Two Faces of Evil: Cancer and Neurodegeneration (Registro nro. 203235)

MARC details
000 -LÍDER
fixed length control field 03991nam a22004455i 4500
001 - NÚMERO DE CONTROL
control field u375355
003 - IDENTIFICADOR DEL NÚMERO DE CONTROL
control field SIRSI
005 - FECHA Y HORA DE LA ULTIMA TRANSACCIÓN
control field 20160812084319.0
007 - CAMPO FIJO DE DESCRIPCIÓN FIJA--INFORMACIÓN GENERAL
fixed length control field cr nn 008mamaa
008 - ELEMENTOS DE LONGITUD FIJA -- INFORMACIÓN GENERAL
fixed length control field 101216s2011 gw | s |||| 0|eng d
020 ## - NÚMERO INTERNACIONAL NORMALIZADO PARA LIBROS
International Standard Book Number 9783642166020
-- 978-3-642-16602-0
040 ## - FUENTE DE CATALOGACIÓN
Transcribing agency MX-MeUAM
050 #4 - SIGNATURA TOPOGRÁFICA DE LA BIBLIOTECA DEL CONGRESO
Classification number RC321-580
082 04 - NÚMERO DE CLASIFICACIÓN DECIMAL DEWEY
Classification number 612.8
Edition number 23
100 1# - ASIENTO PRINCIPAL--NOMBRE PERSONAL
Personal name Curran, Thomas.
Relator term editor.
245 10 - MENCIÓN DE TITULO
Title Two Faces of Evil: Cancer and Neurodegeneration
Medium [recurso electrónico] /
Statement of responsibility, etc. edited by Thomas Curran, Yves Christen.
264 #1 - PRODUCTION, PUBLICATION, DISTRIBUTION, MANUFACTURE, AND COPYRIGHT NOTICE
Place of production, publication, distribution, manufacture Berlin, Heidelberg :
Name of producer, publisher, distributor, manufacturer Springer Berlin Heidelberg :
-- Imprint: Springer,
Date of production, publication, distribution, manufacture, or copyright notice 2011.
300 ## - DESCRIPCIÓN FÍSICA
Extent XIV, 166 p.
Other physical details online resource.
336 ## - CONTENT TYPE
Content type term text
Content type code txt
Source rdacontent
337 ## - MEDIA TYPE
Media type term computer
Media type code c
Source rdamedia
338 ## - CARRIER TYPE
Carrier type term online resource
Carrier type code cr
Source rdacarrier
347 ## - DIGITAL FILE CHARACTERISTICS
File type text file
Encoding format PDF
Source rda
490 1# - MENCIÓN DE SERIE
Series statement Research and Perspectives in Alzheimer's Disease,
International Standard Serial Number 0945-6066
520 ## - NOTA DE RESUMEN, ETC.
Summary, etc. The two greatest medical fears of the aging population are cancer and Alzheimer’s disease. Despite dramatic advances in understanding the molecular etiology of these disorders, therapeutic options for many patients with advanced disease have changed little and outcomes remain dismal. Paradoxically, recent findings suggest that some of the same molecules and biochemical processes underlying cancer may also participate in neurodegeneration. Therefore, it would be very useful to bring together experts from the fields of cancer research and neurodegeneration for discussions of the latest advances and ideas, with a particular emphasis on areas of overlap, to stimulate transdisciplinary interactions with the hope of accelerating progress. Cancer arises as a consequence of a breakdown in the genetic and epigenetic processes governing cell proliferation and cell death. Alterations in several classes of signaling molecules, both oncogenes and tumor suppressor genes, lead to uncontrolled cell growth. Over the past two decades, details of the intricate signaling pathways, from cell surface receptors through protein kinase cascades, transcription factors and modulators of chromatin, as well as the DNA damage response pathways linked to cell cycle control that guard the genome, have been uncovered. In some instances, key regulatory proteins have provided novel targets for development of small molecule inhibitors that are currently being tested in the clinic. The development of the nervous system relies on many of the signaling pathways and growth control processes that go awry in cancer. However, in mature neurons, the very same signaling proteins participate in transduction cascades linking short-term stimuli, elicited by synaptic stimulation, to long-term alterations in neuronal circuits through the regulation of gene expression and chromatin structure. These long-term adaptive modifications lead to changes in synaptic structure and function that contribute to learning and memory. The persistence of growth regulatory molecules in postmitotic neurons provides an opportunity for their contribution to pathophysiological processes resulting in neuronal loss. Recently, evidence has accumulated suggesting an association of cell cycle proteins and signal transduction proteins with neurodegeneration. Indeed, inhibitors of histone deacetylation have shown promise both as anti-cancer agents and in the prevention of neuronal loss
596 ## -
-- 19
650 #0 - ASIENTO SECUNDARIO DE MATERIA - TERMINO TEMÁTICO
Topical term or geographic name as entry element Medicine.
650 #0 - ASIENTO SECUNDARIO DE MATERIA - TERMINO TEMÁTICO
Topical term or geographic name as entry element Oncology.
650 #0 - ASIENTO SECUNDARIO DE MATERIA - TERMINO TEMÁTICO
Topical term or geographic name as entry element Neurosciences.
650 14 - ASIENTO SECUNDARIO DE MATERIA - TERMINO TEMÁTICO
Topical term or geographic name as entry element Biomedicine.
650 24 - ASIENTO SECUNDARIO DE MATERIA - TERMINO TEMÁTICO
Topical term or geographic name as entry element Neurosciences.
650 24 - ASIENTO SECUNDARIO DE MATERIA - TERMINO TEMÁTICO
Topical term or geographic name as entry element Cancer Research.
700 1# - ASIENTO SECUNDARIO - NOMBRE PERSONAL
Personal name Christen, Yves.
Relator term editor.
710 2# - ASIENTO SECUNDARIO - NOMBRE CORPORATIVO
Corporate name or jurisdiction name as entry element SpringerLink (Online service)
773 0# - HOST ITEM ENTRY
Title Springer eBooks
776 08 - ADDITIONAL PHYSICAL FORM ENTRY
Relationship information Printed edition:
International Standard Book Number 9783642166013
830 #0 - ASIENTO SECUNDARIO DE SERIE--TITULO UNIFORME
Uniform title Research and Perspectives in Alzheimer's Disease,
International Standard Serial Number 0945-6066
856 40 - LOCALIZACIÓN Y ACCESO ELECTRÓNICOS
Public note Libro electrónico
Uniform Resource Identifier <a href="http://148.231.10.114:2048/login?url=http://link.springer.com/book/10.1007/978-3-642-16602-0">http://148.231.10.114:2048/login?url=http://link.springer.com/book/10.1007/978-3-642-16602-0</a>
942 ## - TIPO DE MATERIAL (KOHA)
Koha item type Libro Electrónico
Existencias
Estado de retiro Fuente de clasificación Colección Ubicación permanente Ubicación actual Fecha de ingreso Total Checkouts Signatura topográfica Código de barras Date last seen Número de copia Tipo de material
    Colección de Libros Electrónicos Biblioteca Electrónica Biblioteca Electrónica     RC321 -580 375355-2001 12/08/2016 1 Libro Electrónico

Con tecnología Koha