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40
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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.
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URL Address
<a href="http://doi.org/10.1016/j.jneumeth.2008.10.013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jneumeth.2008.10.013</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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Beta-Endorphin Response to an Acute Pain Stimulus
Publisher
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Journal Of Neuroscience Methods
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
Subject
The topic of the resource
Male; Pain Measurement; Time Factors; Reproducibility of Results; Animals; Mice; Acute Disease; Biomarkers of Pain; Physical Stimulation; Animal; beta-Endorphin/analysis/metabolism/secretion; Biological Markers/analysis/blood; Disease Models; Inbred DBA; Neurochemistry/methods; Pain/blood/physiopathology; Radioimmunoassay/methods; Up-Regulation/physiology
Creator
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Rasmussen NA; Farr LA
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jneumeth.2008.10.013" target="_blank" rel="noreferrer noopener">10.1016/j.jneumeth.2008.10.013</a>
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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
Description
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The timing of the measurement of biological samples (e.g. biomarkers) is not always standardized. Biomarkers are the focus of many recent studies and treatments. The purpose of this study was to determine the timing of the release of beta-endorphin (BE), a possible biomarker, after exposure to pain and/or handling stress in order to standardize measurements. Mouse plasma was collected for BE analysis following handling i.e. being picked up by the investigator, exposure to a painful (55 degrees C hot-plate), or exposure to a nonpainful stimulus (room temperature hot-plate). The groups exposed to either a painful or nonpainful stimulus released BE in response to the stimulus, but the duration of the response was longer in mice exposed to a painful stimulus than in mice exposed to a nonpainful stimulus. The BE in the mice exposed to a nonpainful stimulus peaked at 1 min and returned to baseline levels by 5 min while the BE response of the mice exposed to a painful stimulus peaked at 10 min and remained elevated for 25 min. The results of this study indicate that BE can be a biomarker for pain and handling stress, however, the timing of the measurement should differ.
2009
Acute Disease
Animal
Animals
Backlog
beta-Endorphin/analysis/metabolism/secretion
Biological Markers/analysis/blood
Biomarkers of Pain
Disease Models
Farr LA
Inbred DBA
Journal Article
Journal Of Neuroscience Methods
Male
Mice
Neurochemistry/methods
Pain Measurement
Pain/blood/physiopathology
Physical Stimulation
Radioimmunoassay/methods
Rasmussen NA
Reproducibility of Results
Time Factors
Up-Regulation/physiology
-
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.
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Backlog
URL Address
<a href="http://doi.org/10.1111/j.1749-6632.2003.tb03141.x" target="_blank" rel="noreferrer">http://doi.org/10.1111/j.1749-6632.2003.tb03141.x</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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Hypothalamo-pituitary-adrenal axis and chronic immune activation
Publisher
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Annals Of The New York Academy Of Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Humans; Animals; Inflammation/immunology/physiopathology; Animal; Disease Models; Stress/immunology; Autoimmune Diseases/immunology/physiopathology; Corticosterone/secretion; Hypothalamo-Hypophyseal System/physiopathology; Immune System Diseases/physiopathology; Pituitary-Adrenal System/physiopathology
Creator
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Harbuz MS; Chover-Gonzalez AJ; Jessop DS
Description
An account of the resource
Corticosteroids have potent immunosuppressive and anti-inflammatory effects. Although corticosteroids are an important weapon in the clinical arsenal for treating inflammatory episodes, the mechanisms underlying the actions and regulation of endogenous corticosteroids remain obscure. In the late 1980s and early 1990s, a hypothesis was proposed that suggested that susceptibility to autoimmune disease was linked to a hypoactive hypothalamo-pituitary-adrenal (HPA) axis. It was further suggested that this defect in regulation of the HPA axis was situated at the level of the hypothalamus. This compelling hypothesis directly linked control of the HPA axis with susceptibility to disease rather than just severity of inflammation. The initial findings acted as a stimulus to further research, and over the next decade the hypothesis was tested. Recent studies suggest that the original hypothesis is in need of modification and that susceptibility is more complex and requires the involvement of more than a single parameter. These data are discussed together with recent developments concerning regulation of the HPA in disease in preclinical models and patients with rheumatoid arthritis. The latter studies in patients with rheumatoid arthritis provide evidence for the existence of a subpopulation of these patients with altered negative feedback regulation of the HPA axis.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1749-6632.2003.tb03141.x" target="_blank" rel="noreferrer">10.1111/j.1749-6632.2003.tb03141.x</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
2003
Animal
Animals
Annals Of The New York Academy Of Sciences
Autoimmune Diseases/immunology/physiopathology
Backlog
Chover-Gonzalez AJ
Corticosterone/secretion
Disease Models
Harbuz MS
Humans
Hypothalamo-Hypophyseal System/physiopathology
Immune System Diseases/physiopathology
Inflammation/immunology/physiopathology
Jessop DS
Journal Article
Pituitary-Adrenal System/physiopathology
Stress/immunology
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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
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URL Address
<a href="http://doi.org/10.1038/sj.npp.1301393" target="_blank" rel="noreferrer">http://doi.org/10.1038/sj.npp.1301393</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
Inhibition of inflammatory pain by CRF at peripheral, spinal and supraspinal sites: involvement of areas coexpressing CRF receptors and opioid peptides
Publisher
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Neuropsychopharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
Subject
The topic of the resource
Male; Pain Measurement; Animals; Rats; Biomarkers of Pain; Dose-Response Relationship; Drug; Receptors; Freund's Adjuvant; Wistar; Animal; Disease Models; Analgesics/administration & dosage; Drug Administration Routes; Pain Threshold/drug effects; Brain/drug effects/metabolism; Spinal Cord/drug effects/metabolism; Corticotropin-Releasing Hormone/administration & dosage; Opioid Peptides/metabolism; Corticotropin-Releasing Hormone/metabolism; Ganglia; Hormone Antagonists/administration & dosage; Inflammation/chemically induced/complications; Pain/drug therapy/etiology/pathology; Sciatic Nerve/pathology; Spinal/drug effects/metabolism
Creator
An entity primarily responsible for making the resource
Mousa SA; Bopaiah CP; Richter JF; Yamdeu RS; Schafer M
Description
An account of the resource
There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist alpha-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissue--but not peripheral sensory neurons--that coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dose-dependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.
2007
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/sj.npp.1301393" target="_blank" rel="noreferrer">10.1038/sj.npp.1301393</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
2007
Analgesics/administration & dosage
Animal
Animals
Backlog
Biomarkers of Pain
Bopaiah CP
Brain/drug effects/metabolism
Corticotropin-Releasing Hormone/administration & dosage
Corticotropin-Releasing Hormone/metabolism
Disease Models
Dose-Response Relationship
Drug
Drug Administration Routes
Freund's Adjuvant
Ganglia
Hormone Antagonists/administration & dosage
Inflammation/chemically induced/complications
Journal Article
Male
Mousa SA
Neuropsychopharmacology
Opioid Peptides/metabolism
Pain Measurement
Pain Threshold/drug effects
Pain/drug therapy/etiology/pathology
Rats
Receptors
Richter JF
Schafer M
Sciatic Nerve/pathology
Spinal Cord/drug effects/metabolism
Spinal/drug effects/metabolism
Wistar
Yamdeu RS