• Mycobiology
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• v.44 no.1
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• pp.38-47
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• 2016

The ascomycete fungus Mycosphaerella graminicola (synonym Zymoseptoria tritici) is an important pathogen of wheat causing economically significant losses. The primary nutritional mode of this fungus is thought to be hemibiotrophic. This pathogenic lifestyle is associated with an early biotrophic stage of nutrient uptake followed by a necrotrophic stage aided possibly by production of a toxin or reactive oxygen species (ROS). In many other fungi, the genes CREA and AREA are important during the biotrophic stage of infection, while the NOXa gene product is important during necrotrophic growth. To test the hypothesis that these genes are important for pathogenicity of M. graminicola, we employed an over-expression strategy for the selected target genes CREA, AREA, and NOXa, which might function as regulators of nutrient acquisition or ROS generation. Increased expressions of CREA, AREA, and NOXa in M. graminicola were confirmed via quantitative real-time PCR and strains were subsequently assayed for pathogenicity. Among them, the NOXa over-expression strain, NO2, resulted in significantly increased virulence. Moreover, instead of the usual filamentous growth, we observed a predominance of yeast-like growth of NO2 which was correlated with ROS production. Our data indicate that ROS generation via NOXa is important to pathogenicity as well as development in M. graminicola.

• Journal of fish pathology
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• v.3 no.1
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• pp.21-25
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• 1990

In inland aquaculture, a lot of fishes often died cause of touch of L. carteri which is attached on the net cage. In this works, the experiment were carried out on classification of species, toxin test, and extermination with some chemicals. A bryozoa from net cage in lake Okjeong is classified into the Phylactolaemata, Lophopodella carteri Hyatt. A bryozoa broke out firstly on the 30th of June with water temperature up to $31^{\circ}C$ and it reattached on the net with water temperature below $30^{\circ}C$. Size of bryozoa colony is about $0.8{\times}0.6{\sim}1.7{\times}1.5cm$. Water column of attachment was 0~5m and the peak is 2~3m. In toxin test on the israeli carp, goldfish and catfish touched with bryozoa for 1 minute at $25^{\circ}C$ of water temperature, a dead fish appeared at 20 minutes after touched. Mortality was 90% for israeli carp and 100% for goldfish at 100 minuties after touched, but catfish was not died at all. It was supposed that the toxin is from nematocyst being around tentacles and this toxin act a deadly poison on a israeli carp and goldfish. In extermination test, the bryozoa treated with 300ppm of formalin, 5% of sodium chloride, 5ppm of malachite green, 200ppm of potassium permanganate, 1000ppm of potassium iodide, 10ppm of DDVP for minute respectively, all of them were not effected.

• Journal of Life Science
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• v.11 no.4
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• pp.346-353
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• 2001

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) a prototype of the highly toxid halogenated arylhydrocarbons, bioaccumulates in the food chain and induces a complex spectrum of pathological responses. However, its effect on the nerve system is relatively not well studied. In this study we evaluated TCDDs cytotoxicity on the cortical cell and investigated its effect on the expression 2,3-cyclic nucleotide 3-phosphodiesterase(CNPase), a marker for oilgodendrocytes, The survival rates of 4 DIV cortical cells, that are dissociated from E18 rat cortex and maintained in the presence of TCDD, were 88.8, 83.6, 78.5, and 78.6%(5,10, 20 and 50 nM, respectively) where the reduction in 20 and 50mM TCDD were statistically very significant(p<0.01). Imunocytochemistry of cultured cells revealed that the intensities of immunostaining with an anti-CNP1&2 antibody depended on the concentrations of the toxin. Immunoblot analysis also showed differential expression of CNP1 and CNP2 in the presence of TCDD; the CNP1 expression was dose-dependently decreased. Interestingly, the expression of CNP2 in the presence if TDCC; the CNP1 expression was dose-dependently decreased. Interestingly, the expression of CNP2 fluctuated with the TCDD concentration. These results indicated that CNP1 and 2 are differentially regulated by TCDD, implying the functions of oligodendrocytes are modulated by the toxin.

• Food Science of Animal Resources
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• v.25 no.4
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• pp.478-482
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• 2005

Bovine k-casein macropeptide was prepared by adding TCA (3, 6, and $12\%$) treatment after chymosin reaction. Each TCA soluble macropeptide was fractionated into five peak by ion exchange column chromatography. In proportiion to TCA concentrations, the ratio of peak area showed different the elution pattern. At the 6 and $12\%$ TCA concentration, area ratio of P-I which did not content carbohydrates was decreased to 19.9 and $17.0\%$ of total peak area respectively. The area of P-III was changed from $10.2\%\;to\;26.2\;and\;13.2\%$ when the TCA concentration was increased from 3 to 6 and $12\%$ Cholera toxin binding activity of k-casein macropeptide eluted at $0.17\~0.18M$ NaCl gradient was not inhibited by 6 and $12\%$ TCA treatments. The use of $6\%$ TCA as extraction buffer was feasible and led to an effective separation of the peak III.

• Molecules and Cells
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• v.37 no.9
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• pp.656-663
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• 2014

Gintonin, a novel, ginseng-derived G protein-coupled lysophosphatidic acid (LPA) receptor ligand, elicits $[Ca^{2+}]_i$ transients in neuronal and non-neuronal cells via pertussis toxin-sensitive and pertussis toxin-insensitive G proteins. The slowly activating delayed rectifier $K^+$ ($I_{Ks}$) channel is a cardiac $K^+$ channel composed of KCNQ1 and KCNE1 subunits. The C terminus of the KCNQ1 channel protein has two calmodulin-binding sites that are involved in regulating $I_{Ks}$ channels. In this study, we investigated the molecular mechanisms of gintonin-mediated activation of human $I_{Ks}$ channel activity by expressing human $I_{Ks}$ channels in Xenopus oocytes. We found that gintonin enhances $I_{Ks}$ channel currents in concentration- and voltage-dependent manners. The $EC_{50}$ for the $I_{Ks}$ channel was $0.05{\pm}0.01{\mu}g/ml$. Gintonin-mediated activation 1 of the $I_{Ks}$ channels was blocked by an LPA1/3 receptor antagonist, an active phospholipase C inhibitor, an $IP_3$ receptor antagonist, and the calcium chelator BAPTA. Gintonin-mediated activation of both the $I_{Ks}$ channel was also blocked by the calmodulin (CaM) blocker calmidazolium. Mutations in the KCNQ1 $[Ca^{2+}]_i$/CaM-binding IQ motif sites (S373P, W392R, or R539W)blocked the action of gintonin on $I_{Ks}$ channel. However, gintonin had no effect on hERG $K^+$ channel activity. These results show that gintonin-mediated enhancement of $I_{Ks}$ channel currents is achieved through binding of the $[Ca^{2+}]_i$/CaM complex to the C terminus of KCNQ1 subunit.

• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.563-571
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• 2003

Dysfunction of mesangial cells has been contributed to the onset of diabetic nephropathy. Insulin like growth factors (IGFs) are also implicated in the pathogenesis of diabetic nephropathy. However, it is not yet known about the effect of high glucose on IGF-I and IGF-II secretion in the mesangial cells. Furthermore, the relationship between cAMP and high glucose on the secretion of IGFs was not elucidated. Thus, we examined the mechanisms by which high glucose regulates secretion of IGFs in mesangial cells. Glucose increased IGF-I secretion in a time- (>8 hr) and dose- (>15 mM) dependent manner (p<0.05). Stimulatory effect of high glucose on IGF-I secretion is predominantly observed in 25 mM glucose (high glucose), while 25 mM glucose did not affect cell viability and lactate dehydrogenase release. High glucose also increased IGF-II secretion. The increase of IGF-I and IGF-II secretion is not mediated by osmotic effect, since mannitol and L-glucose did not affect IGF-I and IGF-II secretion. 8-Br-cAMP mimicked high glucose-induced secretion of IGF-I and IGF-II. High glucose-induced stimulation of IGF-I and IGF-II secretion was blocked not by pertussis toxin but by SQ 22536 (adenylate cyclase inhibitor). Rp-cAMP (cAMP antagonist), and myristoylated protein kinase A (PKA) inhibitor amide 14-22 (protein kinase A inhibitor). These results suggest that cAMP/PKA pathways independent of Gi protein may mediate high glucose-induced increase of IGF-I and IGF-II secretion in mesangial cells. Indeed, glucose (>15 mM glucose) increased cAMP formation. In conclusion, high glucose stimulates IGF-I and IGF-II secretion via cAMP/PKA pathway in mesangial cells.

• Analytical Science and Technology
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• v.13 no.3
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• pp.399-402
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• 2000

To determine the concentrations of microcystins present in lake water or in tap water using high performance liquid chromatography, it is necessary to concentrate a large volume of water samples (about 20 L) into very small volume (0.1-0.3 mL). Concentration can be conveniently done when disc type solid phase extraction (SPE) apparatus is used. Using this apparatus we have investigated the recovery rates of three kinds of microcystins, RR, YR, LR. The recovery rates were relatively low and the reproducibilities were not good either. It is expected, however, that the appropriate selection of the disc conditioning and eluting solvents and reproducible reconcentration process after SPE will improve both the recovery rates and the reproducibilities.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.77.3-78
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• 2003

We previously shown that sphingosylphosphorylcholine, a lysophosphatidic acid, produced contraction in isolated single cells of cat ilium. We investigated the mechanism of sphingosine-1-phosphate (S1P)-induced contraction of circular smooth muscle cells in cat esophagus. S1P produced esophageal contraction in a dose dependent manner. The maximal contraction (l0$\^$-7/ M) induced at 1min. Pertusis toxin (PTX) inhibited contraction induced by S1P, suggesting that the contraction is mediated to a PTX-sensitive G-protein. (omitted)

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.91-91
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• 2003

We have studied the mechanism of action of TCDD on CYP1A1 promoter activity in both Hepa I and MCF-7 cells using transient transfection system with plAl-Luc reporter gene. When HDAC inhibitors, such as trichostatin A, HC toxin and a novel HDAC inhibitor, IN2001 were cotreated with TCDD to the cells transfected with plAl-Luc reporter gene, the basal promoter activity of CYP1A1 was increased by HDAC inhibitors. Also, in MCF-7 human breast cancer cells, HDAC inhibitors, such as IN2001 and trichostatin A increased the basal activity of CYP1A1 promoter but TCDD stimulated CYP1A1 promoter activity was not changed by HDAC inhibitors. And, in stably-transfected Hepa I cells with plAl-Luc, HDAC inhibitors increased the basal promoter activity only.

• Journal of Environmental Health Sciences
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• v.29 no.1
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• pp.74-83
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• 2003

Microcystin, stable compounds with circular heptapeptides, is presented inside cyanobacterial cell. So far, over 30 types have been known to exist and microcystin-LR, RR among them are the most potent toxin compound. By this reason, a strong oxidant, ozone was used in this study to remove the microcystins produced by cyanobacteria. Removal efficiency of microcystin at M water treatment plant was also evaluated. Microcystin concentration was determined by protein phosphatase inhibition assay. The results showed that dissolved microcystin in raw water detected in the range of 0.011-0.028 ㎍ Microcystin-RR equivalent/l. Above 98% of microcystin was removed through overall treatment system. Therefore, the water treatability of M treatment plant seemed to be excellent. Removal efficiency of microcystin according to unit process varied as characteristics of raw water such as DOC, UV/sub 254/ and turbidity. Removal efficiency of microcystin by ozonation was investigated in laboratory according to contact time and ozone dose. Dissolved microcystin was increased by twice fold according to ozone contact time, but increased by fifth fold according to ozone dose. So, changing of ozone dose more affected microcystin release than changing of ozone contact time. Behavior of microcystin by ozonation was similar to that of DOC, and residual ozone concentration gave influence to removal ratio of microcystin. In conclusion, single ozone treatment wasn't effective on microcystin removal in case of water containing a lot of cells. Therefore, it's more effective to use ozonation process after the removal of cyanobacterial cells in advance.