INT97649

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Context Info
Confidence 0.66
First Reported 2001
Last Reported 2011
Negated 4
Speculated 1
Reported most in Body
Documents 48
Total Number 53
Disease Relevance 13.77
Pain Relevance 8.94

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

mitochondrion (Dlat) transferase activity, transferring acyl groups (Dlat)
Anatomy Link Frequency
sections 1 5
brain 4
neuronal 2
neuron 2
pituitary 2
Dlat (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Neuronal excitability 66 100.00 Very High Very High Very High
bDMF 264 99.84 Very High Very High Very High
Dopamine 120 99.68 Very High Very High Very High
cerebral cortex 11 99.68 Very High Very High Very High
Analgesic 3 98.98 Very High Very High Very High
ischemia 1061 98.84 Very High Very High Very High
agonist 117 98.62 Very High Very High Very High
Hippocampus 307 98.52 Very High Very High Very High
antagonist 125 98.10 Very High Very High Very High
Pyramidal cell 161 98.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypotension 2 99.84 Very High Very High Very High
Aging 29 99.68 Very High Very High Very High
Targeted Disruption 115 99.66 Very High Very High Very High
Cv General 4 Under Development 655 98.84 Very High Very High Very High
Brain Hemorrhage 28 98.72 Very High Very High Very High
Myocardial Infarction 13 98.30 Very High Very High Very High
Stroke 93 97.92 Very High Very High Very High
Apoptosis 126 97.84 Very High Very High Very High
Cv Unclassified Under Development 378 96.64 Very High Very High Very High
Pituitary Cancer 48 94.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Equimolar doses of nor-binaltorphimine (nor-BNI) attenuated analgesic action of E2, but were without hypotensive action produced by E2.
Neg (without) Gene_expression (produced) of E2 associated with analgesic and hypotension
1) Confidence 0.66 Published 2001 Journal Life Sci. Section Abstract Doc Link 11510952 Disease Relevance 0.87 Pain Relevance 0.76
CONCLUSIONS: Both PRGR and PBC are effective techniques for the treatment of trigeminal neuralgia, with PRGR presenting some advantages in terms of milder and fewer complications and allowing lighter anesthesia without compromise of analgesia.
Gene_expression (presenting) of PBC
2) Confidence 0.48 Published 2010 Journal J. Neurosurg. Section Body Doc Link 20187700 Disease Relevance 0 Pain Relevance 0
Effect of E2 on androgen receptor (AR) of prostate with TP (92.6 mg/kg)
Gene_expression (Effect) of E2
3) Confidence 0.47 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2959216 Disease Relevance 0.05 Pain Relevance 0
M E2 produced in HIP neuron) of control, respectively.
Gene_expression (produced) of E2 in neuron
4) Confidence 0.44 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.09
Therefore, the significant inhibition of IGly produced by E2 may have strong effect on the neuronal excitability, suggesting an alternative cellular mechanism by which periodic sex hormone fluctuations affect CNS neuronal excitation and cause mood disorders.
Gene_expression (produced) of E2 in neuronal associated with neuronal excitability and affective disorder
5) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0.78 Pain Relevance 0.42
Regulatory sites for E2 and pregnanolone on GlyRs are separate
Gene_expression (sites) of E2
6) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.07
It remains unexplored whether GlyRs also participate in regulation of neuronal excitability, through E2-induced disinhibition in the mature hippocampus [14].
Gene_expression (unexplored) of E2 in neuronal associated with neuronal excitability and hippocampus
7) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0.55 Pain Relevance 0.40
M), the inactive stereoisomer of E2, mimicked the inhibitory effect of E2 on IGly (Figure 2A6 and 2B1, P > 0.05, Unpaired Student's t-test), suggesting that E2 inhibition on GlyR is independent of classical ERs.


Neg (inhibition) Gene_expression (inhibition) of E2
8) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.07
We further employed tamoxifen, a classical ER antagonist in the hippocampus [15], to examine whether membrane-localized classical ERs were involved in E2 inhibition of IGly.
Neg (inhibition) Gene_expression (inhibition) of E2 in hippocampus associated with antagonist and hippocampus
9) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.10
Effect of different dosages of E2 with TP (0.74 mg/kg)
Gene_expression (dosages) of E2
10) Confidence 0.41 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2959216 Disease Relevance 0 Pain Relevance 0
Effect of different dosages of E2 with TP (92.6 mg/kg)
Gene_expression (dosages) of E2
11) Confidence 0.41 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2959216 Disease Relevance 0 Pain Relevance 0
Effect of different dosages of E2 with TP (3.7 mg/kg)
Gene_expression (dosages) of E2
12) Confidence 0.41 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2959216 Disease Relevance 0 Pain Relevance 0
Effect of different dosages of E2 with TP (18.5 mg/kg)
Gene_expression (dosages) of E2
13) Confidence 0.41 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2959216 Disease Relevance 0 Pain Relevance 0
The membrane capacitance was not changed by E2, indicating that the alteration of plasma membrane capacitance was not involved in E2 inhibition of GlyRs.


Neg (inhibition) Gene_expression (inhibition) of E2 in plasma
14) Confidence 0.38 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.04
Our data suggest that E2 inhibited IGly in a noncompetitive manner because E2 reduced IGly independent of glycine concentrations, and the effect can be additive with that of PGN, a competitive steroid inhibitor of GlyR without changing the membrane viscosity [39,46].
Gene_expression (reduced) of E2
15) Confidence 0.38 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.04
On average, E2 at 1, 3, 6 and 10 ?
Gene_expression (average) of E2
16) Confidence 0.38 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.17
To determine whether acute administration of E2 and synthetic estrogenic compounds such as the GPR30 agonist G1 or the SERM STX are neuroprotective in older animals after prolonged hormonal withdrawal, we tested these compounds in middle-aged females that were OVX for 8 weeks before ischemia (Figure 4).
Gene_expression (administration) of E2 associated with ischemia, agonist and withdrawal
17) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2799530 Disease Relevance 0.76 Pain Relevance 0.55
-cyclodextrin encapsulated E2 (Sigma) dissolved in sterile saline (corresponding to 2.25 µg of free E2), STX (50 µg), G1 (Calbiochem, 50 µg), or the appropriate vehicles (?
Gene_expression (encapsulated) of E2
18) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2799530 Disease Relevance 0.31 Pain Relevance 0.20
, was originally shown to mimic E2 modulation of hypothalamic ion channels and phospholipase C through the activation of a G-protein coupled receptor (for review see [10]).
Gene_expression (modulation) of E2
19) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2799530 Disease Relevance 0.37 Pain Relevance 0.32
Immediately after reperfusion, animals received a single infusion of either E2 (2.25 µg), G1 (50 µg) or STX (50 µg) into the lateral ventricle (ICV) or a single systemic injection of E2 (100 µg/kg).
Gene_expression (injection) of E2 in ICV
20) Confidence 0.31 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2799530 Disease Relevance 0.40 Pain Relevance 0.44

General Comments

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