INT101687

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Context Info
Confidence 0.40
First Reported 2002
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 6
Total Number 15
Disease Relevance 2.95
Pain Relevance 0.95

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

endosome (AVPR1B) plasma membrane (AVPR1B) response to stress (AVPR1B)
signal transducer activity (AVPR1B)
Anatomy Link Frequency
cortex 2
neurons 1
sinus 1
AVPR1B (Homo sapiens)
Pain Link Frequency Relevance Heat
medulla 1 99.24 Very High Very High Very High
Angina 12 97.84 Very High Very High Very High
aspirin 1 96.72 Very High Very High Very High
algil 1 91.84 High High
adenocard 1 74.60 Quite High
Pain 4 69.08 Quite High
nud 1 65.92 Quite High
abdominal pain 1 49.24 Quite Low
behavioral therapy 10 36.24 Quite Low
pruritus 1 31.04 Quite Low
Disease Link Frequency Relevance Heat
Ventricular Tachycardia 3 98.48 Very High Very High Very High
Angina 9 97.84 Very High Very High Very High
Premature Ventricular Beats 1 93.92 High High
Arrhythmias 2 Under Development 1 92.24 High High
Bundle-branch Block 1 90.08 High High
Scotoma 50 89.04 High High
Heart Rate Under Development 30 85.88 High High
Pressure Volume 2 Under Development 16 85.12 High High
Cv General 3 Under Development 9 81.12 Quite High
Toothache 2 76.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3.
Positive_regulation (leads) of V3
1) Confidence 0.40 Published 2002 Journal J. Cardiovasc. Electrophysiol. Section Abstract Doc Link 11900298 Disease Relevance 0.99 Pain Relevance 0.29
As expected, prior to lesioning the entire central sectors of areas V1, V2, and V3 were strongly activated by the retinotopic stimulus.
Positive_regulation (activated) of V3
2) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0 Pain Relevance 0
Surprisingly, the retinotopic organization inside the LPZ of areas V2, V3 remained similar to that of the non-lesioned hemisphere, suggesting that LPZ activation in V2, V3 is not the result of input arising from nearby (non-lesioned) V1 cortex.
Positive_regulation (activation) of V3 in cortex
3) Confidence 0.32 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2677457 Disease Relevance 0.08 Pain Relevance 0
RESULTS: The BR responses (R2 and R3) evoked by stimulation of V3 were significantly smaller than the BR responses evoked by stimulation of V1 and V2 (P < .004).
Positive_regulation (stimulation) of V3
4) Confidence 0.31 Published 2005 Journal J Orofac Pain Section Body Doc Link 16106718 Disease Relevance 0.08 Pain Relevance 0
Finally, we would like to note that time elapsed following the lesion may turn out to be of critical essence: Although our results suggest that activation levels in V2 and V3 remain stable from 1 to 22 months post-lesioning, when compared to the results of transient inactivation studies [1], [3], [25] they also suggest that plasticity processes operating within the first month post lesion likely play a role in modulating the gain of cortical networks responsible for the observed activity.
Positive_regulation (activation) of V3
5) Confidence 0.23 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0 Pain Relevance 0
We conclude that the observed activity patterns are largely mediated by parallel, V1-bypassing, subcortical pathways that can activate areas V2 and V3 in the absence of V1 input.
Positive_regulation (activate) of V3
6) Confidence 0.22 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2677457 Disease Relevance 0.09 Pain Relevance 0
In any event, we can conclude that: 1) as expected, area V2, V3 activity is strongly dependent on area V1 input, yet 2) both areas V2 and V3 can be visually modulated even in the absence of retinotopically corresponding V1 input.
Positive_regulation (dependent) of V3
7) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0 Pain Relevance 0
By contrast, results describing the function of visual areas V2 and V3 after long-standing V1 lesions are limited: 1) there are no electrophysiological studies addressing directly this issue in monkeys, and 2) neuroimaging studies of human “blindsight” patients have not produced definitive results: On the one hand, the fMRI study of hemianopic patients FS and GY by Goebel et al., appears to confirm results from primate electrophysiology suggesting that visually driven activity in areas V2, V3 is strictly dependent on V1 input [29].
Positive_regulation (dependent) of V3
8) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0 Pain Relevance 0
During the pre-lesion experiments visual stimulation with an expanding ring paradigm resulted in strong and reliable activation of the entire visual cortex (areas V1, V2, V3, V4, V5/MT) with single voxel coherence levels >0.7 and z-scores usually reaching values of >15 (Figure 2A).
Positive_regulation (activation) of V3 in cortex
9) Confidence 0.19 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0.06 Pain Relevance 0
It remains to be seen however whether Pulvinar input is capable of activating area V2, V3 neurons in the absence of V1 input.
Spec (whether) Positive_regulation (activating) of V3 in neurons
10) Confidence 0.14 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0 Pain Relevance 0
The ECG performed on hospital admission showed normal sinus rhythm with concave ST-elevation in V2 and V3.
Positive_regulation (elevation) of V3 in sinus
11) Confidence 0.14 Published 2008 Journal Cases J Section Body Doc Link PMC2572045 Disease Relevance 0.55 Pain Relevance 0.25
In order to quantify the strength of visual stimulation inside the area V2, V3 LPZs (Figure 3), the amplitude of the mean BOLD signal over the LPZ at the stimulation frequency (f0) minus the mean amplitude in the noiseband (excluding the stimulation frequency) was normalized using a retinotopically matched control ROI in the intact hemisphere:
Positive_regulation (stimulation) of V3
12) Confidence 0.10 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0 Pain Relevance 0
The strongest argument that V1-bypassing subcortical channels must be involved in generating the observed V2, V3 activity is provided by multi-unit receptive field maps recorded inside the V2 LPZ (Figure 8).
Positive_regulation (generating) of V3
13) Confidence 0.10 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677457 Disease Relevance 0.15 Pain Relevance 0
Physiologically, activation of V3 receptors is associated with adrenocorticotropic hormone and ?
Positive_regulation (activation) of V3
14) Confidence 0.07 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2504060 Disease Relevance 0.17 Pain Relevance 0.09
A 12-lead electrocardiogram (ECG) showed ST segment elevation in leads II, III, aVF, and V3 to V6 (Fig. 2).
Positive_regulation (elevation) of V3
15) Confidence 0.05 Published 2005 Journal BMC Cardiovasc Disord Section Body Doc Link PMC553970 Disease Relevance 0.79 Pain Relevance 0.31

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