• Proceedings of the Korean Vacuum Society Conference
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• 2011.08a
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• pp.373-373
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• 2011

$Cu(In,Ga)Se_2$(CIGS) 박막 태양전지는 Chalcopyrite계 박막 태양전지로 Cu, In, Ga, Se 각 원소의 조성을 적절히 조절하여 박막을 성장시킨다. 성장시킨 CIGS 박막은 광흡수계수가 105cm-1로 다른 물질 보다 뛰어나고 직접 천이형 반도체로서 얇은 두께로도 고효율의 박막 제작이 가능하다. 얇은 두께로도 충분히 빛의 흡수가 가능하지만, cell 표면 반사에 의한 광 손실은 cell 효율을 떨어뜨리게 된다. 본 연구에서는 CIGS 박막 태양전지의 광 흡수 향상을 위해 굴절률이 1.86인 ITO 위에 ITO보다 굴절률이 작은 $MgF_2$ (n=1.377) [1]를 80, 100, 120, 140 nm로 증착하여 $MgF_2$/Al/Ni/ITO/i-ZnO/CdS/CIGS/Mo/SLG 시료를 제작하고, optical reflectance, Quantum Efficiency를 이용하여 분석하였다. optical reflectance 분석 결과, $MgF_2$ AR coating을 한 경우, 두께가 두꺼워짐에 따라 광 반사도가 감소하는 경향을 보였다. 또한 AR coating 두께가 커짐에 따라 fluctuation이 점점 커지며, 파형이 장파장 쪽으로 shift하는 것을 관찰 할 수 있었다. Quantum efficiency (QE)를 분석한 결과 $MgF_2$ AR coating 할 경우, 측정된 대부분의 파장에서 QE가 향상되는 것을 확인할 수 있었다. 하지만 AR coating 두께에 따른 변화는 뚜렷한 차이를 보이지 않았다. AR coating 결과, JSC가 증가하여 efficiency가 향상되는 것을 확인 할 수 있다. 그러나 $MgF_2$ AR coating 80~140 nm 범위에서 cell 효율 변화의 뚜렷한 차이는 관찰할 수 없었다.

• BMB Reports
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• v.56 no.6
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• pp.359-364
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• 2023

KAI1/CD82, a membrane tetraspanin protein, can prevent various cancers and retinal disorders through its anti-angiogenic and anti-metastatic capacity. However, little is known about its anti-inflammatory effect and molecular mechanism. Therefore, the present study aimed to inLPSvestigate effect of a recombinant protein of the large extracellular domain of human KAI1 (Gly 111-Leu 228, rhKAI1) on lipopolysaccharides (LPS)-stimulated RAW264.7 macrophage-like cells and mouse bone marrow-derived macrophages (BMDM) and to identify its underlying mechanism. Our data showed that rhKAI1 suppressed expression levels of classically macrophages (M1) phenotype-related surface markers F4/80+CD86+ in LPS-stimulated BMDM and RAW264.7 cells. In addition, LPS markedly increased mRNA expression and release levels of pro-inflammatory cytokines and mediators such as interleukin (IL)-1β, IL-6, tumor necrosis factor-α, cyclooxygenase-2, nitric oxide and prostaglandin E2, whereas these increases were substantially down-regulated by rhKAI1. Furthermore, LPS strongly increased expression of NF-κB p65 in the nuclei and phosphorylation of ERK, JNK, and p38 MAPK. However, nuclear translocation of NF-κB p65 and phosphorylation of JNK were greatly reversed in the presence of rhKAI1. Especially, rhKAI1 markedly suppressed expression of toll-like receptor (TLR4) and prevented binding of LPS with TLR4 through molecular docking predict analysis. Importantly, Glu 214 of rhKAI1 residue strongly interacted with Lys 360 of TLR4 residue, with a binding distance of 2.9 Å. Taken together, these findings suggest that rhKAI1 has an anti-inflammatory effect on LPS-polarized macrophages by interacting with TLR4 and down-regulating the JNK/NF-κB signaling pathway.