INT8535

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Context Info
Confidence 0.80
First Reported 1992
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 9
Total Number 10
Disease Relevance 2.71
Pain Relevance 9.07

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytosol (Sorbs1) transport (Sorbs1) plasma membrane (Sorbs1)
cytoskeleton (Sorbs1) nucleus (Sorbs1) cytoplasm (Sorbs1)
Anatomy Link Frequency
tubes 1
joint 1
spinal cord 1
Sorbs1 (Mus musculus)
Pain Link Frequency Relevance Heat
Calcitonin gene-related peptide 194 100.00 Very High Very High Very High
qutenza 144 100.00 Very High Very High Very High
Action potential 14 100.00 Very High Very High Very High
Catecholamine 3 100.00 Very High Very High Very High
substance P 35 99.96 Very High Very High Very High
Spinal cord 14 99.56 Very High Very High Very High
Morphine 21 98.72 Very High Very High Very High
trigeminal ganglion 118 98.62 Very High Very High Very High
Nerve growth factor 200 98.36 Very High Very High Very High
Antinociceptive 18 96.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pneumonia 60 100.00 Very High Very High Very High
Ganglion Cysts 146 98.62 Very High Very High Very High
INFLAMMATION 82 95.68 Very High Very High Very High
Bacterial Infection 2 94.48 High High
Sepsis 36 87.60 High High
Chronic Disease 8 85.44 High High
Frailty 6 83.88 Quite High
Infection 34 83.36 Quite High
Nociception 20 81.56 Quite High
Pain 16 78.12 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results suggest that the increase of swimming endurance induced by CAP in mice is caused by an increase in fatty acid utilization due to CAP-induced adrenal catecholamine secretion.
Localization (secretion) of CAP associated with qutenza and catecholamine
1) Confidence 0.80 Published 1997 Journal Biosci. Biotechnol. Biochem. Section Abstract Doc Link 9362118 Disease Relevance 0 Pain Relevance 0.80
Because swimming capacity was enhanced by CAP in mice due to CAP-induced adrenal catecholamine secretion, we investigated the effects of oral administration of C18-VA on swimming capacity using an adjustable-current water pool.
Localization (secretion) of CAP associated with qutenza and catecholamine
2) Confidence 0.74 Published 1998 Journal J. Nutr. Section Abstract Doc Link 9808652 Disease Relevance 0.05 Pain Relevance 0.69
Tibial but not femoral joint preparations from mice with collagenase-induced OA exhibited a significantly enhanced release upon BK stimulation compared to sham controls, while CAP-induced CGRP release did not reveal such difference.
Localization (release) of CAP-induced in joint
3) Confidence 0.48 Published 2004 Journal J. Rheumatol. Section Body Doc Link 15468368 Disease Relevance 0 Pain Relevance 0
Present experiments indicated, however, that i.t. administration of low doses of Cap (0.05-0.5 microgram) in mice preferentially released Dyn and not SP as based on the following results. 1) The antianalgesic action of Cap i.t. against Mor i.c.v. was antagonized by naloxone and nor-binaltorphimine i.t. as was Dyn i.t.
Neg (not) Localization (released) of Cap associated with qutenza, narcan, morphine and substance p
4) Confidence 0.26 Published 1992 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 1374471 Disease Relevance 0 Pain Relevance 2.42
Excellent evidence exists to indicate that, in rats, Cap (30-70 micrograms i.t.) releases SP in the spinal cord and that Mor inhibits this release.
Localization (releases) of Cap in spinal cord associated with qutenza, morphine, spinal cord and substance p
5) Confidence 0.26 Published 1992 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 1374471 Disease Relevance 0 Pain Relevance 2.42
Figure 4 shows the time constant of CAP repolarization (?
Localization (repolarization) of CAP associated with action potential
6) Confidence 0.24 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2952823 Disease Relevance 0.33 Pain Relevance 0.93
Large age-related differences in mortality persisted among survivors of CAP hospitalization at 1-year after hospital discharge.
Localization (hospitalization) of CAP associated with pneumonia
7) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2973976 Disease Relevance 1.03 Pain Relevance 0.17
In conclusion, our results suggest that, once hospitalized for CAP, there is little age-related difference in circulating immune response.
Localization (hospitalized) of CAP associated with pneumonia
8) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2973976 Disease Relevance 0.68 Pain Relevance 0.11
Following washing, TG cultures were exposed for 10 min to the indicated concentrations of CAP, AEA or ACEA or to 50 mM K+ buffer (containing 2.5 mM CaCl2, 50 mM KCl, 1.2 mM MgCl2, 90 mM NaCl, 25 mM NaHCO3, 1 mM NaH2PO4, 10 mM dextrose, 15 mM Hepes, 16 uM thiophan and 0.1% BSA at pH = 7.4), after which the CGRP-containing supernatant was removed and transferred to glass culture tubes (Fisher).
Localization (transferred) of CAP in tubes associated with qutenza, trigeminal ganglion and calcitonin gene-related peptide
9) Confidence 0.04 Published 2005 Journal BMC Neurosci Section Body Doc Link PMC548274 Disease Relevance 0.18 Pain Relevance 0.50
Chronic treatment with NGF and GDNF significantly and concentration-dependently increased 100 nM capsaicin (CAP)-evoked calcitonin gene-related peptide (CGRP) release, reaching approximately 300% at the highest concentration tested (100 ng/ml).
Localization (release) of CAP associated with qutenza, nerve growth factor and calcitonin gene-related peptide
10) Confidence 0.03 Published 2005 Journal BMC Neurosci Section Abstract Doc Link PMC548274 Disease Relevance 0.44 Pain Relevance 1.03

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