• The Korean Journal of Pesticide Science
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• v.7 no.1
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• pp.32-37
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• 2003

Bacterial soft rot by Erwinia carotovora subsp. carotovora is one of the diseases causing the biggest problem in Chinese cabbage. Chemical screening was conducted to select effective agents for controlling bacterial soft rot. Control effect of antibiotics, plant activator, and Biokeeper (avirulent Erwinia) to soft rot were tested by in vitro assay, nursery test, and field experiment. The in vitro assay was done by paper disc method and potato slice method. The nursery test was performed by using mineral oil inoculation method with consistent disease induction. The in vitro assay showed that streptomycin, oxolinic acid, bronopol, and copper hydroxide significantly suppressed the growth of pathogenic bacterium and the decomposition of potato slice. However, plant activators including acibenzolar-S-methyl did not show the suppressive effect on the growth of pathogenic bacterium and the decomposition of potato slice. When applied by the nursery test condition using mineral oil inoculation method with Chinese cabbage 'Kangruckyeurum', Biokeeper, oxolinic acid, antibiotics streptomycin, validamycin, and copper compound provided 83.5%, 95.2%, 91.2%, 57.5% and 79.9% in control efficacy, respectively. However, the control effect of acibenzolar-S-methyl showed to be low to cause phytotoxicity. Also acibenzolar-S-methyl showed a significant control effect in the field experiment with Chinese cabbage 'Sanchon' in 2000, but the field experiment with Chinese cabbage 'Kangruckyeurum' in 2001 revealed it had phytotoxicity to Chinese cabbage. Such a difference was considered to be caused by differences in phytotoxic reaction of Chinese cabbage cultivars to the chemical. Streptomycin+copper, copper hydroxide and Biokeeper showed 79.7%, 71.9% and 60.9% in control efficacy, respectively, in the field experiment with Chinese cabbage 'Sanchon' in 2002.

• Childhood Kidney Diseases
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• v.8 no.1
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• pp.26-32
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• 2004

Purpose : Hypercoagulability is present in patients with nephrotic syndrome. Plasminogen activator inhibitor type 1(PAI-1) is a major inhibitor of plasminogen activators. PAI-1 inactivates both tissue plasminogen activator(tPA) and urokinase plasminogen activator(uPA) by rapid formation of inactive 1:1 stoichiometric complexes. Recently some studies showed that the enhanced PAI-1 expression may be involved in the intraglomerular fibrinogen/fibrinrelated antigen deposition seen in nephrotic syndrome. Methods : PAI-1 gene promoter -844(G/A) polymorphism was evaluated in 146 children with minimal change nephrotic syndrome(MCNS) and 230 control subjects. The patients with MCNS were subdivided into 85 infrequent-relapser(IR) group and 61 frequent relapser(FR) group. PCR of PAI-1 gene promoter region including -844(G/A) and RFLP using the restriction enzyme Xhol were performed for each DNA samples extracted from the groups. Results : The distribution of PAI-1 genotype in the control group was G/G 81(32.5%), A/A 42(16.9%), and G/A 126(50.6%). The distribution of PAI-1 genotypes in the IR group of MCNS was G/G 29(34.1%), A/A 15(17.7%), and G/A 41(48.2%). The distribution of PAI-1 genotype in the FR group of MCNS was G/G 17(27.9%), A/A 18(29.5%), and G/A 26(42.6%). There was a significantly increased frequency of A/A genotype(P=0.0251) in the FR group of MCNS. Conclusion : Our results indicate that the PAI-1 gene promoter A/A genotype may be associated with the FR in MCNS.

• Journal of Chest Surgery
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• v.31 no.9
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• pp.873-876
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• 1998

Background: High-dose aprotinin has been reported to enhance the anticoagulant effects of heparin during cardiopulmonary bypass ; hence, som authors have advocated reducing the dose of heparin in patients treated with aprotinin. Material and Method: The ACT was measured before, during and after cardiopulmonary bypass, with Hemochron 801 system using two activators of celite(C-ACT) and kaolin(K- ACT) as surface activator. From June, 1996 to February, 1997, 22 adult patients who were scheduled for elective operation were enrolled in this study. Result: The ACT without heparin did not differ between C-ACT and K-ACT. At 30 minutes after anticoagulation with heparin and cardiopulmonary bypass, the average C-ACT was 928${\pm}$400 s; K-ACT was 572${\pm}$159s(p<0.05). After administration of protamine, C-ACT was 137${\pm}$26 s; K-ACT was 139${\pm}$28s, which were not statistically significant. Conclusion: Our results showed that the significant increase in the ACT during heparin- induced anticoagulation in the presence of aprotinin was due to the use of celite as surface activator, rather than due to enhanced anticoagulation of heparin by aprotinin. We conclude that the ACT measured with kaolin provides better monitoring of cardiac surgical patients treated with high dose aprotinin than does the ACT measured with celite. The patients treated with aprotinin should receive the usual doses of heparin.

• Journal of Life Science
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• v.30 no.12
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• pp.1092-1100
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• 2020

The six-transmembrane epithelial antigen of prostate 4 (Steap4) is a metalloreductase that plays a role in intracellular iron and cupper homeostasis, inflammatory response, and glucose and lipid metabolism. Previously, Steap4 has been reported to stimulate adipocyte differentiation; however, the underlying mechanisms of this action remain unexplored. In the present study, we investigated the molecular mechanisms involved in Steap4-induced adipocyte differentiation using 3T3-L1 cells, immortalized brown adipocyte (iBA) cells, and mouse embryonic fibroblast C3H10T1/2 cells. The knockdown of Steap4 using adenovirus-containing shRNA attenuated mitotic clonal expansion (MCE), as evidenced by the impaired proliferation of 3T3-L1 cells, iBA cells, and C3H10T1/2 cells within 48 hr after adding the differentiation medium. Steap4 knockdown downregulated G1/S phase transition-related cell cycle regulators (including cyclin A and cyclin D) and upregulated cell cycle inhibitors (including p21 and p27). Furthermore, Steap4 knockdown inhibited the phosphorylation of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, and Akt. Moreover, Steap4 knockdown repressed the expression of early adipogenic activators, such as CCAAT-enhancer-binding protein β (C/EBPβ) and Kruppel-like factor family factor 4 (KLF4). On the other hand, Steap4 knockdown stimulated the expression of adipogenic inhibitors, including KLF2, KLF3, and GATA2. The overexpression of Steap4 using an adenovirus removed the repressive histone marks H3K9me2 and H3K9me3 on the promoter of C/EBPβ. These results indicate that Stepa4 stimulates adipocyte differentiation through the induction of MCE and the modulation of early adipogenic transcription factors, including C/EBPβ, during the early phase of adipocyte differentiation.

• Journal of Life Science
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• v.32 no.11
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• pp.833-840
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• 2022

Chronic inflammation has been shown to be closely associated with tumor development and progression. Nuclear factor kappa B (NF-κB) is composed of a family of five transcription factors. NF-κB signaling plays a crucial role in the inflammatory response and is often found to be dysregulated in various types of cancer, making it an attractive target in cancer therapeutics. In this study, CDC-like kinase 3 (CLK3) was identified as a novel kinase that regulates the NF-κB signaling pathway. Our data demonstrate that CLK3 inhibits the canonical and non-canonical NF-κB pathways. Luciferase assays following the transient or stable expression of CLK3 indicated that this kinase inhibited NF-κB activation mediated by Tumor necrosis factor-alpha (TNFα) and Phorbol 12-myristate 13-acetate (PMA), which are known to activate NF-κB signaling via the canonical pathway. Consistent with data on the ectopic expression of CLK3, CLK3 knockdown using shRNA constructs increased NF-κB activity 1.5-fold upon stimulation with TNFα in HEK293 cells compared with the control cells. Additionally, overexpression of CLK3 suppressed the activation of this signaling pathway induced by NF-κB-inducing kinase (NIK) or CD40, which are well-established activators of the non-canonical pathway. To further examine the negative impact of CLK3 on NF-κB signaling, we performed Western blotting following the TNFα treatment to directly identify the molecular components of the NF-κB pathway that are affected by this kinase. Our results revealed that CLK3 mitigated the phosphorylation/activation of transforming growth factor-α-activated kinase 1 (TAK1), inhibitor of NF-κB kinase alpha/beta (IKKα/α), NF-κB p65 (RelA), NF-κB inhibitor alpha (IκBα), and Extracellular signal-regulated kinase 1/2-Mitogen-activated protein kinase (ERK1/2-MAPK), suggesting that CLK3 inhibits both the NF-κB and MAPK signaling activated by TNFα exposure. Further studies are required to elucidate the mechanism by which CLK3 inhibits the canonical and non-canonical NF-κB pathways. Collectively, these findings reveal CLK3 as a novel negative regulator of NF-κB signaling.