• 한국정보디스플레이학회:학술대회논문집
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• 2002.08a
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• pp.780-783
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• 2002

We report very efficient white OLEDs consisting of a blue-emitting 4,4'bis[N-(1-napthyl)-N-phenyl-amino]-biphenyl (${\alpha}$-NPD), a hole-blocking layer of 2,9-dimethyl-4, 7-diphenyl-1, 10-phenanthroline (BCP) doped with red fluorescent dye of 4-dicyanomethylene-2-methyl-6-[2-(2,3,6,7-tetrahydro- 1H, 5H-benzo[i,j]quinolizin-8-yl) vinyl]-4H-pyran) (DCM2), and green-emitting tris(8-hydroxyquinoline) aluminum ($Alq_3$). The device with the structure of ITO/${\alpha}$-NPD (50 nm)/BCP:DCM2 (0.8 %, 4 nm)/$Alq_3$ (50 nm)/LiF (0.5 nm)/Al shows a white emission with the CIE coordinates (0.329, 0.333). The maximum luminance of 20,800 cd/$m^2$ is obtained at 15.4 V. The power efficiency is 2.6lm/W and the external quantum efficiency is 2.1 % at a luminance of 100 cd/$m^2$ at the bias voltage of 6 V.

• Food Science and Biotechnology
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• v.15 no.1
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• pp.19-23
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• 2006

Effects of cheonggukjang on immunohistochemical reactions in gastrointestinal (GI) tract of rats were investigated. $CD4^+/CD8^+$ immunoreactive cells of cheonggukjang-fed diet groups were more strongly stained in lamina propria of mucosa and submucosa than those of basal diet group. Universal nitric oxide synthase immunoreactive density in colon was mildly stained in surface epithelium and mucous secretory gland, and strongly stained in submucosa and myenteric plexus in muscle layers of all cheonggukjang-fed diet groups. Protein kinase C-${\alpha}$ immunoreactive cells in colons of 15 and 25% cheonggukjang-fed diet groups were more strongly stained in mucosa, submucosa, and muscle layers than those of basal diet group. These results indicate mucosal immune activity, gastrointestinal motility, blood circulation, and physiological activities of enteroendocrine cells in GI tract could be increased with cheonggukjang intake.

• Journal of Pathology and Translational Medicine
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• v.52 no.6
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• pp.416-419
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• 2018

We describe a case of a 61-year-old Korean man who was diagnosed with renal cell carcinoma that was discovered on abdominopelvic computed tomography obtained after the patient complained of back pain. A radical nephrectomy was performed, and the surgical specimen showed a relatively well-circumscribed and yellowish lobulated hard mass. Microscopically, the tumor showed sheets and nests of hypercellular pleomorphic cells with thick fibrous septation, frequent mitoses, and areas of adrenal cortical-like tissue. Immunohistochemical staining revealed that the tumor cells were positive for inhibin-${\alpha}$, vimentin, synaptophysin, and melan A. It also revealed that the tumor cells were negative for pan-cytokeratin, epithelial membrane antigen, paired box 8, ${\alpha}$-methylacyl-coenzyme A racemase, CD10, cytokeratin 7, carbonic anhydrase 9, c-Kit, renal cell carcinoma, transcription factor E3, human melanoma black 45, desmin, smooth muscle actin, S-100, chromogranin A, CD34, anaplastic lymphoma kinase, and integrase interactor 1. Based on these histopathological and immunohistochemical findings, we diagnosed the tumor as intrarenal adrenocortical carcinoma arising in an adrenal rest. Several cases of intrarenal adrenocortical carcinoma have been reported, although they are very rare. Due to its poor prognosis and common recurrence or metastasis, clinicians and pathologists must be aware of this entity.

• Journal of Haehwa Medicine
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• v.18 no.1
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• pp.29-41
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• 2009

Wished to examine closely effect that SoPungDoJeokTang-KaMi (SPDJTK) medicines used to atopy dermatitis disease patient get in atopy eruption control experimentally. SPDJTK medicines controlled $CD4^+/IFN-\gamma$, and $CD4^+/CD25^+/foxp3^+$ revelation that an experiment that motive allergy immune reponse because an in vitro experiment stimulates T cells of a NC/Nga mouse same time by anti-CD40/rmIL-4, and interleukin-$1{\beta}$, IL-6, TNF-$\alpha$, and TGF-$\beta$ mRNA outturn that bear in T and B cells decreased remarkably by SPDJTK medicines. Intracellular staining of splenocytes anti-CD40/rmIL-4 plus rmIL-4 stimulated as described in a, assessed after 24 h, SPDJTK exerts a mainly immunosuppressive effect that acts at least partially through suppression of the transcription factor GATA3 expression in $CD4^+$ T cells. Atopic dermatitis (AD) usually develops in patients with an individual or family history of allergic diseases, and is characterized by chronic relapsing inflammation seen specially in childhood, association with IgE hyperproduction and precipitation by environmental factors. However, the exact etiology of AD has been unclear. To further explore the pathogenesis and treatment of AD, a suitable animal model is required. We found that skin lesions, which were clinically and histologically very similar to human AD, mite antigen-induced dermatitis on the face, neck, ears and dorsal skin of inbred NC/Nga mice. Result that Th1 cell and Th2 cell observe to be shifted by cytokine expression with $CD4^+/CD25^+/foxp3^+$ Treg cells induction by SPDJTK medicines could know that SPDJTK medicines can use usefully in allergy autoimmnune diease.

• Biomolecules & Therapeutics
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• v.17 no.4
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• pp.446-454
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• 2009

1-Furan-2-yl-3-pyridin-2-yl-propenone (FPP-3) has recently been synthesized and characterized to have an anti-inflammatory activity through the inhibition of the production of nitric oxide and tumor necrosis factor-$\alpha$. In the present study, adverse effects of FPP-3 on immune functions were determined in female BALB/c mice. When mice were administered orally with FPP-3 at 125, 250 or 500 mg/kg for 7 consecutive days, FPP-3 suppressed the number of antibody-forming cells and reduced thymus weight at 500 mg/kg. In addition, FPP-3 administered mice exhibited reduced splenic cellularity and numbers of splenocyte subsets, such as $CD3^+$ cells, $CD3^+CD4^+$ cells, $CD3^+CD8^+$ cells and macrophages. IL-4 mRNA expression was significantly suppressed by FPP-3 treatment. Moreover, the number of $CD4^+IL-4^+$ cells was reduced following the treatment of mice with 500 mg/kg of FPP-3. These results suggested that FPP-3 at 500 mg/kg might be immunotoxic, and that FPP-3-induced immunotoxicity might be mediated, at least in part, through the inhibition of cytokine production, such as IL-4.

• Proceedings of the Korean Vacuum Society Conference
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• 1994.02a
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• pp.43-43
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• 1994

We studied chemical reactio of Eu metal on the in situ cleaved CdTe(110) surface by pphotoemission sppectroscoppy using synchrotron radiation. The chamber was maintained with base ppressure $\leq$2${\times}$10-10 mb during the expperiment. The expperiment was carried out in pphoton Factory in Jappan. Core level pphotoemission sppectroscoppy was carried out with Al K${\alpha}$ Line. The CdTe simiconductor was determined to be pp-typpe with low dopping concentration from Hall measurement. We found that there are two reacted pphases of Te with Eu (related to divalent Eu and trivalent Eu, resppectively) from least square fitting of Te 4d sppectra, but three is no indication of Cd reaction. Trivalent Eu exists after roughly one monolayer depposition (600 sec. depposition time is considered as one monolayer), which is also observed at Eu 3d core level sppectra. Overlayer Eu is metallized after roughly 2 monolayers depposition, as can be deduced from the fact that metallic edge near Fermi level begins to appear. The intensity of core-level of Te decreases expponentially at the initial stage (near one monolayer) and after one monolayer depposition it decreases more slowly due to Te out-diffusion. We categorized the growth mode of Eu on CdTe as S-K growth mode (cluster formation after one monolayer deppisition) from the relative intensity pplot of Te 4d normalized to the cleaved surface. At cleaved surface band bending is already established due to surface defects. At first 100 sec. depposition time the shift toward lower binding side by 0.6 eV is found at all core level sppectra of all elements in semiconductor. This shift is considered as the re-adjustment of surface Fermi level to the pposition induced by Eu metal (0.2 eV above the valence band maximum).

• Molecular & Cellular Toxicology
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• v.5 no.3
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• pp.187-192
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• 2009

Toll-like receptors (TLRs) play an important role in host defense by sensing invading microbial pathogens. The stimulation of TLRs by microbial components triggers the activation of the myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter inducing interferon-$\beta$ (TRIF)-dependent downstream signaling pathways. TLR/MyD88 signaling pathway induces the activation of nuclear factor-kappa B (NF-${\kappa}B$) and the expression of inflammatory cytokine genes, including tumor necrosis factor-alpha, interleukin (IL)-6, IL-12, and IL-$1{\beta}$. On the other hand, TLR/TRIF signaling pathway induces the delayed-activation of NF-${\kappa}B$ and interferon regulatory factor 3 (IRF3), and the expression of type I interferons (IFNs) and IFN-inducible genes. The divalent heavy metal cadmium (Cd) is clearly toxic to most mammalian organ systems, especially the immune system. Yet, the underlying toxic mechanism(s) remain unclear. Cd inhibits the MyD88-dependent pathway by ceasing the activity of inhibitor-${\kappa}B$ kinase. However, it is not known whether Cd inhibits the TRIF-dependent pathway. Presently, Cd inhibited NF-${\kappa}B$ and IRF3 activation induced by lipopolysaccharide (LPS) and polyinosinic-polycytidylic acid. Cd inhibited LPS-induced IRF3 phosphorylation and IFN-inducible genes such as interferon inducible protein-10 and regulated on activation normal T-cell expressed and secreted (RANTES). These results suggest that Cd can modulate TRIF-dependent signaling pathways of TLRs.

• Parasites, Hosts and Diseases
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• v.51 no.3
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• pp.289-295
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• 2013

Different functions have been attributed to $CD4^+CD25^+Foxp3^+$ regulatory T-cells (Tregs) during malaria infection. Herein, we describe the disparity in Treg response and pro- and anti-inflammatory cytokines during infection with Plasmodium berghei ANKA between young (3-week-old) and middle-aged (8-month-old) C57BL/6 mice. Young mice were susceptible to cerebral malaria (CM), while the middle-aged mice were resistant to CM and succumbed to hyperparasitemia and severe anemia. The levels of pro-inflammatory cytokines, such as TNF-${\alpha}$, in young CM-susceptible mice were markedly higher than in middle-aged CM-resistant mice. An increased absolute number of Tregs 3-5 days post-inoculation, co-occurring with elevated IL-10 levels, was observed in middle-aged CM-resistant mice but not in young CM-susceptible mice. Our findings suggest that Treg proliferation might be associated with the suppression of excessive pro-inflammatory Th1 response during early malaria infection, leading to resistance to CM in the middle-aged mice, possibly in an IL-10-dependent manner.

• Journal of Haehwa Medicine
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• v.20 no.2
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• pp.1-16
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• 2012

In order to study the effect of CPS in the treatment of atopic dermatitis (AD), its role on various immune related cytokines were tested. Levels of liver and kidney function markers such as ALT, AST, BUN in NC/Nga mice were all normal indicating no toxicity in CPS treated group. Significant recovery from AD could be observed in CPS treated group through naked eye observation. Dermatitis index was significantly decreased after 11, 12, and 13 weeks of treatment. CD4+, CD8+, CD3+ /CD69+ immune cell ratio in DLN were decreased significantly by 37.2%, 49%, 20.8% in CPS treated group. CD4+ and CD11b+ /Gr-1+ immune cell ratio in dorsal skin were decreased significantly by 50.8% and 59.2% in CPS treated group. Expression of IL-4, IL-5, IL-6, IL-13 and TNF-${\alpha}$ in spleen were decreased by 78.8%, 97.8%, 64.7%, 73.6%, and 68.4%, respectively in CPS treated group. The results above strongly indicated the significant immune modulatory effect of CPS and thus clinical application of CPS on AD treatment.

• Journal of Haehwa Medicine
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• v.17 no.2
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• pp.167-183
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• 2008

KCSYJT medicines controlled $CD4^+/IFN-\gamma$, and $CD4^+/CD25^+/foxp3^+$ revelation that an experiment that motive allergy immune reponse because an in vitro experiment stimulates T cells of a NC/Nga mouse same time by anti-CD40/rmIL-4, and interleukin-$1{\beta}$, IL-6, TNF-$\alpha$, and TGF-$\beta$ mRNA outturn that bear in T and B cells decreased remarkably by KCSYJT medicines. Intracellular staining of splenocytes anti-CD40/rmIL-4 plus rmIL-4 stimulated as described in a, assessed after 24 h, KCSYJT exerts a mainly immunosuppressive effect that acts at least partially through suppression of the transcription factor GATA3 expression in $CD4^+$ T cells. We found that skin lesions, which were clinically and histologically very similar to human AD, mite antigen-induced dermatitis on the face, neck, ears and dorsal skin of inbred NC/Nga mice. Result that Th1 cell and Th2 cell observe to be shifted by cytokine expression with GATA3 regulation by KCSYJT medicines could know that KCSYJT medicines can use usefully in allergy autoimmnune diease.