DOCSLIB.ORG

Edited by Elaine Ostrander and Anatoly Ruvinsky the Genetics of the Dog, 2Nd Edition

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Edited by Elaine Ostrander and Anatoly Ruvinsky the Genetics of the Dog, 2Nd Edition Edited by Elaine Ostrander and Anatoly Ruvinsky The Genetics of the Dog, 2nd Edition FSC wwwracorg MIX Paper from responaible sources FSC CO13504 This page intentionally left blank The Genetics of the Dog, 2nd Edition Edited by Elaine A. Ostrander National Human Genome Research Institute National Institutes of Health Maryland USA and Anatoly Ruvinsky University of New England Australia 0 IY) www.cabi.org CABI is a trading name of CAB International CABI CABI Nosworthy Way 875 Massachusetts Avenue Wallingford 7th Floor Oxfordshire OX10 8DE Cambridge, MA 02139 UK USA Tel: +44 (0)1491832111 Tel: +1 6173954056 Fax: +44 (0)1491833508 Fax: +1 6173546875 E-mail: [email protected] E-mail: [email protected] Website: www.cabi.org © CAB International 2012. All rights reserved. No part of this publication may be reproduced in any form or by any means, electronically, mechanically, by photocopying, recording or otherwise, without the prior permission of the copyright owners. A catalogue record for this book is available from the British Library, London, UK. Library of Congress Cataloging-in-Publication Data The genetics of the dog / edited by Elaine A. Ostrander and Anatoly Ruvinsky. -- 2nd ed. P. ;CM. Rev. ed. of: The genetics of the dog / edited by A. Ruvinsky and J. Sampson. c2001. Includes bibliographical references and index. ISBN 978-1-84593-940-3 (hardback : alk. paper) I. Ostrander, Elaine A. II. Ruvinsky, Anatoly. [DNLM: 1. Dogs--genetics. 2. Breeding. SF 427.2] LC classification not assigned 636.7'0821--dc23 2011031350 ISBN-13: 978 1 84593 940 3 Commissioning editor: Sarah Hulbert Editorial assistant: Gwenan Spearing Production editor: Fiona Chippendale Typeset by SPi, Pondicherry, India Printed and bound in the UK by CPI Group (UK) Ltd, Croydon, CR0 4YY I Contents Contributors Preface Elaine A. Ostrander and Anatoly Ruvinsky 1 Canid Phylogeny and Origin of the Domestic Dog 1 Caries Vila and Jennifer A. Leonard 2Experimental Studies of Early Canid Domestication 12 Lyudmila N. Trut, Irina N. Oskina and Anastasiya V Kharlamova 3 The History and Relationships of Dog Breeds 38 Heidi G. Parker 4 Molecular Genetics of Coat Colour, Texture and Length in the Dog 57 Christopher B. Kaelin and Gregory S. Barsh 5Mendelian Traits in the Dog 83 Frank W Nicholas 6 Canine Immunogenetics 91 Lorna J. Kennedy, William E.R. Oilier, Eliane Marti, John L. Wagner and Rainer E Storb 7 The Genetics of Canine Orthopaedic Traits 136 Gert J. Breur, Nicolaas E. Lambrechts and Rory J. Todhunter 8 Genetics of Cancer in Dogs 161 David R. Sargon 9Genetics of Neurological Disease in the Dog 189 Hannes Lohi 10 Genetics of Eye Disorders in the Dog 218 Cathryn S. Mellersh vi Contents) 11Canine Cytogenetics and Chromosome Maps 241 Matthew Breen and Rachael Thomas 12 Canine Genomics 255 Kerstin Lindblad-Toh 13Genetics of Canine Behavioural Disorders 275 Jennifer S. Yokoyama and Steven P Hamilton 14 Biology of Reproduction and Modern Reproductive Technology in the Dog 295 Catharina Linde Forsberg and Karine Reynaud 15 Developmental Genetics 321 Anatoly Ruvinsky and Mark Hill 16Genetics of Morphological Traits in the Domestic Dog 359 Elaine A. Ostrander and Carlos D. Bustamante 17 Canine Olfactory Genetics 375 Pascale Quignon, Stephanie Robin and Francis Galibert 18 Pedigree Analysis, Genotype Testing and Genetic Counselling 394 Anita M. Oberbauer 19Genetics of Quantitative Traits and Improvement of the Dog Breeds 421 Thomas R. Famula 20 Complex Traits in the Dog 435 Karl G. Lark and Kevin Chase 21 The Canine Model in Medical Genetics 458 Alan N. Wilton and Paula S. Henthorn 22 Genetic Aspects of Performance in Working Dogs 477 Heather J. Huson 23 Genetic Nomenclature 496 Zhi-Liang Hu and James M. Reecy Index 505 The colour plate section can be found following p. 244. I Contributors Gregory S. Barsh, Hudson Alpha Institute for Biotechnology, Huntsville, AL 35806 and Department of Genetics, Stanford University, Stanford, CA 94305, USA. Matthew Breen, Department of Molecular Biomedical Sciences, College of Veterinary Medicine and Center for Comparative Medicine and Translational Research, North Carolina State University, Raleigh, NC 27606, USA; also Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA. Gert J. Breur, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA. Carlos D. Bustamante, Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA. Kevin Chase, Department of Biology, University of Utah, Salt Lake City, UT 84112, USA. Thomas R. Famula, Department of Animal Science, University of California Davis, CA 95616, USA. Francis Galibert, Institut de Genetique et Developpement de Rennes, UMR6061 CNRS Universite de Rennes 1, Faculte de Medecine, 2 avenue Prof. Leon Bernard, CS34317, 35043 Rennes Cedex, France. Steven P. Hamilton, Department of Psychiatry and Institute for Human Genetics, University of California, San Francisco, CA 94143-0984, USA. Paula S. Henthorn, Section of Medical Genetics, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104-6010, USA. Mark Hill, Cell Biology Laboratory, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia. Zhi-Liang Hu, Department of Animal Science, Iowa State University, Ames, IA 50011, USA. Heather J. Huson, National Human Genome Research Institute, National Institutes of Health, 50 South Drive, Building 50, Room 5351, Bethesda, MD 20892 and Institute of Arctic Biology, University of Alaska, Fairbanks, AK 99775, USA. Christopher B. Kaelin, Hudson Alpha Institute for Biotechnology, Huntsville, AL 35806 and Department of Genetics, Stanford University, Stanford, CA 94305, USA. Lorna J. Kennedy, Centre for Integrated Genomic Medical Research, University of Manchester, Stopford Building Oxford Road, Manchester, M13 9PT, UK. Anastasiya V. Kharlamova, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 630090, Novosibirsk 630090, Russia. Nicolaas E. Lambrechts, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA. Karl G. Lark, Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, UT 84112, USA. vii viii Contributors) Jennifer A. Leonard, Conservation and Evolutionary Genetics Group, Estacien Biolegica de Doriana (EBD-CSIC), Avd. Americo Vespucio s/n, 41092 Seville, Spain. Kerstin Lindblad-Toh, Broad Institute of MIT and Harvard, Cambridge, MA 02142 and Science for Life Laboratory, Uppsala University, Uppsala Biomedicinska Centrum (BMC), Husargatan 3, 751 23 Uppsala, Sweden. Catharina Linde Forsberg, Department of Clinical Sciences, Division of Reproduction, Faculty of Veterinary Medicine and Animal Sciences, Swedish University of Agricultural Sciences, SE-750 07 Uppsala, Sweden. Hannes Lohi, Department of Veterinary Biosciences, Faculty of Veterinary Medicine and Research Programs Unit, Molecular Medicine, Faculty of Medicine, University of Helsinki; also Folkhalsan Research Center, Helsinki. Biomedicum 1, Room C323b, P.O. Box 63 (Haartmaninkatu 8), FI-00014 University of Helsinki, Finland. Eliane I. Marti, Universitat Bern, Abteilung Experimentelle Klinische Forschung, Langgassstrasse 124, 3001 Bern, Switzerland. Cathryn S. Mellersh, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU, UK. Frank W. Nicholas, Faculty of Veterinary Science, University of Sydney, NSW 2006, Australia. Anita M. Oberbauer, Department of Animal Science, University of California Davis, CA 95616, USA. William E.R. Oilier, Centre for Integrated Genomic Medical Research, University of Manchester, Stopford Building, Oxford Road, Manchester, M13 9PT, UK. Irina N. Oskina, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 630090, Novosibirsk 630090, Russia. Elaine A. Ostrander, Cancer Genetics Section, National Human Genome Research Institute, National Institutes of Health, 50 South Drive, Building 50, Room 5351, Bethesda, MD 20892, USA. Heidi G. Parker, National Human Genome Research Institute, National Institutes of Health, 50 South Drive, Building 50, Room 5351, Bethesda, MD 20892, USA. Pascale Quignon, Institut de Genetique et Developpement de Rennes, UMR6061 CNRS Universite de Rennes 1, Faculte de Medecine, 2 avenue Prof. Leon Bernard, CS34317, 35043 Rennes Cedex, France. James M. Reecy, Department of Animal Science, Iowa State University, Ames, IA 50011, USA. Karine Reynaud, Reproduction and Developmental Biology, UMR 1198 INRA-ENVA, National Institute for Agricultural Research/National Veterinary School of Alfort, 7 Avenue General de Gaulle, 94700 Maisons-Alfort, France. Stephanie Robin, Institut de Genetique et Developpement de Rennes, UMR6061 CNRS Universite de Rennes 1, Faculte de Medecine, 2 avenue Prof. Leon Bernard, CS34317, 35043 Rennes Cedex, France. Anatoly Ruvinsky, University of New England, Armidale, 2351 NSW, Australia. David R. Sargan, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge, CB3 OES, UK. Rainer E Storb, Transplantation Biology, Clinical Research Division, Fred Hutchinson Cancer Research Center, andf University of Washington School of Medicine, Department of Medicine, 1100 Fairview Ave. N., Seattle, WA 98109, USA. Rachael Thomas, Department of Molecular Biomedical Sciences, College of Veterinary Medicine and Center for Comparative Medicine and Translational Research, North Carolina State University, Raleigh,
Load more

Recommended publications
  • Analyses of Allele-Specific Gene Expression in Highly Divergent
    ARTICLES Analyses of allele-specific gene expression in highly divergent mouse crosses identifies pervasive allelic imbalance James J Crowley1,10, Vasyl Zhabotynsky1,10, Wei Sun1,2,10, Shunping Huang3, Isa Kemal Pakatci3, Yunjung Kim1, Jeremy R Wang3, Andrew P Morgan1,4,5, John D Calaway1,4,5, David L Aylor1,9, Zaining Yun1, Timothy A Bell1,4,5, Ryan J Buus1,4,5, Mark E Calaway1,4,5, John P Didion1,4,5, Terry J Gooch1,4,5, Stephanie D Hansen1,4,5, Nashiya N Robinson1,4,5, Ginger D Shaw1,4,5, Jason S Spence1, Corey R Quackenbush1, Cordelia J Barrick1, Randal J Nonneman1, Kyungsu Kim2, James Xenakis2, Yuying Xie1, William Valdar1,4, Alan B Lenarcic1, Wei Wang3,9, Catherine E Welsh3, Chen-Ping Fu3, Zhaojun Zhang3, James Holt3, Zhishan Guo3, David W Threadgill6, Lisa M Tarantino7, Darla R Miller1,4,5, Fei Zou2,11, Leonard McMillan3,11, Patrick F Sullivan1,5,7,8,11 & Fernando Pardo-Manuel de Villena1,4,5,11 Complex human traits are influenced by variation in regulatory DNA through mechanisms that are not fully understood. Because regulatory elements are conserved between humans and mice, a thorough annotation of cis regulatory variants in mice could aid in further characterizing these mechanisms. Here we provide a detailed portrait of mouse gene expression across multiple tissues in a three-way diallel. Greater than 80% of mouse genes have cis regulatory variation. Effects from these variants influence complex traits and usually extend to the human ortholog. Further, we estimate that at least one in every thousand SNPs creates a cis regulatory effect.
    [Show full text]
  • Polymorphisms of the BARX1 and ADAMTS17 Locus Genes in Individuals with Gastroesophageal Reflux Disease
    J Neurogastroenterol Motil, Vol. 25 No. 3 July, 2019 pISSN: 2093-0879 eISSN: 2093-0887 https://doi.org/10.5056/jnm18183 JNM Journal of Neurogastroenterology and Motility Original Article Polymorphisms of the BARX1 and ADAMTS17 Locus Genes in Individuals With Gastroesophageal Reflux Disease Alexandra Argyrou,1 Evangelia Legaki,1 Christos Koutserimpas,2 Maria Gazouli,1* Ioannis Papaconstantinou,3 George Gkiokas,3 and George Karamanolis4 1Department of Basic Medical Sciences, Laboratory of Biology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; 22nd Department of General Surgery, “Sismanoglio General Hospital of Athens, Athens, Greece; 32nd Department of Surgery, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; and 4Gastroenterology Unit, 2nd Department of Surgery, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece Background/Aims Gastroesophageal reflux disease (GERD) represents a common condition having a substantial impact on the patients’ quality of life, as well as the health system. According to many studies, the BARX1 and ADAMTS17 genes have been suggested as genetic risk loci for the development of GERD and its complications. The purpose of this study is to investigate the potential association between GERD and BARX1 and ADAMTS17 polymorphisms. Methods The present is a prospective cohort study of 160 GERD patients and 180 healthy control subjects of Greek origin, examined for BARX1 and ADAMTS17 polymorphisms (rs11789015 and rs4965272) and a potential correlation to GERD. Results The rs11789015 AG and GG genotypes were found to be significantly associated with GERD (P = 0.032; OR, 1.65; 95% CI, 1.06- 2.57 and P = 0.033; OR, 3.00; 95% CI, 1.15-7.82, respectively), as well as the G allele (P = 0.007; OR, 1.60; 95% CI, 1.14- 2.24).
    [Show full text]
  • Supplementary Table 3 Complete List of RNA-Sequencing Analysis of Gene Expression Changed by ≥ Tenfold Between Xenograft and Cells Cultured in 10%O2
    Supplementary Table 3 Complete list of RNA-Sequencing analysis of gene expression changed by ≥ tenfold between xenograft and cells cultured in 10%O2 Expr Log2 Ratio Symbol Entrez Gene Name (culture/xenograft) -7.182 PGM5 phosphoglucomutase 5 -6.883 GPBAR1 G protein-coupled bile acid receptor 1 -6.683 CPVL carboxypeptidase, vitellogenic like -6.398 MTMR9LP myotubularin related protein 9-like, pseudogene -6.131 SCN7A sodium voltage-gated channel alpha subunit 7 -6.115 POPDC2 popeye domain containing 2 -6.014 LGI1 leucine rich glioma inactivated 1 -5.86 SCN1A sodium voltage-gated channel alpha subunit 1 -5.713 C6 complement C6 -5.365 ANGPTL1 angiopoietin like 1 -5.327 TNN tenascin N -5.228 DHRS2 dehydrogenase/reductase 2 leucine rich repeat and fibronectin type III domain -5.115 LRFN2 containing 2 -5.076 FOXO6 forkhead box O6 -5.035 ETNPPL ethanolamine-phosphate phospho-lyase -4.993 MYO15A myosin XVA -4.972 IGF1 insulin like growth factor 1 -4.956 DLG2 discs large MAGUK scaffold protein 2 -4.86 SCML4 sex comb on midleg like 4 (Drosophila) Src homology 2 domain containing transforming -4.816 SHD protein D -4.764 PLP1 proteolipid protein 1 -4.764 TSPAN32 tetraspanin 32 -4.713 N4BP3 NEDD4 binding protein 3 -4.705 MYOC myocilin -4.646 CLEC3B C-type lectin domain family 3 member B -4.646 C7 complement C7 -4.62 TGM2 transglutaminase 2 -4.562 COL9A1 collagen type IX alpha 1 chain -4.55 SOSTDC1 sclerostin domain containing 1 -4.55 OGN osteoglycin -4.505 DAPL1 death associated protein like 1 -4.491 C10orf105 chromosome 10 open reading frame 105 -4.491
    [Show full text]
  • Partial Deletion of Chromosome 6P Causing Developmental Delay and Mild Dysmorphisms in a Child
    Vrachnis et al. Mol Cytogenet (2021) 14:39 https://doi.org/10.1186/s13039-021-00557-y CASE REPORT Open Access Partial deletion of chromosome 6p causing developmental delay and mild dysmorphisms in a child: molecular and developmental investigation and literature search Nikolaos Vrachnis1,2,3* , Ioannis Papoulidis4, Dionysios Vrachnis5, Elisavet Siomou4, Nikolaos Antonakopoulos1,2, Stavroula Oikonomou6, Dimitrios Zygouris2, Nikolaos Loukas7, Zoi Iliodromiti8, Efterpi Pavlidou9, Loretta Thomaidis6 and Emmanouil Manolakos4 Abstract Background: The interstitial 6p22.3 deletions concern rare chromosomal events afecting numerous aspects of both physical and mental development. The syndrome is characterized by partial deletion of chromosome 6, which may arise in a number of ways. Case presentation: We report a 2.8-year old boy presenting with developmental delay and mild dysmorphisms. High-resolution oligonucleotide microarray analysis revealed with high precision a 2.5 Mb interstitial 6p deletion in the 6p22.3 region which encompasses 13 genes. Conclusions: Identifcation and in-depth analysis of cases presenting with mild features of the syndrome will sharpen our understanding of the genetic spectrum of the 6p22.3 deletion. Keywords: 6p22.3 deletion, Syndrome, Developmental delay, Intellectual disability, Dysmorphism, Behavioral abnormalities, High-resolution microarray analysis Background dysmorphic features, and structural organ defects, as well Te interstitial deletion of chromosomal region 6p22.3 as intellectual disability. is a rare condition with variable phenotypic expression. We report herein a case of interstitial deletion of chro- To date, more than 30 children and adolescents with this mosome 6p investigated by array-CGH in a 2.8-year old deletion have been reported [1–11].
    [Show full text]
  • Sequence Analysis of Familial Neurodevelopmental Disorders
    SEQUENCE ANALYSIS OF FAMILIAL NEURODEVELOPMENTAL DISORDERS by Joseph Mark Tilghman A dissertation submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland December 2020 © 2020 Joseph Tilghman All Rights Reserved Abstract: In the practice of human genetics, there is a gulf between the study of Mendelian and complex inheritance. When diagnosis of families affected by presumed monogenic syndromes is undertaken by genomic sequencing, these families are typically considered to have been solved only when a single gene or variant showing apparently Mendelian inheritance is discovered. However, about half of such families remain unexplained through this approach. On the other hand, common regulatory variants conferring low risk of disease still predominate our understanding of individual disease risk in complex disorders, despite rapidly increasing access to rare variant genotypes through sequencing. This dissertation utilizes primarily exome sequencing across several developmental disorders (having different levels of genetic complexity) to investigate how to best use an individual’s combination of rare and common variants to explain genetic risk, phenotypic heterogeneity, and the molecular bases of disorders ranging from those presumed to be monogenic to those known to be highly complex. The study described in Chapter 2 addresses putatively monogenic syndromes, where we used exome sequencing of four probands having syndromic neurodevelopmental disorders from an Israeli-Arab founder population to diagnose recessive and dominant disorders, highlighting the need to consider diverse modes of inheritance and phenotypic heterogeneity. In the study described in Chapter 3, we address the case of a relatively tractable multifactorial disorder, Hirschsprung disease.
    [Show full text]
  • Identification of the Gene and Mutation for Progressive Rod-Cone Degeneration in Dog and Method for Testing Same
    Europäisches Patentamt *EP001609876A1* (19) European Patent Office Office européen des brevets (11) EP 1 609 876 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.7: C12Q 1/68 28.12.2005 Bulletin 2005/52 (21) Application number: 05253831.1 (22) Date of filing: 21.06.2005 (84) Designated Contracting States: • Zangerl, Barbara AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Philadelphia, PA 19104 (US) HU IE IS IT LI LT LU MC NL PL PT RO SE SI SK TR • Goldstein, Orly Designated Extension States: Ithaca, NY 14850 (US) AL BA HR LV MK YU • Pearce-Kelling, Susan Berkshire, NY 13736 (US) (30) Priority: 21.06.2004 US 581499 P • Felix, Jeanette S. Horseheads, NY 14845 (US) (71) Applicant: CORNELL RESEARCH FOUNDATION, • Sidjanin, Duska J. INC. Brookfield, WI 53045 (US) Ithaca, NY 14850 (US) (74) Representative: MacLean, Martin Robert et al (72) Inventors: Mathys & Squire • Aguirre, Gustavo 120 Holborn Philadelphia, PA 19151 (US) London EC1N 2SQ (GB) • Acland, Gregory M. Unionville, PA 19375 (US) (54) Identification of the gene and mutation for progressive rod-cone degeneration in dog and method for testing same (57) Tools and methods are provided for determin- tion of a transversion from G to A at position correspond- ing whether or not a dog is genetically normal, is a carrier ing to nucleotide position 1298 of SEQ ID NO: 1. of, or is affected with or predisposed to progressive rod- cone degeneration. The method is based on the detec- EP 1 609 876 A1 Printed by Jouve, 75001 PARIS (FR) EP 1 609 876 A1 Description FIELD OF THE INVENTION 5 [0001] The present invention relates generally to a class of genetic diseases, observed in canines, termed progres- sive rod-cone degeneration ("prcd").
    [Show full text]
  • Supplementary Table 1: Adhesion Genes Data Set
    Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like,
    [Show full text]
  • Investigation of the Underlying Hub Genes and Molexular Pathogensis in Gastric Cancer by Integrated Bioinformatic Analyses
    bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Investigation of the underlying hub genes and molexular pathogensis in gastric cancer by integrated bioinformatic analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract The high mortality rate of gastric cancer (GC) is in part due to the absence of initial disclosure of its biomarkers. The recognition of important genes associated in GC is therefore recommended to advance clinical prognosis, diagnosis and and treatment outcomes. The current investigation used the microarray dataset GSE113255 RNA seq data from the Gene Expression Omnibus database to diagnose differentially expressed genes (DEGs). Pathway and gene ontology enrichment analyses were performed, and a proteinprotein interaction network, modules, target genes - miRNA regulatory network and target genes - TF regulatory network were constructed and analyzed. Finally, validation of hub genes was performed. The 1008 DEGs identified consisted of 505 up regulated genes and 503 down regulated genes.
    [Show full text]
  • 2013 Trainee Institution Lab/Research Group Division Of
    2014 Trainee Institution Lab/Research Group Division of Basic Sciences Shannon Barbour University of California, Santa Cruz Harmit Malik, PhD Sarah Debs Whitman College Cecilia Moens, PhD Alec Heckert University of Washington Jesse Bloom, PhD Lauren Hillers Hope College Carissa Perez Olsen, PhD Heather Johns Whitman College Robert Bradley, PhD Chris Large University of Puget Sound Harmit Malik, PhD Division of Clinical Research Linda Dao University of Texas at Arlington Edus (Hootie) Warren, MD, PhD Meselle Jeff-Eke University of Chicago Marie Bleakley, MD, PhD, M.Msc Danielle Oliver Hampton University Cameron Turtle, MD, PhD Maya Rosenfield University of Washington James (Jim) Olson, MD, PhD Derek Wong University of Chicago John Pagel, MD, PhD Division of Human Biology Micah Atwood Northwest University Patrick Paddison, PhD Joshua Messer University of Wyoming Denise Galloway, PhD Emma O'Melia Clark University Catherine (Katie) Peichel, PhD Ethan Paddock Northern Arizona University Julie Overbaugh, PhD ± Monica Salazar New Mexico State University Peggy Porter, MD Sophia Stone Mary Baldwin College Stephen Tapscott, MD, PhD Connor Wagner New Mexico State University Nina Salama, PhD Bailey Wooldridge University of Hawaii at Hilo Adam Geballe, MD Division of Public Health Sciences Meghan Gerry New Mexico State University Kerryn Reding, PhD, MPH Riley Hughes Yale University Johanna Lampe, PhD, RD ± Mayra Lovas New Mexico State University Linda Ko, PhD Shirley Beresford, PhD / Lauren Mercer New Mexico State University Beti Thompson, PhD ± Swati
    [Show full text]
  • EPC Exhibit 134-10 May 20, 2011 the LIBRARY of CONGRESS
    EPC Exhibit 134-10 May 20, 2011 THE LIBRARY OF CONGRESS Dewey Section To: Caroline Kent, Chair Decimal Classification Editorial Policy Committee Cc: Members of the Decimal Classification Editorial Policy Committee Karl E. Debus-López, Chief, U.S. General Division From: Giles Martin, Assistant Editor Winton Matthews, Consulting Assistant Editor Dewey Decimal Classification OCLC Online Computer Library Center, Inc Re: 636.72-636.76 Dog breeds Magdalena Svanberg, of the Kungliga biblioteket/National Library of Sweden, pointed out that the arrangement of dog breeds in 636.72-636.76 was different from that used by the Féderation Cynologique Internationale (FCI). The FCI classification is found at http://www.fci.be/nomenclature.aspx, and at the top level is: Group 1 Sheepdogs and Cattle Dogs (except Swiss Cattle Dogs) Group 2 Pinscher and Schnauzer - Molossoid Breeds - Swiss Mountain and Cattle Dogs Group 3 Terriers Group 4 Dachshunds Group 5 Spitz and Primitive types Group 6 Scenthounds and Related Breeds Group 7 Pointing Dogs Group 8 Retrievers - Flushing Dogs - Water Dogs Group 9 Companion and Toy Dogs Group 10 Sighthounds 1 The American Kennel Club (AKC) arrangement, followed by Dewey, is very different at the top level: Sporting Group 636.752 Hound Group 636.753 Working Group 636.73 Terrier Group 636.755 Toy Group 636.76 Non-Sporting Group 636.72 Herding Group 636.737 Miscellaneous Class (breeds which have not yet been put into the other groups) (The order given here is that on the AKC’s webpage, http://www.akc.org/breeds/index.cfm?nav_area=breeds ) The situation is made more complex because 636.72-636.76 contain several references to breeds as “(United Kingdom)” as a shortcut for saying that this group is one of the groupings of the Kennel Club of the United Kingdom (KC).
    [Show full text]
  • The Dog Buyer's Guide
    THE DOG BUYER’S GUIDE The Society for Canine Genetic Health and Ethics www.koiranjalostus.fi Foreword The main purpose of the A dog is a living creature We hope you will find this guidebook is to provide and no one can guarantee that guide useful in purchasing help for anyone planning your dog will be healthy and your dog! the purchase of his or her flawless. Still, it pays to choose first dog. However, it can be a breeder who does his best useful for anyone planning to guarantee it. We hope this to get a dog. Our aim is to guide will help you to actively help you and your family to and critically find and process choose a dog that best suits information about the health, your needs and purposes. characteristics and behaviour of the breed or litter of your Several breeds seem to be choice. plagued with health and character problems. The This guide has been created, Finnish Society for Canine written and constructed by Genetic Health and Ethics the members of the HETI (HETI) aims to influence society: Hanna Bragge, Päivi dog breeding by means of Jokinen, Anitta Kainulainen, information education. Our Inkeri Kangasvuo, Susanna aim is to see more puppies Kangasvuo, Tiina Karlström, born to this world free of Pertti Kellomäki, Sara genetic disorders that would Kolehmainen, Saija Lampinen, deteriorate their quality of life Virpi Leinonen, Helena or life-long stress caused by, Leppäkoski, Anna-Elisa for example, defects in the Liinamo, Mirve Liius, Eira nervous system. Malmstén, Erkki Mäkelä, Katariina Mäki, Anna Niiranen, The demand of puppies is Tiina Notko, Riitta Pesonen, one of the most important Meri Pisto koski, Maija factors that guides the dog Päivärinta, Johanna Rissanen, breeding.
    [Show full text]
  • DOGS in MEDIEVAL ART Text and Illustrations by RIA HÖRTER
    289-304 _289-304 1/27/14 4:08 PM Page 294 HISTORY Medieval illuminated chronicles, breviaries, But at the same time, pestilence, famine, endless codices, psalters and manuals include a wealth dissensions, and bloody wars made it a dark time in of texts and images in which dogs play an impor- medieval Europe. tant role. Here is the story. In the early Middle Ages, the nobility had com- plete authority over a mass of commoners. Farmers BONDSMEN, FARMERS, had to turn over most of their output to the landown- NOBILITY AND CLERGY ers, and respect their privileges, including hunting, fishing and judicial rights. Historians count the Middle Ages as between the The contrasts were huge. While commoners lived 5th and 15th centuries. The development of agricul- in miserable circumstances, the nobility and clergy ture, rise of towns, extension of markets and trade; lived in luxury. the position of bondsmen, farmers, nobility and Images of medieval dogs show an almost exclu- clergy; and the evolution of secular art from the her- sive relationship with the highly placed. Bondsmen, itage of religious art were important events during serfs and farmers had no belongings; they were these centuries. themselves someone’s possession. DOGS IN MEDIEVAL ART text and illustrations by RIA HÖRTER SOURCES The sources I referred to for this article are di- verse: handwritten manuscripts, printed books, books of hours, breviaries, bestiaries and how-to books for the medieval upper class. The Rochester Bestiary is an outstanding example of a manuscript with many pictures of dogs. It is almost unbelievable that, at the beginning of the 13th century, artists could create such a beautiful and accurate work.
    [Show full text]