INT24472

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Context Info
Confidence 0.28
First Reported 1988
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 1.00
Pain Relevance 1.73

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

plasma membrane (Brs3) signal transducer activity (Brs3)
Brs3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
agonist 16 98.50 Very High Very High Very High
qutenza 160 97.74 Very High Very High Very High
sodium channel 10 96.96 Very High Very High Very High
antagonist 2 95.56 Very High Very High Very High
anesthesia 2 95.52 Very High Very High Very High
local anesthetic 3 76.04 Quite High
potassium channel 3 75.00 Quite High
Calcium channel 4 65.48 Quite High
c fibre 32 59.76 Quite High
Action potential 22 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Sudden Death 4 93.40 High High
Arrhythmias 2 Under Development 5 92.40 High High
Heart Rate Under Development 10 89.00 High High
Syncope 8 82.48 Quite High
Nociception 4 82.16 Quite High
Heart Arrhythmia 10 76.16 Quite High
Disease 7 74.44 Quite High
Myocardial Infarction 3 72.08 Quite High
Ventricular Tachycardia 3 71.08 Quite High
Bundle-branch Block 4 69.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The inhibitory effect of BAY on the time-dependent increase in BRS was suppressed by a pretreatment with PN (0.6 micrograms/kg i.c.v.) and by a pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.).
Positive_regulation (increase) of BRS associated with antagonist
1) Confidence 0.28 Published 1988 Journal Arch Mal Coeur Vaiss Section Abstract Doc Link 2461181 Disease Relevance 0 Pain Relevance 0.20
In SHR, i.c.v. injection of BAY (3 microgram/kg) but not PN (0.6 micrograms/kg) suppressed the time dependent increase in BRS.
Positive_regulation (increase) of BRS
2) Confidence 0.28 Published 1988 Journal Arch Mal Coeur Vaiss Section Abstract Doc Link 2461181 Disease Relevance 0 Pain Relevance 0.20
Interestingly, RTX, a high affinity ligand for VR1, did alter regularly discharging BRs even at higher relative concentrations [20].
Positive_regulation (discharging) of BRs
3) Confidence 0.03 Published 2006 Journal J Negat Results Biomed Section Body Doc Link PMC1481593 Disease Relevance 0 Pain Relevance 0.73
CAP, unlike the ultrapotent TRPV1 agonist RTX, had additional non-specific actions to inhibit discharge of pressure activated A-type aortic BRS at very high concentrations.
Positive_regulation (activated) of BRS associated with qutenza and agonist
4) Confidence 0.03 Published 2006 Journal J Negat Results Biomed Section Body Doc Link PMC1481593 Disease Relevance 0.08 Pain Relevance 0.55
In approximately 20% of the cases BrS is caused by mutations in the SCN5A gene on chromosome 3p21-23, encoding the cardiac sodium channel, a protein involved in the control of myocardial excitability.
Positive_regulation (caused) of BrS associated with sodium channel
5) Confidence 0.03 Published 2006 Journal Orphanet J Rare Dis Section Abstract Doc Link PMC1592481 Disease Relevance 0.91 Pain Relevance 0.05

General Comments

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