechanism of action. PCRW (20${\sim}$180 ${\mu}$g/mL), given into an adrenal vein for 90 min, caused inhibition of the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic $N_N$ receptor agonist, 100 ${\mu}$M) and McN-A-343 (a selective muscarinic $M_1$ receptor agonist, 100 ${\mu}$M) in dose- and time-dependent fashion. PCRW itself did not affect basal CA secretion (data not shown). Following the perfusion of PCRW (60 ${\mu}$g/mL), the secretory responses of CA evoked by Bay-K-8644 (a L-type dihydropyridine $Ca^{2+}$ channel activator, 10 ${\mu}$M), cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, 10 ${\mu}$M) and veratridine (an activator of voltage-dependent $Na^+$ channels, 10 ${\mu}$M) were also markedly blocked, respectively. Interestingly, in the simultaneous presence of PCRW (60 ${\mu}$g/mL) and L-NAME (a selective inhibitor of NO synthase, 30 ${\mu}$M), the inhibitory responses of PCRW on the CA secretion evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclpiazonic acid were recovered to considerable level of the corresponding control release compared with those effects of PCRW-treatment alone. Practically, the amount of NO released from adrenal medulla after loading of PCRW (180 ${\mu}$g/mL) was significantly increased in comparison to the corresponding basal released level. Collectively, these results obtained here demonstrate that PCRW inhibits the CA secretory responses evoked by stimulation of cholinergic (both muscarinic and nicotinic) receptors as well as by direct membrane-depolarization from the isolated perfused adrenal gland of the normotensive rats. It seems that this inhibitory effect of PCRW is mediated by blocking the influx of both ions through $Na^+$ and $Ca^+{2$} channels into the rat adrenomedullary chromaffin cells as well as by inhibiting the release of $Ca^{2+}$ from the cytoplasmic calcium store, which are due at least partly to the increased NO production through the activation of nitric oxide synthase. Based on these data, it is also thought that PCRW may be beneficial to prevent or alleviate the cardiovascular diseases, such as hypertension and angina pectoris.
Background: Melanoma is the most fatal form of skin cancer due to its rapid metastasis. Recently, several studies reported that selenium can induce apoptosis in melanoma cells. However, the precise mechanism remains to be elucidated. In this study, we investigated the effect of selenium on cell proliferation in murine melanoma and on tumor growth and metastasis in C57BL/6 mice. Methods: Cell proliferation was measured by MTT assay in selenium-treated melanoma cells. Cell cycle distribution was analysized by staining DNA with propidum iodide (PI). mRNA and protein expression related to cell cycle arrest was measured by reverse transcription PCR and western blot. Tumor growth and metastasis was measured by in vivo model. Results: Selenium was suppressed the proliferation of melanoma cells in a dose dependent manner. The growth inhibition of melanoma by selenium was associated with an arrest of cell cycle distribution at G0/G1 stage. The mRNA and protein level of CDK2/CDK4 was suppressed by treatment with selenium in a time-dependent manner. In vivo, tumor growth was not suppressed by selenium; however tumor metastasis was suppressed by selenium in mouse model. Conclusion: These results suggest that selenium might be a potent agent to inhibit proliferative activity of melanoma cells.
Choi, Hyeun Deok;Baik, Jong Jin;Kim, Sang Hun;Yu, Sun Nyoung;Chun, Sung Hak;Kim, Young Wook;Nam, Hyo Won;Kim, Kwang Youn;Ahn, Soon Cheol
Journal of Life Science
/
v.26
no.4
/
pp.398-405
/
2016
Statins, the inhibitors of 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductase, are widely used in treatments of hypercholesterolemia and newly known as anti-cancer effect of various cancer cells. Recently, several studies suggested that reactive oxygen species (ROS) play a critical role on cell death signaling. However, mechanism of ROS by rosuvastatin is currently unclear. This study aimed to explore the molecular mechanism of apoptosis by rosuvastatin in human prostate cancer PC-3 cells. Cell viability and apoptosis-related protein expression were measured by MTT assay and western blotting, respectively. In addition, the levels of apoptosis and ROS were analyzed. The results showed that rosuvastatin dramatically reduced cell viability in a dose- and time-dependent manner. We confirmed that rosuvastatin induced apoptosis through reduction of procaspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP) in PC-3 cells. In addition, rosuvastatin stimulated ROS production in a dose-dependent manner and pre-treatment with N-acetylcysteine (NAC), a ROS scavenger, significantly recovered rosuvastatin-induced ROS and apoptosis. Thus, we concluded that rosuvastain induces apoptosis through generation of ROS in human prostate cancer PC-3 cells and provides a promising approach to improve the efficacy of cancer therapy.
Neuronal apoptotic events, which result in cell death, are occurred in hypoxic/ischemic conditions. Estradiol is a female sex hormone with steroid structure known to provide neuroprotection through multiple mechanisms in the central nervous system. This study was aimed to investigate the signal transduction pathway of $CoCl_2$-induced neuronal cell death and the inhibitory effects of estradiol. Administration of $CoCl_2$ decreased cell viability in both a dose- and time-dependent manner in PC12 cells. $CoCl_2$-induced cell death produced genomic DNA fragmentation and morphologic changes such as cell shrinkage and condensed nuclei. It was found that $CoCl_2$-treated cells increased the reactive oxygen species (ROS) as well as caspase-8, -9 and -3 activities. However, pretreatment with estradiol before exposure to $CoCl_2$ prevented the reduction in cell viability reduction and attenuated DNA fragmentation and morphologic changes caused by $CoCl_2$. Furthermore, the $CoCl_2$-induced increases of ROS levels and caspases activities were attenuated by estradiol. Gene expression analysis revealed that estradiol blocked the underexpression of the Bcl-2 and ameliorated the increase in the release of cytochrome c from mitochondria into cytoplasm and Fas-ligand (Fas-L) upregulated by $CoCl_2$. These results suggest that $CoCl_2$ induce apoptosis in PC12 cells through both mitochondria- and death receptor-mediated cell death pathway. Estradiol was found to have a neuroprotective effect against $CoCl_2$-induced apoptosis through the inhibition of ROS production and by modulating apoptotic effectors associated with the mitochondria- and death-dependent pathway in PC12 cells.
Leukotrienes(LTs) are hewn to act as a mediator provoking tissue response in inflammation. This finding implicates that LTs also play important roles in the pathogenesis of H, pylori-induced gastritis and gastric ulceration. Rebamipide is being currently used as a therapeutics for gastritis and peptic ulcer, but their mechanisms of action have not been known clearly yet. One possibility is that their therapeutic effects are ascribed to interfering with the H. pylori-induced release of LTs from neutrophils and gastric mucosal cells. In the present study, this possibility was tested using $LTB_4$ as the test material in human neutrophils and Kato III cells(gastric adenoma cells as a substitute for gastric mucosal cells). The release of $LTB_4$ from both neutrophils and Kato III cells was time and H. pylori-dose dependent. The maximum release of $LTB_4$ was induced by neutrophils and Kato III cells when these cells incubated with H. pylori $(4.8{\times}10^8\;cells/ml$ for 30min. But in the presence of rebamipide the release of $LTB_4$ from these cells was suppressed in dose dependent manners. The release was completely suppressed at 1.0 mM of rebamipide in neutrophils and 2.0 mM of this drug in Kato III cells, respectively. We also obtained the results that the release of $LTB_4$ was induced by A23187$(Ca^{2+}\;ionophore)$ and the A23187-induced release was also inhibited by rebamipide. It seems that the machanism of action of rebamipide is through its interaction with the level of intracellular $Ca^{2+}$. In view of the roles of $LTB_4$ in inflammatory reaction and the roles of H. pylori in gastritis and peptic ulcer, the effects of this drug observed in this study may contribute to their therapeutic action in these gastric disorders.
Background: Platelet-activating factor (PAF) induces nuclear factor $(NF)-{\kappa}B$ activation and angiogenesis and increases tumor growth and pulmonary tumor metastasis in vivo. The role of $NF-{\kappa}B$ activation in PAF-induced angiogenesis in a mouse model of Matrigel implantation, and in PAF-mediated pulmonary tumor metastasis were investigated. Methods: Angiogenesis using Matrigel and experimental pulmonary tumor metastasis were tested in a mouse model. Electrophoretic mobility shift assay was done for the assessment of $NF-{\kappa}B$ translocation to the nucleus. Expression of angiogenic factors, such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\alpha}$, basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF) were tested by RT-PCR and ELISA. Results: PAF induced a dose- and time-dependent angiogenic response. PAF-induced angiogenesis was significantly blocked by PAF antagonist, CV6209, and inhibitors of $NF-{\kappa}B$ expression or action, including antisense oligonucleotides to p65 subunit of $NF-{\kappa}B$ (p65 AS) and antioxidants such as ${\alpha}$-tocopherol and N-acetyl-L-cysteine. In vitro, PAF activated the transcription factor, $NF-{\kappa}B$ and induced mRNA expression of $TNF-{\alpha}$, $IL-1{\alpha}$, bFGF, VEGF, and its receptor, KDR. The PAF-induced expression of the above mentioned factors was inhibited by p65 AS or antioxidants. Also, protein synthesis of VEGF was increased by PAF and inhibited by p65 AS or antioxidants. The angiogenic effect of PAF was blocked when anti-VEGF antibodies was treated or antibodies against $TNF-{\alpha}$, $IL-1{\alpha}$, and bFGF was co-administrated, but not by antibodies against $TNF-{\alpha}$, $IL-1{\alpha}$, and bFGF each alone. PAF-augmented pulmonary tumor metastasis was inhibited by p65 AS or antioxidants. Conclusion: These data indicate that PAF increases angiogenesis and pulmonary tumor metastasis through $NF-{\kappa}B$ activation and expression of $NF-{\kappa}B$-dependent angiogenic factors.
Ku, Kyung-Hyung;Lee, Kyung-A;Kim, Young-Lim;Lee, Myung-Gi
Journal of the Korean Society of Food Science and Nutrition
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v.35
no.5
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pp.649-654
/
2006
It was investigated the effects of pre-treatment method on the microbes on the surface of radish (Raphanus sativus L.) leaves. Independent variables put in water washing ($X_1$), microwave treatment ($X_2$) and steam treatment ($X_3$) using central composite design and response surface analysis. It was not detected in the pathogenic microbes, Samonella spp., Camphylobacter spp., Vibrio spp., Shigella spp., Staphyloccocus spp., on the surface of collected radish leaves without pre-treatment. But general microbes showed $3.90{\times}10^5{\sim}1.20{\times}10^7CFU/g$ of total microbes, $1.10{\times}10^2{\sim}2.00{\times}10^5CFU/g$ of E. coli, $2.40{\times}10^3{\sim}3.55{\times}10^6CFU/g$ of yeast/mold on the surface of various radish leaves and lactic acid bacteria was detected or not according to collected samples. The best method of pre-treatment was steam treatment on the microbe reduction effect of samples surface. Also, the multiplex regression coefficients analysis was calculated three independent variables ($X_1,\;X_2,\;X_3$) and dependent variables (total microbes, lactic acid bacteria and yeast/molds). It showed high correlation $R^2$, 0.89, 0.87, 0.85, respectively. For effective reduction of surface microbes, the best method was water washing with microwave or steam treatment at the same time.
Kim, Mi-Hyoung;Rhu, Sang-Young;Lim, Dae-Seog;Song, Jie-Young
Journal of Radiation Protection and Research
/
v.39
no.3
/
pp.134-141
/
2014
Along with the wide use of radiotherapy in cancer treatment, there is growing interest in beneficial effect of low-dose irradiation (LDI) in cancer therapy. Therefore, we investigate how LDI affects immune responses in mice model. Total body irradiation (TBI) on C57BL/6 mice was given at low-dose rate of $1mGy{\cdot}min^{-1}$ using $^{137}Cs$ source at three times for consecutive three days. Hematological examination, total cell numbers of spleen, populations and characteristics of splenocytes were determined. Total numbers of RBC or platelet in irradiated mice showed no significant changes. WBC counts were decreased in a dose-dependent manner 2 days after TBI, however, these differences are gradually waned until 28 days. Dose-dependent decrease in the number of splenocytes of TBI mice at day 2 was also improved as time progressed. While the level of Foxp3 mRNA was decreased, the frequency of $CD4^+$ T cells and $CD69^+$ cells in spleen was increased at day 2 and 14. Fractionated low-dose TBI on mice exhibited normal body weight with no distinguishable behavior during whole experimental periods. These results suggest that some parameters of immune system could be altered and evaluated by fractionated low-dose TBI and be used to broaden boundary of low dose radiation research.
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