• 공업화학
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• 제17권4호
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• pp.397-402
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• 2006

TFT-LCD TV용 백라이트 유니트(BLU)의 각 구성성분이 최종 광확산필름의 물리적, 전기적, 열적, 광학적 특성에 미치는 영향에 관하여 고찰하였다. 블로킹 방지층에 있어서는 $6{\mu}m$의 아크릴 비드를 0.5~1.5 wt%로 첨가했을 때 블로킹 방지성이 우수하였고, 4급 암모니움 염을 0.8 wt%로 첨가하였을 경우 Decay-Time 및 수분에 대한 안정성이 가장 우수한 결과를 나타내었다. 광확산층에 있어서는 아크릴 폴리올을 바인더 수지로서 사용하고, 무황변 타입의 HDI계 경화제를 바인더 수지에 대해 30~35 wt%로 첨가하였을 경우가 PET 필름 표면상에의 접착력, 경화속도 및 유연성 측면에서 가장 우수한 결과를 보였다. 또한 $20{\mu}m$의 다분산형 폴리스티렌($20{\mu}m$ PS) 및 폴리메틸메타크릴레이트($20{\mu}m$ PMMA) 비드를 바인더 수지 대비 250 wt%로 첨가하였을 경우에 가장 높은 법선휘도값을 얻을 수 있었으며, PS 입자를 사용했을 경우보다는 PMMA 입자를 사용했을 경우가 투과율 차이로 인해 더 높은 법선휘도값을 나타내었다.

• 한방안이비인후피부과학회지
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• 제20권2호통권33호
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• pp.89-101
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• 2007

Objectives : This study was carried out to investigate the effects of Jeondo-San(JDS) on anti-Inflammation and anti-Propionibacterium acnes. Methods : The effects of JDS on anti-Inflammation and anti-Propionibacterium acnes were measured by the cytotoxicity of Raw 264.7 cell, the inhibition for NO, $TNF-{\alpha}$, $PGE_2$, iNOS and COX-2, the blocking $NF-{\kappa}B$ into nucleus and the sterilizing power for Propionibacterium acnes. Results : 1. All concentrations of JDS has no cytotoxicity in Raw 264.7 cell. 2. All concentrations of JDS inhibited the production of NO in the Raw 264.7 cell stimulated with LPS. 3. All concentrations of JDS did not significantly inhibit the production of $TNF-{\alpha}$ in the Raw 264.7 cell stimulated with LPS. 4. All concentrations of JDS inhibited the production of $PGE_2$ in the Raw 264.7 cell stimulated with LPS. 5. All concentrations of JDS did not inhibit the expression of COX-2 but concentrations of 50\;{\mu}g/ml$, 100\;{\mu}g/ml$ JDS inhibited iNOS expression in the Raw 264.7 cell stimulated with LPS. 6. Concentrations of 50\;{\mu}g/ml$, 100\;{\mu}g/ml$ JDS has the effect of blocking $NF-{\kappa}B$ into nucleus in LPS-induced macrophage Raw 264.7 cell. 7. All concentrations of IDS did not have the inhibitory effect of Propionibactrium acnes. Conclusions : The present date suggest that JDS has a effect on the stage of inflammation of acne.

• 한국안광학회지
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• 제13권3호
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• pp.7-12
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• 2008

목적: 투명과 착색 안경렌즈의 자외선 차단 특성을 평가하고자 하였다. 방법: 안경렌즈의 투과 스펙트럼은 ANSI Z80.1에 제시된 방법으로 측정하였고, UV(200~380 nm; UVA, UVB, UVC) 및 청색광 영역(380~400 nm)에 대하여 각 렌즈의 투과율을 계산하였다. 결과: 중굴절률, 고굴절률의 투명 플라스틱 렌즈 및 착색 플라스틱 렌즈는 UV에서 우수한 자외선 차단 특성을 보였으나, 자외선 차단제를 처리하지 않은 크라운 유리나 CR39는 그렇지 않았다. 고굴절률 렌즈와 눈부심 방지 야간용 렌즈를 제외한 모든 렌즈는 청색광을 효과적으로 차단하지 않았다. 결론: 크라운 유리와 CR39 렌즈는 UV로부터 눈을 보호하기 위해서 자외선 차단제가 필요하다. 또한 고굴절률 렌즈와 눈부심 방지 야간용 렌즈를 제외한 모든 렌즈는 청색광으로부터 눈을 보호하기 위해서 청색광 차단제가 필요하다.

• 한국산학기술학회논문지
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• 제17권12호
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• pp.482-487
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• 2016

파장 400 nm 이하의 자외선은 눈 건강에 매우 해롭다. 특히 UVA (315 nm ~ 400 nm)는 백내장, 설안염, 초자체경화 등을 유발할 수 있고, UVB (280 nm ~ 315 nm)는 결막염, 각막염 및 설안염 등을 일으킬 수 있다. 따라서 폴리머 안경렌즈를 사용함에 있어서 자외선의 차단 기능과 가시광선 영역에서 투과되는 빛을 증가시키고, 안경렌즈 표면에서 형성되는 허상을 방지하는 반사방지 기능은 매우 중요하다. 본 연구에서는 m-자일릴렌 디이소시아네이트 모노머와 2,3-Bis-1-propanethiol 모노머 및 벤조트리아졸 UV 흡수제 (SEESORB 709), 안료 혼합물, 이염화 이부틸 주석 촉매제, 알킬인산 에스터 이형제 등의 혼합물을 인젝션 몰드 방법으로 열중합 공정을 적용하여, 굴절률 1.67의 고굴절률 폴리머 안경렌즈를 제조하였다. 폴리머 안경렌즈 표면에서의 반사를 줄이기 위하여 렌즈 양면에 다층박막 반사방지 코팅을 E-beam 증착 시스템으로 코팅하였다. 자외선 차단 폴리머 안경렌즈의 광학적 특성을 UV-visible spectrometer로 분석하였고, 반사방지층을 구성하는 박막의 굴절률, 표면거칠기 등과 같은 박막소재 특성을 각각 Ellipsometry 및 원자힘 현미경으로 분석하였다. 분석 결과 제조된 안경렌즈는 395 nm 파장 이하의 자외선을 99% 이상 완벽하게 차단하였다.

• Natural Product Sciences
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• 제10권5호
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• pp.211-216
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• 2004

Citrus unshiu (Rutaceae) has long been known as an anti-inflammatory and anti-allergic agent. In the present study, the inhibitory effect of CUWE (Citus unshiu water extract) on the production of $TNF-{\alpha}$ and tryptase was examined. In addition, a possible mechanism for the inhibition of trypsin-stimulated human leukemic mast cell-1 (HMC- 1 ) activation was determined. To do so, $TNF-{\alpha}$ production from the HMC-1 cells that were stimulated by trypsin (100 nM) in the presence or absence of CUWE $(10,\;100,\;and\;100\;{\mu}g/ml)$ was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-PCR. The tryptase production was evaluated by reverse transcription-PCR. Extracellular signal-regulated kinase (ERK) activation was analyzed by Western blot. Trypsin activity was measured by using Bz-DL-Arg-p-nitroanilide (BAPNA) as substrate. Results showed that the CUWE inhibited production of both $TNF-{\alpha}$ and tryptase from the trypsin-stimulated HMC-1 in a dose-dependent manner. The CUWE a1so inhibited the ERK phosphorylation and trysin activity. These results indicate that the CUWE had an inhibitory effect on $TNF-{\alpha}$ and the tryptase productions by blocking the ERK phosphorylation and trypsin activity.

• Preventive Nutrition and Food Science
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• 제20권4호
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• pp.221-229
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• 2015

Hesperidin has been shown to possess a potential inhibitory effect on vascular formation in endothelial cells. However, the fundamental mechanism for the anti-angiogenic activity of hesperidin is not fully understood. In the present study, we evaluated whether hesperidin has anti-angiogenic effects in mouse embryonic stem cell (mES)-derived endothelial-like cells, and human umbilical vascular endothelial cells (HUVECs), and evaluated their mechanism via the AKT/mammalian target of rapamycin (mTOR) signaling pathway. The endothelial cells were treated with several doses of hesperidin (12.5, 25, 50, and $100{\mu}M$) for 24 h. Cell viability and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. Alteration of the AKT/mTOR signaling in vascular formation was analyzed by western blot. In addition, a mouse aortic ring assay was used to determine the effect of hesperidin on vascular formation. There were no differences between the viability of mES-derived endothelial-like cells and HUVECs after hesperidin treatment. However, hesperidin significantly inhibited cell migration and tube formation of HUVECs (P<0.05) and suppressed sprouting of microvessels in the mouse aortic ring assay. Moreover, hesperidin suppressed the expression of AKT and mTOR in HUVECs. Taken together, these findings suggest that hesperidin inhibits vascular formation by blocking the AKT/mTOR signaling pathways.

• 한국자원식물학회지
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• 제31권6호
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• pp.634-640
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• 2018

Aralia cordata (A. cordata), which belongs to Araliaceae, is a perennial herb widely distributed in East Asia. We evaluated the anti-inflammatory effect of stems (AC-S), roots (AC-R) and leaves (AC-L) extracted with 100% methanol of A. cordata and elucidated the potential signaling pathway in LPS-stimulated RAW264.7 cells. The AC-L showed a strong anti-inflammatory activity through inhibition of NO production. AC-L dose-dependently inhibited NO production by suppressing iNOS, COX-2 and $IL-{\beta}$ expression in LPS-stimulated RAW264.7 cells. AC-L inhibited the degradation and phosphorylation of $I{\kappa}B-{\alpha}$, which donated to the inhibition of p65 nuclear accumulation and $NF-{\kappa}B$ activation. Furthermore, AC-L suppressed the phosphorylation of ERK1/2 and p38. These results suggested that AC-L may utilize anti-inflammatory activity by blocking $NF-{\kappa}B$ and MAPK signaling pathway and indicated that the AC-L can be used as a natural anti-inflammatory drugs.

• Journal of Power Electronics
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• 제17권1호
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• pp.242-252
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• 2017

This paper deals with the blocking of DC-fault current during DC cable short-circuit conditions in HVDC (High-Voltage DC) transmission systems utilizing Modular Multilevel Converters (MMCs), where a new SubModule (SM) topology circuit for the MMC is proposed. In this SM circuit, an additional Insulated-Gate Bipolar Translator (IGBT) is required to be connected at the output terminal of a conventional SM with a half-bridge structure, hereafter referred to as HBSM, where the anti-parallel diodes of additional IGBTs are used to block current from the grid to the DC-link side. Compared with the existing MMCs based on full-bridge (FB) SMs, the hybrid topologies of HBSM and FBSM, and the clamp-double SMs, the proposed topology offers a lower cost and lower power loss while the fault current blocking capability in the DC short-circuit conditions is still provided. The effectiveness of the proposed topology has been validated by simulation results obtained from a 300-kV 300-MW HVDC transmission system and experimental results from a down-scaled HVDC system in the laboratory.

• Journal of information and communication convergence engineering
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• 제10권3호
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• pp.295-299
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• 2012

Defect generation during organic bottom anti-reflective coating (BARC) in the photo lithography process is closely related to humidity control in the BARC coating unit. Defects are related to the water component due to the humidity and act as a blocking material for the etching process, resulting in an extreme pattern bridging in the subsequent BARC etching process of the poly etch step. In this paper, the lower limit for the humidity that should be stringently controlled for to prevent defect generation during BARC coating is proposed. Various images of defects are inspected using various inspection tools utilizing optical and electron beams. The mechanism for defect generation only in the specific BARC coating step is analyzed and explained. The BARC defect-induced gate pattern bridging mechanism in the lithography process is also well explained in this paper.

• IMMUNE NETWORK
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• 제16권2호
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• pp.134-139
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• 2016

Programmed death-1 (PD-1) is a strong negative regulator of T lymphocytes in tumor-microenvironment. By engaging PD-1 ligand (PD-L1) on tumor cells, PD-1 on T cell surface inhibits anti-tumor reactivity of tumor-infiltrating T cells. Systemic blockade of PD-1 function using blocking antibodies has shown significant therapeutic efficacy in clinical trials. However, approximately 10 to 15% of treated patients exhibited serious autoimmune responses due to the activation of self-reactive lymphocytes. To achieve selective activation of tumor-specific T cells, we generated T cells expressing a dominant-negative deletion mutant of PD-1 (PD-1 decoy) via retroviral transduction. PD-1 decoy increased IFN-γ secretion of antigen-specific T cells in response to tumor cells expressing the cognate antigen. Adoptive transfer of PD-1 decoy-expressing T cells into tumor-bearing mice potentiated T cell-mediated tumor regression. Thus, T cell-specific blockade of PD-1 could be a useful strategy for enhancing both efficacy and safety of anti-tumor T cell therapy.