INT65276

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Context Info
Confidence 0.65
First Reported 1996
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 14
Disease Relevance 4.99
Pain Relevance 5.05

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

extracellular region (Fst) nucleus (Fst) cytoplasm (Fst)
Anatomy Link Frequency
myocytes 1
muscle 1
brain 1
Fst (Mus musculus)
Pain Link Frequency Relevance Heat
Eae 90 100.00 Very High Very High Very High
antidepressant 62 100.00 Very High Very High Very High
analgesia 21 100.00 Very High Very High Very High
monoamine 31 99.20 Very High Very High Very High
Dopamine 13 98.88 Very High Very High Very High
depression 27 98.64 Very High Very High Very High
fluoxetine 14 96.68 Very High Very High Very High
opioid receptor 2 95.88 Very High Very High Very High
antinociception 4 92.44 High High
Serotonin 22 92.00 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 128 99.98 Very High Very High Very High
Depression 30 98.64 Very High Very High Very High
Hypertrophy 35 97.60 Very High Very High Very High
Hyperplasia 9 97.28 Very High Very High Very High
Stress 48 93.68 High High
Attention Deficit Hyperactivity Disorder 10 92.48 High High
Cancer 136 87.52 High High
Frailty 64 82.72 Quite High
Gliosis 46 82.56 Quite High
Injury 28 81.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Immobility or despair behavior produced in both FST and TST are taken as paradigm of depression and antidepressant drugs reduce the immobility period.
Gene_expression (produced) of FST associated with antidepressant, depression and eae
1) Confidence 0.65 Published 2007 Journal Prog. Neuropsychopharmacol. Biol. Psychiatry Section Abstract Doc Link 17570574 Disease Relevance 0.18 Pain Relevance 0.50
Overall, the results firstly indicate that folic acid produced an antidepressant-like effect in FST and in TST and that this effect appears to be mediated by an interaction with the serotonergic (5-HT(1A) and 5-HT(2A/2C) receptors) and noradrenergic (alpha(1)- and alpha(2)-adrenoceptors) systems.
Gene_expression (produced) of FST associated with antidepressant
2) Confidence 0.53 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18078962 Disease Relevance 0 Pain Relevance 0.45
Finally, the highly aversive situations in the FST or TST provoked greater active avoidance behavior in GSK-3?
Gene_expression (provoked) of FST associated with eae
3) Confidence 0.37 Published 2009 Journal Mol Brain Section Body Doc Link PMC2785804 Disease Relevance 0.59 Pain Relevance 0.17
A similar behavior in the FST was observed in mice harboring a deletion of one allele of GSK-3?
Gene_expression (behavior) of FST associated with eae
4) Confidence 0.37 Published 2009 Journal Mol Brain Section Body Doc Link PMC2785804 Disease Relevance 0.36 Pain Relevance 0.34
In C2C12 differentiated myocytes, hyperexpression of follistatin, a physiological inhibitor of myostatin, indeed rescues TNF?
Gene_expression (hyperexpression) of follistatin in myocytes
5) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965098 Disease Relevance 0.41 Pain Relevance 0
On the other hand, follistatin overexpression resulted in increased p-Akt levels, irrespective of the presence of TNF?
Gene_expression (overexpression) of follistatin
6) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965098 Disease Relevance 0.40 Pain Relevance 0.03
Of particular relevance, FST produces a variation of the monoamine concentration in the brain while TS does not [40], [41].
Gene_expression (produces) of FST in brain associated with eae and monoamine
7) Confidence 0.26 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565062 Disease Relevance 0.54 Pain Relevance 0.77
Nevertheless, although the effects of follistatin hyperexpression are phenotypically comparable to those exerted by ERK inhibition, the mechanisms involved are quite different.
Gene_expression (hyperexpression) of follistatin
8) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965098 Disease Relevance 0.27 Pain Relevance 0
Groups for Forced Swim Test (FST)
Gene_expression (Groups) of FST associated with eae
9) Confidence 0.15 Published 2008 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2792615 Disease Relevance 0 Pain Relevance 0.26
When myostatin is genetically deleted or inhibited by transgenic expression of the myostatin binding protein follistatin, there is a more profound increase in muscle mass and both hypertrophy and hyperplasia of fibers is observed [4], [5].
Gene_expression (expression) of follistatin in muscle associated with targeted disruption, hypertrophy and hyperplasia
10) Confidence 0.14 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2820101 Disease Relevance 0.79 Pain Relevance 0
In contrast, in the DG, there was an unexpected 50% decrease in average microglial proliferation (labeled over 3 days of BrdU), induced by FS-288 infusion, although the average total microglial population was not significantly changed (Fig. 4D).
Gene_expression (infusion) of FS-288
11) Confidence 0.14 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.46 Pain Relevance 0.16
In the pPV, we found that inhibition of activin A by FS-288 resulted in a 72% average increase of microglial proliferation compared to KA-injected animals that received no FS-288 (Fig. 4C) and this led to an expected 72% increase in the average total microglial population (Fig. 4D).
Neg (no) Gene_expression (received) of FS-288
12) Confidence 0.14 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.53 Pain Relevance 0.15
Thus, we provided evidence that central KATP channels participate in the production of FS-SIA but not production of SW- or PSY-SIA; and we suggest that glibenclamide, through closing of KATP channels, suppresses mu-opioid receptor functions, which subsequently leads to the inhibition of FS-SIA since antinociception is produced by the activation of mu-receptors.
Gene_expression (production) of FS-SIA associated with antinociception, opioid receptor and analgesia
13) Confidence 0.10 Published 1996 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 8854212 Disease Relevance 0.24 Pain Relevance 1.11
Thus, we provided evidence that central KATP channels participate in the production of FS-SIA but not production of SW- or PSY-SIA; and we suggest that glibenclamide, through closing of KATP channels, suppresses mu-opioid receptor functions, which subsequently leads to the inhibition of FS-SIA since antinociception is produced by the activation of mu-receptors.
Gene_expression (production) of FS-SIA associated with antinociception, opioid receptor and analgesia
14) Confidence 0.10 Published 1996 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 8854212 Disease Relevance 0.24 Pain Relevance 1.11

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