• Korean Journal of Weed Science
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• v.14 no.1
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• pp.16-22
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• 1994

Ninty three species of domestic weeds were collected and screened for antimicrobial, antitumor, antioxidant and herbicidal activities. Among them, few showed antifungal activities. Cuscuta japonica showed inhibitory activity against Alternaria mali, Ambrosia artemisiifolia and Geranium sibiricum against Phytophthora capsici, Aster yomema and Aster pilosus against Phytophthora parasitica. Ambrosia artemisiifolia, Artemisia princeps, Artemisia capillaris, Ludwigia prostrata, Chrysanthemum zawadskii, Bidens frondosa, and Geranium sibiricum showed broad antibacterial activities. Carex chordorhiza, Artemisia capillaris, Persicaria nodosa, Senecio koreanus, Pariicum bisulcatum, Geranium sibiricum showed antiblebbing activity on human chronic leukemia K562 cell, among them, Persicaria nodosa was the strongist. Angelica decursiva, Equisetum arvense, Cimicifuga heracleifolia, Persicaria nodosa, Geranium sibiricum, Oenothera odorata, Cyperus sanguinolentus showed antioxidant activities. Ludwigia prostrata and Peucedanum terebinthaceum showed strong herbicidal activities.

• Molecular & Cellular Toxicology
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• v.3 no.2
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• pp.98-106
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• 2007

Genotoxic stress triggers a variety of biological responses including the transcriptional activation of genes regulating DNA repair, cell survival and cell death. In this study, we investigated to examine gene expression profiles and genotoxic response in TK6 cells treated with DNA damaging agents MNNG (N-methyl-N'-nitrosoguanidine) and hydrogen peroxide $(H_2O_2)$. We extracted total RNA in three independent experiments and hybridized cRNA probes with oligo DNA chip (Applied Biosystems Human Genome Survey Microarray). We analyzed raw signal data with R program and AVADIS software and identified a number of deregulated genes with more than 1.5 log-scale fold change and statistical significancy. We indentified 14 genes including G protein alpha 12 showing deregulation by MNNG. The deregulated genes by MNNG represent the biological pathway regarding MAP kinase signaling pathway. Hydrogen peroxide altered 188 genes including sulfiredoxins. These results show that MNNG and $H_2O_2$ have both uniquely regulated genes that provide the potential to serve as biomarkers of exposure to DNA damaging agents.

• Korean Journal of Clinical Laboratory Science
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• v.39 no.1
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• pp.31-36
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• 2007

The purpose of the clinically reportable range (CRR) in clinical chemistry is to estimate linearity in working range. The reportable range includes all results that may be reliably reported, and embraces two types of ranges: the analytical measurement range (AMR) is the range of analyte values that a method can directly measure on the specimen without any dilution, concentration, or other pretreatment not part of the usual assay process. CAP and JCAHO require linearity on analyzers every six months. The clinically reportable range is the range of analyte values that a method can measure, allowing for specimen dilution, concentration, or other pretreatment used to extend the direct analytical measurement range. The AMR cannot exceed the manufacturer's limits. Establishing AMR is easily accomplished with Calibration Verification Assessment and experimental Linearity. For example: The manufacturer states that the limits of the AST on their instrument are 0-1100. The lowest level that could be verified is 2. The upper level is 1241. The verified AMR of the instrument is 2-1241. The lower limit of the range is 2, because that is the lowest level that could be verified by the laboratory. The laboratory could not use the manufacturer's lower limit of 2 because they have not proven that the instrument values below 2 are valid. The upper limit of the range is 1241, because although the lab has shown that the instrument is linear to 1241, the manufacturer does not make that claim. The laboratory needs to demonstrate the accuracy and precision of the analyzer, as well the validation of the patient AMR. Linearity requirements have been eliminated from the CLIA regulations and from the CAP inspection criteria, however, many inspectors continue to feel that linearity studies are a part of good lab practice and should be encouraged. If a lab chooses to continue linearity studies, these studies must fully comply with the calibration/calibration verification requirements of CLIA and/or CAP. The results of lower limit and upper limit of clinically reportable range were total protein (2.1 - 79.9), albumin (1.3 - 39), total bilirubin (0.2 - 106.2), alkaline phosphatase (13 - 6928.2), aspartate aminotransferase (24 - 7446), alanine aminotransferase (13 - 6724.2), gamma glutamyl transpeptidase (16.64 - 9904.2), creatine kinase (15.26 - 4723.8), lactate dehydrogenase (127.66 - 13231.8), creatinine (0.4 - 129.6), blood urea nitrogen (8.67 - 925.8), uric acid (1.6 - 151.2), total cholesterol (48.52 - 3162), triglycerides (36.91 - 3367.8), glucose (31 - 4218), amylase (21 - 6694.2), calcium (3.1 - 118.2), inorganic phosphorus (1.11 - 108), HDL (11.74 - 666), NA (58.3 - 1800), K (1.0 - 69.6), CL (38 - 1230).

• Korean Journal of Head & Neck Oncology
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• v.19 no.2
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• pp.121-126
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• 2003

Objectives: The c-kit gene encodes a transmembrane receptor-type tyrosine kinase, which is known to have a significant role in the normal migration and development of germ cells and melanocytes. In the previous studies of c-kit gene, c-kit expressions showed only in adenoid cystic carcinomas, lymphoepithelioma-like carcinomas and myoepithelial carcinomas, but not in others and mutation was not found in any types of salivary carcinoma. We investigate the c-kit expression which may be useful to differentiating adenoid cystic carcinomas from others, and mutation of the gene which may not be exist nor the mechanism of c-kit activation in salivary carcinomas. Material and Methods: The archival tissue samples from 42 salivary carcinomas of major and minor salivary glands were studied for c-kit expression by immunohistochemistry and gene mutation by polymerase chain reaction amplification and single strand conformational polymorphism. Results: The c-kit expressions were noted in 22/24 adenoid cystic carcinomas, 7/9 mucoepidermoid carcinomas, 2/3 acinic cell carcinomas, 3/4 malignant mixed tumors, and one undifferentiated carcinoma. The mutation of c-kit gene was found in 3/24 adenoid cystic carcinomas, 3/8 mucoepidermoid carcinomas, one acinic cell carcinoma, and 2/4 malignant mixed tumors. Conclusion: c-kit protein overexpression is seen in a variety of salivary gland carcinomas, and the mutation of the gene may be the mechanism of c-kit activation in these neoplasms.

• Korean Journal of Food Science and Technology
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• v.47 no.4
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• pp.525-533
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• 2015

The effect of the hot water extract of defatted green tea seed cake (GTSE) on lipid metabolism and the underlying mechanisms of lipolysis in mature 3T3-L1 adipocytes were investigated. In this study, we found that the naringenin content of GTSE was 5.5 mg/g; however, catechins were not detected. The intracellular lipid droplets were stained with Oil Red O dye and quantified. Compared to the control, lipid accumulation was significantly decreased by 52%, and intracellular triglyceride (TG) level was reduced by 33% after treatment with GTSE at a concentration of $40{\mu}g/mL$. To determine the mechanism of reduction in TG content, we determined the level of fatty acid synthase (FAS), phosphorylation of adenosine monophosphate-activated protein kinase (AMPK), and acetyl-coenzyme A carboxylase (ACC) in the cell model. Incubation of the 3T3-L1 adipocytes with GTSE stimulated AMPK and ACC phosphorylation in a dose-dependent manner, and decreased the expression of FAS.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.521-527
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• 1998

An important property of the intestine is the ability to secrete fluid. The intestinal secretion is regulated by a number of substances including vasoactive intestinal peptide (VIP), ATP and different inflammatory mediators. One of the most important secretagogues is adenosine during inflammation. However, the controversy concerning the underlying mechanism of adenosine-stimulated $Cl^-$ secretion in intestinal epithelial cells still continues. To investigate the effect of adenosine on $Cl^-$ secretion and its underlying mechanism in the rabbit colon mucosa, we measured short circuit current ($I_{SC}$) under automatic voltage clamp with DVC-1000 in a modified Ussing chamber. Adenosine, when added to the basolateral side of the muocsa, increased $I_{SC}$ in a dose-dependent manner. The adenosine-stimulated $I_{SC}$ response was abolished when $Cl^-$ in the bath solution was replaced completely with gluconate. In addition, the $I_{SC}$ response was inhibited by a basolateral Na-K-Cl cotransporter blocker, bumetanide, and by apical $Cl^-$ channel blockers, dephenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), glibenclamide. Amiloride, an epithelial $Na^+$ channel blocker, and 4,4-diisothiocyanato-stilbene-2,2-disulphonate (DIDS), a $Ca^{2+}-activated$ $Cl^-$ channel blocker, had no effect. In the mucosa pre-stimulated with forskolin, adenosine did not show any additive effect, whereas carbachol resulted in a synergistic potentiation of the $I_{SC}$ response. The adenosine response was inhibited by 10 ${\mu}M$ H-89, an inhibitor of protein kinase A. These results suggest that the adenosine-stimulated $I_{SC}$ response is mediated by basolateral to apical $Cl^-$ secretion through a cAMP-dependent $Cl^-$ channel. The rank order of potencies of adenosine receptor agonists was $5'-(N-ethylcarboxamino)adenosine(NECA)＞N^6-(R-phenylisopropyl)adenosine(R-$ PIA)＞2-[p-(2-carbonylethyl)-phenyl-ethylamino]-5'-N-ethylcarboxaminoadenosine(CGS21680). From the above results, it can be concluded that adenosine interacts with the $A_{2b}$ adenosine receptor in the rabbit colon mucosa and a cAMP-dependent signalling mechanism underlies the stimulation of $Cl^-$ secretion.

• Journal of Marine Bioscience and Biotechnology
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• v.2 no.2
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• pp.102-107
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• 2007

Environmental contamination becomes a great public concern as our society gets industrialized rapidly. The present study examine the role of chitosan in a effort to intervene the environmental pollutant-induced toxicity. PCB-induced neurotoxicity with respect to the PKC signaling was examined. Since the developing neuron is particularly sensitive to PCB-induced neurotoxicity, we isolated cerebellar granule cells derived from 7-day old SD rats and grew cells in culture for additional 7 days to mimic PND-14 conditions. PCB showed the alteration of PKC signaling pathway. The alteration was structure-dependent. Mono-ortho-substituted congeners at a high dose showed a significant increase of total PKC activity at [$^3H$]PDBu binding assay, indicating that mono-ortho-substituted congeners are more neuroactive than non-ortho-substituted congeners in neuronal cells. PKC isoforms were immunoblotted with respective monoclonal antibodies. PKC-beta II and -epsilon were activated with mono-ortho-substituted congeners exposure. The result suggests that the position with ortho has a higher potential of altering the signaling pathway. Alteration of PKC was blocked with treatment of high molecular weight of chitosan. The study demonstrated that the ortho position in PCBs are important in assessing the structure-activity relationship. The results suggest a potential use of marine bioactive materials as a means of nutritional intervention to prevent the harmful effects of pollutant-derived toxicity.

• Journal of Life Science
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• v.21 no.11
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• pp.1549-1557
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• 2011

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can selectively induce apoptosis in many types of transformed cells; however, some human hepatocellular carcinoma cells are particularly resistant to the effects of TRAIL. Although genistein, a natural isoflavonoid phytoestrogen, has been shown to have pro-apoptotic activity against human cancer cell lines, little is known about the mechanism of genistein in terms of TRAIL-induced apoptosis. In the present study, it was investigated whether or not combined treatment with genistein and TRAIL synergistically induced apoptosis in Hep3B hepatocarcinoma cells. Results indicate that treatment with TRAIL in combination with nontoxic concentrations of genistein sensitized TRAIL-resistant Hep3B cells to TRAIL-induced apoptosis, which was associated with mitochondrial dysfunction. Further, the inhibition of p38 mitogen-activated protein kinase (MAPK) activation markedly decreased genistein and TRAIL-induced cell viability and apoptosis by enhanced truncation of Bid, increase of pro-apoptotic Bax, decrease of anti-apoptotic Bcl-2, and release of cytochrome c from mitochondria to cytoplasm. Activation of caspases and degradation of poly (ADP-ribose) polymerase induced by the combined treatment was also markedly increased by the inhibition of p38 MAPK, through the mitochondrial amplification step. In conclusion, our data suggest that genistein sensitizes TRAIL-induced-apoptosis via p38 MAPK-dependent pathway.

• Journal of Sasang Constitutional Medicine
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• v.15 no.1
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• pp.72-89
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• 2003

To elucidate the neuroprotective effect of Yeoldahanso-tang(YHT) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT(SODIUM3,3'-{I-[(PHENYLAMINO) CARBONYL]-3,4-TETRAZOLIUM}- BIS (4-METHOXY-6-NITRO) BENZENE SULFONIC ACID HYDRATE), NR(Neutral red), MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and SRB(Sulforhodamin B) asssay. The activity of catalase and SOD(Superoxide dismutase) was measured by spectrophometry, and $TNF-{\alpha}$(Tumor cell necrosis $fector-{\alpha}$) and PKC(Protein kinase C) activity was measured after exposure to hypoxia and treatment of YHTWE. Also the neuroprotective effect of YHTWE was researched for the elucidatioion of neuroprotective mechanism. The results were as follows; 1. Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO2 for $2{\sim}26$ minutes in these cultures and YHTWE inhibited the decrease of cell viability. 2. H2O2 treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 ${\mu}M$ for 6 hours, but YHTWE inhibited the decrease of cell viability. 3. Hypoxia decreased catalase and SOD activity, and also $TNF-{\alpha}$ and PKC activity in these cultured cerebral neurons, but YHTWE inhibited the decrease of the catalase and SOD activity in these cultures. 4. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c forom mitochondria. YHTWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxicity on cultured mouse cerebral neurons, and the YHTWE has the neuroprotective effect in blocking the neurotoxicity induced by hypoxia in cultured mouse cerebral neurons.

• Journal of Life Science
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• v.17 no.7 s.87
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• pp.956-963
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• 2007

The purpose of the present study was to examine the effects of iron shot practice volume based on golf skill level on the indices of muscle damage and fatigue in blood. Twenty four golf players were studied under conditions of different golf skill level (beginners, intermediate, expert) and practice volume (100, 200, 300balls). In this study blood CK and LDH were determined to show the level of muscle damage, and blood phosphorus, lactate, and ammonia were measured to see the level of fatigue. Blood creatinine, and IGF- I generally used to see the rate of protein synthesis were also measured. In summary, these results are interpreted to mean that 1) blood fatigue factors, muscle damages, and creatinine levels increased due to a rise in the practice volume of iron shot, 2) those levels decreased due to rise in the golf skill level, 3) blood fators and creatinine recovered quickly after exercise, however muscle damages did not recover even after 24hr, Therefore, both golf skill lev-el and practice volume should be considered to prevent muscle damage and fatigue during practice iron shot.