INT82841

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Context Info
Confidence 0.68
First Reported 1999
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 3.91
Pain Relevance 2.84

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

lyase activity (Car1) Golgi apparatus (Car1) cytoplasm (Car1)
Anatomy Link Frequency
pyramidal cells 2
neurons 2
molecular layers 1
occipital cortex 1
medial 1
Car1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Pyramidal cell 53 100.00 Very High Very High Very High
Glutamate 4 100.00 Very High Very High Very High
long-term potentiation 72 99.76 Very High Very High Very High
ischemia 176 99.14 Very High Very High Very High
Hippocampus 143 98.64 Very High Very High Very High
tetrodotoxin 5 96.44 Very High Very High Very High
Nerve growth factor 2 87.88 High High
corticosteroid 8 87.36 High High
Inflammation 11 86.36 High High
Neuronal excitability 2 82.32 Quite High
Disease Link Frequency Relevance Heat
Status Epilepticus 57 99.82 Very High Very High Very High
Post-traumatic Stress Disorder 27 99.76 Very High Very High Very High
Cv General 4 Under Development 110 99.14 Very High Very High Very High
Stress 108 95.68 Very High Very High Very High
Cv Unclassified Under Development 64 93.96 High High
Death 43 92.92 High High
Appetite Loss 30 90.16 High High
Intrauterine Growth Retardation 2 87.80 High High
INFLAMMATION 12 86.36 High High
Apoptosis 24 86.32 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In more ventral parts of the hippocampus, all rats showed sparing of the granular, polymorph, and molecular layers of the lateral blade of the dentate gyrus, as well as the most ventral part of the CA1 and CA3, including the stratum oriens, the deep and superficial pyramidal layers, and the stratum radium.
Localization (part) of CA1 in molecular layers associated with hippocampus
1) Confidence 0.68 Published 2010 Journal Behav Neurosci Section Body Doc Link PMC3002222 Disease Relevance 0 Pain Relevance 0.23
The laminar profile of field potentials recorded in CA3 and CA1 suggests that glutamate is released from axons of CA3 pyramidal cells despite the blockade of fast axonal Na(+) channels by TTX.
Localization (released) of CA1 in pyramidal cells associated with tetrodotoxin, glutamate and pyramidal cell
2) Confidence 0.66 Published 1999 Journal J. Neurosci. Section Abstract Doc Link 10407017 Disease Relevance 0 Pain Relevance 0.80
occurred bilaterally in the medial EC after unilateral tetanization of CA1
Localization (tetanization) of CA1 in medial
3) Confidence 0.56 Published 2008 Journal Neural Plasticity Section Body Doc Link PMC2442167 Disease Relevance 0 Pain Relevance 0.29
medial EC of normal eutrophic rats can develop LTP in vivo to tetanization of both the occipital cortex and the CA1
Localization (tetanization) of CA1 in occipital cortex associated with long-term potentiation
4) Confidence 0.56 Published 2008 Journal Neural Plasticity Section Body Doc Link PMC2442167 Disease Relevance 0.25 Pain Relevance 0.13
Thus both of these receptors in CA1 are related with PTSD.
Localization (related) of CA1 associated with post-traumatic stress disorder
5) Confidence 0.43 Published 2008 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2532603 Disease Relevance 0.97 Pain Relevance 0.45
The mechanism of SE-induced CA1 pyramidal cell damage and the role of calcium
Localization (damage) of CA1 in pyramidal cell associated with pyramidal cell and status epilepticus
6) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2873964 Disease Relevance 0.81 Pain Relevance 0.13
Areas of CA1 stratum radiatum were measured in each section using Scion Image software (Scion Corp., Frederick, MD, USA), and the total volume of CA1 stratum radiatum in each rat was estimated as
Localization (radiatum) of CA1
7) Confidence 0.42 Published 2005 Journal Environ Health Perspect Section Body Doc Link PMC1257590 Disease Relevance 0 Pain Relevance 0.06
In contrast, gp91ds-tat administration exerted significant neuroprotection, as indicated by preservation of NeuN-positive neurons in the hippocampal CA1 region (Fig. 4A, panel d).
Localization (region) of CA1 in neurons
8) Confidence 0.30 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935374 Disease Relevance 1.12 Pain Relevance 0.40
Representative photomicrographs of stained hippocampal CA1 sections revealed that GCI induced a significant loss of hippocampal CA1 neurons at 7 d following ischemic reperfusion, as indicated by a significant decrease in NeuN-positive stained cells in saline-treated animals following GCI as compared to sham controls (Fig. 1B).
Localization (decrease) of CA1 in neurons associated with ischemia
9) Confidence 0.30 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935374 Disease Relevance 0.75 Pain Relevance 0.29
AIS localization was also observed within the CA1 layer (Fig. 7, panel CA1) and CA3 (Fig. 7, panel CA3).
Localization (localization) of CA1
10) Confidence 0.13 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2592246 Disease Relevance 0 Pain Relevance 0.04
AIS localization was also observed within the CA1 layer (Fig. 7, panel CA1) and CA3 (Fig. 7, panel CA3).
Localization (localization) of CA1
11) Confidence 0.13 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2592246 Disease Relevance 0 Pain Relevance 0.04

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