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Text
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URL Address
<a href="http://doi.org/10.1016/j.tins.2005.10.001" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.tins.2005.10.001</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Glia: novel counter-regulators of opioid analgesia
Publisher
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Trends In Neurosciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
Subject
The topic of the resource
Humans; Analgesics; Animals; Opioid/administration & dosage; Drug Tolerance; Brain/drug effects/metabolism; Neuroglia/drug effects/metabolism; Neurotransmitter Agents/metabolism; Nociceptors/drug effects/metabolism; Pain/metabolism/prevention & control; Spinal Cord/drug effects/metabolism
Creator
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Watkins LR; Hutchinson MR; Johnston IN; Maier SF
Description
An account of the resource
Development of analgesic tolerance and withdrawal-induced pain enhancement present serious difficulties for the use of opioids for pain control. Although neuronal mechanisms to account for these phenomena have been sought for many decades, their bases remain unresolved. Within the past four years, a novel non-neuronal candidate has been uncovered that opposes acute opioid analgesia and contributes to development of opioid tolerance and tolerance-associated pain enhancement. This novel candidate is spinal cord glia. Glia are important contributors to the creation of enhanced pain states via the release of neuroexcitatory substances. New data suggest that glia also release neuroexcitatory substances in response to morphine, thereby opposing its effects. Controlling glial activation could therefore increase the clinical utility of analgesic drugs.
2005
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.tins.2005.10.001" target="_blank" rel="noreferrer">10.1016/j.tins.2005.10.001</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2005
Analgesics
Animals
Backlog
Brain/drug effects/metabolism
Drug Tolerance
Humans
Hutchinson MR
Johnston IN
Journal Article
Maier SF
Neuroglia/drug effects/metabolism
Neurotransmitter Agents/metabolism
Nociceptors/drug effects/metabolism
Opioid/administration & dosage
Pain/metabolism/prevention & control
Spinal Cord/drug effects/metabolism
Trends In Neurosciences
Watkins LR
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0167-5273(02)00239-5" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0167-5273(02)00239-5</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Neurohormonal factors in the development of catabolic/anabolic imbalance and cachexia
Publisher
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International Journal Of Cardiology
Date
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2002
Subject
The topic of the resource
Humans; Animals; Heart Failure; Cachexia/etiology/metabolism; Neurotransmitter Agents/metabolism; Biological Markers/blood; Congestive/complications/metabolism; Cytokines/metabolism; Glucocorticoids/metabolism; Insulin-Like Growth Factor I/metabolism; Renin-Angiotensin System/physiology
Creator
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Brink M; Anwar A; Delafontaine P
Description
An account of the resource
Mechanisms that lead to cachexia are still poorly understood. The neurohormonal changes that occur in severe disease states may cause an imbalance between protein synthesis and degradation at the cellular level, followed by muscle wasting. Here, we review actions of angiotensin II, TNF-alpha, corticosteroids, insulin-like growth factor-I (IGF-I), and the IGF binding proteins, factors that may each contribute to the metabolic imbalance. The complex endocrine, autocrine and intracellular interactions between these factors will be described with examples from patient, rat and cell culture studies. Moreover, some of the data supporting that each of these hormones may directly affect cellular protein degradation mechanisms will be reviewed. Knowledge on these regulatory mechanisms will facilitate the development of new pharmaceutical strategies to treat cachexia.
2002
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0167-5273(02)00239-5" target="_blank" rel="noreferrer">10.1016/s0167-5273(02)00239-5</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2002
Animals
Anwar A
Backlog
Biological Markers/blood
Brink M
Cachexia/etiology/metabolism
Congestive/complications/metabolism
Cytokines/metabolism
Delafontaine P
Glucocorticoids/metabolism
Heart Failure
Humans
Insulin-Like Growth Factor I/metabolism
International Journal Of Cardiology
Journal Article
Neurotransmitter Agents/metabolism
Renin-Angiotensin System/physiology