• Journal of Information Technology Applications and Management
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• v.19 no.1
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• pp.85-100
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• 2012

The development of technology causes a lot of change. Many researchers have insisted that the proliferation of cyber space changes the physical space. Their insistences have been accumulated into three aspects. Firstly, the proliferation of cyber space brings out the concentration in the physical space, secondly the decentralization and lastly both at the same time. In Korea, the concentration of plastic surgery clinics has taken place in Kangnam-gu area at similar period of the Internet proliferation. In this research, we execute empirical study of whether the concentration of plastic surgery in specific areas correlates with the proliferation of cyber space or not. In order to do this, we verified homogeneity of plastic surgery websites between Kangnam-gu and Non-Kangnam-gu areas. Also, we used three statistical and data-mining techniques which are Multi-discriminant analysis, Decision tree analysis and artificial neural network analysis. As a result, there was homogeneity between two different area plastic surgery clinics websites, but there was not big heterogeneity as well. Therefore, in this case of concentration of plastic surgery in Korea, the proliferation of cyber space restrictively correlates with the concentration of physical space.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.2
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• pp.633-636
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• 2012

Purpose: PRIL (proliferation-inducing ligand) is a newly identified member of the tumor necrosis factor (TNF) family and modulates death ligand-induced apoptosis. Here, we investigated the effect of PRIL on cellular characteristics relating to tumor progression in human gastric cancer. Method: Recombinant lentivirus containing PRIL siRNA was constructed and then infected MGC803 and SGC7901 gastric cancer cells. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] colony formation and cell cycle analysis were used to study the effect of PRIL knockdown on gastric cancer cell proliferation. Results: PRIL expression in lentivirus infected cells was significantly reduced as evidenced by quantitative real-time PCR. Cell viability and colony formation of MGC803 and SGC7901 cells were significantly hampered in PRIL knock-down cells. Moreover, the cell cycle was arrested at G2/M phase, elucidating the mechanism underlying the inhibitory effect of siRNA on cell proliferation. Conclusions: Our study indicated that PRIL functions in promoting cell growth, and lentivirus-mediated PRIL gene knockdown might be a promising strategy in the treatment of gastric cancer.

• Journal of Animal Science and Technology
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• v.53 no.3
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• pp.223-226
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• 2011

The current study was undertaken to determine the effect of retinoic acid (RA) on proliferation and differentiation of preadipocytes from male and female pigs. The preadipocytes were isolated from new-born male and female pigs by collagenase digestion and washed three times one day after seeding (designated as day 0 of culture). RA was included in the media at various concentratives from day 0 to 2. The cell number was measured on day 2 with hematocytometer after trypsin digestion. Cell differentiation was determined on day 6 by measuring glycerol-3-phosphate dehydrogenase activity. RA (0.1, 1 and 10 uM) showed no effect on proliferation of preadipocytes from both male and female pigs. However, RA significantly decreased differentiation of pig preadipocytes. Degree of differentiation with 0.1 uM, 1 uM and 10 uM of RA treatment was 80%, 41% and 29% respectively, compared with control. Similar inhibitory effect was found in the female pigs; 77%, 28% and 16% respectively. It is interesting that RA treated on cell proliferation stage had no effect on proliferation but had a strong inhibitory effect on differentiation which is happening in the late stage of cell culture.

• The Journal of Internal Korean Medicine
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• v.21 no.3
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• pp.433-441
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• 2000

Objective : To analyze the effects of Yukmijihwang-tang, Taeksa-tang, Silbi-um on mesangial cell proliferation, fibronectin synthesis and MHC-class II expression. Methods : Laboratory studies were performed with the method of surface enzyme immunoassays or flow cytometry after addition of peripheral blood mononuclear cells(PBMC) supernatants treated with medications using the cultured human mesangial cells. Results : 1. Silbi-um produces more suppressive effect than control group and hydrocortisone group on the mesangial cell proliferation. In Yukmijihwang-tang, Taeksa-tang and Silbi-um, mesangial cell proliferation significantly decreased than in hydrocortisone group 2. In the 'without fetal bovine serum' study, Yukmijihwang-tang take more suppressive effect than Control group on the fibronectin synthesis. In the 'with fetal bovine serum' study, Yukmijihwang-tang, Taeksa-tang, Silbi-um all have suppressive effect, but it hasn' t any statistical significance. 3. Yukmijihwang-tang, Taeksa-tang, Silbi-um all have a suppressive effect on the MHC-class II expression. Conclusions : Herb medicine generally show a suppressive effect on the suppression of the mesangial cell proliferation, fibronectin synthesis and MHC-class II expression.

• Proceedings of the Korean Vacuum Society Conference
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• 2013.02a
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• pp.526-526
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• 2013

Plasma technology isbeing developed for a range of medical applications including wound healing. However, the effect of plasma on many cells and tissues is unclear. Cell migration and cell proliferation are very important biological processes which are affected by plasma exposure and might be a potential target for plasma therapy during wound healing treatment. In this study, we confirmed the plasma exposure time and incubation time after plasma treatment in skin fibroblast (L-929 cells) to evaluate the optimal conditions forplasma exposure to the cell in-vitro. In addition, we used a scratch method to generate artificial wound for evaluating the cell migration by plasma treatment. Where, the cells were treated with plasma and migration rate was observed by live-cell imaging device. To find the cell proliferation, cell viability assay was executed. The results of this study indicate the increased cell proliferation and migration on mild plasma treatment. The mechanisms for cell migration and cell proliferation after plasma treatment for future studies will be discussed.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1241-1245
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• 2014

Cinobufacin is used clinically to treat patients with many solid malignant tumors. However, the mechanisms underlying action remain to be detailed. Our study focused on miRNAs involved in cinobufacin inhibition of GC cell proliferation. miRNA microarray analysis and real time PCR identified miR-494 as a significant cinobufacin-associated miRNA. In vivo, ectopic expression of miR-494 inhibited the proliferation and induced apoptosis of BGC-823 cells on CCK-8 and flow cytometry analysis. Further study verified BAG-1 (anti-apoptosis gene) to bea target of miR-494 by luciferase reporter assay and Western blotting. In summary, our study demonstrated that cinobufacin may inhibit the proliferation and promote the apoptosis of BGC-823 cells. Cinobufacin-associated miR-494 may indirectly be involved in cell proliferation and apoptosis by targeting BAG-1, pointing to use as a potential molecular target of cinobufacin in gastric cancer therapy.

• Journal of Microbiology and Biotechnology
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• v.30 no.7
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• pp.1044-1050
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• 2020

Abelmoschus manihot (Linn.) is a medicinal herbal plant that is commonly used to treat chronic kidney disease and hepatitis. However, its effect on cell proliferation has not been clearly revealed. In this report, we sought to determine the effect of the flower extract of A. manihot (FA) on cell proliferation. Based on our findings, FA increased the proliferation of human diploid fibroblast (HDF) and HEK293 cells. Through cell cycle analysis, FA was found to increase the number of HDF cells in the S phase and G2/M phase. FA also increased the expression of cyclin D1 and enhanced the migration of HDF cells. By administering FA to HDF cells with ≥30 passages, a decrease in the number of senescence-associated β galactosidase-positive cells was observed, thereby indicating that FA can ameliorate cellular senescence. Collectively, our findings indicate that FA increases cyclin D1 expression and regulates cell proliferation.

• Journal of Korean Neurosurgical Society
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• v.29 no.1
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• pp.28-34
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• 2000

Object : To verify the effect of the lipoxygenase inhibitor and cycloxygenase inhibitor on meningioma cell proliferation. Method : Using two meningioma cell lines, cell proliferation was determined at 96 hrs after adding inhibitor (AA861, Nordihydroguaiaretic acid(NDGA), Indomethacin, acetyl-11-keto-beta-boswellic acid(AKBA) into medium by methyl tetrazolium salt/phenazine methosulfate(MTS/PMS) non-radioactive cell proliferation assay. We checked optical density with 490nm wavelength UV and this value was used as a proliferative index. The percent of inhibition was also calculated from this value. Conclusion : Indomethacin and NDGA showed no effect on meningioma proliferation. AA861 also showed no significant inhibitory effect, but AKBA demonstrated a significant inhibitory effect on meningioma cell proliferation.

• Biomedical Science Letters
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• v.23 no.3
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• pp.194-200
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• 2017

Bone-resorbing osteoclasts play a major role in maintaining bone homeostasis with bone-forming osteoblasts. Although it has been reported that A2B adenosine receptor (A2BAR) regulates osteoclast differentiation, its effects on apoptosis or proliferation of osteoclasts have been less-defined. Here, we demonstrate that A2BAR stimulation regulates macrophage-colony stimulating factor (M-CSF)-mediated osteoclast proliferation. Stimulation with a specific agonist of A2BAR, BAY 60-6583, significantly reduced M-CSF-mediated osteoclast proliferation in a time- and dose-dependent manner. In addition, A2BAR stimulation induced both apoptosis of the cells and cell arrest in the G1 phase with a decrease of cell number in the G2/M phase. Stimulation with BAY 60-6583 inhibited the activation of Akt by M-CSF, whereas M-CSF-induced ERK1/2 activation was not affected. These results suggest that the inhibition of M-CSF-mediated Akt activation by A2BAR stimulation increases apoptotic response of osteoclasts and induces cell cycle arrest in the G1 phase, thus contributing to the down-regulation of osteoclast proliferation.

• Biomolecules & Therapeutics
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• v.24 no.5
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• pp.523-528
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• 2016

Urotensin II (UII) is a potent vasoactive peptide and mitogenic agent to induce proliferation of various cells including vascular smooth muscle cells (VSMCs). In this study, we examined the effects of a novel UII receptor (UT) antagonist, KR-36676, on vasoconstriction of aorta and proliferation of aortic SMCs. In rat aorta, UII-induced vasoconstriction was significantly inhibited by KR-36676 in a concentration-dependent manner. In primary human aortic SMCs (hAoSMCs), UII-induced cell proliferation was significantly inhibited by KR-36676 in a concentration-dependent manner. In addition, KR-36676 decreased UII-induced phosphorylation of ERK, and UII-induced cell proliferation was also significantly inhibited by a known ERK inhibitor U0126. In mouse carotid ligation model, intimal thickening of carotid artery was dramatically suppressed by oral treatment with KR-36676 (30 mg/kg/day) for 4 weeks compared to vehicle-treated group. From these results, it is indicated that KR-36676 suppress UII-induced proliferation of VSMCs at least partially through inhibition of ERK activation, and that it also attenuates UII-induced vasoconstriction and vascular neointima formation. Our study suggest that KR-36676 may be an attractive candidate for the pharmacological management of vascular dysfunction.