INT205949

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Context Info
Confidence 0.15
First Reported 2007
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 1.58
Pain Relevance 0.85

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

Anatomy Link Frequency
hearts 5
neuroblasts 1
neurons 1
Shbdp1 (Mus musculus)
Pain Link Frequency Relevance Heat
Somatosensory cortex 42 100.00 Very High Very High Very High
lidocaine 190 91.04 High High
Action potential 141 85.04 High High
action potential duration 93 78.88 Quite High
Glutamate 7 65.60 Quite High
addiction 6 33.28 Quite Low
Hippocampus 16 5.00 Very Low Very Low Very Low
antiarrhythmic agent 10 5.00 Very Low Very Low Very Low
Eae 10 5.00 Very Low Very Low Very Low
depression 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hypokalemia 172 99.74 Very High Very High Very High
Bartter Syndrome 45 93.68 High High
Neurodegenerative Disease 19 74.32 Quite High
Syndrome 62 62.60 Quite High
Anxiety Disorder 29 50.00 Quite Low
Arrhythmogenic Right Ventricular Dysplasia 21 44.40 Quite Low
Heart Rate Under Development 22 5.00 Very Low Very Low Very Low
Depression 7 5.00 Very Low Very Low Very Low
Coronary Heart Disease 6 5.00 Very Low Very Low Very Low
Heart Arrhythmia 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Normokalemic hearts (Fig. 2a, A–C) again were consistently free from arrhythmic activity after S2 stimulation after any S1S2 interval (n?
Positive_regulation (stimulation) of S2 in hearts
1) Confidence 0.15 Published 2007 Journal Pflugers Arch Section Body Doc Link PMC1839769 Disease Relevance 0.34 Pain Relevance 0.25
This also applied to hypokalemic hearts when S2 stimuli were delivered when MAPs had reached 90% repolarization (Fig. 2b, A, n?
Positive_regulation (stimuli) of S2 in hearts associated with hypokalemia
2) Confidence 0.15 Published 2007 Journal Pflugers Arch Section Body Doc Link PMC1839769 Disease Relevance 0.38 Pain Relevance 0.25
While studies under normokalaemic conditions confirmed an absence of arrhythmic activity at either BCL (0 out of five hearts subjected to regular stimulation, 0 out of seven hearts subjected to S2 stimulation), studies under hypokalaemic conditions (Fig. 1) revealed arrhythmogenicity at the longest (A, five out of five hearts subjected to regular stimulation, seven out of seven hearts subjected to S2 stimulation) but not the shortest (B, 0 out of five hearts subjected to regular stimulation, one out of nine hearts subjected to S2 stimulation) BCL studied.
Positive_regulation (stimulation) of S2 in hearts
3) Confidence 0.13 Published 2007 Journal Pflugers Arch Section Body Doc Link PMC2627988 Disease Relevance 0.25 Pain Relevance 0.08
While studies under normokalaemic conditions confirmed an absence of arrhythmic activity at either BCL (0 out of five hearts subjected to regular stimulation, 0 out of seven hearts subjected to S2 stimulation), studies under hypokalaemic conditions (Fig. 1) revealed arrhythmogenicity at the longest (A, five out of five hearts subjected to regular stimulation, seven out of seven hearts subjected to S2 stimulation) but not the shortest (B, 0 out of five hearts subjected to regular stimulation, one out of nine hearts subjected to S2 stimulation) BCL studied.
Positive_regulation (stimulation) of S2 in hearts
4) Confidence 0.13 Published 2007 Journal Pflugers Arch Section Body Doc Link PMC2627988 Disease Relevance 0.27 Pain Relevance 0.08
While studies under normokalaemic conditions confirmed an absence of arrhythmic activity at either BCL (0 out of five hearts subjected to regular stimulation, 0 out of seven hearts subjected to S2 stimulation), studies under hypokalaemic conditions (Fig. 1) revealed arrhythmogenicity at the longest (A, five out of five hearts subjected to regular stimulation, seven out of seven hearts subjected to S2 stimulation) but not the shortest (B, 0 out of five hearts subjected to regular stimulation, one out of nine hearts subjected to S2 stimulation) BCL studied.
Positive_regulation (stimulation) of S2 in hearts
5) Confidence 0.13 Published 2007 Journal Pflugers Arch Section Body Doc Link PMC2627988 Disease Relevance 0.19 Pain Relevance 0.07
L6 was enhanced in S2 relative to other regions as both a source of synaptic output and a recipient of synaptic input, due to the relatively high density of neurons (Figure S4) and their relatively low photoexcitability (Figure 2C–E).
Positive_regulation (enhanced) of S2 in neurons associated with somatosensory cortex
6) Confidence 0.12 Published 2011 Journal PLoS Biology Section Body Doc Link PMC3014926 Disease Relevance 0 Pain Relevance 0.13
These mice also showed an increase in the number of BrdU/PSA-NCAM double-positive proliferating neuroblasts, presumably derived from the SVZ (see additional file 1, Figure S2B and S2C, right panels); and a notable increase in the number of BrdU-positive cells co-labeled with NeuN in the GCL (see additional file 1, Figure S2D and S2E, right panel).
Positive_regulation (increase) of S2C in neuroblasts
7) Confidence 0.01 Published 2009 Journal Mol Brain Section Body Doc Link PMC2673217 Disease Relevance 0.14 Pain Relevance 0

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