• Journal of the Korea Organic Resources Recycling Association
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• v.7 no.2
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• pp.25-34
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• 1999

The effects of copper on the anaerobic degradation of propionate were studied using anaerobic batch reactors. The apparent inhibitory effects of copper on the anaerobic degradation of propionate could be observed from behaviors of intermediates, ultimate methane yield(UMY) and specific methanogenic activity(SMA) There was little inhibition at the concentration of $2.5mg\;Cu^{2+}/L$. Beyond this concentration, the inhibitory effects increased with increasing dose of coppers. The 50% inhibition of UMY and SMA occurred at copper dosage of 33.8 and $24.1mg\;Cu^{2+}/gVSS$, respectively. The inhibitory effect based on the UMY was gradually reduced with the operation time dueprobably to the acclimation of microorganisms and/or binding of the added copper by ligands(and possibly ion exchange sites)contained on the cell membrane and extracellular polymer matrix whereas it based on the SMA might exclude the this phenomena. Therefore, the methodology for interpretation of inhibition data based on the SMA was more accurated than the UMY. There was no inhibitory effect in batch reactors supplemented with sulfate due to an antagonistic action of the sulfate reducing bacteria. Propionate degradation was initially retarded for copper inhibited samples but it gradually degraded afterward. Based on the mass removal considering take into account the propionate to acetate conversion, propionate degradation may appeal more affected than acetate. This result revealed that the hydrogenotrophic methanogens were the most affected by copper.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.3
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• pp.225-231
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• 1997

As it has been reported that the depolarization-induced norepinephrine (NE) release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor and various lines of evidence indicate the involvement of adenylate cyclase system in $A_1-adenosine$ post-receptor mechanism in hippocampus, it was attempted to delineate the role of adenylate cyclase system in the $A_1-receptor-mediated$ control of NE release in this study. Slices from rat hippocampus were equilibrated with $[^3H]-NE$ and the release of the labelled products was evoked by electrical stimulation.(3 Hz, $5Vcm^{-1}$, 2 ms, rectangular pulses). The influence of various agents on the evoked tritium-outflow was investigated. $N^6-Cyclopentyladenosine$ (CPA), a specific $A_1-adenosine$ receptor agonist, in concentrations Tanging from 0.1 to $10{\mu}M$ decreased the $[^3H]-NE$ release in a dose-dependent mauler without any change of basal rate of release. 8-Cyclopentyl-1,3-dipropylxanthine (DPCPX, $2{\mu}M$), a selective $A_1-receptor$ antagonist, inhibited the CPA effect. The responses to N-ethylmaleimide $(3&10{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked NE-release and the CPA effects were completely abolished by NEM pretreatment. Forskolin, a specific adenylate cyclase activator, in concentrations ranging from 0.1 to $30{\mu}M$ increased the evoked and basal rate of NE release in a dose-dependent manner and the CPA effects were inhibited by forskolin pretreatment. Rolipram $(1&10{\mu}M)$, a phosphodiesterase inhibitor, did not affect the evoked NE release but reduced the CPA effect. And 8-bromo-cAMP $(100&300{\mu}M)$, a membrane permeable cAMP analogue inhibited the CPA effect significantly. These results suggest that the $A_1-adenosine$ heteroreceptor plays an important role in NE-release via nucleotide-binding protein $G_i$ in the rat hippocampus and that the adenylate cyclase system might be participated in this process.

• Bulletin of the Korean Chemical Society
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• v.30 no.12
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• pp.2999-3005
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• 2009

Among the more than 120 different types of human papillomavirus (HPV), types 16 and 18 have been known to be high risk agents that cause cervical cancer. We examined, in an immuno-chromatographic analysis, the potential of using the early gene product, E7 protein, as a diagnostic marker of cervical cancer caused by HPV. We developed monoclonal antibodies specific to HPV-16 and 18 E7 proteins that were produced from bacterial cells using gene recombinant technology. For each E7 protein, the optimal antibody pair was selected using the immuno-chromatographic sandwichtype binding system based on the lateral flow through membrane pores. Under these conditions, this rapid testing assay had a detection capability as low as 2 ng/mL of E7 protein. Furthermore, since viral analysis required the host cell to be lysed using chemicals such as detergents, it was possible that the E7 protein was structurally damaged during this process, which would result in a decrease in detection sensitivity. Therefore, we examined the detrimental effects caused by different detergents on the E7 protein using HeLa cells as the host. In these experiments, we found that the damage caused by the detergent, nonylphenylpolyethylene glycol (NP-40), was minimal relative to Triton X-100 commonly used for the cell lysis. Temperature also affected the stability of the E7 protein, and we found that the E7 protein was stabilized at 4$^{\circ}C$ for about 2 h, which was 4 times longer than at room temperature. Finally, a HPV-infected cervical cancer cell line, which was used as a real sample model, was treated using the optimized conditions and the presence of E7 proteins were analyzed by immuno-chromatography. The results of this experiment demonstrated that this rapid test could specifically detect HPV-infected samples.

• Journal of Periodontal and Implant Science
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• v.37 no.4
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• pp.719-732
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• 2007

Purpose: Various bone graft materials are being used for periodontal tissue regeneration. Th materials are being developed continuously for ideal clinical effects. Therefore, it is necessary to identify the clinical characteristics of each bone graft material through comparing the various bone graft materials statistically and in doing so, proposing a more efficient bone graft material. In this study, the following results were attained through comparing the clinical effects among the bone graft materials, using the statistical method based on the clinical studies published at the department of periodontology of Yonsei hospital. Materials and Method: 6 selected studies of department of Periodontology at Yonsei University Hospital were based on clinical study of bone grafting in intrabony defects. It was compared the clinical parameters among the 6 clinical studies, using the statistical META analysis. Result: When comparing the probing depth reduction, there was a relatively great amount of decease when using the xenograft, Anorganic Bovine Derived Hydroxapatite Bone Matrix/Cell Binding Peptide(ABM/P-15: PepGen $P-15^{(R)}$) and the autogenous bone and absorbable membrane, d, 1-alctide/glycolide copolymer(GC: $Biomesh^{(R)}$). The allogfrafts showed a relatively low decrease in the probing depth and clinical attachment change. It also showed a slight decrease in the bone probing depth. The allografts showed various results according to different bone graft materials. When comparing the ABM/P-15 and bovine bone $powder(BBP^{(R)})$, ABM/P-15 showed a relatively high clinical attachment level and the bovine bone powder showed a relatively high clinical attachment level. The probing depth change and gingival recession change showed a lower value than the mean value between the two bone graft materials. The synthetic bone showed a relatively high decrease in clinical attachment level and periodontal probing depth change. There was a relatively larger amount of gingival recession when using Bioactive Glass(BG) but a relatively low bone regeneration effect was seen. Conclusion: Good restorative results of the periodontal tissue can be attained by applying the various bone graft materials being used today after identifying the accurate clinical effects.

• Korean Journal of Food Science and Technology
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• v.32 no.1
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• pp.218-224
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• 2000

The antimicrobial activities of chitosan oligosaccharide(chitohexaose) and two types of chitosans M.W.(10,000 and M.W. 100,000) were examined against Escherichia coli O157 : H7(ATCC 43894), Staphylococcus aureus(ATCC 144458) and Candida albicans(KFRI 432). Chitosan with molecular weight of 10,000 showed the strongest antimicrobial activities to E. coil O157 : H7 and S. aureus, whereas chitohexaose acted most strongly against C. albicans. The most effective concentration of chitosan was measured to be 0.1 mg/mL for E. coil O157 : H7 and S. aureus, and that of chitohexaose to be 1 mg/mL for C. albicans. Antimicrobial activities of chitosans and chitohexaose were maintained for 60 min after their treatment. They were found to induce leakage of intracellular proteins and nucleic acids from treated microorganisms. The efflux determined by assaying the ${\beta}-galactosidase$ leaked from the lactose-induced E. coli O157 : H7 cells was observed to reach the highest level within 60 min after treatment with the antimicrobial agents and chitosan with 10,000 molecular weight gave the highest ${\beta}-galactosidase$ activity. Therefore, it is supposed that the antimicrobial activity of chitosan with its unique polycationic nature might be caused by its binding to anionic component(s) of the cell envelope and thereby inhibiting the membrane metabolism and/or leaking intracellular materials.

• Applied Microscopy
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• v.30 no.1
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• pp.101-111
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• 2000

In this study, the distribution of lectin receptors in Paragonimus westermani tissue was explored using colloidal gold label complexed with lectin WGA purified from wheat germ (Triticum vulgare). The lectin WGA gold complex, shown to recognize GlcNAc (N-acetylgalactosamine) and NeuNAc (N-acetylneuraminic acid) regions, was applied to detect binding sites in Lowicryl HM 20 sections viewed under electron microscope. Labeled sections of the metacercaria revealed gold particles specifically distributed on the tegumental syncytium and lamella of the excretory canal. Labeling of young adult tissue was then quantified and compared to that of adult worm tissue. Adult worm tissue sections resulted in specific gold particle distribution on the lamella of caecal epithelium and excretory canal. These results indicate that lectin WGA receptors are located in the tegumental syncytium and lamella of the excretory canal of the metacercariae, and in the lamella of the caecum and excretory canal of the young adult and adult. Therefore, the GlcNAc and NeuNAc regions in the tegumental syncytium appear to be functionally associated with cell-recognition and protection from the immune system of the host, and linked with membrane transport and absorption of nutrients in the lamella of the excretaory canal and caecal epithelia.

• Journal of Life Science
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• v.26 no.7
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• pp.758-763
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• 2016

Fatty acid transporters are key mediators of skeletal muscle lipid metabolism. Several protein groups have been implicated in cellular long-chain fatty acid uptake or oxidation, including fatty acid transporter proteins (FATPs), the plasma membrane fatty acid-binding protein (FABPpm), and the fatty acid translocase (FAT/CD36). FAT/CD36 is highly expressed in skeletal muscle and known to be regulated by various factors such as exercise and hormones. Insulin-like growth factor-I (IGF-I) is a well-known regulator of skeletal muscle cells. However, it has not been studied whether there is any interaction between IGF-I and FAT/CD36 in skeletal muscle cells. In this study, the effects of IGF-I treatment on FAT/CD36 induction were examined. Differentiated C2C12 cells were treated with 20 ng/ml of IGF-I at different time points. Treatment of C2C12 cells with IGF-I resulted in increased FAT/CD36 mRNA and protein expression. After 24 and 48 hr of IGF-I treatment, FAT/CD36 mRNA increased 89% and 24% respectively. The increase of both proteins returned to the control level after 72 hr of IGF-I treatment, suggesting that the FAT/CD36 gene is regulated pretranslationally by IGF-I in skeletal muscle cells. These results suggest that IGF-I can regulate the expression of FAT/CD36 in skeletal muscle cells. In conclusion, IGF-I induces a rapid transcriptional modification of the FAT/CD36 gene in C2C12 skeletal muscle cells and has modulating effects on fatty acid uptake proteins as well as oxidative proteins.

• Journal of Life Science
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• v.31 no.10
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• pp.954-959
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• 2021

Apoptosis is an important mechanism that regulates cellular populations to maintain homeostasis, and the caspases, a family of cysteine proteases, are key mediators of the apoptosis pathway. Caspase-8 is an initiator caspase of the extrinsic apoptotic pathway, which is initiated by extracellular stimuli. Caspase-8 have two conserved domains, N-terminal tandem death effector domains (DED) and C-terminal two catalytic domain, which are important for this extrinsic apoptosis pathway. In extrinsic apoptosis pathway, death receptors which members of TNF superfamily are activated by binding of death receptor specific ligands from cell outside. After the activated death receptors recruit adaptor protein Fas-associated death domain protein (FADD), death domains (DD) of death receptor and FADD bind to each other and FADD combined with death receptor recruits procaspase-8, a precursor form of caspase-8. The DED of FADD and procaspase-8 bind to one another and FADD-bound procaspase-8 is activated by cleavage of the prodomain. This death receptor-FADD-caspase-8 complex called death inducing signaling complex (DISC). Cellular FLICE-inhibitory proteins (c-FLIPs) regulate caspase-8 activation by acting both anti- and pro-apoptotically, and caspase-8 activation initiates the activation of executioner caspases such as caspase-3. Finally activated executioner caspases complete the apoptosis by acting critically DNA degradation, nuclear condensation, plasma membrane blebbing, and the proteolysis of certain caspase substrates.

• Journal of Applied Biological Chemistry
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• v.65 no.4
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• pp.239-245
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• 2022

Although normal activation of platelets is important in the process of hemostasis, excessive or abnormal activation of platelets can lead to cardiovascular diseases. Therefore, the discovery of novel substances capable of regulating or inhibiting platelet activation may be helpful in the prevention and treatment of cardiovascular diseases. Artemether is a derivative of artemisinin, known as an active ingredient of Artemisia annua, which has been reported to be effective in treating malaria, and is known to function through antioxidant and metabolic enzyme inhibition. However, the role of artemether in platelet activation and aggregation and the mechanism of action of artemether in collagen-induced human platelets are not known until now. This study investigated the effects of artemether on platelet activation and thrombus formation induced by collagen. As a result, cAMP level was significantly increased by artemether, and VASP and IP3R, substrates of cAMP-dependent kinase, were phosphorylated. IP3R phosphorylation by Artemether inhibited Ca²⁺ recruitment into the cytoplasm, and phosphorylated VASP inhibited fibrinogen binding by inactivating αIIb/β3 located on the platelet membrane. Consequently, artemether inhibited thrombin-induced fibrin clot formation. Therefore, we propose that artemether can act as an effective prophylactic and therapeutic agent for cardiovascular diseases caused by excessive platelet activation and thrombus formation.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.4
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• pp.417-426
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• 2023

The TRPM4 gene encodes a Ca²⁺-activated monovalent cation channel called transient receptor potential melastatin 4 (TRPM4) that is expressed in various tissues. Dysregulation or abnormal expression of TRPM4 has been linked to a range of diseases. We introduced the hemagglutinin (HA) tag into the extracellular S6 loop of TRPM4, resulting in an HA-tagged version called TRPM4-HA. This TRPM4-HA was developed to investigate the purification, localization, and function of TRPM4 in different physiological and pathological conditions. TRPM4-HA was successfully expressed in the intact cell membrane and exhibited similar electrophysiological properties, such as the current-voltage relationship, rapid desensitization, and current size, compared to the wild-type TRPM4. The presence of the TRPM4 inhibitor 9-phenanthrol did not affect these properties. Furthermore, a wound-healing assay showed that TRPM4-HA induced cell proliferation and migration, similar to the native TRPM4. Co-expression of protein tyrosine phosphatase, non-receptor type 6 (PTPN6 or SHP1) with TRPM4-HA led to the translocation of TRPM4-HA to the cytosol. To investigate the interaction between PTPN6 and tyrosine residues of TRPM4 in enhancing channel activity, we generated four mutants in which tyrosine (Y) residues were substituted with phenylalanine (F) at the N-terminus of TRPM4. The YF mutants displayed properties and functions similar to TRPM4-HA, except for the Y256F mutant, which showed resistance to 9-phenanthrol, suggesting that Y256 may be involved in the binding site for 9-phenanthrol. Overall, the creation of HA-tagged TRPM4 provides researchers with a valuable tool to study the role of TRPM4 in different conditions and its potential interactions with other proteins, such as PTPN6.