INT201477

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Context Info
Confidence 0.31
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 11
Disease Relevance 15.00
Pain Relevance 5.38

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

mitochondrion (Acsm3) molecular_function (Acsm3) cellular_component (Acsm3)
ligase activity (Acsm3) biological_process (Acsm3) lipid metabolic process (Acsm3)
Anatomy Link Frequency
neutrophil 2
artery 1
filament 1
basilar artery 1
Acsm3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cva 641 100.00 Very High Very High Very High
Inflammatory mediators 69 99.88 Very High Very High Very High
Kinase C 55 99.28 Very High Very High Very High
chemokine 52 98.84 Very High Very High Very High
Inflammatory marker 4 95.04 Very High Very High Very High
Inflammatory response 32 90.64 High High
Inflammation 168 85.60 High High
cytokine 85 79.24 Quite High
adenocard 5 76.64 Quite High
ischemia 24 73.12 Quite High
Disease Link Frequency Relevance Heat
Subarachnoid Hemorrhage 595 100.00 Very High Very High Very High
Cv General 4 Under Development 28 100.00 Very High Very High Very High
INFLAMMATION 197 99.68 Very High Very High Very High
Stroke 22 99.40 Very High Very High Very High
Adhesions 82 96.80 Very High Very High Very High
Increased Venous Pressure Under Development 115 96.40 Very High Very High Very High
Myocardial Infarction 6 95.36 Very High Very High Very High
Cardiovascular Disease 2 94.04 High High
Body Weight 5 92.24 High High
Stress 90 91.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Male Wistar rats were subjected to the induction of SAH by means of the endovascular filament method.
Positive_regulation (induction) of SAH in filament associated with cva
1) Confidence 0.31 Published 2010 Journal Crit Care Section Abstract Doc Link PMC2945141 Disease Relevance 1.86 Pain Relevance 0.66
Furthermore, we observed marked SAH-induced upregulation of the chemokines MIP-1?
Positive_regulation (marked) of SAH associated with chemokine and cva
2) Confidence 0.29 Published 2010 Journal Crit Care Section Body Doc Link PMC2945141 Disease Relevance 1.62 Pain Relevance 0.66
for four consecutive days starting at two hours after SAH induction.
Positive_regulation (induction) of SAH associated with cva
3) Confidence 0.27 Published 2010 Journal Crit Care Section Abstract Doc Link PMC2945141 Disease Relevance 2.04 Pain Relevance 0.71
SAH was induced at Day 0 in male Wistar rats and treated for four consecutive days with IFN-?.
Positive_regulation (induced) of SAH associated with cva
4) Confidence 0.27 Published 2010 Journal Crit Care Section Body Doc Link PMC2945141 Disease Relevance 0.70 Pain Relevance 0.22
As mentioned by Ersahin et al., treatment with melatonin due to its free radical scavenging properties significantly inhibited SAH-induced lipid peroxidation and neutrophil infiltration of the brain tissue on the second day of SAH induction in rats.
Positive_regulation (induction) of SAH in neutrophil associated with cva
5) Confidence 0.17 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2821769 Disease Relevance 2.04 Pain Relevance 0.56
In both SAH and organ culture this upregulation is attenuated by PKC inhibitors [13-15].
Positive_regulation (upregulation) of SAH associated with kinase c and cva
6) Confidence 0.17 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC1770924 Disease Relevance 1.02 Pain Relevance 0.41
In previous studies, we have demonstrated that in experimental ischemic stroke and subarachnoid hemorrhage (SAH) there is an upregulation of endothelin type B (ETB) receptors in the cerebral arteries [10,11].
Positive_regulation (upregulation) of SAH associated with cv general 4 under development, stroke and cva
7) Confidence 0.17 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC1770924 Disease Relevance 0.86 Pain Relevance 0.42
The main findings of this study are that (1) vascular inflammatory mediators were induced after SAH and could be remarkably repressed when treated with melatonin; (2) the increased lipid peroxidation in the artery tissues could be significantly downregulated after melatonin injections following experimental SAH; (3) after melatonin administration, the postSAH reduced antioxidative status was ameliorated in this two-hemorrhage model; (4) in agreement with the previous research [5], treatment with melatonin prevented cerebral vasospasm of the basilar arteries in rabbits.
Positive_regulation (induced) of SAH in artery associated with inflammatory mediators, cva and increased venous pressure under development
8) Confidence 0.16 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2821769 Disease Relevance 1.12 Pain Relevance 0.52
Our data demonstrated that treatment with melatonin induced the antioxidant defense system, downregulated lipid peroxidation in the basilar artery, and resulted in a significant increase of the cross-sectional area of basilar artery after SAH.
Positive_regulation (increase) of SAH in basilar artery associated with cva
9) Confidence 0.15 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2821769 Disease Relevance 1.15 Pain Relevance 0.43
As mentioned by Ersahin et al., treatment with melatonin due to its free radical scavenging properties significantly inhibited SAH-induced lipid peroxidation and neutrophil infiltration of the brain tissue on the second day of SAH induction in rats.
Positive_regulation (induction) of SAH in neutrophil associated with cva
10) Confidence 0.15 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2821769 Disease Relevance 1.92 Pain Relevance 0.55
The rabbits all survived from the procedure of induction of experimental SAH.

3.2.

Positive_regulation (induction) of SAH associated with cva
11) Confidence 0.15 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2821769 Disease Relevance 0.66 Pain Relevance 0.24

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