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      • SCIESCOPUSKCI등재

        Effects of Oral Intake of Kimchi-Derived Lactobacillus plantarum K8 Lysates on Skin Moisturizing

        ( Hangeun Kim ),( Hye Rim Kim ),( Bong Jun Jeong ),( Seung Su Lee ),( Tae Rahk Kim ),( Ji Hye Jeong ),( Miyeong Lee ),( Sinai Lee ),( Jong Suk Lee ),( Dae Kyun Chung ) 한국미생물 · 생명공학회 2015 Journal of microbiology and biotechnology Vol.25 No.1

        Skin is the soft outer covering of vertebrates that provides protection from pathogenic infection, physical damage, or UV irradiation, and controls body temperature and water content. In this study, we examined the effects of oral intake of kimchi-derived Lactobacillus plantarum K8 lysates on skin moisturizing. In an in vitro study, we observed that the hyaluronic acid content increased in HaCaT cells treated with L. plantarum K8 lysates. Oral administration of L. plantarum K8 lysates effectively attenuated the horny layer formation and decreased epidermal thickening in DNCB-treated SKH-1 hairless mice skin. The damage to barrier function was reduced after 8 weeks of oral administration of L. plantarum K8 lysates as compared with that in the atopic dermatitis mice. For the test with volunteers, we manufactured experimental candy containing 2.1% L. plantarum K8 lysates, while control candy did not contain bacterial lysate. A significant increase in hydration in the experimental candy-administered group as compared with the control candy-administered group was observed on the face after 4 and 8 weeks, and on the forearm after 4 weeks. Decreases in horny layer thickness and TEWL value were observed on the face and forearm of the experimental group. Together, the in vitro cell line and in vivo mouse studies revealed that L. plantarum K8 lysates have a moisturizing effect. A clinical research study with healthy volunteers also showed an improvement in barrier repair and function when volunteers took L. plantarum K8 lysates-containing candy. Thus, our results suggest that L. plantarum K8 lysates may help to improve skin barrier function.

      • SCISCIESCOPUS

        Conventional Dendritic Cells Impair Recovery after Myocardial Infarction

        Lee, Jun Seong,Jeong, Se-Jin,Kim, Sinai,Chalifour, Lorraine,Yun, Tae Jin,Miah, Mohammad Alam,Li, Bin,Majdoubi, Abdelilah,Sabourin, Antoine,Keler, Tibor,Guimond, Jean V.,Haddad, Elie,Choi, Eui-Young,Ep American Association of Immunologists 2018 Journal of Immunology Vol. No.

        <P>Ischemic myocardial injury results in sterile cardiac inflammation that leads to tissue repair, two processes controlled by mononuclear phagocytes. Despite global burden of cardiovascular diseases, we do not understand the functional contribution to pathogenesis of specific cardiac mononuclear phagocyte lineages, in particular dendritic cells. To address this limitation, we used detailed lineage tracing and genetic studies to identify bona fide murine and human CD103<SUP>+</SUP> conventional dendritic cell (cDC)1s, CD11b<SUP>+</SUP> cDC2s, and plasmacytoid DCs (pDCs) in the heart of normal mice and immunocompromised NSG mice reconstituted with human CD34<SUP>+</SUP> cells, respectively. After myocardial infarction (MI), the specific depletion of cDCs, but not pDCs, improved cardiac function and prevented adverse cardiac remodeling. Our results showed that fractional shortening measured after MI was not influenced by the absence of pDCs. Interestingly, however, depletion of cDCs significantly improved reduction in fractional shortening. Moreover, fibrosis and cell areas were reduced in infarcted zones. This correlated with reduced numbers of cardiac macrophages, neutrophils, and T cells, indicating a blunted inflammatory response. Accordingly, mRNA levels of proinflammatory cytokines IL-1β and IFN-γ were reduced. Collectively, our results demonstrate the unequivocal pathological role of cDCs following MI.</P>

      • Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux

        Jeong, Se-Jin,Kim, Sinai,Park, Jong-Gil,Jung, In-hyuk,Lee, Mi-Ni,Jeon, Sejin,Kweon, Hyae Yon,Yu, Dae-Yeul,Lee, Sang-Hak,Jang, Yangsoo,Kang, Sang Won,Han, Ki-Hwan,Miller, Yury I.,Park, Young Mi,Cheong, LANDES BIOSCIENCE 2018 AUTOPHAGY Vol.14 No.1

        <P><B>ABSTRACT</B></P><P>Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous antioxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the antioxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other antioxidant enzymes in monocytes and macrophages. We determined that <I>Prdx1</I> deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages. <I>Prdx1</I>-deficient macrophages had higher intracellular cholesterol mass and lower cholesterol efflux compared with wild type. This perturbation in cholesterol homeostasis was due to impaired lipophagic cholesterol hydrolysis caused by excessive oxidative stress, resulting in the inhibition of free cholesterol formation and the reduction of NR1H3 (nuclear receptor subfamily 1, group H, member 3) activity. Notably, impairment of both lipophagic flux and cholesterol efflux was restored by the 2-Cys PRDX-mimics ebselen and gliotoxin. Consistent with this observation, <I>apoe <SUP>−/−</SUP></I> mice transplanted with bone marrow from <I>prdx1<SUP>−/−</SUP>apoe<SUP>−/−</SUP></I> mice had increased plaque formation compared with <I>apoe<SUP>−/−</SUP></I> BM-transplanted recipients. This study reveals that PRDX1 is crucial to regulating lipophagic flux and maintaining macrophage cholesterol homeostasis against oxidative stress. We suggest that PRDX1-dependent control of oxidative stress may provide a strategy for treating atherosclerosis and autophagy-related human diseases.</P>

      • KCI등재

        밀크세라마이드와 저분자 피쉬콜라겐 복합 섭취에 의한 피부보습 시너지 효과

        시혜정(Hye-Jeong See),김윤석(Yoon Seok Kim),박석준(Seok Jun Park),양진오(Jin Oh Yang),이시내(Sinai Lee),김혜진(Hye-Jin Kim) 한국식품영양과학회 2021 한국식품영양과학회지 Vol.50 No.3

        본 연구에서는 밀크세라마이드와 저분자 피쉬콜라겐의 복합 섭취가 피부의 수분 및 탄력 변화의 시너지 효과를 나타내는지 연구하였다. 만 39~50세 여성을 밀크세라마이드, 저분자 피쉬콜라겐, 밀크세라마이드 및 저분자 피쉬콜라겐 혼합 섭취군으로 나누어 각 7명씩 4주간 섭취하도록 한 후 밀크세라마이드와 저분자 피쉬콜라겐의 혼합 섭취의 시너지 효과를 평가하고자 하였다. 섭취 전후 피부보습 인자(피부수분량, 경피수분손실량) 및 피부탄력 인자(피부탄력, 진피치밀도)의 변화를 측정하여 섭취군 간 및 섭취 전후 변화량을 비교하였다. 피부수분량과 경피수분손실량에서 밀크세라마이드 및 콜라겐 혼합 섭취군의 변화량이 밀크세라마이드군, 저분자 피쉬콜라겐군 단독 섭취 대비 개선된 것으로 나타났다. 또한 피부탄력 변화에서는 밀크세라마이드 및 저분자 콜라겐 혼합 섭취군의 탄력 증가율이 가장 높게 나타났으나, 군 간의 변화량에서 유의적인 변화는 나타내지 않았다. 진피치밀도 역시 밀크세라마이드군, 저분자 피쉬콜라겐군에서 감소하였으나, 밀크세라마이드 및 저분자 피쉬콜라겐 혼합 섭취에서 진피치밀도가 상승하였다. 다만 콜라겐과 세라마이드의 섭취 기간과 농도에 따라 탄력 섬유망의 형성기간, 피부의 수화 정도에 변화를 줄 수 있기 때문에 섭취기간 및 섭취 양에 따른 추가 연구가 필요할 것으로 사료된다. 본 연구에서는 밀크세라마이드와 저분자 피쉬콜라겐의 복합 섭취가 개별 섭취 대비 피부보습 및 피부탄력 향상에 시너지 효과를 나타냄으로써 피부 건강 소재로 활용될 수 있는 근거가 될 것으로 생각된다. The milk-derived milk ceramide (MC) and low molecular fish collagen (LFC) are materials that are effective in skin hydration and elasticity, and are widely used as skin functional ingredients. This study undertook a clinical trial to evaluate the synergistic effects of MC and LFC complex on skin hydration and elasticity. Participants (n=21) were randomly assigned to receive either MC, LFC, or a complex of MC and LFC, twice a day for 4 weeks. Skin hydration, transepidermal water loss (TEWL), elasticity and dermis density were assessed before and after the 4 weeks administration. Compared to the MC and LFC groups, skin hydration and TEWL were significantly improved (P<0.05) in the MC+LFC group after 4 weeks. Both skin elasticity and dermis density also showed improvement in the MC+LFC group after 4 weeks, but was not significantly different. Taken together, these results indicate that the mixture of MC and LFC exerts a synergistic effect in improving human skin hydration, as compared to MC and LFC administration individually.

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