267 research outputs found

    Organic flexible memristor with reduced operating voltage and high stability by interfacial control of conductive filament growth

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    This work was supported in part through the BK21 Program funded by Ministry of Education of Korea.Herein, the underlying mechanisms for the growth of conductive filaments (CFs) at a metal–polymer electrolyte interface through ion migration in organic electrochemical metallization (ECM) memristor are presented. It is observed that the free volume of voids (nanopores) in the polymer electrolyte serves as the pathways of metal‐cations whereas the interfacial topography between an active electrode and a polymer electrolyte determines the nucleation sites of the CFs. The growth kinetics of the CFs and the resultant resistive memory are found to vary with the molecular weight of the polymer electrolyte and the metal protrusions at the interface. Our direct observations show that the free volume of voids of the polymer electrolyte, varied with the molecular weight, dictates the ion transport for the growth and the disruption of the CFs. Our organic ECM‐based memristor with a hetero‐electrolyte exhibits high mechanical flexibility, low switching voltages reduced by about three times compared to those of conventional devices, and stable memory retention for longer than 104 s under repeated cycles of bending.PostprintPeer reviewe

    The Relationship between Lewis/Secretor Genotypes and Serum Carbohydrate Antigen 19-9 Levels in a Korean Population

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    Background : The Lewis histo-blood group system consists of 2 major antigens-Le(a) and Le(b)-and a sialyl Lewis antigen-carbohyd rate antigen (CA) 19-9. We investigated the distribution of Lewis genotypes and evaluated the relationship between the Lewis/Secretor genotypes and the serum level of CA 19-9 in a Korean population to identify whether the serum CA 19-9 levels are influenced by the Lewis/Secretor genotypes. Methods : The study included 242 individuals who had no malignancies. Lewis genotyping was performed for the 59T>G, 508G>A and 1067T>A polymorphic sites. The Secretor genotype was determined through analysis of the 357C>T and 385A>T polymorphic sites and the fusion gene. Serum CA 19-9 level was analyzed using an electrochemiluminescence immunoassay. Results : Individuals carrying the 3 common genotypes-Le/Le, Le/le(59,508), and Le/le(59,1067)-accounted for 95% of the study population. In the Korean population, the allelic frequencies of Le, Le(59)le(59,508) and le(59,1067) were 0.731, 0.010, 0.223, and 0.035, respectiveiy. We found a significant difference in serum CA 19-9 concentrations among the 9 LewislSecretor genotype groups (P<0.001). The serum CA 19-9 levels in subjects with genotype groups 1 and 2 (Le/- and se/se) were higher than those with genotype groups 3-6 (Le/- and Se/-; 15.63 vs 6.64 kU/L, P<0.001). Conclusions : Le/Le(59,508), and Le/le(59,1067) are frequent Lewis genotypes in Koreans. Because serum CA 19-9 levels are significantly influenced by the LewislSecretor genotypes, caution is suggested when interpreting the serum CA 19-9 levels. (Korean J Lab Med 2010;30:51-7)SONG SY, 2008, KOREAN J HEMATOL, V43, P34Park KU, 2005, ANN HEMATOL, V84, P656, DOI 10.1007/s00277-005-1041-5Hayashi N, 2004, PATHOBIOLOGY, V71, P26, DOI 10.1159/000072959Hamajima N, 2002, J MOL DIAGN, V4, P103HAMAJIMA N, 2002, GASTRIC CANCER, V5, P194Liu TC, 2000, ANN HEMATOL, V79, P599Lamerz R, 1999, ANN ONCOL, V10, P145Vestergaard EM, 1999, CLIN CHEM, V45, P54Liu YH, 1999, J HUM GENET, V44, P181Kim MJ, 2002, YONSEI MED J, V43, P427SHIBATA A, 2003, GASTRIC CANCER, V6, P8Liu YH, 1999, J FORENSIC SCI, V44, P82Liu YH, 1998, HUM GENET, V103, P204Pang H, 1998, HUM GENET, V102, P675Narimatsu H, 1998, CANCER RES, V58, P512Liu YH, 1996, J FORENSIC SCI, V41, P1018Koda Y, 1996, AM J HUM GENET, V59, P343Kudo T, 1996, J BIOL CHEM, V271, P9830ROUQUIER S, 1995, J BIOL CHEM, V270, P4632KELLY RJ, 1995, J BIOL CHEM, V270, P4640NISHIHARA S, 1994, J BIOL CHEM, V269, P29271MOLLICONE R, 1994, J BIOL CHEM, V269, P20987

    Association of ATP7B Mutation Detection Rate with Biochemical Characteristics in Korean Patients with Wilson Disease

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    Wilson disease (WD) is an autosomal recessive disorder caused by mutations in the ATP7B gene, yet many patients have either one mutation, or no mutation. We investigated whether the mutation detection rate is associated with any biochemical characteristics of WD. In a study of 71 patients, we used PCR-sequencing to screen for ATP7B mutations in 7 exons (exons 8, 10, 11, 14, 15, 16, and 18) covering 95% of known mutations in Korean patients with WD. We also investigated serum concentrations of various biochemical analytes. Data were analyzed by linear association test and one-way ANOVA. Based on the number of detected ATP7B mutations, a significant difference in serum ceruloplasmin concentration was found among the 3 groups (p < 0.001). Serum ceruloplasmin concentration averaged 3.32 +/- 1.74, 10.8 +/- 5.50, and 14.9 +/- 3.88 mg/dl (mean +/- SD) in the 25, 20, and 26 patients with two, one, and no ATP7B mutations, respectively. We observed 82.9% and 16.7% of mutant allele frequency in WD patients with ceruloplasmin concentration < 10 mg/dl and 10-20 mg/dl, respectively (p < 0.001). Thus serum ceruloplasmin concentrations among WD patients differed according to the number of ATP7B mutations detected.Riordan SM, 2001, J HEPATOL, V34, P165Gow PJ, 2000, GUT, V46, P415Brewer GJ, 2009, NETH J MED, V67, P195Korman JD, 2008, HEPATOLOGY, V48, P1167, DOI 10.1002/hep.22446Mak CM, 2008, CLIN CHEM, V54, P1356, DOI 10.1373/clinchem.2008.103432Mak CM, 2008, CRIT REV CL LAB SCI, V45, P263, DOI 10.1080/10408360801991055Park S, 2007, HUM MUTAT, V28, P1108, DOI 10.1002/humu.20574Kroll CA, 2006, MOL GENET METAB, V89, P134, DOI 10.1016/j.ymgme.2006.03.008Durand F, 2001, GUT, V48, P849Yoo HW, 2002, GENET MED, V4, p43S, DOI 10.1097/01.GIM.0000040260.30727.EBSHIM H, 2003, J NUTR, V133, P1527Roberts EA, 2003, HEPATOLOGY, V37, P1475, DOI 10.1053/jhep.2003.50252Ferenci P, 2003, LIVER INT, V23, P139Cullen LM, 2003, CLIN GENET, V64, P429Seo J, 2004, J TURBUL, V5, DOI 10.1088/1468-5248/5/1/015YANG X, 2005, ZHONGHUA NEI KE ZA Z, V44, P13Brewer GJ, 2005, J HEPATOL, V42, pS13, DOI 10.1016/j.jhep.2004.11.013De Bie P, 2005, J HERED, V96, P803, DOI 10.1093/jhered/esi110CHOI JS, 2006, KOREAN J LAB MED, V26, P449Kim JH, 2006, J GASTROEN HEPATOL, V21, P588, DOI 10.1111/j.1440-1746.2005.04127.xEisenbach C, 2007, WORLD J GASTROENTERO, V13, P1711Kenney SM, 2007, HUM MUTAT, V28, P1171, DOI 10.1002/humu.20586Roberts EA, 2008, HEPATOLOGY, V47, P2089, DOI 10.1002/hep.22261Kok KF, 2008, NETH J MED, V66, P348BREWER GJ, 2009, NETH J MED, V67, P196SALLIE R, 1992, HEPATOLOGY, V16, P1206

    Footwear Design Crowdsourcing Platform Model For Strengthening Of the Competitiveness Of The Footwear Industry

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    The volumes of global footwear production and consumption have been steadily increasing. In particular, the income increases of China and Southeast Asian countries have led to the rapid growth of footwear production and consumption in Asia. However, while advanced countries still include footwear business as one of their growth engines, Korea regard it as stagnant or diminishing. However, beyond the category of simple manufacturing, footwear industry involves the integration of highly functional products, parts manufacturing, and marketing business, and includes expertise in the fields of design, materials, and epidemiology. The strengthening of the shoe industry is an important potential driver of the overall economy. The strengthened competiveness of the footwear industry will play an important role in the overall economic growth. Crowdsourcing is an approach that encourages the participation of specific communities or unspecified masses in a company’s production, service, or problem-solving processes to increase efficiency. To this end, this paper suggests the crowdsourcing platform model built through the integration of footwear design and IT for the ultimate enhancement of the competitiveness of the Korean footwear industry. Following this paper, a study about the practical development, application, and active use of such platform needs to be conducted. One limitation of this study is that the platform is yet to be developed or applied. Future research should focus on developing an actual platform and further studies in its application and vitalization

    Increased O-GlcNAcylation of Drp1 by amyloid-beta promotes mitochondrial fission and dysfunction in neuronal cells.

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    As a dynamic organelle, mitochondria continuously fuse and divide with adjacent mitochondria. Imbalance in mitochondria dynamics leads to their dysfunction, which implicated in neurodegenerative diseases. However, how mitochondria alteration and glucose defect contribute to pathogenesis of Alzheimer's disease (AD) is still largely unknown. Dynamin-related protein 1 (Drp1) is an essential regulator for mitochondria fission. Among various posttranslational modifications, O-GlcNAcylation plays a role as a sensor for nutrient and oxidative stress. In this study, we identified that Drp1 is regulated by O-GlcNAcylation in AD models. Treatment of Aβ as well as PugNAc resulted in mitochondrial fragmentation in neuronal cells. Moreover, we found that AD mice brain exhibits an upregulated Drp1 O-GlcNAcylation. However, depletion of OGT inhibited Drp1 O-GlcNAcylation in Aβ-treated cells. In addition, overexpression of O-GlcNAc defective Drp1 mutant (T585A and T586A) decreased Drp1 O-GlcNAcylation and Aβ-induced mitochondria fragmentation. Taken together, these finding suggest that Aβ regulates mitochondrial fission by increasing O-GlcNAcylation of Drp1

    Association of the programmed cell death 1 (PDCD1) gene polymorphism with ankylosing spondylitis in the Korean population

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    The PD-1 (programmed death 1) molecule is a negative regulator of T cells. PDCD1 (programmed cell death 1) has been reported to have a genetic association in systemic lupus erythematosus and rheumatoid arthritis in Caucasians. However, there are no reports on the association between this gene and ankylosing spondylitis (AS). The present study investigated the association of the PD-1 polymorphisms and the haplotypes with AS in a Korean population sample. In a case-control association study, two single-nucleotide polymorphisms, PD-1.5 C/T and PD-1.9 T/C, were genotyped in 95 AS patients and 130 healthy controls. The T allele of the PD-1.9 polymorphism was more frequent in the Korean male population with AS than in the Korean male controls (21.0% versus 6.9%, odds ratio 1.89, 95% confidence interval 1.483 to 2.408). The frequency of the CT haplotype (PD-1.5 C/T and PD-1.9 T/C) was higher in the AS patients (19%) than the controls (5.4%) (odds ratio 1.83, 95% confidence interval 1.559 to 2.521). The PD-1 polymorphism was demonstrated in Korean AS patients. The results suggest a genetic association between the PD-1 polymorphism and susceptibility to AS

    Heterogeneous nuclear ribonucleoprotein A1 post-transcriptionally regulates Drp1 expression in neuroblastoma cells.

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    Excessive mitochondrial fission is associated with the pathogenesis of neurodegenerative diseases. Dynamin-related protein 1 (Drp1) possesses specific fission activity in the mitochondria and peroxisomes. Various post-translational modifications of Drp1 are known to modulate complex mitochondrial dynamics. However, the post-transcriptional regulation of Drp1 remains poorly understood. Here, we show that the heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) regulates Drp1 expression at the post-transcriptional level. hnRNP A1 directly interacts with Drp1 mRNA at its 3'UTR region, and enhances translation potential without affecting mRNA stability. Down-regulation of hnRNP A1 induces mitochondrial elongation by reducing Drp1 expression. Moreover, depletion of hnRNP A1 suppresses 3-NP-mediated mitochondrial fission and dysfunction. In contrast, over-expression of hnRNP A1 promotes mitochondrial fragmentation by increasing Drp1 expression. Additionally, hnRNP A1 significantly exacerbates 3-NP-induced mitochondrial dysfunction and cell death in neuroblastoma cells. Interestingly, treatment with 3-NP induces subcellular translocation of hnRNP A1 from the nucleus to the cytoplasm, which accelerates the increase in Drp1 expression in hnRNP A1 over-expressing cells. Collectively, our findings suggest that hnRNP A1 controls mitochondrial dynamics by post-transcriptional regulation of Drp1.This research was supported by a grant of the Korea–UK Collaborative Alzheimer's Disease Research Project by Ministry of Health & Welfare, Republic of Korea (A120196, HI14C1913) and was supported by the Basic Science Research Program of the National Research Foundation, Republic of Korea (2014R1A2A1A11053431). We are grateful to Wellcome Trust, Principal Research Fellowship to DCR (095317/Z/11/Z)This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.bbagrm.2015.10.01
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