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Hui-Ju Kim,Mi-Ri Kwon,Hye-Ji Kang,Na-Yeon Kim,Hee-Jeong Hwang,Min-Jung Ko,Myong-Soo Chung 한국산업식품공학회 2017 학술대회 및 심포지엄 Vol.2017 No.11
Citrus fruit is important source of flavonoids, mainly flavanones which are narirutin and hesperidin. Those citrus flavonoids have been found to have health-related properties including antioxidant, anticancer, and anti-inflammatory. The main purpose of this study was to verify that the extraction of narirutin and hesperidin from Citrus peel can be more effective by combining pulsed electric field (PEF) pre-treatment and subcritical water extraction (SWE). Citrus unshiu peels were treated with PEF under conditions of electric field strength (3 kV/cm) and times (1 and 2 min). Subsequent SWE was conducted by using a Dionex Accelerated Solvent Extractor (ASE, Model 350) at extraction temperature 170°C for 10 min. The total flavonoids content was measured by using the aluminum chloride colorimetric method and the antioxidant capacity was analyzed by the Ferric reducing antioxidant power (FRAP) assay using spectrophotometer. The concentrations of narirutin and hesperidin were increased as PEF pre-treatment time increased. The highest concentrations of narirutin and hesperidin were 13.41 mg narirutin/g dry citrus peel and 141.16 mg hesperidin/g dry citrus peel at PEF pre-treatment condition of 3 kV/cm and 2 min. The total flavonoids contents of the extracts increased 105.2% and 123.1% for citrus peel PEF treated at 1 and 2 min, respectively. In addition, compared to the untreated sample, PEF pre-treatments of 1 and 2 min increased the antioxidant capacity of the extracts 109.2% and 160.8%, respectively. Therefore, the results demonstrate the potential of PEF pre-treatment to improve the SWE of flavonoids from citrus unshiu peel.
Ki-Kang Kim,Soo-Min Kim,Yan Cui,Mun-Seok Jeong,Jong-Hun Han,Young-Chul Choi,Kay-Hyeok An,Kyung-Hui Oh,Young-Hee Lee 한국탄소학회 2009 Carbon Letters Vol.10 No.1
We measured the degree of macrodispersion of the various single-walled carbon nanotubes (SWCNTs) and multi-walled carbon nanotubes (MWCNTs) using UV-VIS-NIR absorption spectroscopy. CNTs were dispersed with SDS of 2 wt % in deionized water using the homogenizer and then were further centrifugated at 6000 g for 10 min. The degree of macrodispersion, expressed by Dm(λ)=Aa(λ)/Ab(λ)*100 (%), where λ is the wavelength and Aa(λ) and Ab(λ) are the absorbance of the sample after and before centrifugation, respectively. In the case of MWCNTs, we evaluated the degree of macrodispersion by the average degree of macrodispersion (Dm(λ)) between 1000 and 1200 nm. The degree of macrodispersion of SWCNTs was evaluated at the wavelength in which van Hove singularity-related transition regions were excluded, i.e., the range was chosen between E11S and E22S peaks. We have estimated six samples with the same method. The standard deviation of each sample was lower than 5. Therefore, we presented a reliable evaluation method for the macrodispersion of CNTs for standardization.
Kang, Dong Woo,Lee, Shin Wha,Hwang, Won Chan,Lee, Bo Hui,Choi, Yong-Seok,Suh, Young-Ah,Choi, Kang-Yell,Min, Do Sik American Association for Cancer Research 2017 Cancer Research Vol.77 No.1
<P>A phospholipase that functions as a nodal modifier of colon cancer susceptibility mediates the cross-talk between two major tumor suppressor and oncogenic pathways, with implications for disease-selective therapeutic targeting.</P><P>The RB1/E2F1 signaling pathway is frequently deregulated in colorectal cancer and has been suggested to intersect with Wnt/β-catenin and PI3K/Akt pathways, but molecular evidence for this link is lacking. In this study, we demonstrate that phospholipase D1 (PLD1), a transcriptional target of β-catenin/TCF4, orchestrates functional interactions between these pathways during intestinal tumor development. Overexpression of PLD1 in intestinal epithelial cells protected cells from apoptosis induced by PLD1 ablation in the <I>Apc<SUP>min/+</SUP></I> mouse model of intestinal tumorigenesis. Mechanistic investigations revealed that genetic and pharmacologic targeting of PLD1 promote the E2F1-dependent apoptotic program via both miR-192/4465–mediated downregulation of RB1 and inhibition of Akt–TopBP1 pathways. Moreover, the miRNA–RB1 axis and Akt pathway also contributed to the PLD1-mediated self-renewal capacity of colon cancer–initiating cells. Finally, PLD1-driven E2F1 target gene expression positively correlated with tumor stage in patients with colorectal cancer. Overall, our findings suggest that PLD1 mediates cross-talk between multiple major signaling pathways to promote the survival and malignancy of colon cancer cells and may therefore represent an ideal signaling node for therapeutic targeting. <I>Cancer Res; 77(1); 142–52. ©2016 AACR</I>.</P>
Enabling Community : Disabled Women’s Practice of Changing Disability Values
KANG, Min Hui 이화여자대학교 아시아여성학센터 2010 Asian Journal of Women's Studies(AJWS) Vol.16 No.4
The beginning of disabled women’s political activism can truly be considered an opportunity for them to disclose their experience of discrimination to society as a whole, obtain a chance to empower themselves and embark on a struggle against social injustice. Through their movement, disabled women have developed alternative values whereby they tackle the able-body-centered culture. With these new values, disabled women have also developed the philosophical basis and practical tools for resisting patriarchal disablism in Korean society. This paper aims to examine the significance of the disabled women’s movement and their resistance against patriarchal disablism. It also seeks to investigate these women’s emancipatory politics, which is part of the counter-culture. Disabled women’s politics providesa model for changing discriminative values as well as resisting the oppression of those with disabilities.
Kang, Dong Woo,Lee, Bo Hui,Suh, Young-Ah,Choi, Yong-Seok,Jang, Se Jin,Kim, Yong Man,Choi, Kang-Yell,Min, Do Sik American Association for Cancer Research 2017 Clinical Cancer research Vol.23 No.23
<P><B>Purpose:</B> Dysregulated expression of PLD1 has emerged as a hallmark feature of colorectal cancer, which remains a major cause of mortality worldwide. Aberrant activation of Wnt/β-catenin signaling is a critical event in the development of colorectal cancer. Here, we investigated molecular crosstalk between the Wnt/β-catenin and PI3K/Akt pathways via inhibitor of β-catenin and T-cell factor (ICAT), a negative regulator of Wnt/β-catenin signaling. We also explored the effect of PLD1 inhibition on growth of colorectal cancer hyperactivated by Wnt/β-catenin and PI3K/Akt signaling.</P><P><B>Experimental Design:</B> Expression of ICAT via targeting of PLD1 was assessed <I>in vivo</I> in <I>Apc<SUP>Min/</SUP></I><SUP>+</SUP> mice, an AOM/DSS model, and <I>in vitro</I> using various colorectal cancer cells. The relationship between ICAT/PLD1 expression and prognostic survival value of 153 colorectal cancer patients was examined. The therapeutic efficacy of PLD1 inhibitor was determined using a patient-derived xenograft model carrying <I>APC</I> and <I>PI3K</I> mutations.</P><P><B>Results:</B> PLD1 promoted the Wnt/β-catenin signaling pathway by selectively downregulating ICAT via the PI3K/Akt-TopBP1-E2F1 signaling pathways. Low PLD1 expression and high ICAT expression were significantly associated with increased survival in colorectal cancer patients and vice versa. Furthermore, PLD1 inhibition suppressed growth of colorectal cancer activated by the Wnt/β-catenin and PI3K signaling pathways.</P><P><B>Conclusions:</B> These results suggest that PLD1 linked to ICAT mediates molecular crosstalk between the Wnt/β-catenin and PI3K/Akt pathways and thus could be proposed as a novel colorectal cancer prognostic biomarker. These results may assist in the clinical development of a PLD1 inhibitor for treatment of colorectal cancer patients carrying <I>APC</I> and <I>PI3KCA</I> mutations. PLD1, a nodal modifier, acts as a potential therapeutic target for the treatment of colorectal cancer hyperactivated by the Wnt/β-catenin and PI3K/Akt signaling pathways. <I>Clin Cancer Res; 23(23); 7340–50. ©2017 AACR</I>.</P>
The Role of Dimethyl Sulfoxide in Epigenetic Reprogramming by Mouse Preimplantation Embryos
Min-Hui Kang,DaSom Kim,Yun-Jung Choi,Deug-Nam Kwon,Chankyu Park,Ssang-Goo Cho,Han Geuk Seo,Sangiliyandi Gurunathan,Jin-Hoi Kim 한국동물생명공학회(구 한국동물번식학회) 2013 Reproductive & Developmental Biology(Supplement) Vol.37 No.2s
Dimethyl sulfoxide (DMSO) is one of the most commonly used solvents in drug screening or for cryoprotection. In this study, we exposed mouse-derived zygote to blastocyst to three different concentrations of DMSO [0% (control), 0.5% (medium dose) and 1.0~2% (high dose)] to identify the safest dose that could effectively be used as solvent. We found that DMSO treatment substantially altered the developmental competency of mouse preimplantation embryos in concurrence with a significant reduction in embryo viability in a dose-dependent manner. Furthermore, Gene expression studies revealed a selective expression change of key markers associated with genome-wide DNA methylation reprogramming during preimplantation stages. Immunocytochemistry analysis demonstrated substantial alterations in the levels of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC), increasing of apoptosis, and reduction of total cell numbers. Our study advocates for the first time that DMSO exposure induces significant alteration in gene expression, epigenetic reprogramming, and functionality of the preimplantation embryos. Also, the present study identified DMSO as a novel inducer of Tet1 and Tet2 expressions, and as a novel inhibitor for 5mC/5hmC conversion. Overall, our experiments warrant that mouse preimplantation-based assays can provide timely alerts about the outcome of widespread applications of DMSO as drug solvent and cryoprotectant agent.
Kang, Hye-Min,Jeong, Chang-Bum,Lee, Young Hwan,Cui, Yan-Hong,Kim, Duck-Hyun,Lee, Min-Chul,Kim, Hui-Su,Han, Jeonghoon,Hwang, Dae-Sik,Lee, Su-Jae,Lee, Jae-Seong PERGAMON 2017 MARINE POLLUTION BULLETIN Vol.124 No.2
<P><B>Abstract</B></P> <P>The mitogen-activated protein kinases (MAPKs) family is known to mediate various biological processes in response to diverse environmental pollutants. Although MAPKs are well characterized and studied in vertebrates, in invertebrates the cross-reactivities of MAPKs antibodies were not clearly known in response to environmental pollutants due to limited information of antibody epitopes with material resources for invertebrates. In this paper, we performed phylogenetic analysis of MAPKs genes in the marine rotifer <I>Brachionus koreanus</I> and the copepods <I>Paracyclopina nana</I> and <I>Tigriopus japonicus</I>. Also in rotifer and copepods, several studies of Western blot of MAPK signaling pathways were shown in response to environmental pollutants, including multi-walled carbon nanotubes (MWCNTs), water-accommodated fractions (WAFs) of crude oil, and microplastics. This paper will provide a better understanding of the underlying mechanistic scenario in terms of cross-reactivities of mammalian antibodies in rotifer and copepod.</P> <P><B>Highlight</B></P> <P> <UL> <LI> Phylogenetic analysis of MAPKs genes was performed in rotifer and copepods. </LI> <LI> Western blot of MAPKs were reproducible upon MWCNTs, WAFs, and microplastics exposure. </LI> </UL> </P>