1
40
6
-
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/10.1152/jappl.2000.89.4.1561" target="_blank" rel="noreferrer">http://doi.org/10.1152/jappl.2000.89.4.1561</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
Systemic hypoxia increases leukocyte emigration and vascular permeability in conscious rats.
Publisher
An entity responsible for making the resource available
Journal Of Applied Physiology (bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
Subject
The topic of the resource
Male; Animals; Rats; Sprague-Dawley; Endothelium; Vascular/ph [Physiology]; Anoxia/pp [Physiopathology]; Capillary Permeability/ph [Physiology]; Endothelium; Leukocytes/ph [Physiology]; Venules/ph [Physiology]; Antioxidants/pd [Pharmacology]; Capillary Permeability/de [Drug Effects]; Catalase/pd [Pharmacology]; Cell Adhesion; Consciousness; Leukocytes/de [Drug Effects]; Nitric Oxide Donors/pd [Pharmacology]; Nitrogen Oxides; Reactive Oxygen Species/ph [Physiology]; Spermine/aa [Analogs & Derivatives]; Spermine/pd [Pharmacology]; Splanchnic Circulation/ph [Physiology]; Superoxide Dismutase/pd [Pharmacology]; Vascular/pp [Physiopathology]; Venules/pp [Physiopathology]
Creator
An entity primarily responsible for making the resource
Wood JG; Johnson JS; Mattioli LF; Gonzalez NC
Description
An account of the resource
We recently observed that acute systemic hypoxia produces rapid increases in leukocyte adherence in the mesenteric microcirculation of the anesthetized rat Wood JG, Johnson JS, Mattioli LF, and Gonzalez NC. J Appl Physiol 87: 1734-1740, 1999; Wood JG, Mattioli LF, and Gonzalez NC. J Appl Physiol 87: 873-881, 1999. Hypoxia-induced leukocyte adherence is associated with an increase in reactive oxygen species (ROS) generation and is attenuated by antioxidants or interventions that increase tissue levels of nitric oxide (NO). These results suggest that the acute effects of hypoxia on leukocyte-endothelial interactions are caused by a change in the ROS-NO balance. The present experiments were designed to extend our observations of the initial microcirculatory response to hypoxia; specifically, we wanted to determine whether the response to systemic hypoxia involves increased microvascular permeability and leukocyte emigration and whether ROS generation and decreased NO levels contribute to these responses. At this time, there is conflicting evidence, from in vitro studies, regarding the effect of hypoxia on these indexes of vascular function. Our studies were carried out in the physiological setting of the conscious animal, in which a prolonged hypoxic exposure is possible without the adverse effects that may develop under anesthesia. The central observation of these studies is that conscious animals exposed for 4 h to environmental hypoxia show increased microvascular permeability and emigration of leukocytes into the extravascular space of the mesenteric circulation. Furthermore, these events are dependent on increased ROS generation and, possibly, a subsequent decrease in tissue NO levels during systemic hypoxia. Our results show that systemic hypoxia profoundly affects vascular endothelial function through changes in the ROS-NO balance in the conscious animal.
2000
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.2000.89.4.1561" target="_blank" rel="noreferrer">10.1152/jappl.2000.89.4.1561</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
2000
Animals
Anoxia/pp [Physiopathology]
Antioxidants/pd [Pharmacology]
Backlog
Capillary Permeability/de [Drug Effects]
Capillary Permeability/ph [Physiology]
Catalase/pd [Pharmacology]
Cell Adhesion
Consciousness
Endothelium
Gonzalez NC
Johnson JS
Journal Article
Journal Of Applied Physiology (bethesda, Md. : 1985)
Leukocytes/de [Drug Effects]
Leukocytes/ph [Physiology]
Male
Mattioli LF
Nitric Oxide Donors/pd [Pharmacology]
Nitrogen Oxides
Rats
Reactive Oxygen Species/ph [Physiology]
Spermine/aa [Analogs & Derivatives]
Spermine/pd [Pharmacology]
Splanchnic Circulation/ph [Physiology]
Sprague-Dawley
Superoxide Dismutase/pd [Pharmacology]
Vascular/ph [Physiology]
Vascular/pp [Physiopathology]
Venules/ph [Physiology]
Venules/pp [Physiopathology]
Wood JG
-
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/10.1016/0928-4257(93)90034-q" target="_blank" rel="noreferrer">http://doi.org/10.1016/0928-4257(93)90034-q</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
Brain and gut neuropeptides in peripheral blood mononuclear cells
Publisher
An entity responsible for making the resource available
Journal Of Physiology, Paris
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
Subject
The topic of the resource
Humans; Male; Adult; Aged; Middle Aged; Brain; Animals; Rats; 80 and over; Sprague-Dawley; Aging/metabolism; beta-Endorphin/blood/pharmacology; Chemotaxis/drug effects; Cholecystokinin/blood/pharmacology; Digestive System; Headache/blood; Lymphocytes/metabolism; Neuropeptides/blood; Schizophrenia/blood; Vasoactive Intestinal Peptide/blood/pharmacology
Creator
An entity primarily responsible for making the resource
Panerai AE; Sacerdote P
Description
An account of the resource
Neuropeptides, initially thought to be common features of gut and brain, are only synthesized in immune cells and modulate immune functions. The presence and possible functions of these peptides in immune cells in both physiological or pathological conditions have been investigated in our laboratory in the last years. Some of the data obtained are reviewed here, and future developments of the field are indicated.
1993
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0928-4257(93)90034-q" target="_blank" rel="noreferrer">10.1016/0928-4257(93)90034-q</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
1993
80 And Over
Adult
Aged
Aging/metabolism
Animals
Backlog
beta-Endorphin/blood/pharmacology
Brain
Chemotaxis/drug effects
Cholecystokinin/blood/pharmacology
Digestive System
Headache/blood
Humans
Journal Article
Journal Of Physiology, Paris
Lymphocytes/metabolism
Male
Middle Aged
Neuropeptides/blood
Panerai AE
Rats
Sacerdote P
Schizophrenia/blood
Sprague-Dawley
Vasoactive Intestinal Peptide/blood/pharmacology
-
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/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">http://doi.org/10.1006/brbi.1994.1023</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
Intermittent but not continuous inescapable footshock stress affects immune responses and immunocyte beta-endorphin concentrations in the rat
Publisher
An entity responsible for making the resource available
Brain, Behavior, And Immunity
Date
A point or period of time associated with an event in the lifecycle of the resource
1994
Subject
The topic of the resource
Male; Time Factors; Animals; Acute Disease; Rats; Comparative Study; Receptors; beta-Endorphin/analysis; Corticosterone/blood; Corticotropin-Releasing Hormone/antagonists & inhibitors; Corticotropin-Releasing Hormone/blood/pharmacology/physiology; Electroshock/adverse effects; Foot; Helplessness; Killer Cells; Learned; Lymphocyte Activation; Lymphoid Tissue/chemistry; Natural/immunology; Neuroimmunomodulation/physiology; Peptide Fragments/pharmacology; Spleen/immunology; Sprague-Dawley; Stress/etiology/immunology
Creator
An entity primarily responsible for making the resource
Sacerdote P; Manfredi B; Bianchi M; Panerai AE
Description
An account of the resource
It is well known that a variety of stressors influence immune responses. The opioid peptide-beta-endorphin (BE) is deeply involved in stress responses, is synthesized in cells of the immune system, and participates in the modulation of immune function. We analyzed the ability of two different stress paradigms to modulate the beta-endorphin concentrations in the immune cells and the immune response in the rat. Two and 24 h after the exposure to inescapable intermittent footshock (1.6 mA, 60 Hz, 1 s, every 5 s for 20 min) the concentrations of beta-endorphin in splenocytes, peripheral blood mononuclear cells and lymph node cells were significantly increased. In contrast, the exposure to a continuous footshock for 3 min did not affect the concentrations of the opioid peptide. Similarly, phytohemoagglutinin-induced proliferation of splenocytes and natural killer activity were significantly impaired only after the exposure to intermittent footshock stress. On the contrary, plasma corticosterone levels were similarly elevated after both paradigms of stress. The pretreatment with the corticotropin-releasing hormone (CRH) receptor antagonist prevented both the stress-induced increase of immunocyte BE and immunosuppression. In conclusion, our data suggest that intermittent and continuous footshock stressors activate different neuroendocrine responses and that CRH plays a central role in mediating the immune effects of the intermittent footshock stress. The possible relationship between the beta-endorphin changes and immunosuppression is discussed.
1994
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">10.1006/brbi.1994.1023</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
1994
Acute Disease
Animals
Backlog
beta-Endorphin/analysis
Bianchi M
Brain, Behavior, And Immunity
Comparative Study
Corticosterone/blood
Corticotropin-Releasing Hormone/antagonists & inhibitors
Corticotropin-Releasing Hormone/blood/pharmacology/physiology
Electroshock/adverse effects
Foot
Helplessness
Journal Article
Killer Cells
Learned
Lymphocyte Activation
Lymphoid Tissue/chemistry
Male
Manfredi B
Natural/immunology
Neuroimmunomodulation/physiology
Panerai AE
Peptide Fragments/pharmacology
Rats
Receptors
Sacerdote P
Spleen/immunology
Sprague-Dawley
Stress/etiology/immunology
Time Factors
-
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/10.1152/jn.00353.2003" target="_blank" rel="noreferrer">http://doi.org/10.1152/jn.00353.2003</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
Activation of peripheral NMDA receptors contributes to human pain and rat afferent discharges evoked by injection of glutamate into the masseter muscle
Publisher
An entity responsible for making the resource available
Journal Of Neurophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Female; Humans; Male; Adult; Analysis of Variance; Animals; Double-Blind Method; Cross-Over Studies; Rats; Non-U.S. Gov't; Research Support; Nonparametric; Statistics; Dose-Response Relationship; Drug; Receptors; Sprague-Dawley; Afferent Pathways/drug effects/physiology; Glutamic Acid/pharmacology; Masseter Muscle/drug effects/physiology; N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/metabolism; Pain/chemically induced/physiopathology
Creator
An entity primarily responsible for making the resource
Cairns BE; Svensson P; Wang K; Hupfeld S; Graven-Nielsen T; Sessle BJ; Berde CB; Arendt-Nielsen L
Description
An account of the resource
Peripheral N-methyl-d-aspartate (NMDA) receptors are found in deep tissues and may play a role in deep tissue pain. Injection of the endogenous NMDA receptor agonist glutamate into the masseter muscle excites deep craniofacial afferent fibers in rats and evokes pain in human subjects. It is not clear whether peripheral NMDA receptors play a role in these effects of glutamate. Accordingly, the effect of NMDA on afferent activity as well as the effect of locally administered NMDA receptor antagonists on glutamate-evoked afferent discharges in acutely anesthetized rats and muscle pain in human subjects was examined. Injection of NMDA into the masseter muscle evoked afferent discharges in a concentration-related manner. It was found that the NMDA receptor antagonists 2-amino-5-phosphonvalerate (APV, 10 mM), ketamine (10 mM), and dextromethorphan (40 mM) significantly decreased glutamate-evoked afferent discharges. The effects of APV and ketamine, but not dextromethorphan, were selective for glutamate-evoked afferent discharges and did not affect hypertonic saline-evoked afferent discharges. In human experiments, it was found that 10 mM ketamine decreased glutamate-evoked muscle pain but had no effect on hypertonic saline-evoked muscle pain. These results indicate that injection of glutamate into the masseter muscle evokes afferent discharges in rats and muscle pain in humans in part through activation of peripheral NMDA receptors. It is conceivable that activation of peripheral NMDA receptors may contribute to masticatory muscle pain and that peripherally acting NMDA receptor antagonists could prove to be effective analgesics for this type of pain.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jn.00353.2003" target="_blank" rel="noreferrer">10.1152/jn.00353.2003</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
Adult
Afferent Pathways/drug effects/physiology
Analysis of Variance
Animals
Arendt-Nielsen L
Backlog
Berde CB
Cairns BE
Cross-Over Studies
Dose-Response Relationship
Double-Blind Method
Drug
Female
Glutamic Acid/pharmacology
Graven-Nielsen T
Humans
Hupfeld S
Journal Article
Journal Of Neurophysiology
Male
Masseter Muscle/drug effects/physiology
N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/metabolism
Non-U.S. Gov't
Nonparametric
Pain/chemically induced/physiopathology
Rats
Receptors
Research Support
Sessle BJ
Sprague-Dawley
Statistics
Svensson P
Wang K
-
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/10.1073/pnas.0409888102" target="_blank" rel="noreferrer">http://doi.org/10.1073/pnas.0409888102</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
CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids
Publisher
An entity responsible for making the resource available
Proceedings Of The National Academy Of Sciences Of The United States Of America
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; Male; Animals; Rats; Biomarkers of Pain; Cells; Cultured; Analgesics/pharmacology; Sprague-Dawley; beta-Endorphin/secretion; Cannabinoid; Cannabinoids; CB2/agonists/physiology; Endothelin B/physiology; Receptor
Creator
An entity primarily responsible for making the resource
Ibrahim MM; Porreca F; Lai J; Albrecht PJ; Rice FL; Khodorova A; Davar G; Makriyannis A; Vanderah TW; Mata HP; Malan TP
Description
An account of the resource
CB(2) cannabinoid receptor-selective agonists are promising candidates for the treatment of pain. CB(2) receptor activation inhibits acute, inflammatory, and neuropathic pain responses but does not cause central nervous system (CNS) effects, consistent with the lack of CB(2) receptors in the normal CNS. To date, there has been virtually no information regarding the mechanism of CB(2) receptor-mediated inhibition of pain responses. Here, we test the hypothesis that CB(2) receptor activation stimulates release from keratinocytes of the endogenous opioid beta-endorphin, which then acts at opioid receptors on primary afferent neurons to inhibit nociception. The antinociceptive effects of the CB(2) receptor-selective agonist AM1241 were prevented in rats when naloxone or antiserum to beta-endorphin was injected in the hindpaw where the noxious thermal stimulus was applied, suggesting that beta-endorphin is necessary for CB(2) receptor-mediated antinociception. Further, AM1241 did not inhibit nociception in mu-opioid receptor-deficient mice. Hindpaw injection of beta-endorphin was sufficient to produce antinociception. AM1241 stimulated beta-endorphin release from rat skin tissue and from cultured human keratinocytes. This stimulation was prevented by AM630, a CB(2) cannabinoid receptor-selective antagonist and was not observed in skin from CB(2) cannabinoid receptor-deficient mice. These data suggest that CB(2) receptor activation stimulates release from keratinocytes of beta-endorphin, which acts at local neuronal mu-opioid receptors to inhibit nociception. Supporting this possibility, CB(2) immunolabeling was detected on beta-endorphin-containing keratinocytes in stratum granulosum throughout the epidermis of the hindpaw. This mechanism allows for the local release of beta-endorphin, where CB(2) receptors are present, leading to anatomical specificity of opioid effects.
2005
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1073/pnas.0409888102" target="_blank" rel="noreferrer">10.1073/pnas.0409888102</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
Albrecht PJ
Analgesics/pharmacology
Animals
Backlog
beta-Endorphin/secretion
Biomarkers of Pain
Cannabinoid
Cannabinoids
CB2/agonists/physiology
Cells
Cultured
Davar G
Endothelin B/physiology
Humans
Ibrahim MM
Journal Article
Khodorova A
Lai J
Makriyannis A
Malan TP
Male
Mata HP
Porreca F
Proceedings Of The National Academy Of Sciences Of The United States Of America
Rats
Receptor
Rice FL
Sprague-Dawley
Vanderah TW
-
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/j.smrv.2005.08.001" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.smrv.2005.08.001</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
Sleep deprivation and pain perception
Publisher
An entity responsible for making the resource available
Sleep Medicine Reviews
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
Subject
The topic of the resource
Humans; Attitude; Animals; Rats; Sleep; Sprague-Dawley; Pain/epidemiology/physiopathology; REM/physiology; Sleep Deprivation/epidemiology/physiopathology
Creator
An entity primarily responsible for making the resource
Lautenbacher S; Kundermann B; Krieg JC
Description
An account of the resource
Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. To fathom the causal direction from sleep to pain we have reviewed experimental human and animal studies on the effects of sleep deprivation on pain processing. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.
2006
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.smrv.2005.08.001" target="_blank" rel="noreferrer">10.1016/j.smrv.2005.08.001</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
2006
Animals
Attitude
Backlog
Humans
Journal Article
Krieg JC
Kundermann B
Lautenbacher S
Pain/epidemiology/physiopathology
Rats
REM/physiology
Sleep
Sleep Deprivation/epidemiology/physiopathology
Sleep Medicine Reviews
Sprague-Dawley