• Microbiology and Biotechnology Letters
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• v.39 no.4
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• pp.364-373
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• 2011

Human embryonic stem cells have been highlighted as a valuable cellular source in the regenerative medicine field, due to their pluripotency. However, there is the challenge of the establishment of specific functional cell type forms of undifferentiated human embryonic stem cells (hESC). To establish and purify functional cell types from hESCs, we differentiated undifferentiated hESCs into vascular lineage cells and sorted the specific cell population from the whole cell population, depending on their cell volume, and compared them with the non-sorted cell population. We observed that about 10% of the PECAM positive population existed in the VEGF induced differentiating human embryoid body (hEB), and differentiated hEBs were made into single cells for cell transplantation. After making single cells, we performed cell sorting using a fluorescence-activated cell sorter (FACs), according to their cell volume on the basis of FSC region gating, and compared their therapeutic capacity with the non-sorted cell population through cell transplantation into hindlimb ischemic disease model mice. 4 Weeks after cell transplantation, the recovery rate of blood perfusion reached 54% and 17% in the FSC regions of sorted cells- and non-sorted cells, respectively. This result suggests that derivation of a functional cell population from hESCs can be performed through cell sorting on the basis of cell volume after preliminary differentiation induction. This approach may then greatly contribute to overcoming the limitations of marker sorting.

• Journal of Chest Surgery
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• v.29 no.9
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• pp.1031-1035
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• 1996

International Ass ciation for the Study of Lung Cancer(IASLC) recommended the following classification of small cell lung carcinoma(SCLC) : (1) Small cell carcinoma (2) Mixed small cell/large cell carcinoma (3) Combined small cell carcinoma. Combined small cell carcinomas contain a squamous cell carcinoma or adenocarcinoma component. The prognostic significance of these elements is not known, but since the frequency and extent of non-small cell elements are considerably greater in posttherapy and autopsy tissues, it is possible that the non-SCLC elements are more resistant to therapy than the SCLC cells. Metaplasia & dysplasia of the bronchial surface epithelium are frequently observed in the bronchial biopsy specimens that contain small cell carcinoma of the lung. We report a case of combined small cell carcinoma with squamous element associated with microinvasive squamous cell carcinoma of the bronchial surface epithelium in 68 year old male patient, stage was IIIa. The two lesion are not connected n serial sections.

• Parasites, Hosts and Diseases
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• v.54 no.2
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• pp.147-154
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• 2016

Toxoplasma gondii infection induces alteration of the host cell cycle and cell proliferation. These changes are not only seen in directly invaded host cells but also in neighboring cells. We tried to identify whether this alteration can be mediated by exosomes secreted by T. gondii-infected host cells. L6 cells, a rat myoblast cell line, and RH strain of T. gondii were selected for this study. L6 cells were infected with or without T. gondii to isolate exosomes. The cellular growth patterns were identified by cell counting with trypan blue under confocal microscopy, and cell cycle changes were investigated by flow cytometry. L6 cells infected with T. gondii showed decreased proliferation compared to uninfected L6 cells and revealed a tendency to stay at S or G2/M cell phase. The treatment of exosomes isolated from T. gondii-infected cells showed attenuation of cell proliferation and slight enhancement of S phase in L6 cells. The cell cycle alteration was not as obvious as reduction of the cell proliferation by the exosome treatment. These changes were transient and disappeared at 48 hr after the exosome treatment. Microarray analysis and web-based tools indicated that various exosomal miRNAs were crucial for the regulation of target genes related to cell proliferation. Collectively, our study demonstrated that the exosomes originating from T. gondii could change the host cell proliferation and alter the host cell cycle.

• BMB Reports
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• v.45 no.3
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• pp.159-164
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• 2012

CD99 is known to be involved in the regulation of cell-cell adhesion. However, it remains unclear whether CD99 controls cell-extracellular matrix adhesion. In this study, the effects of CD99 activation on cell-extracellular matrix adhesion were investigated. It was found that engagement of CD99 with the stimulating antibody YG32 downregulated the adhesion of MCF-7 cells to fibronectin, laminin and collagen IV in a dose-dependent manner. The CD99 effect on cell-ECM adhesion was inhibited by overexpression of the dominant negative form of CD99 or CD99 siRNA transfection. Treatment of cells with $Mn^{2+}$ or by ${\beta}_1$ integrin-stimulating antibody restored the inhibitory effect of CD99 on cell-ECM adhesion. Cross-linking CD99 inactivated ${\beta}_1$ integrin through conformational change. CD99 activation caused dephosphorylation at Tyr-397 in FAK, which was restored by the ${\beta}_1$ stimulating antibody. Taken together, these results provide the first evidence that CD99 inhibits cell-extracellular matrix adhesion by suppressing ${\beta}_1$ integrin affinity.

• Transactions on Electrical and Electronic Materials
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• v.16 no.5
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• pp.268-273
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• 2015

While analyzing the specimens before and after the thermal shock test, we found that the power drop rate of the bare cell was 5.08%, while the power drop rate of the ribboned cell was 16.49%. In comparative terms, the efficiency was lower at the ribboned cell than at the bare cell. While analyzing through EL (Electroluminescence) shots and cross sections, we tried to decipher the exact cause of the power drop. Although mere color change of the cell was observed at the surface of the bare cell, no abnormality could be found inside the cell. On the surface of the ribboned cell, the short circuit of gridfinger extended from the front part of the front electrode of the ribboned cells. Therefore, cracks occurred on the surface of the cell. Cracks also appeared inside the cell. While analyzing the I-V curve, we determined an increase in the leakage current and an increase of resistances in series in the bare cell. In the ribboned cell, the resistances in parallel reduced remarkably. An increase of resistances in series could also be verified. Conclusively, we deduced that the power drop rate in the bare cell is a life span of the cell itself; aging is the cause of power drop rate in cells. In case of ribboned cell, the power drop rate was directly influenced by internal cracks and an intermetallic compound layer joining the ribbon at the front electrode.

• Transactions of the Korean hydrogen and new energy society
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• v.16 no.2
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• pp.170-179
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• 2005

Electrolyte loss is considered as one of the major obstacles limiting the life time of molten carbonate fuel cells (MCFCs). Unit cells with an effective area of 100 $cm^2$ were prepared and were operated to determine the optimum matrix thickness which contains the maximum amount of electrolyte without serious preformance loss caused by high resistance. Matrices with different thickness, 1.45, 1.8, and 2.3 mm, were used in unit cells and those cells were operared about 5000, 10000, and 4000 hrs. The unit cell used 1.8 mm thick matrix showed 0.85 V (at 150 mA/$cm^2$) as the intial performance and this cell voltage is not lower than the cell voltage obtained in the cell with 1 mm thick matrix. This cell was operated for 10000 hrs. The cell used 1.45 mm thick matrices showed 16.6 % in the electrolyte loss after 5000 hr operation. In the case of the cell with 2.3 mm thick matrix, the initial cell voltage was below 0.80 V (at 150 mA/$cm^2$). For thermal cycle test, the gas crossover amount of unit cell used 1.8 mm thick matrix was much less than that of the cell with 1.0 mm thick matrix.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.35 no.2
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• pp.66-73
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• 2009

Tumor angiogenesis is a process leading to formation of blood vessels within tumors and is crucial for maintaining a supply of oxygen and nutrients to support tumor growth and metastasis. Vascular endothelial growth factor(VEGF) plays a key role in tumor angiogenesis including induction of endothelial cell proliferation, migration, survival and capillary tube formation. VEGF binds to two distinct receptors on endothelial cells. VEGFR-2 is considered to be the dominant signaling receptor for endothelial cell permeability, proliferation, and differentiation. Bevacizumab(Avastin, Genetech, USA) is a monoclonal antibody against vascular endothelial growth factor. It is used in the treatment of cancer, where it inhibits tumor growth by blocking the formation of new blood vessels. The goal of this study is to identify the anti-tumor effect of Bevacizumab(Avastin) for oral squamous cell carcinoma cell lines. Human squamous cell carcinoma cell line(HN4) was used in this study. We examined the sensitivity of HN4 cell line to Bevacizumab(Avastin) by using in vitro proliferation assays. The results were as follows. 1. In the result of MTT assay according to concentration of Bevacizumab(Avastin), antiproliferative effect for oral squamous cell carcinoma cell lines was observed. 2. The growth curve of cell line showed the gradual growth inhibition of oral squamous cell carcinoma cell lines after exposure of Bevacizumab(Avastin). 3. In the apoptotic index, groups inoculated Bevacizumab(Avastin) were higher than control groups. 4. In condition of serum starvation, VEGFR-2 did not show any detectable autophosphorylation, whereas the addition of VEGF activated the receptor. Suppression of phosphorylated VEGFR-2 and phosphorylated MAPK was observed following treatment with Bevacizumab(Avastin) in a dose-dependent manner. 5. In TEM view, dispersed nuclear membrane, scattered many cytoplasmic vacuoles and localized chromosomal margination after Bevacizumab(Avastin) treatment were observed. These findings suggest that Bevacizumab(Avastin) has the potential to inhibit MAPK pathway in proliferation of oral squamous cell carcinoma cell lines via inhibition of VEGF-dependent tumor growth.

• Natural Product Sciences
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• v.15 no.1
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• pp.1-7
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• 2009

This study was performed to investigate the cell growth inhibitory effect of tissue cultured root of wild Panax ginseng C.A. Mayer (tcwPG). The human stomach carcinoma cell line, MKN 74, was incubated with 70% EtOH extract of tcwPG or Panax ginseng C.A. Mayer (PG) for 24 hrs. tcwPG inhibited cell growth at a concentration of $250{\mu}g/ml$. However, Panax ginseng extract did not inhibit cell growth at the same concentration. We also tested the ethyl acetate and $H_2O$ fractions of tcwPG. The inhibitory effect of the ethyl acetate fraction on cell proliferation in MKN 74 cells was more potent than that of the crude extract, and the inhibitory effect of the $H_2O$ fraction was less than that of the ethyl acetate fraction. When we separated tcwPG into polar and non-polar saponin fractions and then measured cell growth inhibition, the non-polar saponin in tcwPG exhibited cytotoxicity. To compare the effects of tcwPG on various cancer cell lines, we measured cytotoxicity in MKN 74 (stomach cancer cell line), SW 620 (colon cancer cell line) and PC 3 (prostate cancer cell line). All three cell lines showed cell growth inhibition, and the cell growth inhibitory effects were not quite different in the various cell lines. The non-polar saponins of tcwPG arrested PC 3 cells at G1-phase as did Panax ginseng.

• Journal of the Korea institute for structural maintenance and inspection
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• v.20 no.2
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• pp.60-66
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• 2016

Polyurethane foam index a of the cell structure and the absorption change by using the foam stabilizer of six to investigate the polyurethane foam index producing the agent to the siloxane analyzed with silicon foam stabilizer with FE-SEM in accordance with the characteristics of the silicon-based foam stabilizer cell structure of the primary DC-193 on the chain ends is PO n dog bond, DC-2585, DC-5125, DC-198 has been confirmed as a close cell, silicone surfactant is combined EO n dog to a siloxane main chain terminus DC-5043 and DC-5598 that appeared to open cell structure. In addition, most absorption of the DC-5043 appeared was the size of the open cell greatest formed by the absorption of the cell structure change this absorption of the size of the close cell most detailed and uniform DC-193 appeared small household water-resistant best many showed. The performance test of the water was found to be excellent.

• The Journal of Internal Korean Medicine
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• v.40 no.3
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• pp.425-442
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• 2019

Objectives: This study aimed to reveal the pharmacological properties of the newly prescribed herbal mixture, Chenmadansamgamibokhap-tang(CDBT), against hypoxia-induced neuronal cell injury (especially mouse hippocampal neuronal cell line, HT-22 cells) and their corresponding mechanisms. Methods: A cell-based in vitro experiment, in which a hypoxia condition induced neuronal cell death, was performed. Various concentrations of the CDBT were pre-treated to the HT-22 cells for 4 h before 18 h in the hypoxia chamber. The glial cell BV-2 cells were stimulated with $IFN{\gamma}$ and LSP to produce inflammatory cytokines and reactive oxygen species. When the neuronal HT-22 cells were treated with this culture solution, the drug efficacy against neuronal cell death was examined. Results: CDBT showed cytotoxicity in the normal condition of HT-22 cells at a dose of $125{\mu}g/mL$ and showed a protective effect against hypoxia-induced neuronal cell death at a dose of $31.3{\mu}g/mL$. CDBT prevented hypoxia-induced neuronal cell death in a dose-dependent manner in the HT-22 cells by regulating $HIF1{\alpha}$ and cell death signaling. CDBT prevented neuronal cell death signals and DNA fragmentation due to the hypoxia condition. CDBT significantly reduced cellular oxidation, cell death signals, and caspase-3 activities due to microglial cell activations. Moreover, CDBT significantly ameliorated LPS-induced BV-2 cell activation and evoked cellular oxidation through the recovery of redox homeostasis. Conclusions: CDBT cam be considered as a vital therapeutic agent against neuronal cell deaths. Further studies are required to reveal the other functions of CDBT in vivo or in the clinical field.