• Microbiology and Biotechnology Letters
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• v.44 no.4
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• pp.540-549
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• 2016

Plant residues serve as substrates for the proliferation and overwintering of plant pathogenic fungi in soil. Effects of the biocontrol fungus Trichoderma harzianum on the colonization of wheat straw by the plant pathogenic fungus Fusarium solani were investigated under different soil moisture regimes (-50 vs. -500 kPa) in non-sterile soil. T. harzianum ThzID1-M3 and/or F. solani were added along with wheat straw to non-sterile soils. ThzID1-M3, other Trichoderma species, and F. solani were monitored for a 21-day period using quantitative PCR. ThzID1-M3 reduced the colonization of F. solani on wheat straw (p < 0.05) under both moisture regimes, and F. solani reduced the colonization by ThzID1-M3 and other Trichoderma species (p < 0.05), thus suggesting competitive inhibition between ThzID1-M3 and F. solani. Colonization by ThzID1-M3 and generic Trichoderma was improved in the wet soil (p < 0.05), but colonization by F. solani did not differ between the two moisture conditions. Thus, the inhibitory effect of ThzID1-M3 was greater in the wet soil (p < 0.05). The growth competition between ThzID1-M3 and F. solani to colonize plant debris suggests that the biocontrol fungus T. harzianum may reduce the potential of the plant pathogen, F. solani, to survive and proliferate on crops.

• Journal of Korean Society of Environmental Engineers
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• v.28 no.2
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• pp.128-136
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• 2006

This study was conducted for developing the stability parameter in uncontrolled landfill by using a biomolecular investigation on the microbial community growing through leachate plume. Landfill J(which is in Cheonan) and landfill T(which is in Wonju) were chosen for this study among a total of 244 closed uncontrolled landfills. It addressed the genetic diversity of the microbial community in the leachate by 165 rDNA gene cloning using PCR and compared quantitative analysis of denitrifiers and methanotrophs with the conventional water quality parameters. From the BLAST search, genes of 47.6% in landfill J, and 32.5% in landfill T, respectively, showed more than 97% of the similarity where Proteobacteria phylum was most significantly observed. It showed that the numbers of denitrification genes, i.e. nirS gene and cnorB gene in the J site are 7 and 4 times higher than those in T site, which is well reflecting from a difference of site closure showing 7 and 13 years after being closed, respectively. In addition, the quantitative analysis on methane formation gene showed that J1 spot immediately bordering with the sources has the greatest number of methane formation bacteria, and it was decreased rapidly according to distribute toward the outer boundary of landfill. The comparative investigation between the number of genes, i.e. nirS gene, cnorB gene and MCR gene, md the conventional monitoring parameters, i.e. TOC, $NH_3-N,\;NO_3-N,\;NO_2-N,\;Cl^-$, alkalinity, addressed that more than 99% of the correlation was observed except for the $NO_3-N$. It was concluded that biomolecular investigation was well consistent with the conventional monitoring parameters to interpret their influences and stability made by leachate plume formed in downgradient around the uncontrolled sites.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.3
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• pp.197-208
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• 2023

Dysregulation of certain long non-coding RNAs may facilitate tumor initiation and progression. However, numerous carcinogenesis-related long noncoding RNAs have not been characterized. The goal of this study was to elucidate the role of LINC00562 in gastric cancer (GC). The expression of LINC00562 was analyzed using real-time quantitative PCR and Western blotting. The proliferative capacity of GC cells was determined using Cell Counting Kit-8 and colony-formation assays. The migration of GC cells were evaluated using wound-healing assays. The apoptosis of GC cells was assessed by measuring the expression levels of apoptosis-related proteins (Bax and Bcl-2). Xenograft models in nude mice were constructed for in vivo functional analysis of LINC00562. The binding relationship between miR-4636 and LINC00562 or adaptor protein complex 1 sigma 3 (AP1S3), obtained from public databases, was confirmed using dual-luciferase and RNA-binding protein immunoprecipitation experiments. LINC00562 was expressed in GC cells at high levels. Knockdown of LINC00562 repressed GC cell growth and migration, promoted apoptosis in vitro, and inhibited tumor growth in nude mouse models. LINC00562 directly targeted miR-4636, and miR-4636 depletion restored the GC cell behavior inhibited by LINC00562 absence. AP1S3, an oncogene, binds to miR-4636. MiR-4636 downregulation increased AP1S3 level, restoring GC cell malignant behaviors inhibited by AP1S3 downregulation. Thus, LINC00562 exerts carcinogenic effects on GC development by targeting miR-4636-mediated AP1S3 signaling.

• Journal of Life Science
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• v.15 no.1 s.68
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• pp.38-44
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• 2005

Infection with hepatitis B virus (HBV) is a major health problem worldwide. Although a tremendous amount has been known about HBV, there have been obstacles in the study of HBV due to the narrow host range of HBV limited to humans and primates. In the present study, we investigated the susceptibility to HBV infection of mouse hepatoma cell line, Hepa-1c1c7. In addition, based on that human hepatocytes infected by HBV increase the expression of the pro-inflammatory cytokine TNF-a, the inducibility of TNF-a expression by HBV in the cells was determined. HBV surface antigen (HBsAg) secretion was measured by the microparticle enzyme immunoassay and steady state mRNA expression was analyzed by quantitative competitive RT-PCR. Transient transfection of Hepa-1c1c7 cells with HBV expression vector resulted in a dose-dependent induction of TNF-a expression. Infection of Hepa-1c1c7 cells with the serum of HBV carrier also increased TNF-a mRNA expression. Both in the transfected and infected cells, HBV mRNA was expressed and significant HBsAg secretion was detected. There was no significant variation in $\beta-actin$ mRNA expression by HBV. These results demonstrate that HBV is infectious to Hepa-lc1c7 in vitro and the viral infection induces TNF-a expression, which suggests that Hepa-lc1c7, a mouse hepatoma cell line, may be a possible model system for analysis of various molecular aspects of HBV infection.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.32 no.1
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• pp.8-18
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• 2006

Purpose: The purpose of this study was to verify that the expressions of angiogenin, transforming growth factor-beta(TGF-${\beta}$), vascular endothelial growth factor(VEGF), human apurinic/apyrimidinic endonuclease(APEX) and tumor necrosis factor-alpha(TNF-${\alpha}$) were associated with the tumorigenesis of the oral squamous cell carcinoma(OSCC). Materials and Methods: Fifty-one samples of OSCC and fifteen normal oral mucosae were obtained to analyze the expression levels of above five factors. mRNA expressions were quantified by the quantitative competitive PCR(QC-PCR) method. After 2% agarose gel electrophoresis stained with ethidium bromide, the concentration of mRNA was calculated by a digital image analysis system. The expression levels of angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ were compared by unpaired Student's t-tests between cancer and normal tissues. We analyzed statistically to find the cut-off values that would be useful as diagnostic markers, and the linear regression analysis between every two factors of these five factors by SAS system. Results: All of these five factors (angiogenin: P<0.0037, TGF-${\beta}$: P<0.0001, VEGF: P<0.0102, APEX: P<0.0023, TNF-${\alpha}$: P<0.0074) were significantly correlated with OSCC. In the analysis to find the cut-off values for the diagnosis, we could not find any value that had a reasonable sensitivity and specificity. In the linear regression analysis, there were correlations between angiogenin and TNF-${\alpha}$, TGF-${\beta}$ and VEGF, TGF-${\beta}$ and APEX, TGF-${\beta}$ and TNF-${\alpha}$, VEGF and APEX, VEGF and TNF-${\alpha}$, APEX and TNF-${\alpha}$. Conclusion: Our results suggest that not only angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ are significantly associated with the tumorigenesis, but also the close relationship between these factors might enhance the tumorigenesis of OSCC. We can not find clinical availability for diagnosis.

• Clinical and Experimental Pediatrics
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• v.46 no.8
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• pp.795-802
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• 2003

Purpose : We investigated the hormonal control of OB gene expression and leptin secretion in cultured human visceral adipose tissue. Methods : Visceral adipose tissues were cultured for up to 48 hrs in modified Eagle's medium with varying concentration of hormones : Control(no hormone), bovine insulin(100 nM), Dexamethasone(DEX, 100 nM), growth hormone(GH, 40 ng/mL), insulin+DEX(100 nM each), insulin+DEX+GH(100 nM insulin and DEX, 40 ng/mL GH). Quantitative analysis of leptin mRNA was performed by competitive reverse transcription polymerase chain reaction, and leptin secretion in culture medium was measured by IRMA using a commercial kit. Results : The addition of dexamethasone to the medium significantly increased OB gene expression and leptin secretion(P<0.05). Unlike dexamethasone, insulin did not affect OB gene expression and leptin secretion. Both insulin and dexamethasone, at high concentration, significantly stimulated leptin secretion compared with basal values(P<0.05). Leptin gene expression was not significantly increased by GH treatment alone, however GH, in combination with high concentrations of insulin and dexamethasone, attenuated the stimulatory effects of high concentrations of insulin and dexamethasone. Conclusion : Insulin cannot increase leptin secretion without the presence of dexamethasone. The mechanism suggested is that insulin may increase leptin secretion in cytoplasm only after dexamethasone increases the expression of OB gene. Further studies are necessary to elucidate the mechanism of the action of insulin on leptin secretion after increasing OB gene expression by dexamethasone.