INT97649

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

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 bDMF 264 99.84 Dopamine 120 99.68 cerebral cortex 11 99.68 Analgesic 3 98.98 ischemia 1061 98.84 agonist 117 98.62 Hippocampus 307 98.52 antagonist 125 98.10 Pyramidal cell 161 98.08

Disease Link Frequency Relevance Heat Hypotension 2 99.84 Aging 29 99.68 Targeted Disruption 115 99.66 Cv General 4 Under Development 655 98.84 Brain Hemorrhage 28 98.72 Myocardial Infarction 13 98.30 Stroke 93 97.92 Apoptosis 126 97.84 Cv Unclassified Under Development 378 96.64 Pituitary Cancer 48 94.64

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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