Identification of Three Novel Mutations in FRMD7 Gene for X-Linked Idiopathic Congenital Nystagmus

Total Page:16

File Type:pdf, Size:1020Kb

Identification of Three Novel Mutations in FRMD7 Gene for X-Linked Idiopathic Congenital Nystagmus Identification of Three Novel Mutations in FRMD7 gene for X-linked Idiopathic Congenital Nystagmus Xiao Zhang, Xianglian Ge, Ying Yu, Yilan Zhang, Yaming Wu, Yin Luan, Ji Sun, Jia Qu, Zi-Bing Jin and Feng Gu* Table S1. Capture Next Generation Sequencing of CASK gene Position: Position: Number Sequencing Chromosome Start Stop Length of tags Depth Mutation chrX 41379641 41379880 239 172 72.0 No chrX 41383186 41383305 119 80 67.2 No chrX 41390241 41390480 239 189 79.1 No chrX 41393939 41394058 119 175 147.1 No chrX 41394119 41394238 119 92 77.3 No chrX 41401882 41402061 179 106 59.2 No chrX 41412950 41413189 239 332 138.9 No chrX 41414811 41414930 119 95 79.8 No chrX 41416259 41416378 119 202 169.7 No chrX 41418928 41419167 239 511 213.8 No chrX 41420795 41420914 119 52 43.7 No chrX 41428900 41429019 119 11 9.2 No chrX 41437567 41437806 239 210 87.9 No chrX 41446140 41446259 119 54 45.4 No chrX 41448747 41448866 119 86 72.3 No chrX 41469110 41469337 227 223 98.2 No chrX 41481819 41481938 119 115 96.6 No chrX 41483466 41483585 119 293 246.2 No chrX 41485847 41485966 119 75 63.0 No chrX 41495813 41495932 119 73 61.3 No chrX 41519678 41519872 194 246 126.8 No chrX 41524498 41524737 239 252 105.4 No chrX 41530672 41530791 119 69 58.0 No chrX 41554860 41556059 1199 1932 161.1 No chrX 41586245 41587324 1079 1044 96.8 No chrX 41598613 41598732 119 27 22.7 No chrX 41604756 41604875 119 27 22.7 No chrX 41646424 41646543 119 124 104.2 No chrX 41712364 41712483 119 37 31.1 No chrX 41782152 41782271 119 5 4.2 No Table S2.
Recommended publications
  • Strategies to Increase ß-Cell Mass Expansion
    This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Strategies to increase -cell mass expansion Drynda, Robert Lech Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Strategies to increase β-cell mass expansion A thesis submitted by Robert Drynda For the degree of Doctor of Philosophy from King’s College London Diabetes Research Group Division of Diabetes & Nutritional Sciences Faculty of Life Sciences & Medicine King’s College London 2017 Table of contents Table of contents .................................................................................................
    [Show full text]
  • Mitochondrial Dynamics During Spermatogenesis Grigor Varuzhanyan and David C
    © 2020. Published by The Company of Biologists Ltd | Journal of Cell Science (2020) 133, jcs235937. doi:10.1242/jcs.235937 REVIEW SUBJECT COLLECTION: MITOCHONDRIA Mitochondrial dynamics during spermatogenesis Grigor Varuzhanyan and David C. Chan* ABSTRACT Mitophagy is an additional layer of quality control that utilizes Mitochondrial fusion and fission (mitochondrial dynamics) are autophagy (Mizushima, 2007; Mizushima et al., 1998; Tsukada and homeostatic processes that safeguard normal cellular function. This Ohsumi, 1993) to remove excessive mitochondria or damaged relationship is especially strong in tissues with constitutively high energy mitochondria that are beyond repair (Pickles et al., 2018). During demands, such as brain, heart and skeletal muscle. Less is known about mitophagy, microtubule-associated protein 1A/1B light chain 3 the role of mitochondrial dynamics in developmental systems that involve (collectively LC3; also known as MAP1LC3A, MAP1LC3B and changes in metabolic function. One such system is spermatogenesis. MAP1LC3C) is recruited to the autophagosomal membrane and binds The first mitochondrial dynamics gene, Fuzzy onions (Fzo), was to mitochondria that selectively express mitophagy receptors on their discovered in 1997 to mediate mitochondrial fusion during Drosophila outer membrane. This molecular recognition designates damaged spermatogenesis. In mammals, however, the role of mitochondrial fusion mitochondria as cargo for autophagosomes, and the resulting during spermatogenesis remained unknown for nearly two decades after mitophagosomes subsequently fuse with lysosomes for degradation discovery of Fzo. Mammalian spermatogenesis is one of the most and recycling of the engulfed organelles. Much of the molecular complex and lengthy differentiation processes in biology, transforming workings of mitophagy have been parsed in cultured cells, and spermatogonial stem cells into highly specialized sperm cells over a recently developed mouse models are enabling the analysis of 5-week period.
    [Show full text]
  • Edinburgh Research Explorer
    Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S.
    [Show full text]
  • Aplicación De La Biología De Sistemas Al Estudio De La Malaria Y Búsqueda De Biomarcadores Y Dianas Terapéuticas
    Aplicación de la biología de sistemas al estudio de la malaria y búsqueda de biomarcadores y dianas terapéuticas Autora: Mireia Ferrer Almirall Máster en Bioinformática y Bioestadística Area 1-Bioinformática farmacéutica Tutores: Melchor Sánchez Martínez y Alex Sánchez Pla Profesor responsable de la asignatura: Carles Ventura Royo 02/01/2019 Esta obra está sujeta a una licencia de Reconocimiento-NoComercial- SinObraDerivada 3.0 España de Creative Commons FICHA DEL TRABAJO FINAL Aplicación de la biología de sistemas al Título del trabajo: estudio de la malaria y búsqueda de biomarcadores y dianas terapéuticas Nombre del autor: Mireia Ferrer Almirall Melchor Sánchez Martínez y Nombre del consultor/a: Alex Sánchez Pla Nombre del PRA: Carles Ventura Royo Fecha de entrega (mm/aaaa): 01/2019 Titulación: Máster en Bioinformática y Bioestadística Área del Trabajo Final: 1-Bioinformática farmacéutica Idioma del trabajo: castellano Malaria, Biología-de-sistemas, Palabras clave dianas-terapéuticas Resumen del Trabajo (máximo 250 palabras): Con la finalidad, contexto de aplicación, metodología, resultados i conclusiones del trabajo. La finalidad de este trabajo es aplicar herramientas de biología de sistemas para investigar los mecanismos implicados en la infección por el parásito de la malaria e identificar posibles biomarcadores y dianas terapéuticas. Se ha partido de una serie temporal de datos de microarrays del bazo de ratones infectados con dos cepas del parásito (NL y L) para determinar los genes que se encuentran diferencialmente expresados (DEG) respecto a ratones control. A partir de las listas de DEG obtenidas, se han utilizado herramientas de biología de sistemas en combinación con análisis de significación biológica para obtener una visión integrada de los procesos biológicos que se encuentran alterados en la enfermedad e identificar posibles biomarcadores/dianas terapéuticas.
    [Show full text]
  • Low Abundance of the Matrix Arm of Complex I in Mitochondria Predicts Longevity in Mice
    ARTICLE Received 24 Jan 2014 | Accepted 9 Apr 2014 | Published 12 May 2014 DOI: 10.1038/ncomms4837 OPEN Low abundance of the matrix arm of complex I in mitochondria predicts longevity in mice Satomi Miwa1, Howsun Jow2, Karen Baty3, Amy Johnson1, Rafal Czapiewski1, Gabriele Saretzki1, Achim Treumann3 & Thomas von Zglinicki1 Mitochondrial function is an important determinant of the ageing process; however, the mitochondrial properties that enable longevity are not well understood. Here we show that optimal assembly of mitochondrial complex I predicts longevity in mice. Using an unbiased high-coverage high-confidence approach, we demonstrate that electron transport chain proteins, especially the matrix arm subunits of complex I, are decreased in young long-living mice, which is associated with improved complex I assembly, higher complex I-linked state 3 oxygen consumption rates and decreased superoxide production, whereas the opposite is seen in old mice. Disruption of complex I assembly reduces oxidative metabolism with concomitant increase in mitochondrial superoxide production. This is rescued by knockdown of the mitochondrial chaperone, prohibitin. Disrupted complex I assembly causes premature senescence in primary cells. We propose that lower abundance of free catalytic complex I components supports complex I assembly, efficacy of substrate utilization and minimal ROS production, enabling enhanced longevity. 1 Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK. 2 Centre for Integrated Systems Biology of Ageing and Nutrition, Newcastle University, Newcastle upon Tyne NE4 5PL, UK. 3 Newcastle University Protein and Proteome Analysis, Devonshire Building, Devonshire Terrace, Newcastle upon Tyne NE1 7RU, UK. Correspondence and requests for materials should be addressed to T.v.Z.
    [Show full text]
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • Supplementary Materials
    Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine
    [Show full text]
  • Multi-Functionality of Proteins Involved in GPCR and G Protein Signaling: Making Sense of Structure–Function Continuum with In
    Cellular and Molecular Life Sciences (2019) 76:4461–4492 https://doi.org/10.1007/s00018-019-03276-1 Cellular andMolecular Life Sciences REVIEW Multi‑functionality of proteins involved in GPCR and G protein signaling: making sense of structure–function continuum with intrinsic disorder‑based proteoforms Alexander V. Fonin1 · April L. Darling2 · Irina M. Kuznetsova1 · Konstantin K. Turoverov1,3 · Vladimir N. Uversky2,4 Received: 5 August 2019 / Revised: 5 August 2019 / Accepted: 12 August 2019 / Published online: 19 August 2019 © Springer Nature Switzerland AG 2019 Abstract GPCR–G protein signaling system recognizes a multitude of extracellular ligands and triggers a variety of intracellular signal- ing cascades in response. In humans, this system includes more than 800 various GPCRs and a large set of heterotrimeric G proteins. Complexity of this system goes far beyond a multitude of pair-wise ligand–GPCR and GPCR–G protein interactions. In fact, one GPCR can recognize more than one extracellular signal and interact with more than one G protein. Furthermore, one ligand can activate more than one GPCR, and multiple GPCRs can couple to the same G protein. This defnes an intricate multifunctionality of this important signaling system. Here, we show that the multifunctionality of GPCR–G protein system represents an illustrative example of the protein structure–function continuum, where structures of the involved proteins represent a complex mosaic of diferently folded regions (foldons, non-foldons, unfoldons, semi-foldons, and inducible foldons). The functionality of resulting highly dynamic conformational ensembles is fne-tuned by various post-translational modifcations and alternative splicing, and such ensembles can undergo dramatic changes at interaction with their specifc partners.
    [Show full text]
  • THE FUNCTIONAL SIGNIFICANCE of MITOCHONDRIAL SUPERCOMPLEXES in C. ELEGANS by WICHIT SUTHAMMARAK Submitted in Partial Fulfillment
    THE FUNCTIONAL SIGNIFICANCE OF MITOCHONDRIAL SUPERCOMPLEXES in C. ELEGANS by WICHIT SUTHAMMARAK Submitted in partial fulfillment of the requirements For the degree of Doctor of Philosophy Dissertation Advisor: Drs. Margaret M. Sedensky & Philip G. Morgan Department of Genetics CASE WESTERN RESERVE UNIVERSITY January, 2011 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of _____________________________________________________ candidate for the ______________________degree *. (signed)_______________________________________________ (chair of the committee) ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. Dedicated to my family, my teachers and all of my beloved ones for their love and support ii ACKNOWLEDGEMENTS My advanced academic journey began 5 years ago on the opposite side of the world. I traveled to the United States from Thailand in search of a better understanding of science so that one day I can return to my homeland and apply the knowledge and experience I have gained to improve the lives of those affected by sickness and disease yet unanswered by science. Ultimately, I hoped to make the academic transition into the scholarly community by proving myself through scientific research and understanding so that I can make a meaningful contribution to both the scientific and medical communities. The following dissertation would not have been possible without the help, support, and guidance of a lot of people both near and far. I wish to thank all who have aided me in one way or another on this long yet rewarding journey. My sincerest thanks and appreciation goes to my advisors Philip Morgan and Margaret Sedensky.
    [Show full text]
  • Analyzing the Function of TRAP1 in Models of Parkinson's Disease
    Analyzing the function of TRAP1 in models of Parkinson’s disease Von der Fakultät für Mathematik, Informatik und Naturwissenschaften der RWTH Aachen University zur Erlangung des akademischen Grades einer Doktorin der Naturwissenschaften genehmigte Dissertation vorgelegt von Li Zhang aus Changchun, Jilin (China) Berichter: Universitätsprofessor Dr. med. Jörg B. Schulz Universitätsprofessor Dr. rer. nat. Marc Spehr Tag der mündlichen Prüfung: 29.01.2016 Diese Dissertation ist auf den Internetseiten der Universitätsbibliothek online verfügbar. Eidesstattliche Versicherung ___________________________Zhang, Li ___________________________ Name, Vorname Matrikelnummer (freiwillige Angabe) Ich versichere hiermit an Eides Statt, dass ich die vorliegende Arbeit/Bachelorarbeit/ Masterarbeit* mit dem Titel __________________________________________________________________________Analyzing the function of TRAP1 in models of Parkinson’s disease __________________________________________________________________________Uebersetzung: Analyse der TRAP1-Funktion in Modellen fuer Morbus Parkinson __________________________________________________________________________ selbständig und ohne unzulässige fremde Hilfe erbracht habe. Ich habe keine anderen als die angegebenen Quellen und Hilfsmittel benutzt. Für den Fall, dass die Arbeit zusätzlich auf einem Datenträger eingereicht wird, erkläre ich, dass die schriftliche und die elektronische Form vollständig übereinstimmen. Die Arbeit hat in gleicher oder ähnlicher Form noch keiner Prüfungsbehörde vorgelegen.
    [Show full text]
  • The Human Gene Connectome As a Map of Short Cuts for Morbid Allele Discovery
    The human gene connectome as a map of short cuts for morbid allele discovery Yuval Itana,1, Shen-Ying Zhanga,b, Guillaume Vogta,b, Avinash Abhyankara, Melina Hermana, Patrick Nitschkec, Dror Friedd, Lluis Quintana-Murcie, Laurent Abela,b, and Jean-Laurent Casanovaa,b,f aSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065; bLaboratory of Human Genetics of Infectious Diseases, Necker Branch, Paris Descartes University, Institut National de la Santé et de la Recherche Médicale U980, Necker Medical School, 75015 Paris, France; cPlateforme Bioinformatique, Université Paris Descartes, 75116 Paris, France; dDepartment of Computer Science, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel; eUnit of Human Evolutionary Genetics, Centre National de la Recherche Scientifique, Unité de Recherche Associée 3012, Institut Pasteur, F-75015 Paris, France; and fPediatric Immunology-Hematology Unit, Necker Hospital for Sick Children, 75015 Paris, France Edited* by Bruce Beutler, University of Texas Southwestern Medical Center, Dallas, TX, and approved February 15, 2013 (received for review October 19, 2012) High-throughput genomic data reveal thousands of gene variants to detect a single mutated gene, with the other polymorphic genes per patient, and it is often difficult to determine which of these being of less interest. This goes some way to explaining why, variants underlies disease in a given individual. However, at the despite the abundance of NGS data, the discovery of disease- population level, there may be some degree of phenotypic homo- causing alleles from such data remains somewhat limited. geneity, with alterations of specific physiological pathways under- We developed the human gene connectome (HGC) to over- come this problem.
    [Show full text]
  • Functional Annotation of the Human Retinal Pigment Epithelium
    BMC Genomics BioMed Central Research article Open Access Functional annotation of the human retinal pigment epithelium transcriptome Judith C Booij1, Simone van Soest1, Sigrid MA Swagemakers2,3, Anke HW Essing1, Annemieke JMH Verkerk2, Peter J van der Spek2, Theo GMF Gorgels1 and Arthur AB Bergen*1,4 Address: 1Department of Molecular Ophthalmogenetics, Netherlands Institute for Neuroscience (NIN), an institute of the Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 47, 1105 BA Amsterdam, the Netherlands (NL), 2Department of Bioinformatics, Erasmus Medical Center, 3015 GE Rotterdam, the Netherlands, 3Department of Genetics, Erasmus Medical Center, 3015 GE Rotterdam, the Netherlands and 4Department of Clinical Genetics, Academic Medical Centre Amsterdam, the Netherlands Email: Judith C Booij - [email protected]; Simone van Soest - [email protected]; Sigrid MA Swagemakers - [email protected]; Anke HW Essing - [email protected]; Annemieke JMH Verkerk - [email protected]; Peter J van der Spek - [email protected]; Theo GMF Gorgels - [email protected]; Arthur AB Bergen* - [email protected] * Corresponding author Published: 20 April 2009 Received: 10 July 2008 Accepted: 20 April 2009 BMC Genomics 2009, 10:164 doi:10.1186/1471-2164-10-164 This article is available from: http://www.biomedcentral.com/1471-2164/10/164 © 2009 Booij et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
    [Show full text]