• 제목/요약/키워드: Flow-through Cell

검색결과 650건 처리시간 0.029초

고분자 전해질 연료전지용 수소극 촉매층의 이오노머 함량 영향 (Effect of Ionomer Content on the Anode Catalyst Layers of PEM Fuel Cells)

  • 박범준;이선호;우승희;박석희;정남기;임성대
    • 한국수소및신에너지학회논문집
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    • 제30권6호
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    • pp.523-530
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    • 2019
  • For the low-Pt electrodes for polymer electrolyte fuel cells (PEMFCs), the optimization of ionomer content for anode catalyst layers was carried out. A commercial catalyst of 20 wt.% Pt/C was used instead of 50 wt.% Pt/C which is commonly used for PEMFCs. The ionomer content varies from 0.6 to 1.2 based on ionomer to carbon ratio (I/C) and the catalyst layer is formed over the electrolyte by the ultrasonic spray process. Evaluation of the prepared MEA in the unit cell showed that the optimal ionomer content of the air electrode was 0.8 on the I/C basis, while the hydrogen electrode was optimal at the relatively high ionomer content of 1.0. In addition, a large difference in cell performance was observed when the ionomer content of the hydrogen electrode was changed. Increasing the ionomer content from 0.6 to 1.0 by I/C in a hydrogen electrode with 0.05 mg/㎠ platinum loading resulted in more than double cell performance improvements on a 0.6 V. Through the analysis of various electrochemical properties in the single cell, it was assumed that the change in ionomer content of the hydrogen electrode affects the water flow between the hydrogen and air electrodes bounded by the membrane in the cell, which affects the overall performance of the cell. A more specific study will be carried out to understand the water flow mechanism in the future, and this study will show that the optimization process of hydrogen electrode can also be a very important cell design variable for the low-Pt and high-performance MEA.

세포 크기 차이를 이용한 유세포 분석을 통한 인간배아줄기세포 유래 기능성 혈관세포의 확립 (Establishment of Functional Cells for Vascular Defect Disease from Human Embryonic Stem Cell via Region Sorting Depending on Cell Volume)

  • 이지혜;김주미;정형민;채정일
    • 한국미생물·생명공학회지
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    • 제39권4호
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    • pp.364-373
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    • 2011
  • 인간배아줄기세포는 인간배아줄기세포가 가지는 전 분화능 등의 특이적 특성으로 인해 재생의학 분야에서 세포 치료제의 근원으로 널리 각광받고 있다. 그러나, 미분화 상태의 인간배아줄기세포를 세포치료제로 이용하기 위해서는 인간배아줄기세포 주 유래 기능성 세포를 확립이 반드시 요구된다. 본 연구에서는, 미분화 상태의 인간배아줄기세포주로부터 기능성 세포의 확립을 위해, 혈관계통의 세포로 분화를 유도하였으며, 분화 유도 후 세포의 크기 차이를 이용하여 특정 세포군 만을 분리하여 그 기능성을 비교 분석하였다. 그 결과, VEGF를 이용하여 분화 시킨 세포군에서 약 10%의 PECAM 양성 세포군을 확인할 수 있었으며, 분리 및 세포 이식을 위해 세포를 단일 세포군으로 만들었다. 단일 세포군의 형성 후, 유세포 분석기를 이용한 세포 분리 기법을 이용하여 FCS를 기준으로 한 세포 크기의 차이를 이용하여 특정 세포군 만을 분리하여, 하지 허혈 동물 모델로의 이식을 통해, 비 분리 세포군과 치료 효능을 비교 분석을 실시하였다. 세포 이식 4주 후, 혈류량 복구율이 FSC 기준 분리 군의 경우 54%, 비 분리군의 경우 17%를 보이는 것을 확인하였다. 이 결과는, 초기 분화 유도 후 세포 크기차이를 이용한 세포 분리법이 기능성 세포 획득에 이용될 수 있음을 시사한다. 이와 같은 방법을 통해 다양한 종류의 기능성 세포 분리에 이용될 수 있을 것이라 생각된다.

Role of soy lecithin combined with soy isoflavone on cerebral blood flow in rats of cognitive impairment and the primary screening of its optimum combination

  • Hongrui Li;Xianyun Wang;Xiaoying Li;Xueyang Zhou;Xuan Wang;Tiantian Li;Rong Xiao;Yuandi Xi
    • Nutrition Research and Practice
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    • 제17권2호
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    • pp.371-385
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    • 2023
  • BACKGROUND/OBJECTIVES: Soy isoflavone (SIF) and soy lecithin (SL) have beneficial effects on many chronic diseases, including neurodegenerative diseases. Regretfully, there is little evidence to show the combined effects of these soy extractives on the impairment of cognition and abnormal cerebral blood flow (CBF). This study examined the optimal combination dose of SIF + SL to provide evidence for improving CBF and protecting cerebrovascular endothelial cells. MATERIALS/METHODS: In vivo study, SIF50 + SL40, SIF50 + SL80 and SIF50 + SL160 groups were obtained. Morris water maze, laser speckle contrast imaging (LSCI), and hematoxylin-eosin staining were used to detect learning and memory impairment, CBF, and damage to the cerebrovascular tissue in rat. The 8-hydroxy-2'-deoxyguanosine (8-OHdG) and the oxidized glutathione (GSSG) were detected. The anti-oxidative damage index of superoxide dismutase (SOD) and glutathione (GSH) in the serum of an animal model was also tested. In vitro study, an immortalized mouse brain endothelial cell line (bEND.3 cells) was used to confirm the cerebrovascular endothelial cell protection of SIF + SL. In this study, 50 µM of Gen were used, while the 25, 50, or 100 µM of SL for different incubation times were selected first. The intracellular levels of 8-OHdG, SOD, GSH, and GSSG were also detected in the cells. RESULTS: In vivo study, SIF + SL could increase the target crossing times significantly and shorten the total swimming distance of rats. The CBF in the rats of the SIF50 + SL40 group and SIF50 + SL160 group was enhanced. Pathological changes, such as attenuation of the endothelium in cerebral vessels were much less in the SIF50 + SL40 group and SIF50 + SL160 group. The 8-OHdG was reduced in the SIF50 + SL40 group. The GSSG showed a significant decrease in all SIF + SL pretreatment groups, but the GSH showed an opposite result. SOD was upregulated by SIF + SL pretreatment. Different combinations of Genistein (Gen)+SL, the secondary proof of health benefits found in vivo study, showed they have effective anti-oxidation and less side reaction on protecting cerebrovascular endothelial cell. SIF50 + SL40 in rats experiment and Gen50 + SL25 in cell test were the optimum joint doses on alleviating cognitive impairment and regulating CBF through protecting cerebrovascular tissue by its antioxidant activity. CONCLUSIONS: SIF+SL could significantly prevent cognitive defect induced by β-Amyloid through regulating CBF. This kind of effect might be attributed to its antioxidant activity on protecting cerebral vessels.

Blocking Bcl-2 Leads to Autophagy Activation and Cell Death of the HEPG2 Liver Cancer Cell Line

  • Du, Peng;Cao, Hua;Wu, Hao-Rong;Zhu, Bao-Song;Wang, Hao-Wei;Gu, Chun-Wei;Xing, Chun-Gen;Chen, Wei
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권10호
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    • pp.5849-5854
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    • 2013
  • Background: Apoptosis may be induced after Bcl-2 expression is inhibited in proliferative cancer cells. This study focused on the effect of autophagy activation by ABT737 on anti-tumor effects of epirubicin. Methods: Cytotoxic effects of ABT737 on the HepG2 liver cancer cell line were assessed by MTT assay and cell apoptosis through flow cytometry. Mitochondrial membrane potential was measured by fluorescence microscopy. Monodansylcadaverin (MDC) staining was used to detect activation of autophagy. Expression of p53, p62, LC3, and Beclin1, apoptotic or autophagy related proteins, was detected by Western blotting. Results: ABT737 and epirubicin induced growth inhibition in HepG2 cells in a dose- and time-dependent manner. Both ABT737 and epirubicin alone could induce cell apoptosis with a reduction in mitochondrial membrane potential as well as increased apoptotic protein expression. Further increase of apoptosis was detected when HepG2 cells were co-treated with ABT373 and epirubicin. Furthermore, our results demonstrated that ABT373 or epirubicin ccould activate cell autophagy with elevated autophagosome formation, increased expression of autophagy related proteins and LC3 fluorescent puncta. Conclusions: ABT737 influences cancer cells through both apoptotic and autophagic mechanisms, and ABT737 may enhance the effects of epirubicin on HepG2 cells by activating autophagy and inducing apoptosis.

Effects of MicroRNA-106 on Proliferation of Gastric Cancer Cell through Regulating p21 and E2F5

  • Yao, Yong-Liang;Wu, Xiao-Yang;Wu, Jian-Hong;Gu, Tao;Chen, Ling;Gu, Jin-Hua;Liu, Yun;Zhang, Qing-Hui
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권5호
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    • pp.2839-2843
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    • 2013
  • Objective: To investigate the effects of miR-106b on malignant characteristics of gastric cancer cells, and explore possible mechanisms. Methods: Expression of miR-106b, p21 and E2F was determined by real-time PCR. Transfection with miR-106b mimics was conducted, and gastric cancer cells with miR-106b overexpression were obtained. Cells transfected with mimic mutants and those without transfection served as negative and blank controls, respectively. Flow cytometry and transwell assays were adopted to detect the effects of miR-106b overexpression on cell cycle, migration and invasion of gastric cancer cells. Results:. The expression of miR- 106b in gastric cancer cells was significantly higher than that in normal gastric mucosa cells. Furthermore, the expression level of miR-106b rose according to the degree of malignacy among the three GC cell strains (MKN- 45 > SGC-7901 > MKN-28). Overexpression of miR-106b shortened the G0/G1 phase and accelerated cell cycle progression, while reducing p21 and E2F5, without any significant effects on the capacity for migration and invasion of gastric cancer cells. Conclusions: miR-106b may promote cell cycling of gastric cancer cells through regulation of p21 and E2F5 target gene expression.

Identification of stemness and differentially expressed genes in human cementum-derived cells

  • Lee, EunHye;Kim, Young-Sung;Lee, Yong-Moo;Kim, Won-Kyung;Lee, Young-Kyoo;Kim, Su-Hwan
    • Journal of Periodontal and Implant Science
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    • 제51권5호
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    • pp.329-341
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    • 2021
  • Purpose: Periodontal treatment aims at complete regeneration of the periodontium, and developing strategies for periodontal regeneration requires a deep understanding of the tissues composing the periodontium. In the present study, the stemness characteristics and gene expression profiles of cementum-derived cells (CDCs) were investigated and compared with previously established human stem cells. Candidate marker proteins for CDCs were also explored. Methods: Periodontal ligament stem cells (PDLSCs), pulp stem cells (PULPSCs), and CDCs were isolated and cultured from extracted human mandibular third molars. Human bone marrow stem cells (BMSCs) were used as a positive control. To identify the stemness of CDCs, cell differentiation (osteogenic, adipogenic, and chondrogenic) and surface antigens were evaluated through flow cytometry. The expression of cementum protein 1 (CEMP1) and cementum attachment protein (CAP) was investigated to explore marker proteins for CDCs through reverse-transcription polymerase chain reaction. To compare the gene expression profiles of the 4 cell types, mRNA and miRNA microarray analysis of 10 samples of BMSCs (n=1), PDLSCs (n=3), PULPSCs (n=3), and CDCs (n=3) were performed. Results: The expression of mesenchymal stem cell markers with a concomitant absence of hematopoietic markers was observed in PDLSCs, PULPSCs, CDCs and BMSCs. All 4 cell populations also showed differentiation into osteogenic, adipogenic, and chondrogenic lineages. CEMP1 was strongly expressed in CDCs, while it was weakly detected in the other 3 cell populations. Meanwhile, CAP was not found in any of the 4 cell populations. The mRNA and miRNA microarray analysis showed that 14 mRNA genes and 4 miRNA genes were differentially expressed in CDCs vs. PDLSCs and PULPSCs. Conclusions: Within the limitations of the study, CDCs seem to have stemness and preferentially express CEMP1. Moreover, there were several up- or down-regulated genes in CDCs vs. PDLSCs, PULPSCs, and BMSCs and these genes could be candidate marker proteins of CDCs.

고분자전해질형 연료전지 가스확산층의 탄소 부식에 관한 실험적 분석 (Experimental Study on Carbon Corrosion of Gas Diffusion Layer in PEM Fuel Cell)

  • 하태훈;조준현;박재만;민경덕;이은숙;정지영
    • 한국신재생에너지학회:학술대회논문집
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    • 한국신재생에너지학회 2010년도 추계학술대회 초록집
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    • pp.76.1-76.1
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    • 2010
  • Recently, many efforts to solve the durability problem of PEM fuel cell are carried on constantly. However, despite this attention, durability researches of gas diffusion layer (GDL) are not much reported yet. Generally, GDL of PEM fuel cell experiences three external attacks, which are dissolution of water, erosion of gas flow, corrosion of electric potential. In this study, among these degradation factors, carbon corrosion of electric potential was focused and investigated with accelerated carbon corrosion test. Through the test, it is confirmed that carbon corrosion occurred at GDL, and corroded GDL decreased a performance of operating fuel cell. The property changes of GDL were measured with various methods such as air permeability meter, pore distribution analyzer, thermo gravimetric analyzer, and tensile stress test to discover the effects of carbon corrosion. Carbon corrosion caused not only loss of weight and thickness, but also degradation of mechanical strength of GDL. In addition, to analysis the reason of GDL property changes, a surface and a cross section of GDL were observed with scanning electron microscope. After 100 hours test, the GDL showed serious damage in center of layer.

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EJ 인간 방광암 세포에서 bufalin 의 TRAIL 저항성 극복 효과 (The Effect of overcoming the TRAIL resistance through bufalin in EJ human bladder cancer cell)

  • 홍수현
    • 대한한의학방제학회지
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    • 제25권2호
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    • pp.145-154
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    • 2017
  • Objectives : Bufalin is one of the bioactive component of 'Sum Su (蟾酥)', which is obtained from the skin and parotid venom gland of toad. Bufalin has been known to possess the inhibitory effects on cell proliferation and inducing apoptosis in various cancer cells. The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has concerned, because it can selectively induce apoptotic cell death in many types of malignant cells, while it is relatively non-toxic to normal cells. Here, we investigated whether bufalin can trigger TRAIL-induced apoptotic cell death in EJ human bladder cancer cells. Methods : Effects on the cell viability and apoptotic activity were quantified using MTT assay and flow cytometry analysis, respectively. To investigate the morphological change of nucleus, DAPI staining was performed. Protein expressions were measured by immunoblotting. Results : A combined treatment with bufalin (10 nM) and TRAIL (50 ng/ml) significantly promoted TRAIL-mediated growth inhibition and apoptosis in EJ cells. The apoptotic effects were associated with the up-regulation of death receptor proteins, and the down-regulation of cFLIP and XIAP. Moreover, our data showed that bufalin and TRAIL combination activated caspases and subsequently increased degradation of poly(ADP-ribose) polymerase. Conclusions : Taken altogether, the nontoxic doses of bufalin sensitized TRAIL-mediated apoptosis in EJ cells. Therefore, bufalin might be an effective therapeutic strategy for the safe treatment of TRAIL-resistant bladder cancers.

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

  • Zhou, Jing;Luo, Yan-Hong;Wang, Ji-Rong;Lu, Bin-Bin;Wang, Ke-Ming;Tian, Ye
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권12호
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    • pp.7601-7605
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    • 2013
  • Background: Gambogenic acid is a major active compound of gamboge which exudes from the Garcinia hanburyi tree. Gambogenic acid anti-cancer activity in vitro has been reported in several studies, including an A549 nude mouse model. However, the mechanisms of action remain unclear. Methods: We used nude mouse models to detect the effect of gambogenic acid on breast tumors, analyzing expression of apoptosis-related proteins in vivo by Western blotting. Effects on cell proliferation, apoptosis and apoptosis-related proteins in MDA-MB-231 cells were detected by MTT, flow cytometry and Western blotting. Inhibitors of caspase-3,-8,-9 were also used to detect effects on caspase family members. Results: We found that gambogenic acid suppressed breast tumor growth in vivo, in association with increased expression of Fas and cleaved caspase-3,-8,-9 and bax, as well as decrease in the anti-apoptotic protein bcl-2. Gambogenic acid inhibited cell proliferation and induced cell apoptosis in a concentration-dependent manner. Conclusion: Our observations suggested that Gambogenic acid suppressed breast cancer MDA-MB-231 cell growth by mediating apoptosis through death receptor and mitochondrial pathways in vivo and in vitro.

Mangiferin Induces Apoptosis by Regulating Bcl-2 and Bax Expression in the CNE2 Nasopharyngeal Carcinoma Cell Line

  • Pan, Li-Li;Wang, Ai-Yan;Huang, Yong-Qi;Luo, Yu;Ling, Min
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권17호
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    • pp.7065-7068
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    • 2014
  • To investigate the anti-proliferative mechanism of mangiferin in a human nasopharyngeal carcinoma cell line, CNE2 cells were incubated with different concentrations of mangiferin (12.5, 25, 50, 100, 150 and $200{\mu}M$) or with PBS as a control for 72 hours. Analyses were made of the cell cycle and apoptosis with measurement of mRNA and protein levels of two apoptosis-related genes, Bcl-2 and Bax. Flow cytometry assays showed mangiferin could inhibit CNE2 cell proliferation via G2/M arrest and induction of early apoptosis. Real time PCR and Western blotting showed the mRNA and protein level of Bcl-2 to be down-regulated, while those of Bax were upregulated, when CNE2 cells were treated with mangiferin. This investigation indicated anti-proliferation effects of mangiferin through induction of cell apoptosis regulated by Bcl-2 and Bax expression.