INT148884

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Context Info
Confidence 0.23
First Reported 2007
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 7
Total Number 8
Disease Relevance 7.23
Pain Relevance 0.53

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

plasma membrane (HCRTR1) signal transducer activity (HCRTR1)
Anatomy Link Frequency
T-cell 2
puncture 1
cortex 1
HCRTR1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 20 82.76 Quite High
Neuropeptide 16 79.96 Quite High
Somatostatin 6 59.32 Quite High
Opioid 4 57.04 Quite High
opioid receptor 5 55.60 Quite High
reflex sympathetic dystrophy 5 50.00 Quite Low
Inflammatory mediators 1 50.00 Quite Low
antidepressant 9 48.24 Quite Low
sSRI 9 44.64 Quite Low
Substantia nigra 2 43.60 Quite Low
Disease Link Frequency Relevance Heat
Idiopathic Hypersomnolence 101 99.72 Very High Very High Very High
Sleep Disorders 442 99.60 Very High Very High Very High
Disease 161 99.56 Very High Very High Very High
Lumbar Puncture Related Headaches 4 98.74 Very High Very High Very High
Hypersomnia 152 98.10 Very High Very High Very High
Dystonia 2 94.32 High High
Complex Regional Pain Syndromes 5 93.40 High High
Neurodegenerative Disease 13 90.20 High High
Neurological Disease 2 88.72 High High
Parkinson's Disease 155 85.76 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Further evidence has accumulated supporting the causal role of hypocretin deficiency in the origin of NC [8], however, participation of hypocretin signaling in other forms of central hypersomnia including narcolepsy without cataplexy (NWC) or idiopathic hypersomnia (HI) is less understood, although a partial hypocretin deficiency is possible in the former condition [9], [10].
Spec (partial) Negative_regulation (deficiency) of hypocretin associated with idiopathic hypersomnolence, hypersomnia and sleep disorders
1) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954157 Disease Relevance 1.15 Pain Relevance 0.04
Further evidence has accumulated supporting the causal role of hypocretin deficiency in the origin of NC [8], however, participation of hypocretin signaling in other forms of central hypersomnia including narcolepsy without cataplexy (NWC) or idiopathic hypersomnia (HI) is less understood, although a partial hypocretin deficiency is possible in the former condition [9], [10].
Negative_regulation (deficiency) of hypocretin associated with idiopathic hypersomnolence, hypersomnia and sleep disorders
2) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954157 Disease Relevance 1.10 Pain Relevance 0.04
Selective loss or reduction of hypocretin neurons in NC together with the tight association with HLA DQB1*0602, the recent finding of polymorphisms in the T-cell receptor alpha locus and the presence of elevated Tribbles homolog 2 antibody levels suggest a possible autoimmune mechanism which so far remains elusive [11], [12], [13].
Negative_regulation (reduction) of hypocretin in T-cell associated with sleep disorders
3) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954157 Disease Relevance 1.17 Pain Relevance 0.03
A lumbar puncture was performed in 35 patients (19 NC, 7 NWC, 9 HI) in order to measure the CSF hypocretin-1/orexin A levels.
Negative_regulation (measure) of CSF hypocretin-1 in puncture associated with idiopathic hypersomnolence, sleep disorders and lumbar puncture related headaches
4) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954157 Disease Relevance 1.08 Pain Relevance 0
A recent study conducted on PD subjects found a 40% decrease of hypocretin-1 in the prefrontal cortex and a 25% decrease in the ventricular CSF when compared to controls [122].
Negative_regulation (decrease) of hypocretin-1 in cortex associated with disease
5) Confidence 0.08 Published 2010 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2965495 Disease Relevance 1.35 Pain Relevance 0.31
This explanation requires that the branch leading to the outside member be correspondingly short, which becomes increasingly problematic over very long periods of time, but as observed in the orexin receptor example above has occurred to some extent.
Negative_regulation (observed) of orexin receptor
6) Confidence 0.05 Published 2007 Journal Evolutionary Bioinformatics Online Section Body Doc Link PMC2684142 Disease Relevance 0 Pain Relevance 0.11
We measured interleukin-1beta, interleukin-6, interferon-gamma inducible protein-10, RANTES (regulated upon activation, normal T-cell expressed and secreted), complement C3, mannose-binding lectin, complement C1q, soluble intercellular adhesion molecule-1, endothelin-1, nitric oxide, human lactoferrin, and hypocretin-1 levels in these samples.
Negative_regulation (measured) of hypocretin-1 in T-cell
7) Confidence 0.04 Published 2008 Journal Clin J Pain Section Body Doc Link 18180633 Disease Relevance 0.19 Pain Relevance 0
However, it is clear that mutations in the hypocretin (orexin) receptor 2 gene cause genetic narcolepsy in several animal species (Chemelli et al 1999; Lin et al 1999) and there is no doubt that hypocretin/orexin deficiency is the most frequent cause of narcolepsy with cataplexy in humans (Peyron et al 2000; Thannickal et al 2000).
Negative_regulation (deficiency) of hypocretin associated with sleep disorders
8) Confidence 0.02 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2526380 Disease Relevance 1.17 Pain Relevance 0

General Comments

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