• Journal of Life Science
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• v.25 no.2
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• pp.237-242
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• 2015

The use of calcite-forming bacteria (CFB) in crack remediation and durability improvements in construction materials creates a permanent and environmentally-friendly material. Therefore, research into this type of application is stimulating interdisciplinary studies between microbiology and architectural engineering. However, the mechanisms giving rise to these materials are dependent on calcite precipitation by the metabolism of the CFB, which raises concerns about possible hazards to cement-based construction due to microbial metabolic acid production. The aim of this study was to determine target microorganisms that possibly can have bio-corrosive effects on cement mortar and to assess multi-functional CFBs for their safe application to cement structures. The chalky test was first used to evaluate the $CaCO_3$ solubilization feature of construction sites by fungi, yeast, bacterial strains. Not all bacterial strains are able to solubilize $CaCO_3$, but C. sphaerospermum KNUC253 or P. prolifica KNUC263 showed $CaCO_3$ solubilization activity. Therefore, these two strains were identified as target microorganisms that require control in cement structures. The registered patented strains Bacillus aryabhatti KNUC205, Arthrobacter nicotianae KNUC2100, B. thuringiensis KNUC2103 and Stenotrophomonas maltophilia KNUC2106, reported as multifunctional CFB (fungal growth inhibition, crack remediation, and water permeability reduction of cement surfaces) and isolated from Dokdo or construction site were unable to solubilize $CaCO_3$. Notably, B. aryabhatti KNUC205 and A. nicotianae KNUC2100 could not hydrolyze cellulose or protein, which can be the major constituent macromolecules of internal materials for buildings. These results show that several reported multi-functional CFB can be applied to cement structures or diverse building environments without corrosive or bio-deteriorative risks.

• The korean journal of orthodontics
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• v.27 no.2
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• pp.349-357
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• 1997

Epidermal growth factor(EGF), a single chain polypeptide of 53 amino acids with a molecular weight of 6,045 Da, was first isolated from the male mouse submandibular glands. EGF stimulates cellular proliferation and differentiation in several tissues and accelerates the rate of wound healing. EGF is bound to the specific receptor(EGFR) on the cell membrane of its target cell. EGFR is a transmembrane glycoprotein with a molecular weight of 170,000 Da and is detectable on a large variety of cell types and tissues. The authors investigated the expression of EGFR in the normal and inflamed human gingival epithelium to study the role of EGFR in the inflammation of the gingival epithelium, and the expression of EGFR in the dental follicle by using in situ mRNA hybridization and immunohistochenistry. The results weree as follows : 1. The expression of EGFR mRNA in the normal gingival epithelium on in situ mRNA hybridization was mainly localized on the basal cell layer, and the spinous layer was weakly positive The granular and cornified layers were negative 2. The expression of EGFR protein in the normal gingival epithelium on inmunohistochemistry was localized on the cornified and granular layers, and the spinous layer was weakly positive. The basal cell layer was completely negative 3. The expression of EGFR mRNA in the inflamed gingival epithelium on in situ mRNA hybridization was evenly and homogeneously distributed in the whole layers of the gingival epithelium except the cornified layer. The staining intensity appeared to increase progressively from the basal cell layer to the cornified layer. 4. The expression of EGFR protein in the inflamed gingival epithelium on immunohistochemistry was evenly and homogeneously distributed in the whole layers of the gingival epithelium. The staining intensity appeared to increase progressively from the cornified layer to the basal cell layer. 5. Strong positive reaction was seen in the epithelial cell rests of Malassez, whereas only background staining was seen in other cells of the dental follicle. In conclusion, the up-regulation of EGFR in the inflamed gingival epithelium and the high amounts of EGFR in the epthelial cell rests of Malassez in the dental follicle can be regarded as responses to the possible damages to the oral environment to maintain the homeostatic conditions.

• Microbiology and Biotechnology Letters
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• v.29 no.3
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• pp.181-185
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• 2001

The naturally occurring chemical indole-3-carbinol (13C), found in vegetables of the Brassica genus, is a promising anticancer agent that was shown previ- ously to induce a Gl cell cycle arrest of human breast cancer cell lines, independent of estrogen receptor signaling. The anticancer activity of 13C and the possible mechanisms of its action were explored in a human hepatocellular carcinoma cell line, HepG2. Treatment of HepG2 cells with 13C suppressed the growth of the cells. The growth sup- pression caused by 13C ($IC_{50}$/: 444$\mu$M) was found to be partially due to its ability to stop the cell cycle in HepG2 cells. Western blot analysis for the Gl phase artiest demonstrated that the expression-levels of cyclin-dependent kinase (Cdk4, Cdk6) and cyclic D were reduced strongly after treatment of Hep72 cells with 13C (4007M) for 24- 72 hrs. Furthermore, I3C selectively abolished the expression of Cdk6 in a dose- and time-dependent manner, and accordingly, inhibited the phosphorylation of retinoblastoma. Interestingly, after the HepG2 cells reached their max- imal growth arrest, the level of the p21, a well-known Cdk inhibitor, increased significantly. Therefore, it could be considered that the Gl arrest of HepG2 cells treated with 13C was due to the indirect inhibition of Cdk4/6 activities by p21 Western blot analysis for G2/M phase arrest of demonstrated the levels of Cdc2 and cyclin Bl werer reduced dramatically after the treatment of HepG2 cells with 13C ($40\mu$M) for 24-72 hrs. flow cytometry of propidium iodide-stained HepG2 cells revealed that 13C induces a Gl (53%,72hr incubation) and G2 (25%,24hr incubation) cell cycle arrest. Thus, our observations have uncovered a previously undefined antiproliferative pathway for r3C that implicates Cdk4/6 and Cdc2 as a target for cell cycle control in human HepG2 cells. However, the 13C-medi- ated cell cycle arrest and repression of Cdk4/6 production did not affect the apoptotic induction of HepG2 cell.

• Radiation Oncology Journal
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• v.21 no.4
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• pp.306-314
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• 2003

Purpose : In our Previous study, we have shown the main cel1 death pattern Induced by irradiation or protein tyrosine kinase (PTK) inhibitors in K562 human myeiogenous leukemic cell line. Death of the cells treated with irradiation alone was characterized by mitotic catastrophe and typical radiation-induced apoptosis was accelerated by herblmycin A (HMA). Both types of cell death were inhibited by genistein. In this study, we investigated the effects of HMA and genistein on cell cycle regulation and its correlation with the alterations of radiation-induced cell death. Materials and Methods: K562 cells In exponential growth phase were used for this study. The cells were Irradiated with 10 Gy using 6 MeV Linac (200-300 cGy/min). Immediately after irradiation, cells were treated with 250 nM of HMA or 25 $\mu$N of genistein. The distributions of cell cycle, the expressions of cell cycle-related protein, the activities of cyclin-dependent kinase, and the yield of senescence and differentiation were analyzed. Results: X-irradiated cells were arrested In the G2 phase of the cell cycle but unlike the p53-positive cells, they were not able to sustain the cell cycle arrest. An accumulation of cells in G2 phase of first ceil-cycle post-treatment and an increase of cyclin Bl were correlated with spontaneous, premature, chromosome condensation and mitotic catastrophe. HMA induced rapid G2 checkpoint abrogation and concomitant p53-independent Gl accumulation. HMA-induced cell cycle modifications correlated with the increase of CDK2 kinase activity, the decrease of the expressions of cyclins I and A and of CDK2 kinase activity, and the enhancement of radiation-induced apoptosis. Genistein maintained cells that were arrested in the G2-phase, decreased the expressions of cyclin Bl and cdc25c and cdc25C kinase activity, increased the expression of pl6, and sustained senescence and megakaryocytic differentiation. Conclusion: The effects of HMA and genistein on the radiation-induced cell death of KS62 cells were closely related to the cell cycle regulatory activities. In this study, we present a unique and reproducible model in which for investigating the mechanisms of various, radiation-induced, cancer cell death patterns. Further evaluation by using this model will provide a potent target for a new strategy of radiotherapy.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2659-2664
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• 2015

Background: To examine the expression of cysteine-rich 61 (Cyr61/CCN1) protein in laryngeal squamouscell carcinoma (LSCC) tissues, and its relationship with the tumor epithelial-mesenchymal transition (EMT), invasion, metastasis, and prognosis. Materials and Methods: Immunohistochemistry was used to detect the expressions of Cyr61, Vimentin (Vim), and E-cadherin (E-cad) in 88 cases of LSCC tissues and 30 cases of tumor-adjacent normal tissues. Vim and E-cad were used as mesenchymal and epithelial markers, respectively, to determine the relationship between Cyr61 expression and the EMT of LSCC cells. In addition, clinical and histopathological data were combined to analyze the relationship between the positive-expression rates of Cyr61, Vim and E-cad and LSCC invasion, metastasis and prognosis. Results: In LSCC tissues, Vim expression rate was significantly higher than that of the tumor-adjacent tissues, whereas E-cad expression rate was significantly lower than that of the tumor-adjacent tissues. The Vim expression rate was significantly higher in stages T3 and T4 than in stages T1 and T2 LSCC tissues, whereas E-cad expression rate was significantly lower in stages T3 and T4 than in stages T1 and T2 LSCC tissues. Compared to the group without lymph node metastasis, the Vim expression rate was significantly higher and the E-cad expression rate was significantly lower in the group with lymph node metastasis. The expression rate of Cyr61 was significantly higher in LSCC tissues than in the tumor-adjacent normal tissues. In addition, the Cyr61 expression rate was higher in stages T3 and T4 than in stages T1 and T2 LSCC, and higher in the group with lymph node metastasis than in the group without lymph node metastasis. The Vim expression rate was significantly higher in the Cyr61 positive group than in the Cyr61 negative group, whereas the E-cad expression rate was significantly higher in the Cyr61 negative group than in the Cyr61 positive group. Survival analysis indicated that survival rates of Cyr61 positive, Vim positive and E-cad negative groups were significantly lower than that of Cyr61 negative, Vim negative and E-cad positive groups, respectively. Conclusions: Cyr61 expression is closely associated with LSCC invasion and lymph node metastasis. Overexpression of Cyr61 may induce EMT and therefore leads to LSCC invasion and metastasis and poor prognosis. Cyr61 may become a new maker for clinical prediction of LSCC invasion and metastasis and a new target for LSCC treatment.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.32 no.3
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• pp.218-228
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• 2010

Components of dental resin-based restorative materials are reported to leach from the filling materials even after polymerization. Hydroquinone (HQ) is one of the major monomers used in the dental resin and is known as a carcinogen. Thus, carcinogenic risk of HQ leaching from the dental resin becomes a public health concern. The present study attempted to examine the carcinogenic potentials of HQ on the human epithelial cell, which is the target cell origin of the most of oral cancers. Cytotoxicity of HQ was observed above 50${\mu}M$ as measured by LDH assay, indicating a relatively low toxicity of this substance in human epithelial cells. The parameters of neoplastic cellular transformation such as cell saturation density, soft agar colony formation and cell aggregation were analyzed to examine the carcinogenic potential of HQ. The study showed that 2-week exposure of HQ showed the tendency of increase in the saturation density and the significant enhancement of soft agar colony formation at the highest dose, 50 ${\mu}M$ only. It is suggested that HQ has a weak potential of carcinogenicity. When cells were treated with HQ and TPA, a well-known tumor promoter, the parameters of neoplastic cellular transformation was significantly increased. This result indicates that the potential risk of carcinogenicity from HQ is largely dependent upon the presence of promoter. Exposure of 50 ${\mu}M$ HQ increased the time-dependent apoptosis as measured by the ELISA kit. This concentration coincides with a dose of neoplastic transformation, indicating a possible link between apoptosis and HQ-induced cellular transformation. Hydroquinone generated Reactive Oxygen Species (ROS) which was evidenced by the treatment of antioxidants such as trolox and N-acetyl cysteine and the GSH depleting agent, BSO. Antioxidants blocked the generation of ROS and the GSH depleting agent, BSO dramatically increased the ROS production. Since HQ is known to increase ROS production thru activation of transcriptional factor such as c-Myb and Pim-1, it is speculated that ROS generation by HQ plays a role in the activation of oncogene, which may lead to neoplastic transformation. In addition, ROS is involved in the alteration of signal transduction, which regulates the apoptosis in many cellular systems. Thus, ROS-mediated apoptosis may be involved in the HQ-induced carcinogenic processes. Protein kinase C (PKC) is known to play pivotal roles in neoplastic transformation of cells and its high expression is often found in a variety of types of tumors including oral cancer. PKC translocation of PKC-${\alpha}$ was observed following HQ exposure. Altered signaling system may also play a role in the transformation process. Taken together, HQ leached from the dental resin does not pose a significant threat as a cancer causing agent, but its carcinogenic potential can be significantly elevated in the presence of promoter. The mechanism of HQ-induced carcinogenesis involved ROS generation, apoptosis and altered signaling pathway. The present study will provide a valuable data to estimate the potential risk of HQ as a carcinogen and understand mechanism of HQ-induced carcinogenesis in human epithelial cells.

• Journal of Life Science
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• v.22 no.1
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• pp.41-48
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• 2012

Bee venom (BV) has been used in medicine to treat a variety of diseases including arthritis, rheumatism, and various cancers. Recent reports indicate that BV has anti-angiogenic effects, but the precise molecular mechanism underlying the effects of BV against colorectal cancer remains to be elucidated. We examined the effects of BV and its major components (melittin and apamin) on tumor angiogenesis and found that BV significantly decreased protein levels of hypoxia-inducible factor-$1{\alpha}$ (HIF-$1{\alpha}$), an important factor involved in angiogenesis and tumor progression, in human colorectal carcinoma HCT116 cells. BV also suppressed the transcription of HIF-$1{\alpha}$ under hypoxia, leading to a decrease in the expression of vascular endothelial growth factor (VEGF), a major target gene of HIF-$1{\alpha}$. We also found that these effects were mainly elicited by apamin, but not melittin. BV specifically inhibited the phosphorylation of ERK1/2 without changing the total levels of this protein, but had no effect on kinases of p38/JNK and AKT. Our results suggest that BV may inhibit human colorectal cancer progression and angiogenesis by inhibiting HIF-$1{\alpha}$ and VEGF expression, thereby providing a novel potential mechanism for the anticancer action of BV.

• Journal of Life Science
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• v.30 no.11
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• pp.999-1006
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• 2020

The suppression of neuroinflammatory responses in microglial cells, well known as the main immune cells in the central nervous system (CNS), are considered a key target for improving the progression of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Teleogryllus emma is widely consumed around the world for its broad-spectrum therapeutic effect. In a previous work, we performed transcriptome analysis on T. emma in order to obtain the diversity and activity of its antimicrobial peptides (AMPs). AMPs are found in a variety of species, from microorganisms to mammals. They have received much attention as candidates oftherapeutic drugs for the treatment of inflammation-associated diseases. In this study, we investigated the anti-neuroinflammatory effect of Teleogryllusine (VKWKRLNNNKVLQKIYFVKI-NH₂) derived from T. emma on lipopolysaccharide (LPS) induced BV-2 microglia cells. Teleogryllusine significantly inhibited nitric oxide (NO) production without cytotoxicity, and reducing pro-inflammatory enzymes expression such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In addition, Telegryllusine also inhibited the expression of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) through down-regulation of the mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) signaling pathway. These results suggest that T. emma-derived Teleogryllusine could be a good source of functional substances that prevent neuroinflammation and neurodegenerative diseases.

• Journal of Aquaculture
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• v.17 no.4
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• pp.275-281
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• 2004

The present study was conducted to evaluate dietary requirements for essential fatty acids (EFAs) such as linoleic acid (LA, l8:2n-6), -lenolenic acid (LNA, 18:3n-3), or docosahexaenoic acid (DHA, 22:6n-3), eicosapentaenoic acid (EPA, 20:5n-3) and arachidonic acid (ARA, 20:4n-6) in juvenile eel Anguilla japonica cultured in a recirculating system for 16 weeks. The experimental diets contained 50% crude protein, 10% crude lipid and 3800 kcal/kg energy.Brown fish meal and blood meal were used as the main protein sources, while coconut oil, com oil and linseed oil were used as the lipid source to yield target fatty acids ratios. At the end of the trial, the effects of essential fatty acids supplementation on weight gain (WG), specific growth rate (SGR), feeding efficiency (FE), proximate composition andwhole body fatty acids contents were examined. WG, SGR, and FEof eels fed diet D2, D3, was significantly higher (P<0.05) than those of fish fed the other diets. Whole body HUFA concentration of eels fed D 1 was significantly lower (P<0.05) than those fed the other diets. HUFA/SFA (saturated fatty acids) ratio of whole body in eels fed diets D2, D3 and D6 were significantly higher than that of eels fed diet D1 (P<0.05).DHA/EPA ratio of whole body in eels fed diet D7was significantly higher than those fed the other diets; and eels fed diet D5 showed the lowest DHA/EPA ratio among all the dietary treatments (P<0.05).Based on the experimental results, we concluded that LNA (n-3) and LA (n-6) were necessary for optimum growth of juvenile eel, and the dietary requirement of LNA and LA were 0.35∼0.5% and 0.5∼0.65%, respectively.

• Journal of Life Science
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• v.25 no.4
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• pp.463-472
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• 2015

Adrenomedullin (AM) is a peptide expressed in all body tissues, and its related receptors are increased in liver fibrosis. In this study, we evaluated the effect of AM deficiency on liver fibrogenesis induced by $CCl_4$ using AM heterozygous (HT) mice. The animals received a single injection of $CCl_4$ or olive oil for the acute experiment, and received $CCl_4$ or olive oil three times a week for 6 weeks for the chronic experiment. Fibrosis was accessed using histopathological analysis and the western blot. The AM HT mice showed mild pericentrilobular degeneration when compared to the AM wild type (WT) mice. In the acute experiment, there was no significant difference between the AM WT and AM HT mice. However, in the chronic experiment, the $CCl_4$-treated AM HT mice showed more severe liver fibrosis than that of the CCl₄-treated AM WT mice. The AST and ALT levels of the AM HT $CCl_4$ group were higher than those of the AM WT CCl₄ group. Additionally, the collagen deposition, $\alpha$- SMA protein and TGF-$\beta$ protein were increased in the AM HT $CCl_4$ group when compared to the AM WT $CCl_4$ group. The AM HT mice also exhibited severe lipid peroxidation through the GSH decrement. Taken together, our data suggest that AM deficiency increases the susceptibility to liver fibrosis induced by $CCl_4$, indicating a novel therapeutic target for patients with liver fibrosis.