• Journal of Korean Society of Water and Wastewater
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• v.25 no.3
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• pp.399-405
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• 2011

In a desalination technology using RO membranes, chemical cleaning makes damage for membrane surface and membrane life be shortened. In this research cleaning technology using direct osmosis (DO) was introduced to apply it under the condition of high pH and high concentration of feed. When the high concentration of feed is injected to the concentrate side after release of operating pressure, then backward flow occurred from treated water toward concentrated for osmotic pressure. This flow reduces fouling on the membrane surface. Namely, flux of DO was monitored under pH 3, 5, 10 and 12 conditions at feed concentrations of NaCl 40,000 mg/L, 120,000 mg/L and 160,000 mg/L. As a result, DO flux in pH 12 increased about 21% than pH 3. DO cleaning was performed under the concentrate NaCl 160,000 mg/L of pH 12 during 20 minutes. Three kinds of synthetic feed water were used as concentrates. They consisted of organic, inorganic and seawater; chemicals of SiO2 (200 mg/L), humic acid (50 mg/L) sodium alginate (50 mg/L) and seawater. As a result, fluxes were recovered to 17% in organic fouling, 15% in inorganic fouling and 14% of seawater fouling after cleaning using DO under the condition of concentrate NaCl 160,000 mg/L of pH 12.

• Asian-Australasian Journal of Animal Sciences
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• v.25 no.7
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• pp.1021-1028
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• 2012

Peripheral blood mononuclear cells (PBMCs) discriminate microbial pathogens and induce T-cell responses of appropriate effector phenotype accordingly. Toll-like receptors (TLRs), in part, mediate this microbial recognition and differentiation while the development of T-cell effector functions critically depends on the release of Th1- or Th2- type cytokines. In the present study, buffalo PBMCs were stimulated under in vitro culture conditions by Bacillus subtilis cell wall petidoglycan, a TLR2 ligand, in a dose- and time- dependent manner. The expression of TLR2 as well as the subsequent differential induction of the Th1 and Th2 type cytokines was measured. Stimulation was analyzed across five doses of peptidoglycan ($10{\mu}g/ml$, $20{\mu}g/ml$, $30{\mu}g/ml$, $40{\mu}g/ml$ and $50{\mu}g/ml$) for 3 h, 12 h, 24 h and 36 h incubation periods. We observed the induction of TLR2 expression in a dose- and time-dependent manner and the peptidoglycan induced tolerance beyond $30{\mu}g/ml$ dose at all incubation periods. The correlation between peptidoglycan stimulation and TLR2 induction was found positive at all doses and for all incubation periods. Increased production of all the cytokines was observed at low doses for 3 h incubation, but the expression of IL-4 was relatively higher than IL-12 at the higher antigen doses, indicating tailoring towards Th2 response. At 12 h incubation, there was a pronounced decrease in IL-4 and IL-10 expression relative to IL-12 in a dose- dependent manner, indicating skewing to Th1 polarization. The expression of IL-12 was highest for all doses across all the incubation intervals at 24 h incubation, indicating Th1 polarization. The relative expression of TNF-${\alpha}$ and IFN-${\gamma}$ was also higher while that of IL-4 and IL-10 showed a decrease. For 36 h incubation, at low doses, relative increase in the expression of IL-4 and IL-10 was observed which decreased at higher doses, as did the expression of all other cytokines. The exhaustion of cytokine production at 36 h indicated that PBMCs became refractory to further stimulation. It can be concluded from this study that the cytokine response to sPGN initially was of Th2 type which skews, more pronouncedly, to Th1 type with time till the cells become refractory to further stimulation.

• Biomolecules & Therapeutics
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• v.23 no.1
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• pp.84-89
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• 2015

We investigated the question of whether 7-oxygenated cholesterol derivatives could affect inflammatory and/or immune responses in atherosclerosis by examining their effects on expression of IL-23 in monocytic cells. $7{\alpha}$-Hydroxycholesterol ($7{\alpha}OHChol$) induced transcription of the TLR6 gene and elevated the level of cell surface TLR6 protein in THP-1 monocytic cells. Addition of an agonist of TLR6, FSL-1, to TLR6-expressing cells by treatment with $7{\alpha}OHChol$ resulted in enhanced production of IL-23 and transcription of genes encoding the IL-23 subunit ${\alpha}$ (p19) and the IL-12 subunit ${\beta}$ (p40). However, treatment with 7-ketocholesterol (7K) and $7{\beta}$-hydroxycholesterol ($7{\beta}OHChol$) did not affect TLR6 expression, and addition of FSL-1 to cells treated with either 7K or $7{\beta}OHChol$ did not influence transcription of the genes. Pharmacological inhibition of ERK, Akt, or PI3K resulted in attenuated transcription of TLR6 induced by $7{\alpha}OHChol$ as well as secretion of IL-23 enhanced by $7{\alpha}OHChol$ plus FSL-1. Inhibition of p38 MAPK or JNK resulted in attenuated secretion of IL-23. These results indicate that a certain type of 7-oxygenated cholesterol like $7{\alpha}OHChol$ can elicit TLR6-mediated expression of IL-23 by monocytic cells via PI3K/Akt and MAPKs pathways.

• Journal of Yeungnam Medical Science
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• v.23 no.1
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• pp.26-35
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• 2006

Background: Luteolin, a flavone found in various Chinese herbal medicines is known to possess anti-inflammatory properties through its ability to inhibit various proinflammatory signaling pathways including NF-${\kappa}B$ and p38 MAPK. In this study, we investigated the potential therapeutic effect of luteolin on dextran sodium sulfate (DSS)-induced colitis. Materials and Methods: We used a transgenic mouse model expressing the enhanced green fluorescent protein (EGFP) under the transcriptional control of NF-${\kappa}B$ $cis$-elements. C57BL/6 NF-${\kappa}B^{EGFP}$ mice received 2.5% DSS in their drinking water for six days in combination with daily luteolin administration (1mg/kg body weight, 0.1ml vol, intragastric) or vehicle. NF-${\kappa}B$ activity was assessed macroscopically with a Charge-Coupled Device (CCD) camera and microscopically by confocal analysis. Results: A significant increase in the Disease Activity Index (DAI), histological score (p<0.05), IL-12 p40 secretion in colonic stripe culture (p<0.05) and EGFP expression was observed in luteolin and/or DSS-treated mice compared to water-treated mice. Interestingly, a trend toward a worse colitis (DAI, IL-12p40) was observed in luteolin-treated mice compared to non-treated DSS-exposed mice. In addition, EGFP expression (NF-${\kappa}B$ activity) strongly increased in the luteolin-treated mice compared to control mice. Confocal microscopy showed that EGFP positive cells were primarily lamina propria immune cells. Conclusions: These results suggest that luteolin is not a therapeutic alternative for intestinal inflammatory disorders derived for primary defects in barrier function. Thus, therapeutic intervention targeting these signaling pathways should be viewed with caution.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.46 no.2
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• pp.78-83
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• 2001

Two rice cultivars of the japonica type, ozone-resistant Ilpumbyeo (IL) and ozone-susceptible Keu-mobyeo#l (KM) were exposed to ozone ($O_3$) at 0.15 ppm for 30 days. The available nutrient regimes were varied by doubling the supply of nitrogen (N), phosphorus (P) and potassium (K) within a basic fertilizer status (N, P, K; 15, 12, 12 kg l0$a^{-1}$). There was little difference on plant height between ozone-treated and nontreated plants. The most significant ozone stress on tiller number was shown on the 30th day of ozone exposure. Slight recovery from ozone stress was noted on the 60th day. On the 30th day, tiller number was greatly decreased by 40.8% in IL and 64.6% in KM, whereas at a high nitrogen supply regime (2N), it was decreased by 21.4% in IL and 42.7% in KM as compared to the control not treated with ozone at basic fertilizer status. The inhibition of tiller production caused by ozone exposure was alleviated on the 60th day. In both cultivars, number of spikelets per plant and weight of 100 grains were affected little by the ozone treatment irrespective of nutrient regime. However, the number of panicles per plant and yield were reduced significantly. In both cultivars, yield of ozone-treated plants with 2N status was 12.4-16.1 % higher than that of the ozone-treated plants with basic nutrient status. A significant yield decrease of 47.8% and 33.4% was observed for IL and KM, respectively, in ozone-treated plants with higher potassium (2K) status.

• Clinical and Experimental Pediatrics
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• v.53 no.12
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• pp.1000-1005
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• 2010

Purpose: This study aimed to determine the optimal initial vancomycin dose to achieve appropriate trough levels in pediatric patients. Methods: We analyzed clinical data for 309 children treated with intravenous vancomycin between 2004 and 2009 at 2 different hospitals in South Korea. The patients were 1-16 years old and exhibited normal renal function. Patient data, including reason for treatment and initial dosing regimen, were reviewed. Two subgroups were identified and compared according to initial vancomycin dose: 40 (35-45) mg/kg/day and 60 (55-65) mg/kg/day. Trough levels were obtained at steady state after at least 4 doses of vancomycin. Results: Patients who received vancomycin had post-operation or wound-related infections (37.2%), localized infection (12.9%), catheter-related infections (9.4%), meningitis (8.7%), or endocarditis (6.8%). Pathogens were confirmed in 79 cases: 28 cases of methicillin-resistant $Staphylococcus$ $epidermidis$ (35.4%) and 25 of methicillin-resistant $Staphylococcus$ $aureus$ (31.6%). Out of the 309 patients, 201 (65%) received vancomycin at 40 mg/kg/day and 108 (35%) at 60 mg/kg/day. Average trough concentrations were significantly different between the groups ($P$<0.001). Trough levels over 10 mg/L were less likely to be achieved in the 40 mg/kg/day group (14%) than in the 60 mg/kg/day group (49%) ($P$<0.001). There were no differences in renal function deterioration between the groups. Conclusion: A common vancomycin dosing regimen, 40 mg/kg/day, was not high enough to achieve trough levels of over 10 mg/L in pediatric patients. Careful drug monitoring must be performed, and increasing initial dose of vancomycin should be considered in pediatric patients.

• International Journal of Oral Biology
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• v.42 no.3
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• pp.117-121
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• 2017

We have previously shown that the specific phosphatidylinositol 3-kinase inhibitor LY294002 (LY29), and its inactive analog LY303511 (LY30), inhibit a monocyte chemoattractant protein-1 (MCP-1) expression in human umbilical vein endothelial cells; these results suggest the potential of LY30 as an anti-inflammatory drug. In this study, we determined the effects of LY30 on the production of various inflammatory cytokines in human macrophagic THP-1 cells which were stimulated with lipopolysaccharide (LPS). LY30 selectively suppressed the mRNA expression of IL-12 p40, $TNF-{\alpha}$, and MCP-1 without affecting the expression of $IL-1{\alpha}$, IL-6, and IL-8. Inhibition of the production of IL-12 and $TNF-{\alpha}$ by LY30 was also demonstrated using ELISA assays. In order to elucidate the mechanisms of the action of LY30, we examined the role played by the mitogen-activated protein kinases and the key transcription factors, AP-1 and $NF-{\kappa}B$ in LPS-stimulated THP-1 cells. The results revealed that LY30 inhibited LPS-induced activation of ERK, but not p38 or JNK. Furthermore, the AP-1 DNA binding activity was suppressed by LY30 based upon the dosage, whereas $NF-{\kappa}B$ DNA binding was not affected. These results suggest that LY30 selectively inhibits cytokine production in the LPS-stimulated macrophagic THP-1 cells by down-regulating the activation of ERK and AP-1.

• Journal of Microbiology
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• v.40 no.4
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• pp.331-334
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• 2002

The substance 0116p, which exhibits cytotoxicity against human macrophage cell line THP-1, was isolated from a mycelial extract of Streptomyces scabiei subsp. chosunensis M0137. The cytotoxic substance was purified by Diaion-HP2O adsorption, solvent extraction, Sephadex LH-20 column chromatography, and silica-gel column chromatography. The molecular formula is C$\_$19/H$\_$38/O$\_$2/ (MW301.10) based on elemental and spectrometric analysis. It was identified as nonadecanoic acid by NMR spectral data. It exhibits cytotoxic activities in various human cancer cell lines, including A549, SK-OV-3, SK-MEL-2 and HCT-15. In addition, 0116p also inhibits IL-12 production in lipopolysaccharide-activated macrophages.

• Toxicological Research
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• v.14 no.4
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• pp.465-474
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• 1998

This study was examined on the effect of ex-vivo immunotherapy in 7, 12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary carcinogenesis. Sprague-Dawley female 40 rats were divided into Jour groups. As a positive control, Group I was intubated with DMBA, 5 mg /100 g body weight and single dose, at experimental onset. Group II was treated ex-vivo immunotherapy with polyinosinic-polycytidylic acid (Poly I : C) and Group III was treated with Interleukin-2 (IL-2). Group IV was negative control. All rats were sacrificed at 16 weeks after DMBA intubation. Mammary gland wet weight, dry fat free tissue weight, incidence of tumor, and the number of lobules, alveolar buds, terminal end buds, and terminal ducts were examined. Morphological changes of the mammary gland after treated with DMBA were analyzed by whole mount and histopathological method. As results, the induced mammary tumors of Group I, II and III were 60%, 33% and 0%, respectively. Histopathological types of induced-mammary tumors were adenoma, adenocarcinoma and carcinosarcoma. In analysis of the whole mount method, the number of the terminal end buds, terminal ducts and lobules were significantly lower in Group II (p<0.01) and III (p<0.01) than DMBA alone treated Group I. In microscopic observation, hyperplastic alveolar nodules were significantly lower in Group III than Group I (p<0.01). In conclusion, IL-2 had strong inhibitory effect on the mammary gland tumorigenesis induced by DMBA in rats. Whole mount method may be a useful technique to assess the mammary carcinogenesis. Moreover, hyperplastic alveolar nodules were very sensitive parameter to assess the mammary carcinogenesis.

• Molecules and Cells
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• v.23 no.2
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• pp.198-206
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• 2007

Hydroquinone is a toxic compound and a major benzene metabolite. We report that it strongly inhibits the activation of macrophages and associated cells. Thus, it suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$, IL-3, IL-6, IL-10, IL-12p40, IL-23], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)] and the activation and expression of CD29 as judged by cell-cell adhesion and surface staining experiments. The inhibition was due to the induction of heme oxygenase (HO)-1 in LPS-activated macrophages, since blocking HO-1 activity with ZnPP, an HO-1 specific inhibitor, abolished hydroquinone's NO inhibitory activity. In addition, hydroquinone and inhibitors (wortmannin and LY294002) of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway had very similar inhibitory effects on LPS-induced and CD29-mediated macrophage responses, including the phoshorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune responses by modulating intracellular signaling and protective mechanisms.