• Korean Journal of Agricultural Science
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• v.13 no.2
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• pp.168-175
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• 1986

Leaf segments of tomato (Lycopersicum escullentum Mill) were cultured on the MS medium supplemented with the concentration of 0, 0.2, 0.5, 2.0 or $5.0mg/{\ell}$ NAA, 2,4-D and/or BA. The treatments were able to induced callus, however the best combinations for the induction of callus were $2.0mg/{\ell}$ BA and 2.0 or $0.5mg/{\ell}$ NAA. Shoot formation was stimulated at the treatment of 2.0 or $5.0mg/{\ell}$ BA, and root formation was stimulated on the medium of 0.2, 0.5, 2.0 or $5.0mg/{\ell}$ NAA plus 0, 0.2 or $0.5mg/{\ell}$ BA.

• Journal of dental hygiene science
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• v.15 no.3
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• pp.295-300
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• 2015

Odontoclasts and osteoclasts resorb tooth root and alveolar bone, respectively. Many studies have focused on osteoclast formation in periodontitis, but effect of periodontitis on odontoclast formation is not clearly clarified. In this study, we observed formation of odontoclasts as well as osteoclasts in rats with ligature-induced periodontitis. To induce periodontitis, ligatures were placed around the first molars in left mandibles of rats. Rats were sacrificed at days 1, 3, and 10 after ligation. After tartrate resistant acid phosphatase (TRAP) staining in mandible section, the number of TRAP-positive odontoclasts and osteoclasts were histologically counted along the root and the alveolar bone surfaces of tooth, respectively. Odontoclasts increased until day 10 in mesial and furcation root surface, but did not increase in distal root surface. When compared odontoclast formation to osteoclast formation in mesial surface, osteoclasts peaked at day 3, and then decreased gradually, whereas odontoclasts were continuously increased until day 10. The number of odontoclasts was lower than that of osteoclasts before and after periodontitis induction. These indicate that periodontitis increased formation of odontoclasts as well as osteoclasts, but odontoclast formation occurs slower and weaker than that of osteoclasts.

• Korean Journal of Veterinary Research
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• v.31 no.3
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• pp.343-353
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• 1991

In order to investigate the histopathological, mechanism of Rompun-induced shock, the development of mammary carcinoma, the numerical changes and the morphological findings of the mast cells appeared in the carcinoma were microscopically observed in the rat treated with DMBA and each chemical of compound 48/80 and Rompun. Also mast cell degranulation induced by Rompun was observed with electron microscope. The results observed were summarized as follows: Tumor appeared in 100% of the animals. Tumors grew more rapidly to $10{\times}10mm$ in rats depleted of mast cells ($37.7{\pm}4.2$ days) than was observed in the control group ($42.5{\pm}4.7$ days) (p<0.005). The mean number of tumors per rat was $2.8{\pm}1.3$ in the compound 48/80- treated group in contrast to $3.4{\pm}1.3$ in the control group. No significant difference was apparent in the tumor induction time of Rompun treated group compared with the compound 48/80-treated group, but the tumor measuring at least $10{\times}10mm$ appeared more quickly in the Rompun treated group than in the control group (p<0.005). The numbers of mast cells in the control group were inclined to increase significantly according to the mammary tumor development (p<0.005). In contrast, the mast cells were fewer significantly in the compound 48/80-treated group and Rompun-treated group than in the control group (p<0.005). The numbers of mast cells in the compound 48/80-treated group and Rompun-treated group were inclined to reduce significantly according to the stages of the mammary carcinoma growth in contrast to the control group respectively. The ultrastructural morphologies of mast cells at 30 minutes after Rompun injection were appeared many normal granules in the cytoplasm, but many normal and degranulated granules were scattered along the cell membrane. And at 1 hour after Rompun injection mast cell granules were disappeared nearly or rarely seen. many long cytoplasmic projections were folded back to adhere to their own surface membrane. and mast cells resulted in a reduced size of these cells. Otherwise. compound 48/80 caused extensive degranulation of mast cells by disrupting cell membrane. but mast cell degranulation by Rompun was observed exocytosis of granules through a channel. From the above results. it is concluded that the Rompun may give rise to the dealth of animals as a shock caused by mast cell degranulation.

• Journal of Life Science
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• v.17 no.1 s.81
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• pp.132-136
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• 2007

When alginate lyase gene (aly) from Pseudoalteromonas elyakovii was expressed in E. coli, most of the gene product was produced as aggregated insoluble particles known as inclusion bodies. In order to produce a soluble and active form of alginate lyase, E. coli cells fore cotransformed with the plasmids designed to permit coexpression of aly together with molecular chaperones such as DnaK/DnaJ/GrpE or GroEL/ES chaperones. The results revealed that the coexpression of aly together with DnaK/DnaJ/GrpE chaperone had a marked effect on the production of this protein as a soluble and active form, presumably through facilitating correct folding of alginate lyase protein. The optimal concentration of L-arabinose for the induction of DnaK/DnaJ/GrpE chaperone was found to be 0.05 mg/ml. When DnaK/DnaJ/GrpE chaperone was coexpressed, about 34% in the total alginate lyase was produced in the soluble fraction. By addition of 10% cetylpyridinium chloride, a clear zone around the colony coexpressing aly and DnaK/DnaJ/GrpE chaperone was formed, indicating that the alginate in the medium was hydrolyzed by active alginate lyase enzyme.

• Journal of Life Science
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• v.17 no.7 s.87
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• pp.996-1001
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• 2007

To investigate whether sulindac, sulindac sulfone, and sulindac sulfide could affect cancer cell viabilities, human colorectal HCTl16 cells were treated with 10 ${\mu}M$ of each NSAID. Among treated NSAms, sulindac sulfide dramatically decreased the cell viabilities detected by MTS and the cytotoxic effect showed dose-dependent manner. To understand the molecular mechanism of cell death in response to sulindac sulfide treatment, we performed oligo DNA microarray analysis. We found that 23 genes were up-regulated more than 2 folds, whereas 33 genes were down-regulated more than 2 folds by treatment of 10 ${\mu}M$ sulindac sulfide. Among the up-regulated genes, we selected 3 genes (NAG-1, DDIT3, PCK2) and performed RT-PCR and quantitative real-time PCR to cofirm microarray data. The results of RT-PCR and real-time PCR were highly accorded with those of microarray experiment. As NAG-1 is well-known gene as tumor suppressor, we detected changes of NAG-1 expression by 10 ${\mu}M$ of sulindac, sulindac sulfone, and sulindac sulfide. The results of RT-PCR and quantitacve real-time PCR indicated that sulindac sulfide was the strongest inducer of NAG-1 among treated NSAIDS. This result implies that induction of NAG-1 by sulindac sulfide plays important role in cell death of colorectal cancer. Overall, we speculate that these results may be helpful in understanding the molecular mechanism of the cancer chemoprevention by sulindac sulfide in human colorectal cancer.

• Radiation Oncology Journal
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• v.18 no.4
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• pp.329-336
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• 2000

Backgrounds : The purpose of this study was to identify drugs that can enhance radioresponse of murine fepatocarcinorna. Methods : CSH/HeJ mice bearing 8 mm tumors of murine fepatocarcinorna, HCa-1, were treated with 25 Gy radiation and one of the following drugs: 5-Fu, 150 mghg; adriamycin, 8 mg/kg; cisplatin, 6 mg/kg; paclitaxel, 40 mg/kg; and gemcitabine, 50 mg/kg. Tumor response to the treatment was determined by tumor growth delay assay and by enhancement factor. Apoptotic level was assessed in tissue sections. Expression of regulating molecules was analyzed by western blotting for p53, Bcl-2, Bax, Bcl-XL, Bcl-XS, and p21$^{WAF1/CIP1}$. Results :Among the drugs tested, only gemcitabine enhanced the antitumor effect of radiation, with enhancement factor of 1.6. Induction of apoptosis by a combination of gemcitabine and radiation was shown as only additive level. In analysis of radiation-induced expression of regulating molecules, the most significant change by combining gemcitabine was activation of p21$^{WAF1/CIP1}$ Conclusion :Gemcitabine is the first drug showing an enhancement of radioresponse in murine hepatocarcinoma, when combined with radiation. The key element of enhancement is thought to be p21$^{WAF1/CIP1}$.

• Korean Journal of Food Science and Technology
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• v.26 no.4
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• pp.464-470
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• 1994

The biological activities of Humulus japonicus were extracted by water and methanol. Methanol was better solvent than water in the extraction for antimicrobial activities against six different species of bacteria and two yeasts. The methanol extract was systematically fractionated with various organic solvents which have different polarities. From the result of antimicrobial activities against six species of bacteria and two species of yeasts, methanol extract was superior to water extract. The methanol extract of Humulus japonicus showed antimicrobial activity against the all species of microorganisms tested except Escherichia coli . The butanol fraction of methanol extract showed antimicrobial effect on the all species tested. The minimal inhibition concentration(MIC) of the butanol fraction on the growth of microorganisms was ranged between $0.1{\sim}0.4%$. The water extract of Humulus japonicus did not show inhibition of the activity of trypsin but methanol extract showed inhibitory activity. The chloroform fraction of methanol extract showed comparatively higher trypsin inhibitory activity than other fractions. The concentration of 50% inhibition$(IC_{50})$ by chloroform fraction was 1.0 mg/ml. Enzyme-inhibitor complex formation was above 90% of the while for 20 min. It was revealed that methanol extract of Humulus japonicus inhibited peroxide production of lard and soybean oil as substrate by antioxidative test. The chloroform fraction of methanol extract had the highest activity. When 0.2% of chloroform fraction was added, induction period of soybean oil and lard were extended 15, 9 days, respectively.

• Membrane Journal
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• v.22 no.5
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• pp.332-341
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• 2012

We studied the effects of induction of natural convection instability flow (NCIF) according to the gravitational orientation (inclined angle) of the membrane cell on the reduction of membrane fouling in the constant-flow ultrafiltration (UF) of colloidal silica solutions. Five colloidal silica solutions with different silica size (average size = 7, 12, 22, 50 nm and 78 nm) were used as UF test solutions. The silica particles in colloidal solutions form cakes on the membrane surface thereby causing severe membrane fouling. The constant-flow UF performance according to the gravitational orientation of the membrane cell (from $0^{\circ}$ to $180^{\circ}$ inclined angle), was examined in an unstirred dead-end cell. We evaluate the effects of NCIF on the suppression of fouling formation by measuring the variation of transmembrane pressure (TMP) and the increase of critical flux by using the flux-stepping method. In the constant-flow dead-end UF for the smaller size (7, 12 nm and 22 nm) silica colloidal solutions, changing the gravitational orientation (inclined angle) of the membrane cell above the $30^{\circ}$ angle induces NCIF in the membrane module. This induced NCIF enhances back transport of the deposited silica solutes away from the membrane surface, therefore gives for the reduction of TMP. But in the constant-flow UF for the more larger size (50 nm and 78 nm) silica colloidal solutions, NCIF effects are not appearing. The critical flux is increased as increasing the module angle and decreasing the silica size. Those results show that the intesity of NCIF occurrence in membrane module is more higher as increasing the module angle and decreasing the silica size.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.33-41
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• 1993

Central analgesic effect of capsaicin was assessed by the tail flick reflex (TFR) test, using male Sprague-Dawley rats under anesthesia with pentobarbital sodium (induction with 40 mg/kg and maintenance with $4{\sim}8\;mg/kg/hr$). Level of norepinephrine in the spinal cord was also measured. Capsaicin, $35{\sim}150\;{\mu}g$, was injected intrathecally, and the TFR latency was measured before, 10, 30, and 60 minutes after the drug administration. TFR latency was increased 100% or more immediately by intrathecal capsaicin, from 2.9 seconds to the maximum of 7.0 seconds at 10 minute after the drug; P<0.01. The increase in TFR latency was maintained during the course of experiment of 2 hours. Concomitant reduction of NE content in the spinal cord was observed; from 16 ng/mg protein to 7 ng/mg protein. On the other hand, subcutaneous injection of capsaicin of 50 mg/kg did not change the TFR latency although the NE content reduced similarly to the case of intrathecal injection. Pretreatment of the animal with 0.5 mg/kg of MK-801 reversed the increase of TFR latency and NE reduction induced by intrathecal capsaicin. These results suggest that capsaicin causes analgesia at the spinal cord level by activating the excitatory amino acid-NE-dorsal horn interneurons axis of the descending inhibitory pain modulation pathway.

• Journal of Microbiology and Biotechnology
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• v.26 no.2
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• pp.287-294
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• 2016

The effect of kaempferol (3,5,7,4-tetrahydroxyflavone), a flavonoid compound that was identified in barnyard millet (Echinochloa crus-galli var. frumentacea) grains, on G₂-checkpoint and apoptotic pathways was investigated in human acute leukemia Jurkat T cell clones stably transfected with an empty vector (J/Neo) or a Bcl-xL expression vector (J/Bcl-xL). Exposure of J/Neo cells to kaempeferol caused cytotoxicity and activation of the ATM/ATR-Chk1/Chk2 pathway, activating the phosphorylation of p53 (Ser-15), inhibitory phosphorylation of Cdc25C (Ser-216), and inactivation of cyclin-dependent kinase 1 (Cdk1), with resultant G₂-arrest of the cell cycle. Under these conditions, apoptotic events, including upregulation of Bak and PUMA levels, Bak activation, mitochondrial membrane potential (Δψm) loss, activation of caspase-9, -8, and -3, anti-poly (ADP-ribose) polymerase (PARP) cleavage, and accumulation of apoptotic sub-G₁ cells, were induced without accompanying necrosis. However, these apoptotic events, except for upregulation of Bak and PUMA levels, were completely abrogated in J/Bcl-xL cells overexpressing Bcl-xL, suggesting that the G₂-arrest and the Bcl-xL-sensitive mitochondrial apoptotic events were induced, in parallel, as downstream events of the DNA-damage-mediated G₂-checkpoint activation. Together these results demonstrate that kaempferol-mediated antitumor activity toward Jurkat T cells was attributable to G₂-checkpoint activation, which caused not only G₂-arrest of the cell cycle but also activating phosphorylation of p53 (Ser-15) and subsequent induction of mitochondria-dependent apoptotic events, including Bak and PUMA upregulation, Bak activation, Δψm loss, and caspase cascade activation.