Summer Research Symposium 2019
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Reframing Psychiatry for Precision Medicine
Reframing Psychiatry for Precision Medicine Elizabeth B Torres 1,2,3* 1 Rutgers University Department of Psychology; [email protected] 2 Rutgers University Center for Cognitive Science (RUCCS) 3 Rutgers University Computer Science, Center for Biomedicine Imaging and Modelling (CBIM) * Correspondence: [email protected]; Tel.: (011) +858-445-8909 (E.B.T) Supplementary Material Sample Psychological criteria that sidelines sensory motor issues in autism: The ADOS-2 manual [1, 2], under the “Guidelines for Selecting a Module” section states (emphasis added): “Note that the ADOS-2 was developed for and standardized using populations of children and adults without significant sensory and motor impairments. Standardized use of any ADOS-2 module presumes that the individual can walk independently and is free of visual or hearing impairments that could potentially interfere with use of the materials or participation in specific tasks.” Sample Psychiatric criteria from the DSM-5 [3] that does not include sensory-motor issues: A. Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive, see text): 1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions. 2. Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures; to a total lack of facial expressions and nonverbal communication. -
Download the Fall 2020 Virtual Commencement Program
FALL 2020 VIRTUAL COMMENCEMENT DECEMBER 18 Contents About the SIU System .............................................................................................................................................. 3 About Southern Illinois University Edwardsville ................................................................................................. 4 SIUE’s Mission, Vision, Values and Statement on Diversity .............................................................................. 5 Academics at SIUE ................................................................................................................................................... 6 History of Academic Regalia ................................................................................................................................. 8 Commencement at SIUE ......................................................................................................................................... 9 Academic and Other Recognitions .................................................................................................................... 10 Honorary Degree ................................................................................................................................................... 12 Distinguished Service Award ............................................................................................................................... 13 College of Arts and Sciences: Undergraduate Ceremony ............................................................................. -
Oil Sketches and Paintings 1660 - 1930 Recent Acquisitions
Oil Sketches and Paintings 1660 - 1930 Recent Acquisitions 2013 Kunsthandel Barer Strasse 44 - D-80799 Munich - Germany Tel. +49 89 28 06 40 - Fax +49 89 28 17 57 - Mobile +49 172 890 86 40 [email protected] - www.daxermarschall.com My special thanks go to Sabine Ratzenberger, Simone Brenner and Diek Groenewald, for their research and their work on the text. I am also grateful to them for so expertly supervising the production of the catalogue. We are much indebted to all those whose scholarship and expertise have helped in the preparation of this catalogue. In particular, our thanks go to: Sandrine Balan, Alexandra Bouillot-Chartier, Corinne Chorier, Sue Cubitt, Roland Dorn, Jürgen Ecker, Jean-Jacques Fernier, Matthias Fischer, Silke Francksen-Mansfeld, Claus Grimm, Jean- François Heim, Sigmar Holsten, Saskia Hüneke, Mathias Ary Jan, Gerhard Kehlenbeck, Michael Koch, Wolfgang Krug, Marit Lange, Thomas le Claire, Angelika and Bruce Livie, Mechthild Lucke, Verena Marschall, Wolfram Morath-Vogel, Claudia Nordhoff, Elisabeth Nüdling, Johan Olssen, Max Pinnau, Herbert Rott, John Schlichte Bergen, Eva Schmidbauer, Gerd Spitzer, Andreas Stolzenburg, Jesper Svenningsen, Rudolf Theilmann, Wolf Zech. his catalogue, Oil Sketches and Paintings nser diesjähriger Katalog 'Oil Sketches and Paintings 2013' erreicht T2013, will be with you in time for TEFAF, USie pünktlich zur TEFAF, the European Fine Art Fair in Maastricht, the European Fine Art Fair in Maastricht. 14. - 24. März 2013. TEFAF runs from 14-24 March 2013. Die in dem Katalog veröffentlichten Gemälde geben Ihnen einen The selection of paintings in this catalogue is Einblick in das aktuelle Angebot der Galerie. Ohne ein reiches Netzwerk an designed to provide insights into the current Beziehungen zu Sammlern, Wissenschaftlern, Museen, Kollegen, Käufern und focus of the gallery’s activities. -
Sensory Deficits in a Mouse Model of Christianson Syndrome Tarheen
Sensory Deficits in a Mouse Model of Christianson Syndrome Tarheen Fatima Department of Physiology McGill University, Montreal April 2019 A thesis submitted to McGill University in partial fulfillment of the requirements of the degree of Master of Science. © Tarheen Fatima 2019 Abstract Christianson Syndrome (CS) is a recently characterized X-linked neurodevelopmental disorder caused by loss-of-function mutations in the gene slc9a6, encoding the endosomal Na+/H+ Exchanger 6 (NHE6). The disorder is associated with developmental delay, intellectual disability, loss of motor coordination, mutism, ataxia, epilepsy, as well as autistic features. In addition to these symptoms, CS patients exhibit elevated pain thresholds to noxious stimuli as well as discomfort at normally innocuous stimuli. The underlying causes of these sensory deficits are yet to be determined. Hence, this study aims at understanding how loss-of-function of NHE6 affects transmission and processing of pain. To this end, we examined the expression of NHE6 in peripheral and central neurons implicated in sensation and interpretation of pain. Additionally, we characterized the nociceptive behaviour of NHE6 knockout (KO) mice using a battery of behaviour tests. Our immunohistochemical experiments demonstrate that NHE6 is highly expressed in nociceptive, small-diameter dorsal root ganglia (DRG) neurons. Moreover, mice lacking NHE6 display decreased responses to noxious mechanical, thermal and chemical stimuli but are more responsive to noxious cold than wild-type littermates. Interestingly, immunohistochemical characterization of DRG tissue from aged NHE6 null mice indicates a decrease in some neuronal subsets suggesting cell death. Finally, using light brush-induced Fos activation in the dorsal horn, we found that the spinal processing of innocuous stimuli is not different between wildtype and NHE6 knockout mice. -
What Is Christianson Syndrome? by Dr
What is Christianson Syndrome? By Dr. Eric Morrow Christianson syndrome is a genetic disorder that affects brain development. It is an “X-linked” disorder (see “Why is CS found only in boys?” section for a description of what X-linked means). Symptoms of CS usually appear in infancy and include epilepsy and intellectual disability. Although the exact prevalence of Christianson syndrome is unknown, a genetic study by Tarpey and colleagues identified Christianson Syndrome in 2 of about 200 families (about 1% of families with apparent X-linked developmental disabilities). This was among the most common genetic change in X-linked forms of intellectual disability. What are the causes of Christianson syndrome? Christianson syndrome is caused by changes in the gene, SLC9A6. Genes are important because they code for proteins, which carry out essential processes in the cells of our bodies. The SLC9A6 gene codes for the NHE6 protein. NHE6 is part of a family of proteins that are sodium (Na+)/hydrogen (H+) exchangers. The NHE6 protein is found in endosomes, which take up molecules to be destroyed or recycled for other processes in our body. NHE6 makes sure that these endosomes have the correct intra-endosomal acid level by letting in Na into the endosome and getting rid of hydrogen, which is the acid molecule. The acid level regulates protein turnover. My analogy our stomach acid, the acidity in endosomes helps degrade cellular proteins. These genetic changes in SLC9A6 cause the NHE6 protein to not work properly. You may have heard words such as “loss-of-function”, “truncation” or “frame- shift”, which describe how the NHE6 protein cannot be made in the cells to carry out these processes in the endosome. -
Mark Twain's Theories of Morality. Frank C
Louisiana State University LSU Digital Commons LSU Historical Dissertations and Theses Graduate School 1941 Mark Twain's Theories of Morality. Frank C. Flowers Louisiana State University and Agricultural & Mechanical College Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_disstheses Recommended Citation Flowers, Frank C., "Mark Twain's Theories of Morality." (1941). LSU Historical Dissertations and Theses. 99. https://digitalcommons.lsu.edu/gradschool_disstheses/99 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Historical Dissertations and Theses by an authorized administrator of LSU Digital Commons. For more information, please contact [email protected]. MARK TWAIN*S THEORIES OF MORALITY A dissertation Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College . in. partial fulfillment of the requirements for the degree of Doctor of Philosophy in The Department of English By Prank C. Flowers 33. A., Louisiana College, 1930 B. A., Stanford University, 193^ M. A., Louisiana State University, 1939 19^1 LIBRARY LOUISIANA STATE UNIVERSITY COPYRIGHTED BY FRANK C. FLOWERS March, 1942 R4 196 37 ACKNOWLEDGEMENT The author gratefully acknowledges his debt to Dr. Arlin Turner, under whose guidance and with whose help this investigation has been made. Thanks are due to Professors Olive and Bradsher for their helpful suggestions made during the reading of the manuscript, E. C»E* 3 7 ?. 7 ^ L r; 3 0 A. h - H ^ >" 3 ^ / (CABLE OF CONTENTS ABSTRACT . INTRODUCTION I. Mark Twain— philosopher— appropriateness of the epithet 1 A. -
Luca Bartolini, MD 1 8/9/2021 CURRICULUM VITAE LUCA
8/9/2021 CURRICULUM VITAE LUCA BARTOLINI, MD Director, Pediatric Epilepsy Program Hasbro Children’s Hospital Assistant Professor of Pediatrics Assistant Professor of Neurology Assistant Professor of Neurosurgery The Warren Alpert Medical School of Brown University Email: [email protected] EDUCATION: Undergraduate Liceo Classico “Tito Livio”, Padova, Italy Medical School University of Padova School of Medicine, Padova, Italy 09/2000 – 07/2006 Doctor of Medicine (M.D.) POSTGRADUATE TRAINING: Residency Obstetrics and Gynecology University of Parma, Italy 07/2007 – 01/2008 Pediatrics (Pediatric Neurology Track) University of Padova, Italy 04/2008 – 10/2013 Pediatrics Children’s National Medical Center / The George Washington University, Washington DC 07/2012 – 06/2013 Child Neurology Children’s National Medical Center / The George Washington University, Washington DC 07/2013 – 06/2016 Luca Bartolini, MD 1 Fellowship Neuroscience Research Children’s National Medical Center / The George Washington University, Washington DC National Institutes of Health, Bethesda, MD 07/2016 – 06/2017 Epilepsy National Institutes of Health, Bethesda, MD 07/2017 – 06/2018 Clinical Neurophysiology National Institutes of Health, Bethesda, MD 07/2018 – 06/2019 POSTGRADUATE HONORS AND AWARDS: Research Career Symposium Scholarship American Academy of Neurology 02/2015 Pediatric Epilepsy Fellow Pipeline Travel Scholarship Epilepsy Foundation of America 12/2015 Sentinel of Science Award (Top 10% of Researchers contributing to the peer-review of the field of Medicine) -
Amyloid Clearance Defect in Apoe4 Astrocytes Is Reversed by Epigenetic Correction of Endosomal Ph
Amyloid clearance defect in ApoE4 astrocytes is reversed by epigenetic correction of endosomal pH Hari Prasada and Rajini Raoa,1 aDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205 Edited by Reinhard Jahn, Max Planck Institute for Biophysical Chemistry, Goettingen, Germany, and approved June 6, 2018 (received for review January 28, 2018) Endosomes have emerged as a central hub and pathogenic driver ability (7–9). Patients who have CS also show striking age- of Alzheimer’s disease (AD). The earliest brain cytopathology in dependent neurodegeneration, with prominent glial pathology neurodegeneration, occurring decades before amyloid plaques and phosphorylated tau deposits (7). Female carriers have and cognitive decline, is an expansion in the size and number of learning difficulties and behavioral issues, and some present with endosomal compartments. The strongest genetic risk factor for low Mini-Mental State Examination scores suggestive of early sporadic AD is the e4 allele of Apolipoprotein E (ApoE4). Previous cognitive decline (10). Interestingly, NHE6 was among the most studies have shown that ApoE4 potentiates presymptomatic endo- highly down-regulated genes (up to sixfold) in the elderly (70 y) somal dysfunction and defective endocytic clearance of amyloid brain, compared with the adult (40 y) brain (11). These obser- beta (Aβ), although how these two pathways are linked at a cel- vations led us to consider a broader role for NHE6 in neuro- lular and mechanistic level has been unclear. Here, we show that degenerative disorders, including Alzheimer’s disease (AD), a aberrant endosomal acidification in ApoE4 astrocytes traps the major cause of dementia in the elderly. -
Geologic Map of the Victoria Quadrangle (H02), Mercury
H01 - Borealis Geologic Map of the Victoria Quadrangle (H02), Mercury 60° Geologic Units Borea 65° Smooth plains material 1 1 2 3 4 1,5 sp H05 - Hokusai H04 - Raditladi H03 - Shakespeare H02 - Victoria Smooth and sparsely cratered planar surfaces confined to pools found within crater materials. Galluzzi V. , Guzzetta L. , Ferranti L. , Di Achille G. , Rothery D. A. , Palumbo P. 30° Apollonia Liguria Caduceata Aurora Smooth plains material–northern spn Smooth and sparsely cratered planar surfaces confined to the high-northern latitudes. 1 INAF, Istituto di Astrofisica e Planetologia Spaziali, Rome, Italy; 22.5° Intermediate plains material 2 H10 - Derain H09 - Eminescu H08 - Tolstoj H07 - Beethoven H06 - Kuiper imp DiSTAR, Università degli Studi di Napoli "Federico II", Naples, Italy; 0° Pieria Solitudo Criophori Phoethontas Solitudo Lycaonis Tricrena Smooth undulating to planar surfaces, more densely cratered than the smooth plains. 3 INAF, Osservatorio Astronomico di Teramo, Teramo, Italy; -22.5° Intercrater plains material 4 72° 144° 216° 288° icp 2 Department of Physical Sciences, The Open University, Milton Keynes, UK; ° Rough or gently rolling, densely cratered surfaces, encompassing also distal crater materials. 70 60 H14 - Debussy H13 - Neruda H12 - Michelangelo H11 - Discovery ° 5 3 270° 300° 330° 0° 30° spn Dipartimento di Scienze e Tecnologie, Università degli Studi di Napoli "Parthenope", Naples, Italy. Cyllene Solitudo Persephones Solitudo Promethei Solitudo Hermae -30° Trismegisti -65° 90° 270° Crater Materials icp H15 - Bach Australia Crater material–well preserved cfs -60° c3 180° Fresh craters with a sharp rim, textured ejecta blanket and pristine or sparsely cratered floor. 2 1:3,000,000 ° c2 80° 350 Crater material–degraded c2 spn M c3 Degraded craters with a subdued rim and a moderately cratered smooth to hummocky floor. -
Research Resources: Brown University
7/31/2019 This resource listing is intended as a source of information that can be selectively cut, pasted and edited into Facilities and Other Resources sections of grant submissions. BROWN ENVIRONMENT AND RESOURCES (QUICK SECTION LINKS) ACADEMIC INSTITUTIONS ACADEMIC HEALTH CENTERS ACADEMIC SCHOOLS, COLLEGES, DEPARTMENTS, CENTERS, INSTITUTES AND PROGRAMS CLINICAL RESEARCH SUPPORT COLLABORATING INSTITUTIONS COMMUNITY ENGAGEMENT ORGANIZATIONS COMPUTING AND INFORMATION SERVICES CORE AND SHARED RESEARCH FACILITIES DIVERSITY PROGRAMS EDUCATION AND MENTORING RESOURCES EDUCATION PROGRAMS EDUCATION TECHNOLOGY RESOURCES LIBRARY RESOURCES MULTISPECIALTY PRACTICE GROUPS RESEARCH ADMINISTRATION RESEARCH BUILDINGS RHODE ISLAND & RESEARCH ENVIRONMENT RHODE ISLAND STATEWIDE COLLABORATIVE PROGRAMS BROWN ENVIRONMENT AND RESOURCES – DETAILED TABLE OF CONTENTS WITH LINKS ACADEMIC INSTITUTIONS Brown University – Long Brown University - Short University of Rhode Island (URI) ACADEMIC HEALTH CENTERS Lifespan Health System Care New England (CNE) Health System Providence VA Medical Center (PVAMC) ACADEMIC SCHOOLS, COLLEGES, DEPARTMENTS, CENTERS, INSTITUTES AND PROGRAMS Center - Advance-CTR: Comprehensive Center - Advance-CTR: Comprehensive - Alternative Center - Advance-CTR: Summary Center - Advance Predictive Biology Center - Alcohol and Addiction Studies (CAAS) Center - Biology of Aging Center - Brown Center for Biomedical Informatics (BCBI) Center - Brown Center for the Study of Children at Risk Center - Center for Biomedical Engineering (CBME) Center - -
![Catalogue Number [Of the Bulletin]](https://docslib.b-cdn.net/cover/3412/catalogue-number-of-the-bulletin-1433412.webp)
Catalogue Number [Of the Bulletin]
BULLETIN OF WELLESLEY COLLEGE CATALOGUE NUMBER 1967-1968 JULY 1967 CATALOGUE NUMBER BULLETIN OF WELLESLEY COLLEGE July 1967 Bulletins published six times a year by Wellesley College, Green Hall, Wellesley, Massachusetts 02181. January, one; April, one; July, one; Ocober, one; Novem- ber, two. Second-Class postage paid at Boston, Massachusetts and at additional mailing offices. Volume 57 Number 1 CALENDAR Academic Year 1967-1968 Term I Registration of new students, 9:00 a.m. to 11:00 p.m Sunday, September 10 Registration closes for all students, 11:00 p.m Tuesday, September 12 Opening Convocation, 8:30 a.m Wednesday, September 13 Classes begin Thursday, September 14 _, , . C Wednesday, November 22 . after classes iiianksgivmg recess ° <. , ^^ a^ j m i a-r ^ ) to 1:00 A.M Monday, November 27 _, ( from Tuesday, December 12 Exammations: <,, , c i. j rA u ic y through Saturday, December lb Christmas vacation begins after the student's last examination. Term II Registration closes for all students, 1:00 a.m. .Thursday, January 4 „ (after classes Wednesday, February 21 /to 1:00 a.m Monday, February 26 from Tuesday, April 2 Examinations: <., , through Saturday,c i. i Aprila i bc I Spring vacation begins after the student's last examination. Term III Registration closes for all students, 1:00 a.m. .Tuesday, April 16 ^ ( from Monday, May 27 Exammations: <^, , t- j a/t oc ) through Tuesday, May 28 Commencement Saturday, June 1 2 TABLE OF CONTENTS Visitors; Correspondence 5 Board of Trustees . 6 Officers of Instruction and Administration 7 The College 21 The Curriculum 26 Requirements for the Degree of Bachelor of Arts; Exemp- tion; Advanced Placement; Credit Outside the Regular Course Program; Course and Special Examinations; Research or In- dividual Study; Academic Distinctions and Honors; Require- ments for Master of Arts Degree Special Programs and Preparation for Careers . -
A Potential Gain-Of-Function Variant of SLC9A6 Leads to Endosomal T Alkalinization and Neuronal Atrophy Associated with Christianson Syndrome Alina Iliea, Andy Y.L
Neurobiology of Disease 121 (2019) 187–204 Contents lists available at ScienceDirect Neurobiology of Disease journal homepage: www.elsevier.com/locate/ynbdi A potential gain-of-function variant of SLC9A6 leads to endosomal T alkalinization and neuronal atrophy associated with Christianson Syndrome Alina Iliea, Andy Y.L. Gaob, Annie Bouchera, Jaeok Parkc, Albert M. Berghuisc, ⁎ Mariëtte J.V. Hofferd, Yvonne Hilhorst-Hofsteed, R. Anne McKinneyb, John Orlowskia, a Department of Physiology, McGill University, Montreal, Canada b Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada c Department of Biochemistry, McGill University, Montreal, Canada d Department of Clinical Genetics, Leiden University Medical Center, Leiden, the Netherlands ARTICLE INFO ABSTRACT Keywords: Loss-of-function mutations in the recycling endosomal (Na+,K+)/H+ exchanger gene SLC9A6/NHE6 result in Christianson Syndrome overacidification and dysfunction of endosomal-lysosomal compartments, and cause a neurodevelopmental and X-linked intellectual disability degenerative form of X-linked intellectual disability called Christianson Syndrome (CS). However, knowledge of Alkali cation/proton exchangers –SLC9A6/ the disease heterogeneity of CS is limited. Here, we describe the clinical features and underlying molecular and NHE6 cellular mechanisms associated with a CS patient carrying a de novo missense variant (p.Gly218Arg; G218R) of a Endosomal pH homeostasis conserved residue in its ion translocation domain that results in a potential gain-of-function. The patient Membrane trafficking Neurodegeneration manifested several core symptoms typical of CS, including pronounced cognitive impairment, mutism, epilepsy, ataxia and microcephaly; however, deterioration of motor function often observed after the first decade of life in CS children with total loss of SLC9A6/NHE6 function was not evident.