• Current Photovoltaic Research
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• v.11 no.4
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• pp.103-107
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• 2023

A Nickel oxide (NiO_x) thin films were prepared via sol-gel process on a transparent conductive oxide glass substrate. The NiO_x thin films were spin-coated in ambient air and subsequently annealed for 30 minutes at temperatures ranging from 150℃ to 450℃. The structural and optical characteristics of the NiO_x thin films annealed at various temperatures were measured using X-ray diffraction, field emission scanning electron microscopy, and ultraviolet-visible spectroscopy. After optimizing the NiO_x coating conditions, perovskite solar cells were fabricated with p-i-n inverted structure, and its photovoltaic performance was evaluated. NiO_x thin films annealed at 350℃ exhibited the most favorable characteristics as a hole transport layer, resulting in the highest power conversion efficiency of 17.88 % when fabricating inverted perovskite solar cells using this film.

• Microbiology and Biotechnology Letters
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• v.18 no.3
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• pp.233-238
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• 1990

The mechanism of intracellular accumulation of cadmium in a cadmium-ion tolerant yeast, Hansenula ammala B-7, which is an extreme cadmium tolerant strain and has the ability to take up a large amount of cadmium was investigated. The amounts of cadmium taken up by the scalded yeast cells were 2 to 3 times more than the value of the living cells. The living Hansenula anomala B-7 cells adsorbed 74% of cadmium taken up onto the other layer of the cells and 26% of it accumulated inside the cells. But the scalded cells adsorbed 98.3% of cadmium taken up and accumulated 1.7% of it inside the cells. A cadmium uptake and its accumulation were accelerated up to 162.3% and 275.4% by Triton X-100 in the living cells, respectively. Whereas in the scalded cell cadmium uptake was not affected by Triton X-100. Furthermore the cadmium uptake and its accumulation were strongly inhibited by metabolic inhibitors like 2,4-dinitrophenol, sodium azide and potassium cyanide in the living cells, but in the scalded cells cadmium uptake was not affected by metabolic inhibitors. These results suggested that the intracellular accumulation of cadmium by the cadmium-tolerant Hansenula anomala B-7 cells was apparently dependent of biological activity, and also gave evidence of the existance of energy-dependent system.

• Journal of Food Hygiene and Safety
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• v.25 no.3
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• pp.258-262
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• 2010

Radiotherapy is one of the major therapies for cancer treatment. p53 acts as a central mediator of the cellular response to stressful stimuli, such as radiation. Recently it has been known that activation of the phosphatidylinositol-3-kinase (PI3K) pathway is associated with radioresistance. In this study, we investigated whether X-irradiation up-regulates PI3K in a p53-dependent manner in human colon cancer cells. In order to study this phenomenon, we have treated p53-wild type and p53-mutant type HCT116 cells with X-ray. Treatment of wild type HCT116 cells with 8 Gy resulted in a marked increase in PI3K (p85), which paralleled an increase in PTEN, a counterpart of PI3K. However, these effects of X-rays in the p53-mutant cells were not observed. These results suggest that the X-irradiation-induced up-regulation of PI3K/PTEN pathway is p53-dependent.

• Animal cells and systems
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• v.1 no.3
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• pp.491-496
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• 1997

When olfactory placodes are transplanted at stages 23/24 from Xenopus laevis to Xenopus borealis hosts of the same age, it is possible to distinguish the cell populations of the host and donor due to the peculiar nuclear Q bands specific to X. borealis. I have replaced the eye anlage in each of a number of X. borealis with the transplanted olfactory placode of an individual X. laevis, or vice versa. In most instances, the placode of the donor fuses with that of the host. When fusion occurs, but not when the host and donor orqans grow separately, the cells of the donor were replaced gradually and according to a characteristic pattern by cells of the host. The basal cells of the donor were the first to be replaced, followed by the more matured cells of the sensory epithelium. This cellular substitution, proceeding in an orderly fashion from bottom to upper layers of the epithelium, depends on the fusion of the two organs. This observation suggests intercellular contacts in the mitotic zone of the two organs favor the host's cells over those of the donor.

• Journal of Radiation Protection and Research
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• v.32 no.4
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• pp.140-156
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• 2007

This research was performed to investigate the morphological changes of folliculus ovary according to the radiation dose. The whole body radiation of 200 cGy, 400 cGy, and 600 cGy was given to the each groups of 5 months-aged female mouse. Various staining methods used in this research are: Hematosylin-Eosin method, and immunohistochemistrical methods using BrdU, TUNEL, p53, p21, PCNA and inhibin. The minute structural changes of folliculus ovary were observed through an electron microscope with high magnification. The morphological changes of growing folliculus ovary became distinct as the dose of X-rays increased. Especially, the nuclei of granular cells showed manifest condensation and the changes of the transparent zone were distinct. As a result of histochemical reaction according to Masson's trichrome method and reticular fiber method, the changed granular cells, the deformed basilar membrane of folliculus ovary and the abnormal arrangement of the reticular fiber were observed. In the reaction of BrdU, the granular cells of normal folliculus ovary with positive reaction rapidly decreased according to the increase of the dose of X-rays. In TUNEL study, granular cells showing positive reaction in retarded folliculus ovary were expanded to growing folliculus ovary and primordial folliculus ovary according to the increase of the dose of X-rays. In case of 600 cGy of X-rays, oocyte underwent apoptosis. In p53 immunohistochemistry, p53 manifested to be stronger as the dose of X-rays increased. p53 reactivity was manifested distinctively in all cells comprising folliculus ovary following irradiation of 600 cGy. p21 was manifested in granular cells of folliculus ovary and showed very positive reaction around follicular antrum according to the increase of the dose of X-rays. In PCNA, positive reaction was manifested in growing folliculus ovary, mature folliculus ovary and primordial folliculus ovary, but the extent of the reaction decreased as the dose of the X-rays decreased. The finding that the reaction of granular cells around folliculus ovary was stronger than that near follicular membrane indicates that what was damaged first by X-ray was the cells near folliculus ovary and follicular antrum. The reactivity of $inhibin-{\alpha}$ showed difference according to the growing stage of folliculus ovary: $inhibin-{\alpha}$ showed the most strong reaction in mature folliculus ovary with follicular antrum. There was strong reaction in granular cells around follicular membrane but $inhibin-{\alpha}$ did not occur at all in theca cells comprising follicular membrane. $Inhibin-{\alpha}$ in ovary tissue exposed to 400 cGy of X-rays was manifested more strongly than in ovary tissue exposed to 600 cGy of X-rays, which was related to the phenomenon that granular cells of mature folliculus ovary underwent necrosis or apoptosis increasingly due to X-rays. In an electron microscope with high magnification, nuclei and protoplasm of granular cells in growing folliculus ovary abruptly underwent minute structural changes according to the increase of dose of X-rays. Cell residue, by-product of cell decease, neutrophil and macrophage around follicular antrum were observed. The minute structural changes in granular cells showed typical characteristics of apoptosis: the increase of electronic density due to nuclear condensation, fragmentation of nuclei and atrophy of protoplasm. Necrosis of cells was identified but it was not so remarkable. Macrophage with apoptotic bodies was scattered. Proportional to the radiation dose, we found that the generation of heterogeneous substance of normal ovary texture's follicular fluid, the emergence of dyeing characteristic in the basilar membrane of folicle, the generation of apoptosis, and the transformation of macrophages, etc. From this results, we can infer the possible radiation hazard on the ovary of cervix cancer patient with radiation therapy.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.3
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• pp.175-179
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• 2009

High concentrations of ATP induce membrane blebbing. However, the underlying mechanism involved in epithelial cells remains unclear. In this study, we investigated the role of the P2X7 receptor (P2X7R) in membrane blebbing using Par C5 cells. We stimulated the cells with 5 mM of ATP for 1${\sim}$2 hrs and found the characteristics of membrane blebbing, a hallmark of apoptotic cell death. In addition, 500 ${\mu}M$ Bz-ATP, a specific P2X7R agonist, induced membrane blebbing. However, 300 ${\mu}M$ of Ox-ATP, a P2X7R antagonist, inhibited ATP-induced membrane blebbing, suggesting that ATP-induced membrane blebbing is mediated by P2X7R. We found that ATP-induced membrane blebbing was mediated by ROCK I activation and MLC phosphorylation, but not by caspase-3. Five mM of ATP evoked a biphasic $[Ca^{2+}]_i$ response; a transient $[Ca^{2+}]_i$ peak and sustained $[Ca^{2+}]_i$ increase secondary to ATP-stimulated $Ca^{2+}$ influx. These results suggest that P2X7R plays a role in membrane blebbing of the salivary gland epithelial cells.

• International Journal of Oral Biology
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• v.33 no.1
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• pp.1-5
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• 2008

Adenosine 5'-triphosphate (ATP) is an important extracellular signaling molecule which is involved in a variety of physiological responses in many different tissues and cell types, by acting at P2 receptors, either ionotropic (P2X) or G protein-coupled metabotropic receptors (P2Y). P2X receptors have seven isoforms designated as $P2X_{1^-}P2X_7$. In this study, we investigated the electrophysiological and pharmacological properties of rat $P2X_{1^-}P2X_4$ currents by using whole-cell patch clamp technique in a heterologous expression system. When ATP-induced currents were analyzed in human embryonic kidney (HEK293) cells following transient transfection of rat $P2X_{1^-}P2X_4$, the currents showed different pharmacological and electrophysiological properties. ATP evoked inward currents with fast activation and fast desensitization in $P2X_{^1-}$ or $P2X_{3^-}$ expressing HEK293 cells, but in $P2X_{2^-}$ or $P2X_{4^-}$ expressing HEK293 cells, ATP evoked inward currents with slow activation and slow desensitization. While PPADS and suramin inhibited $P2X_2$ or $P2X_3$ receptor-mediated currents, they had little effects on $P2X_4$ receptor-mediated currents. Ivermectin potentiated and prolonged $P2X_4$ receptor-mediated currents, but did not affect $P2X_2$ or $P2X_3$ receptor-mediated currents. We suggest that distinct pharmacological and electrophysiological properties among P2X receptor subtypes would be a useful tool to determine expression patterns of P2X receptors in the nervous system including trigeminal sensory neurons and microglia.

• Journal of Life Science
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• v.13 no.1
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• pp.118-127
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• 2003

$\rho$-Fluorophenylalanine (FPA), a phenylalanine analog, is able to induce apoptotic cell death of human acute leukemia Jurkat T cells. To better understand the mechanism by which FPA induces apoptotic cell death, the effect of ectopic expression of antiapoptotic proteins, Bcl-2 and Bcl-xL, on FPA-induced apoptosis was investigated by employing lurkat T cells transfected with Bcl-2 gene (JT/Bcl-2) or Bcl-xL gene (1/Bcl-xL) and Jurkat T cells transfected with vector (JT/Neo or J/Neo). When Jurkat T cells, JT/Neo or J/Neo, were exposed to FPA at concentrations ranging from 0.63 to 5.0 mM, the cell viability determined by MTT assay declined in a dose-dependent manner. In addition, apoptotic DNA fragmentation along with several apoptotic events such as caspase-8 activation, Bid cleavage, mitochondrial cytochrome c release, caspase-9 activation, caspase-3 activation, and degradation of PARP was induced. However, the FPA-induced cytotoxic effect, activation of caspase-8, and cleavage of Bid were significantly abrogated by ectopic expression of Bcl-2 or Bcl-xL. At the same time, there was marked reduction in the level of cytochrome c release from mitorhondria, caspase-9 activation, caspase-3 activation, and degradation of PARP. These results indicate that caspase-8 activation, Bid cleavage, and mitochondrial cytochrome c release with subsequent activation of the caspase cascade are negatively regulated by Bcl-2 or Bcl-xL, and are thus required for FPA-induced apoptosis in Jurkat T cells

• Archives of Pharmacal Research
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• v.29 no.11
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• pp.1032-1041
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• 2006

Extracellular adenosine 5'-triphosphate (ATP) affects the function of many tissues and cells. To confirm the biological activity of ATP on human myeloid leukemic cells, F-36P and HL-60, cells were treated with a variety of concentrations of ATP. The stimulation with extracellular ATP induced the arrest of cell proliferation and cell death. from the analysis of Annexin-V staining and caspase activity by flow cytometry. The Annexin-V positive cells in both cell lines were dramatically increased following ATP stimulation. The expression of P2 purinergic receptor genes was confirmed, such as P2X1, P2X4, P2X5, P2X7 and P2Y1, P2Y2, P2Y4, P2Y5, P2Y6, P2Y11 in both leukemic cell lines. Interestingly, ATP induced intracellular calcium flux in HL-60 cells but not in F-36P cells, as determined by Fluo-3 AM staining. Cell cycle analysis revealed that ATP treatment arrested both F-36P and HL-60 cells at G1/G0. Taken together, these data showed that extracellular ATP via P2 receptor genes was involved in the cell proliferation and survival in human myeloid leukemic cells, HL-60 and F-36P cells by the induction of apoptosis and control of cell cycle. Our data suggest that treatment with extracellular nucleotides may be a novel and powerful therapeutic avenue for myeloid leukemic disease.

• Radiation Oncology Journal
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• v.18 no.1
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• pp.51-58
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• 2000

Purpose :The effect of PTK inhibitors (herbimycin A and genistein) on the induction of radiation-induced apoptosis in Ph-positive KS62 leukemia cell line was investigated. Materials and Methods :K562 cells in exponential growth phase were irradiated with a linear accelerator at room temperature. For 6 MV X-ray irradiation and drug treatment, cultures were initiated at 2×106 cells/mL. The cells were irradiated with 10 Gy. Stock solutions of herbimycin A and genistein were prepared in dimethyl sulphoxide (DMSO). After incubation at 37$^{\circ}C$ for 0$\~$48 h, the extent of apoptosis was determined using agarose gel electrophoresis and TUNEL assay. The progression of cells through the cell cycle after irradiation and drug treatment was also determined with flow cytometry. Western blot analysis was used to monitor bel-2, bel-X$_{L}$ and bax protein levels. Results :Treatment with 10 Gy X-irradiation did not result in the induction of apoptosis. The HMA alone (500 nM) also failed to induce apoptosis. By contrast, incubation of K562 cells with HMA after irradiation resulted in a substantial induction of nuclear condensation and fragmentation by agarose gel electro-phoresis and TUNEL assay. Genistein failed to enhance the ability of X-irradiation to induce DNA fragmentation. Enhancement of apoptosis by HMA was not attributable to downregulation of the bel-2 or bel-X$_{L}$ anti-apoptotic proteins. When the cells were irradiated and maintained with HMA, the percentage of cells in G2/M phase decreased to 30$\~$40$\%$ at 48 h. On the other hand, cells exposed to 10 Gy X-irradiation alone or maintained with genistein did not show marked cell cycle redistribution. Conclusion : We have shown that nanomolar concentrations of the PTK inhibitor HMA synergize with X-irradiation in inducing the apoptosis in Ph (+) K562 leukemia cell line. While, genistein, a PTK inhibitor which is not selective for p210$^{bcr/abl}$ failed to enhance the radiation induced apoptosis in KS62 cells. It is unlikely that the ability of HMA to enhance apoptosis in K562 cells is attributable to bel-2 family. It is plausible that the relationship between cell cycle delays and cell death is essential for drug development based on molecular targeting designed to modify radiation-induced apoptosis.