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Harris Mylonas
HARRIS MYLONAS Department of Political Science, George Washington University 2115 G street, NW, Suite 440, Washington, DC 20052 [email protected] RESEARCH AND TEACHING INTERESTS Nationalism, Nation- and State-Building, Social Order, Diaspora Policies, European Politics, Qualitative Methods. POSITIONS Editor-in-Chief of Nationalities Papers--peer-reviewed journal published by Cambridge University Press [2018-present]. George Washington University, Washington, DC Associate Professor of Political Science and International Affairs [2015- present]. Associate Dean for Research, Elliott School of International Affairs [2017-2018]. Assistant Professor of Political Science and International Affairs [2009-2015]. Harvard University, Cambridge, MA Academy Scholar, Harvard Academy for International and Area Studies, Weatherhead Center for International Affairs [2008-2009 and 2011-2012 academic years]. EDUCATION Yale University, New Haven, CT Ph.D., with Distinction, Political Science, 2008 M.A. (2004) and M.Phil. (2005) in Political Science The University of Chicago, Chicago, IL M.A. in Political Science, 2003 The University of Athens, Athens, Greece M.Sc. in Political Science & Sociology, 2002 B.A. in Political Science & Public Administration, 2000 PUBLICATIONS Books Diaspora Management Logics, Unpublished book manuscript. Forthcoming. Nationalism Reawakened: The Good, the Bad, and the Ugly, under contract with Cambridge University Press. (w/ Maya Tudor) 2012. The Politics of Nation-Building: Making Co-Nationals, Refugees, and Minorities. New York, NY: Cambridge University Press. ¬ Winner, 2014 European Studies Book Award, Council for European Studies, for the best first book on any subject in European Studies published within a two-year period. ¬ Winner, 2013 Peter Katzenstein Book Prize, Cornell University, for an outstanding first book in International Relations, Comparative Politics, or Political Economy. -
Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma
Anatomy and Pathology Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma Sarah L. Lake,1 Sarah E. Coupland,1 Azzam F. G. Taktak,2 and Bertil E. Damato3 PURPOSE. To detect deletions and loss of heterozygosity of disease is fatal in 92% of patients within 2 years of diagnosis. chromosome 3 in a rare subset of fatal, disomy 3 uveal mela- Clinical and histopathologic risk factors for UM metastasis noma (UM), undetectable by fluorescence in situ hybridization include large basal tumor diameter (LBD), ciliary body involve- (FISH). ment, epithelioid cytomorphology, extracellular matrix peri- ϩ ETHODS odic acid-Schiff-positive (PAS ) loops, and high mitotic M . Multiplex ligation-dependent probe amplification 3,4 5 (MLPA) with the P027 UM assay was performed on formalin- count. Prescher et al. showed that a nonrandom genetic fixed, paraffin-embedded (FFPE) whole tumor sections from 19 change, monosomy 3, correlates strongly with metastatic death, and the correlation has since been confirmed by several disomy 3 metastasizing UMs. Whole-genome microarray analy- 3,6–10 ses using a single-nucleotide polymorphism microarray (aSNP) groups. Consequently, fluorescence in situ hybridization were performed on frozen tissue samples from four fatal dis- (FISH) detection of chromosome 3 using a centromeric probe omy 3 metastasizing UMs and three disomy 3 tumors with Ͼ5 became routine practice for UM prognostication; however, 5% years’ metastasis-free survival. to 20% of disomy 3 UM patients unexpectedly develop metas- tases.11 Attempts have therefore been made to identify the RESULTS. Two metastasizing UMs that had been classified as minimal region(s) of deletion on chromosome 3.12–15 Despite disomy 3 by FISH analysis of a small tumor sample were found these studies, little progress has been made in defining the key on MLPA analysis to show monosomy 3. -
The Sources of Islamic Revolutionary Conduct
Joint Military Intelligence College LAMBERT Y Y The Sources of Islamic Revolutionary Conduct TEL IN LIG Y E R N A C T E I L C I O M L L T E N G I E O J 1962 Major Stephen P. Lambert U.S. Air Force TEL IN LIG Y E R N A C ISBN 1-932946-02-0 T E PCN 56747 I L C I O M L L T E N G I E O J 1962 The Joint Military Intelligence College supports and encourages research on intelligence issues that distills lessons and improves Intelligence Community capabilities for policy-level and operational consumers Y: The Sources of Islamic Revolutionary Conduct, Major Stephen P. Lambert, U.S. Air Force This product has been reviewed by senior experts from academia and government, and has been approved for unrestricted distribution by the Directorate for Freedom of Information and Security Review, Washington Headquarters Services. It is available to the public through the National Technical Information Service (www.ntis.gov). The author has also arranged for publication of this study through the Hoover Institution at Stanford University. The projected publication date is 2005. The Hoover Institution book includes commentar- ies on Major Lambert’s work by an even greater variety of scholars than included in the present book. [email protected], Editor and Director Center for Strategic Intelligence Research Library of Congress Control Number 2004114330 ISBN 1-932946-02-0 Y The Sources of Islamic Revolutionary Conduct Major Stephen P. Lambert, U.S. Air Force Research Fellow In g ic t e e g ll t ii a g e r n tt c SS c ee rr R R o o e e f f s s e e r r a a e e t r t r n c n Joint Military c e h e h C Intelligence College C WASHINGTON, DC April 2005 With the cooperation and support of the Institute for National Security Studies (INSS) USAF Academy, Colorado Springs The views expressed in this book are those of the author and do not reflect the official policy or position of the Department of Defense or the U.S. -
SETMAR Antibody
Product Datasheet SETMAR Antibody Catalog No: #43086 Orders: [email protected] Description Support: [email protected] Product Name SETMAR Antibody Host Species Rabbit Clonality Polyclonal Purification Antigen affinity purification. Applications WB IHC Species Reactivity Hu Specificity The antibody detects endogenous levels of total SETMAR protein. Immunogen Type protein Immunogen Description Fusion protein of human SETMAR Target Name SETMAR Other Names Mar1; HsMar1; METNASE Accession No. Swiss-Prot#: Q53H47Gene ID: 6419 Calculated MW 78kd Concentration 1mg/ml Formulation Rabbit IgG in pH7.4 PBS, 0.05% NaN3, 40% Glycerol. Storage Store at -20°C Application Details Western blotting: 1:200-1:1000 Immunohistochemistry: 1:20-1:100 Images Gel: 6%SDS-PAGE Lysate: 40 µg Lane: Jurkat cell Primary antibody: 1/400 dilution Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution Exposure time: 30 seconds Address: 8400 Baltimore Ave., Suite 302, College Park, MD 20740, USA http://www.sabbiotech.com 1 Immunohistochemical analysis of paraffin-embedded Human liver cancer tissue using #43086 at dilution 1/20. Immunohistochemical analysis of paraffin-embedded Human thyroid cancer tissue using #43086 at dilution 1/20. Background This gene encodes a fusion protein that contains an N-terminal histone-lysine N-methyltransferase domain and a C-terminal mariner transposase domain. The encoded protein binds DNA and functions in DNA repair activities including non-homologous end joining and double strand break repair. The SET domain portion of this protein specifically methylates histone H3 lysines 4 and 36. This gene exists as a fusion gene only in anthropoid primates, other organisms lack mariner transposase domain. Note: This product is for in vitro research use only and is not intended for use in humans or animals. -
Mouse Setmar Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Setmar Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Setmar conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Setmar gene (NCBI Reference Sequence: NM_178391 ; Ensembl: ENSMUSG00000034639 ) is located on Mouse chromosome 6. 2 exons are identified, with the ATG start codon in exon 1 and the TAG stop codon in exon 2 (Transcript: ENSMUST00000049246). Exon 2 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Setmar gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP23-93D20 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 2 covers 82.85% of the coding region. Start codon is in exon 1, and stop codon is in exon 2. The size of intron 1 for 5'-loxP site insertion: 10466 bp. The size of effective cKO region: ~2167 bp. The cKO region does not have any other known gene. Page 1 of 7 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 2 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Setmar Homology arm cKO region loxP site Page 2 of 7 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats. -
Birth of a Chimeric Primate Gene by Capture of the Transposase Gene
Birth of a chimeric primate gene by capture of the SEE COMMENTARY transposase gene from a mobile element Richard Cordaux*, Swalpa Udit†, Mark A. Batzer*, and Ce´ dric Feschotte†‡ *Department of Biological Sciences, Biological Computation and Visualization Center, Center for BioModular Multi-Scale Systems, Louisiana State University, 202 Life Sciences Building, Baton Rouge, LA 70803; and †Department of Biology, University of Texas, Arlington, TX 76019 Edited by Susan R. Wessler, University of Georgia, Athens, GA, and approved March 27, 2006 (received for review February 10, 2006) The emergence of new genes and functions is of central impor- SETMAR transcript, which consists of these three exons, is tance to the evolution of species. The contribution of various types predicted to encode a protein of 671 amino acids and is of duplications to genetic innovation has been extensively inves- supported by 48 human cDNA clones from 18 different normal tigated. Less understood is the creation of new genes by recycling and͞or cancerous tissues (Table 1, which is published as sup- of coding material from selfish mobile genetic elements. To inves- porting information on the PNAS web site; refs. 14 and 15). tigate this process, we reconstructed the evolutionary history of These data suggest that the SETMAR protein is broadly ex- SETMAR, a new primate chimeric gene resulting from fusion of a pressed and has an important, yet unknown, function in human. SET histone methyltransferase gene to the transposase gene of a Recently, it was shown that the SET domain of the SETMAR mobile element. We show that the transposase gene was recruited protein exhibits histone methyltransferase activity (15), as do all as part of SETMAR 40–58 million years ago, after the insertion of known SET domains (16, 17). -
A Role for Setmar in Gene Regulation
A ROLE FOR SETMAR IN GENE REGULATION: INSIGHTS FROM STRUCTURAL ANALYSIS OF THE DNA-BINDING DOMAIN IN COMPLEX WITH DNA Qiujia Chen Submitted to the faculty of the University Graduate School in partial fulfillment of the requirements for the degree Doctor of Philosophy in the Department of Biochemistry and Molecular Biology Indiana University August 2016 Accepted by the Graduate Faculty, Indiana University, in partial fulfillment of the requirements for the degree of Doctor of Philosophy. ___________________________ Millie M. Georgiadis, Ph. D., Chair ___________________________ Thomas D. Hurley, Ph. D. Doctoral Committee ___________________________ Ronald C. Wek, Ph. D. June 30, 2016 ___________________________ John J. Turchi, Ph. D. ___________________________ Mark R. Kelley, Ph. D. ii DEDICATION This thesis is dedicated to my parents Chuhui and Xuanna. Thank you for giving me the best education you could and great support. To my brother Jiamin, sister-in-law Xiaoqiong, and my niece Yuhan, for helping me survive all the stress. I would like to dedicate this thesis to Dr. Jinsong Liu, who opened the door for me to the intriguing world of X-ray crystallography and structural biology. Special dedication of this thesis must be given to Dr. Millie M. Georgiadis, a very talented and inspiring scientific mentor and advisor, for her patience, enthusiasm, and encouragement throughout this project. iii ACKNOWLEDGEMENTS Firstly, I would like to express deepest appreciation to my advisor, Professor Millie M. Georgiadis, for her continuous support of my Ph.D research work, for her motivation, patience, and immense knowledge. Her excitement in regard to protein-DNA crystallography helped me in all the time of research and writing of this thesis. -
A Single Genetic Locus Associated with Pediatric Fractures: a Genome-Wide Association Study on 3,230 Patients
1716 EXPERIMENTAL AND THERAPEUTIC MEDICINE 20: 1716-1724, 2020 A single genetic locus associated with pediatric fractures: A genome-wide association study on 3,230 patients ROOPE PARVIAINEN1, SINI SKARP2,3, LINDA KORHONEN1, WILLY SERLO1, MINNA MÄNNIKKÖ2 ��� JUHA-JAAKKO SINIKUMPU1 1D�p���m��� �� C������� ��� A����������, O��� C�������� F������� ��� Sp���� I�j��y S���y, R������� U��� ��� P���������, P�������� N�������y, P�������� Surgery, C���� P�y������y, D��m������y, C������� G�������, O��������� ��� Gy�������y, O����������y������y ��� Op�����m����y (PEDEGO), O��� M������ R������� C����� (MRC), U��������y �� O��� ��� O��� U��������y H��p����, FI-90029 O���; 2N������� F������ B���� C�����, F�����y �� M�������, U��������y �� O���; 3C����� ��� L��� C����� H����� R�������, F�����y �� M�������, U��������y �� O���, FI-90014 O���, F������ Received July 13, 2019; Accepted April 29, 2020 DOI: 10.3892/etm.2020.8885 Abstract. The�� understanding������������� ��of the��� biological���������� and��� environ�������- RNA 1 (PROSER2-AS1) and PROSER2, thus suggesting that mental risk factors of fractures in pediatrics is limited. Previous these m�y be novel candidate genes associated with the risk of studies have reported that fractures involve heritable traits, but pediatric fractures. the genetic factors contributing to the risk of fractures remain elusive. Furthermore, genetic influences specific to immature Introduction bone have not been thoroughly studied. Therefore, the aim of the present study was to identify genetic variations that are The incidence of fractures is highest �mong the young and associated with fractures in early childhood. The present study older p�pulations (1). O� note, fractures in pediatric patients used � prospective Northern Finland Birth Cohort (year 1986; are common injuries that result in pain, as well as short‑ and �=9,432). -
Assemblée Générale GENERALE
NATIONS UNIES A Distr. Assemblée générale GENERALE A/AC.96/986 2 octobre 2003 Original: ANGLAIS/FRANCAIS COMITE EXECUTIF DU PROGRAMME DU HAUT COMMISSAIRE Cinquante-quatrième session (Genève, 29 septembre - 3 octobre 2003) EXECUTIVE COMMITTEE OF THE HIGH COMMISSIONER'S PROGRAMME Fifty-fourth session (Geneva, 29 September -3 October 2003) LISTE DES PARTICIPANTS LIST OF PARTICIPANTS GE.03-02713 A/AC.96/986 Page 2 TABLE DES MATIERES Pages I. ETATS 3 A. Etats membres 3 B. Etats représentés par des observateurs 37 II. OBSERVATEUR 58 III AUTRES OBSERVATEURS 58 IV. ORGANISATIONS INTERGOUVERNEMENTALES 60 A. Système des Nations Unies 60 1. Nations Unies 60 2. Institutions spécialisées 62 B. Autres organisations intergouvernementales 63 V. ORGANISATIONS NON GOUVERNEMENTALES 65 TABLE OF CONTENTS I. STATES 3 A. Member States 3 B. States represented by observers 37 II. OBSERVER 58 III. OTHER OBSERVERS 58 IV. INTERGOVERNMENTAL ORGANIZATIONS 60 A. United Nations system 60 1. United Nations 60 2. Specialized agencies 62 B. Other intergovernmental organizations 63 V. NON-GOVERNMENTALES ORGANIZATIONS 65 A/AC.96/986 Page 3 I. ETATS - STATES A. Etats membres/Member States AFRIQUE DU SUD - SOUTH AFRICA Representatives Mr. Pitso Montwedi Chargé d’affaires a.i., Permanent Mission to the United Nations Office at Geneva Alternate Representatives Mr. Claude Schravesande Acting Chief Director, Refugee Affairs and Migration, Department of Home Affairs Dr. Moleboge Machele Deputy Director, Refugee Affairs and Migration, Department of Home Affairs Mr. Graham Anderson Deputy Director, Refugee Affairs and Migration, Department of Foreign Affairs Ms Laura Joyce First Secretary, Permanent Mission to the United Nations Office at Geneva ALGERIE - ALGERIA Représentant S.E. -
The UN Security Council and the Responsibility to Protect
The UN Security Council and the Responsibility to Protect FAVORITA PapeRs 01/2010 01/2010 S The UN Security Council PAPER A and the Responsibility to Protect FAVORIT Policy, Process, and Practice DA 39th IPI VIenna SemInar BN 978-3-902021-67-0 s I "FAVORITA PAPERS" OF THE DIPLOMATIC ACADEMY OF VIENNA The ‘Favorita Papers’ series is intended to complement the academic training for international careers which is the core activity of the Diplomatic Academy. It reflects the expanding conference and public lectures programme of the Academy by publishing substantive conference reports on issues that are of particular relevance to the understanding of contemporary international problems and to the training for careers in diplomacy, international public service and business. The series was named ‘Favorita Papers’ after the original designation of the DA’s home, the imperial summer residence ‘Favorita’ donated by Empress Maria Theresia to the ‘Theresianische Akademie’ in 1749. Contributions to this series come from academics and practitioners actively engaged in the study, teaching and practice of international affairs. All papers reflect the views of the author. THE UN SECURITY COUNCIL AND THE RESPONSIBILITY TO PROTECT: POLICY, PROCESS, AND PRACTICE 39th IPI Vienna Seminar Diplomatic Academy of Vienna Favorita Papers 01/2010 Edited by: Hans Winkler (DA), Terje Rød-Larsen (IPI), Christoph Mikulaschek (IPI) ISBN 978-3-902021-67-0 ©2010 The Diplomatic Academy of Vienna The Diplomatic Academy of Vienna is one of Europe’s leading schools for post-graduate studies in international relations and European affairs. It prepares young university graduates for the present-day requirements of successful international careers in diplomacy, public administration and business. -
Anti-SETMAR-Antibody Pack Size
TECHNICAL DATA SHEET Cat No: Kab07773 Product Particulars: anti-SETMAR-antibody Pack Size: 100μg Pack Size: Pack Size: 100μg Purify: Immunogen affinity purified Host: Rabbit Isotype: IgG Storage: PBS with 0.02% sodium azide and 50% glycerol pH 7.3 , -20Ԩ for 24 months (Avoid repeated freeze / thaw cycles.) Background (Function): Protein derived from the fusion of a methylase with the transposase of an Hsmar1 transposon that plays a role in DNA double-strand break repair, stalled replication fork restart and DNA integration. DNA-binding protein, it is indirectly recruited to sites of DNA damage through protein-protein interactions. Has also kept a sequence-specific DNA-binding activity recognizing the 19- mer core of the 5'-terminal inverted repeats (TIRs) of the Hsmar1 element and displays a DNA nicking and end joining activity (PubMed:16332963, PubMed:16672366, PubMed:17877369, PubMed:17403897, PubMed:18263876, PubMed:22231448, PubMed:24573677, PubMed:20521842). In parallel, has a histone methyltransferase activity and methylates 'Lys-4' and 'Lys-36' of histone H3. Specifically mediates dimethylation of H3 'Lys-36' at sites of DNA double-strand break and may recruit proteins required for efficient DSB repair through non-homologous end-joining (PubMed:16332963, PubMed:21187428, PubMed:22231448). Also regulates replication fork processing, promoting replication fork restart and regulating DNA decatenation through stimulation of the topoisomerase activity of TOP2A (PubMed:18790802, PubMed:20457750). Immunogen: SET domain and mariner transposase fusion gene Synonyms: Calculated MW: Uniprot ID: Q53H47 Specificity: Human Tested Application: ELISA,WB,IP Recommended Dilution: Gene ID: 6419 Gene Location: Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE" OUR KINESISDX COMMITMENT : GUARANTEED QUALITY WITH EXPERT TECHNICAL SUPPORT . -
Evolutionary Tinkering with Transposable Elements
COMMENTARY Evolutionary tinkering with transposable elements I. King Jordan* National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD 20894 t was almost 30 years ago when with to create novel forms. Indeed, de- Franc¸oisJacob declared that evolu- spite the early notion of TEs as being tionary innovation (the emergence strictly selfish (parasitic) elements that of novel form and function over serve no function for their hosts (7), Itime) occurred primarily via a process there now exist numerous examples of of ‘‘tinkering’’ (1). By tinkering, Jacob formerly mobile TE sequences that have essentially meant the creation of novelty been ‘‘domesticated’’ (8) to serve some through random combinations of pre- functional role for the host genomes in existing forms. Two fundamental and which they reside (9, 10). However, countervailing notions are implicit in there is still a relative paucity of de- this view of evolution: optimality versus tailed studies that address both the evo- constraint. Were evolution to perform lutionary dynamics of TE-derived host optimally, a more apt metaphor might genes as well as the functional roles of be that of an engineer. An engineer the proteins that they encode. The work works according to a plan, with a pre- of Cordaux et al. (3) on the SETMAR cise goal for the desired end, and uses gene represents an important step to- material designed specifically toward ward alleviating this knowledge gap. that end. Evolution, on the other hand, SETMAR, originally discovered by must work without the benefit of fore- Robertson and Zumpano (11), is a chi- sight and is subject to very real con- meric gene made up of a SET histone straints with respect to the material at methyltransferase transcript fused to the its disposal; as such, evolutionary biol- transposase domain of a formerly mo- ogy is replete with examples of subopti- bile TE sequence.