Neuroprotection: Rescue from Neuronal Death in the Brain (Record no. 2984926)

MARC details
000 -LEADER
fixed length control field 06144naaaa2201477uu 4500
001 - CONTROL NUMBER
control field https://directory.doabooks.org/handle/20.500.12854/76898
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20220714164334.0
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number books978-3-0365-1995-1
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9783036519944
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9783036519951
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.3390/books978-3-0365-1995-1
Terms of availability doi
041 0# - LANGUAGE CODE
Language code of text/sound track or separate title English
042 ## - AUTHENTICATION CODE
Authentication code dc
072 #7 - SUBJECT CATEGORY CODE
Subject category code GP
Source bicssc
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Lee, Bae Hwan
Relator code edt
9 (RLIN) 1579728
245 10 - TITLE STATEMENT
Title Neuroprotection: Rescue from Neuronal Death in the Brain
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT)
Place of publication, distribution, etc Basel, Switzerland
Name of publisher, distributor, etc MDPI - Multidisciplinary Digital Publishing Institute
Date of publication, distribution, etc 2021
300 ## - PHYSICAL DESCRIPTION
Extent 1 electronic resource (408 p.)
506 0# - RESTRICTIONS ON ACCESS NOTE
Terms governing access Open Access
Source of term star
Standardized terminology for access restriction Unrestricted online access
520 ## - SUMMARY, ETC.
Summary, etc Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE
Terms governing use and reproduction Creative Commons
-- https://creativecommons.org/licenses/by/4.0/
-- cc
-- https://creativecommons.org/licenses/by/4.0/
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Language note English
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Topical term or geographic name as entry element Research & information: general
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9 (RLIN) 928234
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700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Lee, Bae Hwan
Relator code oth
9 (RLIN) 1579728
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://mdpi.com/books/pdfview/book/4368">https://mdpi.com/books/pdfview/book/4368</a>
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Public note DOAB: download the publication
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://directory.doabooks.org/handle/20.500.12854/76898">https://directory.doabooks.org/handle/20.500.12854/76898</a>
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