Neuron-glia interaction in neuroinflammation / (Titelsatznr. 58484)

[ MARC ]
000 -LEADER
fixed length control field 04426cam a2200553 i 4500
001 - CONTROL NUMBER
control field 17856518
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20170913120551.0
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 130819s2013 nyua g b 001 0 eng c
010 ## - LIBRARY OF CONGRESS CONTROL NUMBER
LC control number 2013948228
016 7# - NATIONAL BIBLIOGRAPHIC AGENCY CONTROL NUMBER
Record control number 101624940
Source DNLM
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9781461483120 (alk. paper)
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 1461483123 (alk. paper)
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
Canceled/invalid ISBN 9781461483137 (eBook)
035 ## - SYSTEM CONTROL NUMBER
System control number (OCoLC)ocn847348501
041 ## - LANGUAGE CODE
Language code of text/sound track or separate title eng
042 ## - AUTHENTICATION CODE
Authentication code pcc
050 00 - LIBRARY OF CONGRESS CALL NUMBER
Classification number QP363.2
Item number .N53 2013
060 00 - NATIONAL LIBRARY OF MEDICINE CALL NUMBER
Classification number 2014 B-075
060 10 - NATIONAL LIBRARY OF MEDICINE CALL NUMBER
Classification number WL 102
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number 612.81045
Edition number 23
Item number S N
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Suzumura, Akio
9 (RLIN) 1454
245 10 - TITLE STATEMENT
Title Neuron-glia interaction in neuroinflammation /
Statement of responsibility, etc. Akio Suzumura, Kazuhiro Ikenaka, editors.
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT)
Place of publication, distribution, etc. new york :
Name of publisher, distributor, etc. springer sience + business media ;
Date of publication, distribution, etc. 2013 .
265 ## - SOURCE FOR ACQUISITION/SUBSCRIPTION ADDRESS [OBSOLETE]
Source for acquisition/subscription address [OBSOLETE] اقرأ للنشر و التوزيع
300 ## - PHYSICAL DESCRIPTION
Extent x, 187 pages :
Other physical details illustrations (some color) ;
Dimensions 24 cm.
490 1# - SERIES STATEMENT
Series statement Advances in neurobiology,
International Standard Serial Number 2190-5215 ;
Volume/sequential designation volume 7
504 ## - BIBLIOGRAPHY, ETC. NOTE
Bibliography, etc Includes bibliographical references and index.
505 00 - FORMATTED CONTENTS NOTE
Title Acute, Chronic, and Nonclassical Neuroinflammation: Definitions in a Changing Scientific Environment /
Statement of responsibility Robert P. Lisak, Joyce A. Benjamin --
Title Neuroinflammation in Neurological Disorders /
Statement of responsibility Jun-ichi Kira --
Title Factors from Intact and Damaged Neurons /
Statement of responsibility Tetsuya Mizuno --
Title Interactions Between Neurons and Microglia During Neuroinflammation /
Statement of responsibility Akio Suzumura --
Title Neuron-Astrocyte Interactions in Neuroinflammation /
Statement of responsibility Jasna Kriz --
Title Neuron-Oligodendrocyte Interactions in Neuroinflammation /
Statement of responsibility Kazuhiro Ikenaka --
Title Neuron-Glia Interaction via Neurotrophins /
Statement of responsibility Cinthia Farina --
Title Glial Communication via Gap Junction in Neuroinflammation /
Statement of responsibility Hideyuki Takeuchi --
Title Toll-Like Receptors and Neuroinflammation /
Statement of responsibility Sung Joong Lee --
Title The Blood-Brain Barrier in Neuroinflammation /
Statement of responsibility Fumitaka Shimizu.
520 ## - SUMMARY, ETC.
Summary, etc. Accumulation of glia, gliosis, in various neurological disorders is not a static scar, but actively involved in pathogenesis of various neurological and psychiatric disorders, where glial cells produce both inflammatory and neurotrophic factors. These factors may play a role in neuronal damage, but also have a protective and reparative function by inducing neuroinflammation. However, definition as well as the mechanisms of neuroinflammation is not yet clear. We first define acute, chronic and non-classical neuroinflammation. Glial cells are activated by a variety of stimuli via receptors on glial cells. Toll like receptors (TLR) are one of these receptors. In response to harmful stimuli, neurons produce factors as either eat-me or help-me signals. These factors include cytokines, chemokines and damage-associated molecular pattern (DAMP). Some of them activate glial cells via TLR, and function to protect neurons or further induce neuroinflammation. Thus, the interaction between neuron-glia and glia-glia is a main feature of neuroinflammation. Glial cells communicate with other glial or neural cells via gap-junctions. The communication may also be important for the understanding of neuroinflammation. Oligodendrocytes-neurons communication may be critical in either myelination or demyelination. Damage of blood-brain barrier (BBB) is common feature of both inflammatory and degenerative neurological disorders. Thus, relation of BBB damage and functions of glial cell may also be important in the development of neuroinflammation. In this book, we focused on neuron-glia interaction of various aspects for understanding of pathophysiology of neuroinflammation in development of inflammatory as well as degenerative neurological disorders.
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neuroglia.
9 (RLIN) 1456
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neural transmission.
9 (RLIN) 1457
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Nervous system
General subdivision Degeneration.
9 (RLIN) 1458
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Inflammation.
9 (RLIN) 1459
650 12 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neuroglia
General subdivision physiology.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Inflammation
General subdivision physiopathology.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Nervous System Physiological Phenomena.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neurodegenerative Diseases.
650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neuroimmunomodulation.
650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Inflammation.
Source of heading or term fast
650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Nervous system
General subdivision Degeneration.
Source of heading or term fast
650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neural transmission.
Source of heading or term fast
650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name as entry element Neuroglia.
Source of heading or term fast
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Suzumura, Akio,
Relator term editor.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Ikenaka, Kazuhiro,
Relator term editor.
830 #0 - SERIES ADDED ENTRY--UNIFORM TITLE
Uniform title Advances in neurobiology ;
Volume number/sequential designation v. 7.
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Source of classification or shelving scheme
Koha item type Books
Item part Faculty of Engineering كلية الهندسة
Exemplare
Withdrawn status Lost status Source of classification or shelving scheme Damaged status Not for loan Collection code Permanent location Current location Shelving location Date acquired Cost, normal purchase price Full call number Barcode Date last seen Copy number Price effective from Koha item type
          معرض الكتاب 2017 6october 6october 1104 2017-08-16 1540.00 612.81045 S N SOULE104006012 2021-08-31 1 2017-08-16 Books
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