Neuron-Glia Interaction in Neuroinflammation (Record no. 96046)
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fixed length control field | 03898nam a22004695i 4500 |
001 - CONTROL NUMBER | |
control field | 978-1-4614-8313-7 |
003 - CONTROL NUMBER IDENTIFIER | |
control field | DE-He213 |
005 - DATE AND TIME OF LATEST TRANSACTION | |
control field | 20140220082831.0 |
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION | |
fixed length control field | cr nn 008mamaa |
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION | |
fixed length control field | 130913s2013 xxu| s |||| 0|eng d |
020 ## - INTERNATIONAL STANDARD BOOK NUMBER | |
International Standard Book Number | 9781461483137 |
-- | 978-1-4614-8313-7 |
024 7# - OTHER STANDARD IDENTIFIER | |
Standard number or code | 10.1007/978-1-4614-8313-7 |
Source of number or code | doi |
050 #4 - LIBRARY OF CONGRESS CALL NUMBER | |
Classification number | RC321-580 |
072 #7 - SUBJECT CATEGORY CODE | |
Subject category code | PSAN |
Source | bicssc |
072 #7 - SUBJECT CATEGORY CODE | |
Subject category code | MED057000 |
Source | bisacsh |
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER | |
Classification number | 612.8 |
Edition number | 23 |
100 1# - MAIN ENTRY--PERSONAL NAME | |
Personal name | Suzumura, Akio. |
Relator term | editor. |
245 10 - TITLE STATEMENT | |
Title | Neuron-Glia Interaction in Neuroinflammation |
Medium | [electronic resource] / |
Statement of responsibility, etc | edited by Akio Suzumura, Kazuhiro Ikenaka. |
264 #1 - | |
-- | New York, NY : |
-- | Springer New York : |
-- | Imprint: Springer, |
-- | 2013. |
300 ## - PHYSICAL DESCRIPTION | |
Extent | X, 187 p. 25 illus., 24 illus. in color. |
Other physical details | online resource. |
336 ## - | |
-- | text |
-- | txt |
-- | rdacontent |
337 ## - | |
-- | computer |
-- | c |
-- | rdamedia |
338 ## - | |
-- | online resource |
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-- | rdacarrier |
347 ## - | |
-- | text file |
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-- | rda |
490 1# - SERIES STATEMENT | |
Series statement | Advances in Neurobiology, |
International Standard Serial Number | 2190-5215 ; |
Volume number/sequential designation | 7 |
505 0# - FORMATTED CONTENTS NOTE | |
Formatted contents note | Acute, Chronic, and Non-classical Neuroinflammation: Definitions in a Changing Scientific Environment -- Neuroinflammation in Neurological Disorders -- Factors from Intact and Damaged Neurons -- Interactions between Neurons and Microglia During Neuroinflammation -- Neuron-Astrocyte Interactions in Neuroinflammation -- Neuron-oligodendrocyte Interactions in Neuroinflammation -- Neuron-glia Interaction via Neurotrophins -- Glial Communication via Gap Junction in Neuroinflammation -- Toll-Like Receptors and Neuroinflammation -- The Blood-Brain-Barrier in Neuroinflammation. |
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 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
Topical term or geographic name as entry element | Medicine. |
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
Topical term or geographic name as entry element | Neurosciences. |
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
Topical term or geographic name as entry element | Neurology. |
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
Topical term or geographic name as entry element | Biomedicine. |
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
Topical term or geographic name as entry element | Neurosciences. |
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
Topical term or geographic name as entry element | Neurology. |
700 1# - ADDED ENTRY--PERSONAL NAME | |
Personal name | Ikenaka, Kazuhiro. |
Relator term | editor. |
710 2# - ADDED ENTRY--CORPORATE NAME | |
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 | |
Display text | Printed edition: |
International Standard Book Number | 9781461483120 |
830 #0 - SERIES ADDED ENTRY--UNIFORM TITLE | |
Uniform title | Advances in Neurobiology, |
-- | 2190-5215 ; |
Volume number/sequential designation | 7 |
856 40 - ELECTRONIC LOCATION AND ACCESS | |
Uniform Resource Identifier | http://dx.doi.org/10.1007/978-1-4614-8313-7 |
912 ## - | |
-- | ZDB-2-SBL |
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