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Context Info
Confidence 0.73
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 1.11
Pain Relevance 0.94

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
chromaffin cells 1
synapses 1
neural 1
Car1 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 12 99.82 Very High Very High Very High
Hippocampus 88 96.20 Very High Very High Very High
long-term potentiation 91 94.08 High High
ketamine 79 87.48 High High
Pyramidal cell 80 72.68 Quite High
opioid receptor 1 58.24 Quite High
GABAergic 13 50.00 Quite Low
Action potential 5 49.52 Quite Low
nMDA receptor 12 37.76 Quite Low
addiction 3 29.64 Quite Low
Disease Link Frequency Relevance Heat
Unconsciousness 14 98.28 Very High Very High Very High
Schizophrenia 44 96.36 Very High Very High Very High
Congenital Anomalies 13 93.28 High High
Osteoporosis 3 89.08 High High
Cognitive Disorder 46 82.08 Quite High
Stress Fractures 53 81.84 Quite High
Anaerobic Bacterial Infections 3 67.20 Quite High
Obesity 28 63.44 Quite High
Body Weight 10 63.12 Quite High
Genetic Predisposition To Disease 1 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In our study, the CTR allele C together with a VDR C-A haplotype appeared to protect subjects from fractures.
Localization (haplotype) of C-A
1) Confidence 0.73 Published 2010 Journal BMC Genet Section Body Doc Link PMC2975640 Disease Relevance 0.36 Pain Relevance 0
Ensemble in vivo recording from hippocampal CA1
Localization (hippocampal) of CA1
2) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2999569 Disease Relevance 0.10 Pain Relevance 0.37
Thus, the behavioral correlates of deficits in CA3 neural circuitry would be decreased novelty recognition and impaired spatial learning[58], and for CA1, decreased spatial working memory[56], [57]; and both areas are believed necessary for effective performance on the probe component of the Morris water maze.
Localization (decreased) of CA1 in neural
3) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.20 Pain Relevance 0.07
Two electrodes, one on the subicular side and another on the CA3 side of the recording location in CA1 were chosen to activate control and test pathways respectively (Fig. 5A).
Localization (location) of CA1
4) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1574331 Disease Relevance 0.17 Pain Relevance 0.10
Collectively, these results suggest that dysbindin modulates the kinetics, amount, and probability of single presynaptic vesicle release in hippocampal CA1 glutamatergic synapses, just as in chromaffin cells.
Localization (release) of CA1 in chromaffin cells
5) Confidence 0.39 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2396815 Disease Relevance 0 Pain Relevance 0.03
Because we here found several defects in glutamate vesicle release in hippocampal CA1, combined with the fact that dysbindin reduction occurs in the glutamatergic terminals of the hippocampus in schizophrenia (Talbot et al., 2004), we set out to examine the excitatory asymmetrical synapses on CA1 dendritic spines in sdy mice by electron microscopy.
Localization (release) of CA1 in synapses associated with glutamate, hippocampus and schizophrenia
6) Confidence 0.36 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2396815 Disease Relevance 0.29 Pain Relevance 0.24
The left CA1 was not injected and was therefore utilized for an untreated control.
Localization (utilized) of CA1
7) Confidence 0.16 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2612658 Disease Relevance 0 Pain Relevance 0.13

General Comments

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