• Title/Summary/Keyword: bio-potential

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Review on Proton Exchange Membranes for Microbial Fuel Cell Application (미생물 연료 전지 적용을 위한 양성자 교환막에 대한 검토)

  • Kim, Ji Min;Patel, Rajkumar
    • Membrane Journal
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    • v.30 no.4
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    • pp.213-227
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    • 2020
  • As unrenewable energy resources have depleted over the years, the demand for renewable energy has increased promoting research for more effective methods to produce renewable energy. The field of fuel cell development, specifically microbial fuel cells (MFCs), has developed because of the dual performance potential of the technology. MFCs convert power by facilitating electrode-reducing organisms such as bacteria (microbes) as a catalyst to produce electrical energy. MFCs use domestic and industrial wastewater as fuel to initiate the process, purifying the wastewater as a result. Proton exchange membranes (PEM) play a crucial role in MFCs as a separator between the anodes and cathodes chambers allowing only protons to effectively pass through. Nafion is the commercially used PEM for MFCs, but there are many setbacks: such as cost, production time, and less effective proton conductivity properties. In this review there will be largely two parts. Firstly, several newly developed PEM are discussed as possible replacements of Nafion. Secondly, MFC based on PEM, blended PEM and composite PEM are summarized.

Stabilization of Quinonoid Intermediate E-Q by Glu32 of D-Amino Acid Transaminase

  • Ro Hyeon-Su;Jeon Che-Ok;Kim Hak-Sung;Sung Moon-Hee
    • Journal of Microbiology and Biotechnology
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    • v.16 no.9
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    • pp.1434-1440
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    • 2006
  • The stable anchorage of pyridoxal 5'-phosphate (PLP) in the active site of D-amino acid transaminase (D-AT) is crucial for the enzyme catalysis. The three-dimensional structure of D-AT revealed that Glu32 is one of the active site groups that may playa role in PLP binding. To prove the role of Glu32 in PLP stability, we firstly checked the rate of the potential rate-limiting step. The kinetic analysis showed that the rate of the ${\alpha}$-deprotonation step reduced to 26-folds in E32A mutant enzyme. Spectral analyses of the reaction of D-AT with D-serine revealed that the E32A mutant enzyme failed to stabilize the key enzyme-substrate intermediate, namely a quinonoid intermediate (E-Q). Finally, analysis of circular dichroism (CD) on the wild-type and E32A mutant enzymes showed that the optical activity of PLP in the enzyme active site was lost by the removal of the carboxylic group, proving that Glu32 is indeed involved in the cofactor anchorage. The results suggested that the electrostatic interaction network through the groups from PLP, Glu32, His47, and Arg50, which was observed from the three-dimensional structure of the enzyme, plays a crucial role in the stable anchorage of the cofactor to give necessary torsion to the plane of the cofactor-substrate complex.

JPH203, a selective L-type amino acid transporter 1 inhibitor, induces mitochondria-dependent apoptosis in Saos2 human osteosarcoma cells

  • Choi, Dae Woo;Kim, Do Kyung;Kanai, Yoshikatsu;Wempe, Michael F.;Endou, Hitoshi;Kim, Jong-Keun
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.6
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    • pp.599-607
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    • 2017
  • Most normal cells express L-type amino acid transporter 2 (LAT2). However, L-type amino acid transporter 1 (LAT1) is highly expressed in many tumor cells and presumed to support their increased growth and proliferation. This study examined the effects of JPH203, a selective LAT1 inhibitor, on cell growth and its mechanism for cell death in Saos2 human osteosarcoma cells. FOB human osteoblastic cells and Saos2 cells expressed LAT1 and LAT2 together with their associating protein 4F2 heavy chain, but the expression of LAT2 in the Saos2 cells was especially weak. JPH203 and BCH, a non-selective L-type amino acid transporter inhibitor, potently inhibited L-leucine uptake in Saos2 cells. As expected, the intrinsic ability of JPH203 to inhibit L-leucine uptake was far more efficient than that of BCH in Saos2 cells. Likewise, JPH203 and BCH inhibited Saos2 cell growth with JPH203 being superior to BCH in this regard. Furthermore, JPH203 increased apoptosis rates and formed DNA ladder in Saos2 cells. Moreover, JPH203 activated the mitochondria-dependent apoptotic signaling pathway by upregulating pro-apoptotic factors, such as Bad, Bax, and Bak, and the active form of caspase-9, and downregulating anti-apoptotic factors, such as Bcl-2 and Bcl-xL. These results suggest that the inhibition of LAT1 activity via JPH203, which may act as a potential novel anti-cancer agent, leads to apoptosis mediated by the mitochondria-dependent intrinsic apoptotic signaling pathway by inducing the intracellular depletion of neutral amino acids essential for cell growth in Saos2 human osteosarcoma cells.

The Anti-Adipogenic Activity of a New Cultivar, Pleurotus eryngii var. ferulae 'Beesan No. 2', through Down-Regulation of PPAR γ and C/EBP α in 3T3-L1 Cells

  • Kang, Min-Jae;Kim, Keun Ki;Son, Byoung Yil;Nam, Soo-Wan;Shin, Pyung-Gyun;Kim, Gun-Do
    • Journal of Microbiology and Biotechnology
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    • v.26 no.11
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    • pp.1836-1844
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    • 2016
  • Adipogenesis is one of the cellular processes and a highly controlled program. Nowadays, inhibition of adipogenesis has received attention as an effective way to regulate obesity. In the current study, we investigated the inhibition effect of a chloroform extract of Pleurotus eryngii var. ferulae 'Beesan No. 2' (CEBT) on adipogenesis in 3T3-L1 murine preadipocytes. Pleurotus eryngii var. ferulae is one of many varieties of King oyster mushroom and has been reported to have various biological activities, including antitumor and anti-inflammation effects. Biological activities of 'Beesan No. 2', a new cultivar of Pleurotus eryngii var. ferulae, have not yet been reported. In this study, we found that CEBT suppressed adipogenesis in 3T3-L1 cells through inhibition of key adipogenic transcription factors, such as peroxisome proliferatoractivated receptor ${\gamma}$ and CCAAT/enhancer binding protein ${\alpha}$. Additionally, CEBT reduced the expression of the IRS/PI3K/Akt signaling pathway and its downstream factors, including mammalian target of rapamycin and p70S6 kinase, which stimulate adipogenesis. Furthermore, ${\beta}-catenin$, a suppressor of adipogenesis, was increased in CEBT-treated cells. These results indicate that Pleurotus eryngii var. ferulae 'Beesan No. 2' effectively inhibited adipogenesis, so this mushroom has potential as an anti-obesity food and drug.

Genome Characteristics of Lactobacillus fermentum Strain JDFM216 for Application as Probiotic Bacteria

  • Jang, Sung Yong;Heo, Jaeyoung;Park, Mi Ri;Song, Min-Ho;Kim, Jong Nam;Jo, Sung Ho;Jeong, Do-Youn;Lee, Hak Kyo;Kim, Younghoon;Oh, Sangnam
    • Journal of Microbiology and Biotechnology
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    • v.27 no.7
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    • pp.1266-1271
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    • 2017
  • Lactobacillus fermentum strain JDFM216, isolated from a Korean infant feces sample, possesses the ability to enhance the longevity and immune response of a Caenorhabditis elegans host. To explore the characteristics of strain JDFM216 at the genetic level, we performed whole-genome sequencing using the PacBio system. The circular draft genome has a total length of 2,076,427 bp and a total of 2,682 encoding sequences were identified. Five phylogenetically featured genes possibly related to the longevity and immune response of the host were identified in L. fermentum strain JDFM216. These genes encode UDP-N-acetylglucosamine 1-carboxyvinyltransferase (E.C. 2.5.1.7), ErfK/YbiS/YcfS/YnhG family protein, site-specific recombinase XerD, homocysteine S-methyltransferase (E.C. 2.1.1.10), and aspartate-ammonia ligase (E.C. 6.3.1.1), which are involved in peptidoglycan synthesis and amino acid metabolism in the gut environment. Our findings on the genetic background of L. fermentum strain JDFM216 and its potential candidate genes for host longevity and immune response provide new insight for the application of this strain in the food industry as newly isolated functional probiotic.

Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways

  • Lee, Min Jung;Chang, Byung Joon;Oh, Seikwan;Nah, Seung-Yeol;Cho, Ik-Hyun
    • Journal of Ginseng Research
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    • v.42 no.4
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    • pp.436-446
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    • 2018
  • Background: The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. Methods: We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanism of KRGE on spinal myelination. Results: Pretreatment with KRGE (100 mg/kg, orally) for 10 days before immunization with myelin basic protein $(MBP)_{68-82}$ peptide exerted a protective effect against demyelination in the spinal cord, with inhibited recruitment and activation of immune cells including microglia, decreased mRNA expression of detrimental inflammatory mediators (interleukin-6, interferon-${\gamma}$, and cyclooxygenase-2), but increased mRNA expression of protective inflammatory mediators (insulin-like growth factor ${\beta}1$, transforming growth factor ${\beta}$, and vascular endothelial growth factor-1). These results were associated with significant downregulation of p38 mitogen-activated protein kinase and nuclear factor-${\kappa}B$ signaling pathways in microglia/macrophages, T cells, and astrocytes. Conclusion: Our findings suggest that KRGE alleviates spinal demyelination in acute experimental autoimmune encephalomyelitis through inhibiting the activation of the p38 mitogen-activated protein kinase/nuclear factor-${\kappa}B$ signaling pathway. Therefore, KRGE might be used as a new therapeutic for autoimmune disorders such as multiple sclerosis, although further investigation is needed.

Biomimetic Copper Complex Containing Polymer Modified Electrode for Electrocatalytic Reduction of Oxygen

  • Saravanakumar, D.;Nagarale, Rajaram Krishna;Jirimali, Harish Chandra;Lee, Jong Myung;Song, Jieun;Lee, Junghyun;Shin, Woonsup
    • Journal of Electrochemical Science and Technology
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    • v.7 no.4
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    • pp.298-305
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    • 2016
  • The development of non-precious metal based electrocatalysts is highly desired for the oxygen reduction reaction (ORR) as alternates to noble metal based ORR electrocatalysts. Herein, we report mononulcear copper(II) complex $[CuLbpy]ClO_4$ (L=4-[(2-hydroxyphenylimino)methyl]benzoic acid) containing poly(allylamine.HCl) polymer (PAlACuLbpy) as an electrocatalyst for oxygen reduction reaction (ORR). PAlACuLbpy was mixed with poly(acrylic acid) and tetraethylortho silicate to prepare a composite and then deposited on the screen printed electrode surface. The modified electrode (PAlACuLbpy/PCE) is highly stable and showed a quasi-reversible redox behavior with $E_{1/2}=-0.2V$ vs. Ag/AgCl(3 M KCl) in 0.1 M phosphate buffer at pH 7 under argon atmosphere. PAlACuLbpy/PCE exhibited a remarkable ORR activity with an onset potential of -0.1 V vs Ag/AgCl in 0.1 M PB (pH 7) in the presence of oxygen. The kinetics for ORR was studied by rotating disk voltammetry in neutral aqueous medium and the results indicated that the number of electrons involving in the ORR is four and the conversion products are water and hydrogen peroxide.

Effect of Ponciri Fructus Extracts Fermented with Ganoderma lucidum on the Collagen Synthesis and Expression of Matrix Metalloproteinase-1 (콜라겐 합성과 MMP-1 발현에 대한 생물전환 지실 추출물의 효과)

  • Lee, Gye Won;Park, Sung Min;Yoo, Yung Choon;Cho, Young Ho
    • KSBB Journal
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    • v.28 no.2
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    • pp.106-114
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    • 2013
  • Ponciri fructus, the unripe fruits of Poncirus trifoliata, are widely used in oriental traditional medicine as a remedy for inflammation, gastritis, emesis, digestive ulcers, allergy, and dysentery. To study the anti-wrinkle effects of Ponciri fructus extract (PFE) containing flavanone glycosides, PFE was fermented with Ganoderma lucidum mycelia and its biological activities were investigated. In Ponciri fructus extracts fermented with G. lucidum (G-PFE), polyphenol content was $1,021.00{\pm}0.50{\mu}g/mL$ and flavonoid content was $589.41{\pm}0.21{\mu}g/mL$. G-PFE was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals and superoxide anion radical by a dose dependent manner, respectively. G-PFE showed higher antioxidant activity than that of PFE. In addition, the photoprotective properties of G-PFE was tested in human dermal fibroblasts (HDF) exposed to UVA radiation. G-PFE inhibited the activity of matrix metalloproteinase-1 (MMP-1) and showed a dose dependent decrease in the expression level of MMP-1. G-PFE also increased collagen biosynthesis in HDF. These results demonstrate that G-PFE could be useful as a potential cosmetic ingredient for anti-wrinkle.

Mutational Analysis of Extranodal NK/T-Cell Lymphoma Using Targeted Sequencing with a Comprehensive Cancer Panel

  • Choi, Seungkyu;Go, Jai Hyang;Kim, Eun Kyung;Lee, Hojung;Lee, Won Mi;Cho, Chun-Sung;Han, Kyudong
    • Genomics & Informatics
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    • v.14 no.3
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    • pp.78-84
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    • 2016
  • Extranodal natural killer (NK)/T-cell lymphoma, nasal type (NKTCL), is a malignant disorder of cytotoxic lymphocytes of NK or T cells. It is an aggressive neoplasm with a very poor prognosis. Although extranodal NKTCL reportedly has a strong association with Epstein-Barr virus, the molecular pathogenesis of NKTCL has been unexplored. The recent technological advancements in next-generation sequencing (NGS) have made DNA sequencing cost- and time-effective, with more reliable results. Using the Ion Proton Comprehensive Cancer Panel, we sequenced 409 cancer-related genes to identify somatic mutations in five NKTCL tissue samples. The sequencing analysis detected 25 mutations in 21 genes. Among them, KMT2D, a histone modification-related gene, was the most frequently mutated gene (four of the five cases). This result was consistent with recent NGS studies that have suggested KMT2D as a novel driver gene in NKTCL. Mutations were also found in ARID1A, a chromatin remodeling gene, and TP53, which also recurred in recent NGS studies. We also found mutations in 18 novel candidate genes, with molecular functions that were potentially implicated in cancer development. We suggest that these genes may result in multiple oncogenic events and may be used as potential bio-markers of NKTCL in the future.

Systemic and Cell-Type Specific Profiling of Molecular Changes in Parkinson's Disease

  • Lee, Yunjong
    • Interdisciplinary Bio Central
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    • v.4 no.3
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    • pp.6.1-6.12
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    • 2012
  • Parkinson's disease (PD) is a complicated neurodegenerative disorder although it is oftentimes defined by clinical motor symptoms originated from age dependent and progressive loss of dopaminergic neurons in the midbrain. The pathogenesis of PD involves dopaminergic and nondopaminergic neurons in many brain regions and the molecular mechanisms underlying the death of different cell types still remain to be elucidated. There are indications that PD causing disease processes occur in a global scale ranging from DNA to RNA, and proteins. Several PD-associated genes have been reported to play diverse roles in controlling cellular functions in different levels, such as chromatin structure, transcription, processing of mRNA, translational modulation, and posttranslational modification of proteins. The advent of quantitative high throughput screening (HTS) tools makes it possible to monitor systemic changes in DNA, RNA and proteins in PD models. Combined with dopamine neuron isolation or derivation of dopamine neurons from PD patient specific induced pluripotent stem cells (PD iPSCs), HTS techonologies will provide opportunities to draw PD causing sequences of molecular events in pathologically relevant PD samples. Here I discuss previous studies that identified molecular functions in which PD genes are involved, especially those signaling pathways that can be efficiently studied using HTS methodologies. Brief descriptions of quantitative and systemic tools looking at DNA, RNA and proteins will be followed. Finally, I will emphasize the use and potential benefits of PD iPSCs-derived dopaminergic neurons to screen signaling pathways that are initiated by PD linked gene mutations and thus causative for dopaminergic neurodegneration in PD.