DOCSLIB.ORG

Characterization of Human Stem Cells and Therapeutic Strategies Involving IGF-1 and Shrna in Huntington's Disease

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Characterization of Human Stem Cells and Therapeutic Strategies Involving IGF-1 and Shrna in Huntington's Disease Imagem Carla Maria Nunes Lopes Characterization of human stem cells and therapeutic strategies involving IGF-1 and shRNA in Huntington's disease Tese de Doutoramento em Biologia Experimental e Biomedicina, Ramo de Neurociências e Doença, orientada por Doutora Ana Cristina Rego e apresentada ao Instituto de Investigação Interdisciplinar da Universidade de Coimbra (IIIUC) 2015 Characterization of human stem cells and therapeutic strategies involving IGF-1 and shRNA in Huntington's disease Dissertação apresentada ao Instituto de Investigação Interdisciplinar da Universidade de Coimbra para cumprimento dos requisitos necessários à obtenção do Grau de Doutor em Biologia Experimental e Biomedicina na especialidade de Neurociências e Doença Orientada por: Professora Doutora Ana Cristina Carvalho Rego – Faculdade de Medicina da Universidade de Coimbra e Centro de Neurociências e Biologia Celular, Universidade de Coimbra, Coimbra, Portugal Co-orientada por: Professor Doutor Luis Pereira de Almeida –Faculdade de Farmácia e Centro de Neurociências e Biologia Celular, Universidade de Coimbra, Coimbra, Portugal The research described in the present thesis was performed at the Center for Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal. Carla Lopes received a PhD fellowship from Fundação para a Ciência e Tecnologia (FCT), Portugal (fellowship: SFRH / BD / 51192 / 2010, financed by national founds of MEC CRM:0044390 ). The research work was funded by European community fund FEDER through “Programa Operacional Temático Factores de Competitividade – COMPETE” and “Fundação para a Ciência e a Tecnologia” (FCT), Portugal. ACKNOWLEDGEMENTS Table of Contents SUMMARY ............................................................................................................................................ V RESUMO ............................................................................................................................................ VIII CHAPTER I - GENERAL INTRODUCTION ................................................................................................... 1 1.1. HUNTINGTON’S DISEASE .......................................................................................................... 2 1.1.1. HISTORICAL BACKGROUND........................................................................................................... 2 1.1.2. EPIDEMIOLOGY ......................................................................................................................... 3 1.1.3. GENETICS ................................................................................................................................ 5 1.1.4. NEUROPATHOLOGY ................................................................................................................... 7 1.1.5. SYMPTOMS ........................................................................................................................... 12 1.1.6. CENTRAL AND PERIPHERAL METABOLIC CHANGES IN HD .................................................................... 14 1.1.6.1. Diabetes mellitus in HD ............................................................................................. 18 1.2. NORMAL FUNCTION OF HUNTINGTIN ...................................................................................... 2 1.2.1. DEVELOPMENT ......................................................................................................................... 2 1.2.2. STRUCTURE ............................................................................................................................. 3 1.2.3. INTERACTORS ........................................................................................................................... 4 1.2.4. FUNCTIONS ............................................................................................................................. 5 1.2.5. MITOSIS ............................................................................................................................... 24 1.2.5.1. Cell cycle ................................................................................................................... 24 1.2.5.2. The mitotic spindle .................................................................................................... 25 1.2.5.3. In development and cell fate specification ................................................................. 28 1.3. HUNTINGTIN AND HD............................................................................................................. 30 1.3.1. LOSS OF WILD-TYPE HUNTINGTIN................................................................................................. 30 1.3.2. MISFOLDING AND AGGREGATION OF MUTANT HUNTINGTIN ............................................................... 31 1.3.3. INTRACELLULAR MECHANISMS OF TOXICITY .................................................................................... 33 1.3.3.1. Protein misfolded and inhibition of protein degradation ............................................ 34 1.3.3.2. Caspase activation .................................................................................................... 35 1.3.3.3. Transcription deregulation ........................................................................................ 36 1.3.3.4. Disruption of axonal transport ................................................................................... 38 1.3.3.5. Synaptic dysfunction.................................................................................................. 38 1.3.3.6. Mitochondrial dysfunction and oxidative stress .......................................................... 40 1.4. MODELING HD ....................................................................................................................... 42 1.4.1. ANIMAL MODELS .................................................................................................................... 43 i 1.4.1.1. N-terminal fragment mouse models .......................................................................... 43 1.4.1.2. Full-length mouse model ........................................................................................... 45 1.4.2. CELLULAR MODELS .................................................................................................................. 46 1.4.2.1. Characteristics of embryonic and induced pluripotent stem cells ................................ 46 1.4.3. MITOCHONDRIAL FUNCTION AND METABOLISM IN STEM CELLS ........................................................... 50 1.4.3.1. Altered metabolic profile and mitochondrial function following reprogramming to pluripotency ................................................................................................................................ 50 1.4.4. METABOLIC PROFILE OF PLURIPOTENT STEM CELLS ........................................................................... 55 1.4.5. STEM CELL DIFFERENTIATION – ROLE OF MITOCHONDRIAL FUNCTION AND ROS ....................................... 56 1.4.6. MITOCHONDRIAL MODIFICATIONS AND STEM CELL BIOLOGY – CURRENT KNOWLEDGE IN NEUROLOGICAL DISORDERS .......................................................................................................................................... 59 1.5. THERAPEUTIC STRATEGIES IN HD ........................................................................................... 63 1.5.1. GENETIC STRATEGIES ............................................................................................................... 63 1.5.1.1. Gene addition............................................................................................................ 63 1.5.1.2. Silencing.................................................................................................................... 63 1.5.2. REPAIR ................................................................................................................................. 70 1.5.2.1. Homologous recombination....................................................................................... 70 1.5.2.2. Zinc finger nucleases ................................................................................................. 70 1.5.2.3. TAL effectors ............................................................................................................. 72 1.5.2.4. Crispr/CAS ................................................................................................................. 73 1.5.3. IGF-1 AS A POTENTIAL THERAPEUTIC DRUG ................................................................................... 75 1.6. HYPOTHESIS AND SPECIFIC AIMS OF THE PRESENT WORK ..................................................... 79 CHAPTER II - IGF-1 INTRANASAL ADMINISTRATION RESCUES HUNTINGTON’S DISEASE PHENOTYPES IN YAC128 MICE ....................................................................................................................................... 81 2.1. INTRODUCTION ...................................................................................................................... 82 2.2. MATERIALS AND METHODS .................................................................................................... 85 2.2.1. MATERIALS ........................................................................................................................... 85 2.2.2. EXPERIMENTAL ANIMALS .........................................................................................................
Load more

Recommended publications
  • The Kid Kit: All You Need to Interview Your Grandparents
    The Kid Kit: All you need to interview your grandparents INCLUDED: • 45 FAMILY HISTORY QUESTIONS • 3 BONUS ACTIVITIES • INTERVIEW RECORDING TIPS • THE HISTORY YOUR GRANDPARENTS LIVED THROUGH • TIPS FOR WHAT TO DO POST-INTERVIEW Recommended for children ages 8-12. Recommended for children A resource from ModernHeirloomBooks.com. ©2020 Modern Heirloom Books LLC. For personal use only. The Kid Kit Dear Grandma/Grandpa/Poppy/Nana/Oma/Bubbe, I can’t wait to interview you and learn more about your life before you were my grandparent. Could you please: • Tell me when you need a break during our interview? • Consider my questions an invitation to tell me everything—don’t feel like you should just answer what I ask, but rather use the questions as a springboard to travel back in time, remember, and tell me all the stories that come to mind—please!! • Have fun! I hope you enjoy this process, and know that I and the rest of the family value you and all that you have experienced. Love, CUT OUT, SIGN & GIVE TO YOUR GRANDPARENT & PARENT BEFORE YOUR INTERVIEW. The Kid Kit Dear Mom/Dad, Thank you for giving me this idea and for helping me to set up my interviews with my grandparent! Could you please: • Let me use one of the family’s smart phones or tablets to record my interviews? I am told that using two might be even better (just in case something goes wrong with one). • Find a few old photos of your parents that I can show them to prompt memories? • Suggest some questions I might ask that you know will spark good stories from your parent(s)? • Help me figure out how to transcribe the interview after it is done? Thank you!! Love, personal use only.
    [Show full text]
  • Galac Recent Dev Cushing.Indd
    Recent developments in canine Cushing’s syndrome Nieuwe ontwikkelingen met betrekking tot het syndroom van Cushing bij de hond (met een samenvatting in het Nederlands) Novejša dognanja o Cushingovem sindromu pri psu (z izvlečkom v slovenščini) Proefschrift ter verkrijging van de graad van doctor aan de Universiteit Utrecht op gezag van de rector magnificus, prof.dr. J.C. Stoof, ingevolge het besluit van het college voor promoties in het openbaar te verdedigen op dinsdag 22 juni 2010 des middags te 12.45 uur door Sara Galac geboren op 16 januari 1968 te Slovenj Gradec, Slovenië Promotor: Prof.dr. J. Rothuizen Co-promotoren: Dr. H.S. Kooistra Dr.ir. J.A. Mol The studies described in this thesis were conducted at and financially supported by the Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands Publication of this thesis was made possible by generous support of: AUV Dierenartsencoöperatie Boehringer Ingelheim B.V. Dechra Veterinary Products Eurovet Animal Health J.E. Jurriaanse stichting Novartis Animal Health Royal Canin Virbac Ontwerp en grafische begeleiding: Kees van Veenendaal, Haarlem Omslagillustratie: Ruby de Goede, Heemstede Druk: Drukkerij de Bij, Amsterdam CIP-DATA KONINKLIJKE BIBLIOTHEEK, DEN HAAG Galac, Sara Recent developments in canine Cushing`s syndrome Sara Galac, Utrecht Universiteit Utrecht, Faculteit Diergeneeskunde Thesis Universiteit Utrecht. – With ref. – With summary in Dutch and Slovene. ISBN 978-90-393-5347-9 Subject headings: hypercortisolism,
    [Show full text]
  • Autosomal Dominant Leukodystrophy with Autonomic Symptoms
    List of Papers This thesis is based on the following papers, which are referred to in the text by their Roman numerals. I MR imaging characteristics and neuropathology of the spin- al cord in adult-onset autosomal dominant leukodystrophy with autonomic symptoms. Sundblom J, Melberg A, Kalimo H, Smits A, Raininko R. AJNR Am J Neuroradiol. 2009 Feb;30(2):328-35. II Genomic duplications mediate overexpression of lamin B1 in adult-onset autosomal dominant leukodystrophy (ADLD) with autonomic symptoms. Schuster J, Sundblom J, Thuresson AC, Hassin-Baer S, Klopstock T, Dichgans M, Cohen OS, Raininko R, Melberg A, Dahl N. Neurogenetics. 2011 Feb;12(1):65-72. III Bedside diagnosis of rippling muscle disease in CAV3 p.A46T mutation carriers. Sundblom J, Stålberg E, Osterdahl M, Rücker F, Montelius M, Kalimo H, Nennesmo I, Islander G, Smits A, Dahl N, Melberg A. Muscle Nerve. 2010 Jun;41(6):751-7. IV A family with discordance between Malignant hyperthermia susceptibility and Rippling muscle disease. Sundblom J, Mel- berg A, Rücker F, Smits A, Islander G. Manuscript submitted to Journal of Anesthesia. Reprints were made with permission from the respective publishers. Contents Introduction..................................................................................................11 Background and history............................................................................... 13 Early studies of hereditary disease...........................................................13 Darwin and Mendel................................................................................
    [Show full text]
  • The Role of the C-Terminus Merlin in Its Tumor Suppressor Function Vinay Mandati
    The role of the C-terminus Merlin in its tumor suppressor function Vinay Mandati To cite this version: Vinay Mandati. The role of the C-terminus Merlin in its tumor suppressor function. Agricultural sciences. Université Paris Sud - Paris XI, 2013. English. NNT : 2013PA112140. tel-01124131 HAL Id: tel-01124131 https://tel.archives-ouvertes.fr/tel-01124131 Submitted on 19 Mar 2015 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. 1 TABLE OF CONTENTS Abbreviations ……………………………………………………………………………...... 8 Resume …………………………………………………………………………………… 10 Abstract …………………………………………………………………………………….. 11 1. Introduction ………………………………………………………………………………12 1.1 Neurofibromatoses ……………………………………………………………………….14 1.2 NF2 disease ………………………………………………………………………………15 1.3 The NF2 gene …………………………………………………………………………….17 1.4 Mutational spectrum of NF2 gene ………………………………………………………..18 1.5 NF2 in other cancers ……………………………………………………………………...20 2. ERM proteins and Merlin ……………………………………………………………….21 2.1 ERMs ……………………………………………………………………………………..21 2.1.1 Band 4.1 Proteins and ERMs …………………………………………………………...21 2.1.2 ERMs structure ………………………………………………………………………....23 2.1.3 Sub-cellular localization and tissue distribution of ERMs ……………………………..25 2.1.4 ERM proteins and their binding partners ……………………………………………….25 2.1.5 Assimilation of ERMs into signaling pathways ………………………………………...26 2.1.5. A. ERMs and Ras signaling …………………………………………………...26 2.1.5. B. ERMs in membrane transport ………………………………………………29 2.1.6 ERM functions in metastasis …………………………………………………………...30 2.1.7 Regulation of ERM proteins activity …………………………………………………...31 2.1.7.
    [Show full text]
  • Studies and Sources in Islamic Art and Architecture
    STUDIES AND SOURCES IN ISLAMIC ART AND ARCHITECTURE SUPPLEMENTS TO MUQARNAS Sponsored by the Aga Khan Program for Islamic Architecture at Harvard University and the Massachusetts Institute of Technology, Cambridge, Massachusetts. VOLUME IX PREFACING THE IMAGE THE WRITING OF ART HISTORY IN SIXTEENTH-CENTURY IRAN BY DAVID J. ROXBURGH BRILL LEIDEN • BOSTON • KÖLN 2001 This book is printed on acid-free paper. Library of Congress Cataloging-in-Publication Data Roxburgh, David J. Prefacing the image : the writing of art history in sixteenth-century Iran / David J. Roxburgh. p. cm. — (Studies and sources in Islamic art and architecture. Supplements to Muqarnas, ISSN 0921 0326 ; v. 9) Includes bibliographical references and index. ISBN 9004113762 (alk. papier) 1. Art, Safavid—Historiography—Sources. 2. Art, Islamic—Iran– –Historiography—Sources. 3. Art criticism—Iran—History—Sources. I. Title. II. Series. N7283 .R69 2000 701’.18’095509024—dc21 00-062126 CIP Die Deutsche Bibliothek - CIP-Einheitsaufnahme Roxburgh, David J.: Prefacing the image : the writing of art history in sixteenth century Iran / by David J. Roxburgh. – Leiden; Boston; Köln : Brill, 2000 (Studies and sources in Islamic art and architectue; Vol 9) ISBN 90-04-11376-2 ISSN 0921-0326 ISBN 90 04 11376 2 © Copyright 2001 by Koninklijke Brill NV, Leiden, The Netherlands All rights reserved. No part of this publication may be reproduced, translated, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without prior written permission from the publisher. Authorization to photocopy items for internal or personal use is granted by Brill provided that the appropriate fees are paid directly to The Copyright Clearance Center, 222 Rosewood Drive, Suite 910 Danvers MA 01923, USA.
    [Show full text]
  • Exploring Extracellular Vesicles Biogenesis in Hypothalamic Cells Through a Heavy Isotope Pulse/Trace Proteomic Approach
    cells Article Exploring Extracellular Vesicles Biogenesis in Hypothalamic Cells through a Heavy Isotope Pulse/Trace Proteomic Approach Chee Fan Tan 1,2 , Hui San Teo 2, Jung Eun Park 2, Bamaprasad Dutta 2, Shun Wilford Tse 2, Melvin Khee-Shing Leow 3,4,5 , Walter Wahli 3,6 and Siu Kwan Sze 2,* 1 NTU Institute for Health Technologies, Interdisciplinary Graduate School, Nanyang Technological University, Singapore 637335, Singapore; [email protected] 2 School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore; [email protected] (H.S.T.); [email protected] (J.E.P.); [email protected] (B.D.); [email protected] (S.W.T.) 3 Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 636921, Singapore; [email protected] (M.K.-S.L.); [email protected] (W.W.) 4 Department of Endocrinology, Tan Tock Seng Hospital, Singapore 308433, Singapore 5 Cardiovascular and Metabolic Disorder Program, Duke-NUS Medical School, Singapore 169857, Singapore 6 Center for Integrative Genomics, University of Lausanne, Le Génopode, CH-1015 Lausanne, Switzerland * Correspondence: [email protected]; Tel.: +65-6514-1006; Fax: +65-6791-3856 Received: 24 March 2020; Accepted: 21 May 2020; Published: 25 May 2020 Abstract: Studies have shown that the process of extracellular vesicles (EVs) secretion and lysosome status are linked. When the lysosome is under stress, the cells would secrete more EVs to maintain cellular homeostasis. However, the process that governs lysosomal activity and EVs secretion remains poorly defined and we postulated that certain proteins essential for EVs biogenesis are constantly synthesized and preferentially sorted to the EVs rather than the lysosome.
    [Show full text]
  • Summary of Sexual Abuse Claims in Chapter 11 Cases of Boy Scouts of America
    Summary of Sexual Abuse Claims in Chapter 11 Cases of Boy Scouts of America There are approximately 101,135sexual abuse claims filed. Of those claims, the Tort Claimants’ Committee estimates that there are approximately 83,807 unique claims if the amended and superseded and multiple claims filed on account of the same survivor are removed. The summary of sexual abuse claims below uses the set of 83,807 of claim for purposes of claims summary below.1 The Tort Claimants’ Committee has broken down the sexual abuse claims in various categories for the purpose of disclosing where and when the sexual abuse claims arose and the identity of certain of the parties that are implicated in the alleged sexual abuse. Attached hereto as Exhibit 1 is a chart that shows the sexual abuse claims broken down by the year in which they first arose. Please note that there approximately 10,500 claims did not provide a date for when the sexual abuse occurred. As a result, those claims have not been assigned a year in which the abuse first arose. Attached hereto as Exhibit 2 is a chart that shows the claims broken down by the state or jurisdiction in which they arose. Please note there are approximately 7,186 claims that did not provide a location of abuse. Those claims are reflected by YY or ZZ in the codes used to identify the applicable state or jurisdiction. Those claims have not been assigned a state or other jurisdiction. Attached hereto as Exhibit 3 is a chart that shows the claims broken down by the Local Council implicated in the sexual abuse.
    [Show full text]
  • Genetic Status of the Swedish Central Collection of Heirloom Apple Cultivars
    Scientia Horticulturae 272 (2020) 109599 Contents lists available at ScienceDirect Scientia Horticulturae journal homepage: www.elsevier.com/locate/scihorti Genetic Status of the Swedish Central collection of heirloom apple cultivars T Jonas Skytte af Sätraa,*, Michela Troggiob, Firuz Odilbekova, Jasna Sehicc, Helena Mattissona, Inger Hjalmarssond, Pär K. Ingvarssone, Larisa Garkava-Gustavssona a Department of Plant Breeding, Swedish University of Agricultural Sciences, Alnarp, Sweden b Research and Innovation Centre, Fondazione Edmund Mach, San Michele all’Adige, Trento, Italy c Department of Plant Breeding – Balsgård, Swedish University of Agricultural Sciences, Fjälkestadsvägen 459, 29194, Kristianstad, Sweden d Department of Landscape Architecture, Planning and Management, Swedish University of Agricultural Sciences, Alnarp, Sweden e Department of Plant Biology, Swedish University of Agricultural Sciences, 750 07, Uppsala, Sweden ARTICLE INFO ABSTRACT Keywords: Cultivated apple is one of the most widely grown fruit crops worldwide. With the introduction of modern apple Malus domestica cultivars, from foreign and national breeding programs, the use of local cultivars decreased during the 20th SNP array century. In order to minimize genetic erosion and avoid loss of special genotypes, a number of local clonal Genotyping archives were established across Sweden, with the goal of retaining old and local cultivars. About 220 apple Pedigree cultivars, appointed for preservation, obtained the status of mandate cultivars. Initially, they were identified Gene bank based on pomological traits, but prior to the establishment of the Swedish Central Collection they were geno- Local cultivars SSR markers typed with simple sequence repeat (SSR) markers. SSR markers helped to evaluate the status of the preserved material, as well as to find the best possible true-to-type source for propagation, thus guiding the establishment of the Central Collection.
    [Show full text]
  • Oklahoma State Radiological Society State Legislative Report - First Session 53Rd Legislature Prepared by Lynne White - [email protected]
    Oklahoma State Radiological Society State Legislative Report - First Session 53rd Legislature Prepared by Lynne White - [email protected] The First Session of Oklahoma’s 53rd Legislature convened on Feb. 7 and adjourned on May 27. In the first session, or 2011 session, of the Legislature: 969 Senate bills and 44 Joint Resolutions were introduced. 1,168 House bills and 41 Joint Resolutions were introduced. Governor Fallin signed 388 bills into law. Bills and resolutions that were not heard in committee or on the floor or voted “do not pass” may be considered in the Second Session beginning in February 2012. Workers’ Compensation Reform HB 2038, Sykes/Sullivan, authorizes the Workers’ Compensation Court administrator to compile annual reports relating to characteristics of cases including the amount of surgeries, length of temporary total disability, permanent partial disability, and other medical treatments and therapies. Effective date: Aug. 26, 2011. Status: Signed by the governor. SB 878, Sykes/Sullivan, is comprehensive legislation that significantly changes the Oklahoma workers’ compensation law. The 222-page measure is a result of a proposal brought forward by a working group representing workers’ compensation lawyers, the business community, and the medical community. The overall goal of the measure is to reduce the cost of workers’ compensation to businesses while revising processes for injured workers receiving medical treatment. It was clear during negotiations of this measure that treatment guidelines and medical fees would be the most contentious part for the medical community. SB 878 contains the following key provisions: Medical Fees The measure requires the Workers’ Compensation Court administrator to develop a new medical fee schedule by Jan.
    [Show full text]
  • The Undergraduate Scholars Program Acknowledges the Following Sponsors and Partners for Their Ongoing Support of Student Research
    The Undergraduate Scholars Program Acknowledges the Following Sponsors and Partners for their Ongoing Support of Student Research: American Indian Research Opportunities (AIRO) Center for Biofilm Engineering McNair Scholars Program Montana INBRE Program Montana Space Grant Consortium College of Agriculture College of Arts & Architecture College of Business College of Education, Health & Human Development College of Engineering College of Letters & Science College of Nursing Honors College Office of the Provost The Graduate School Vice President for Research & Economic Development 1 Table of Contents Map ............................................................................................................................ 3 Topical Sessions .................................................................................................. 4 McNair Scholars ................................................................................................................................4 Plant Science & Agricultural Research .....................................................................................5 Morning Poster Presentations ......................................................................... 6 Afternoon Poster Presentations...................................................................... 18 Graduate Abstracts College of Agriculture........................................................................................................................ 31 College of Arts & Architecture.......................................................................................................
    [Show full text]
  • Karaoke Catalog Updated On: 09/04/2018 Sing Online on Entire Catalog
    Karaoke catalog Updated on: 09/04/2018 Sing online on www.karafun.com Entire catalog TOP 50 Tennessee Whiskey - Chris Stapleton My Way - Frank Sinatra Wannabe - Spice Girls Perfect - Ed Sheeran Take Me Home, Country Roads - John Denver Broken Halos - Chris Stapleton Sweet Caroline - Neil Diamond All Of Me - John Legend Sweet Child O'Mine - Guns N' Roses Don't Stop Believing - Journey Jackson - Johnny Cash Thinking Out Loud - Ed Sheeran Uptown Funk - Bruno Mars Wagon Wheel - Darius Rucker Neon Moon - Brooks & Dunn Friends In Low Places - Garth Brooks Fly Me To The Moon - Frank Sinatra Always On My Mind - Willie Nelson Girl Crush - Little Big Town Zombie - The Cranberries Ice Ice Baby - Vanilla Ice Folsom Prison Blues - Johnny Cash Piano Man - Billy Joel (Sittin' On) The Dock Of The Bay - Otis Redding Bohemian Rhapsody - Queen Turn The Page - Bob Seger Total Eclipse Of The Heart - Bonnie Tyler Ring Of Fire - Johnny Cash Me And Bobby McGee - Janis Joplin Man! I Feel Like A Woman! - Shania Twain Summer Nights - Grease House Of The Rising Sun - The Animals Strawberry Wine - Deana Carter Can't Help Falling In Love - Elvis Presley At Last - Etta James I Will Survive - Gloria Gaynor My Girl - The Temptations Killing Me Softly - The Fugees Jolene - Dolly Parton Before He Cheats - Carrie Underwood Amarillo By Morning - George Strait Love Shack - The B-52's Crazy - Patsy Cline I Want It That Way - Backstreet Boys In Case You Didn't Know - Brett Young Let It Go - Idina Menzel These Boots Are Made For Walkin' - Nancy Sinatra Livin' On A Prayer - Bon
    [Show full text]
  • Type of Horizontal Deviation in Consanguinity
    Original Article Type of Horizontal Deviation in Consanguinity Samia Iqbal, Hakim Anjum Nadeem Pak J Ophthalmol 2018, Vol. 34, No. 2 . .. .. See end of article for Purpose: To find out the association and types of horizontal deviation in authors affiliations consanguinity. …..……………………….. Study Design: Cross-sectional study. Place and duration of Study: Department of Ophthalmology, The University Correspondence to: of Lahore teaching hospital from September to December 2017. Samia Iqbal Department of Ophthalmology, Material and Methods: In this study, 93 patients of 3 to 15 years, with The University of Lahore diagnosis of horizontal deviation and positive history of consanguinity were Email: [email protected] included in the study. While the patients with vertical deviation and negative history of consanguinity were excluded from study. Data was collected by self- designed proforma after taking consent from patients having history of consanguinity. The visual acuity screening and orthoptic assessment were performed on the sample of 93 patients using snellen chart for visual acuity and pen torch for Hirschberg test, cover uncover test and alternate cover test and prisms for krimsky test. Data was analyzed using SPSS version 20. Results: Out of 93 patients, 55 (59.1) had exotropia and 38 (40.8%) had esotropia. 17 (18.2%) had emmetropia, 22 (23.65%) had myopia, 7 (7.5%) had hyperopia, 25 (26.8%) had myopic astigmatism, 10 (10.7%) had hyperopic astigmatism and the remaining 12 (12.9%) had mixed astigmatism. Conclusion: Consanguinity is related with horizontal deviation and refractive errors. Exotropia is found to be more common in these cases. …..……………………….. Key Word: Consanguinity, Horizontal deviation, Myopia.
    [Show full text]