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Context Info
Confidence 0.73
First Reported 1979
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 4.53
Pain Relevance 0.85

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

isomerase activity (GPI) small molecule metabolic process (GPI) carbohydrate metabolic process (GPI)
cytoplasm (GPI) cytosol (GPI) extracellular space (GPI)
Anatomy Link Frequency
putamen 1
GPI (Homo sapiens)
Pain Link Frequency Relevance Heat
metalloproteinase 46 100.00 Very High Very High Very High
gABA 2 100.00 Very High Very High Very High
agonist 1 93.72 High High
Dopamine 1 93.40 High High
chemokine 3 81.36 Quite High
cytokine 19 80.40 Quite High
aspirin 1 76.16 Quite High
Inflammation 49 75.64 Quite High
GABA receptor 1 75.00 Quite High
cINOD 11 65.80 Quite High
Disease Link Frequency Relevance Heat
Disorder Of Lipid Metabolism 14 99.52 Very High Very High Very High
Paroxysmal Nocturnal Hemoglobinuria 158 99.46 Very High Very High Very High
Targeted Disruption 6 98.30 Very High Very High Very High
Dyskinesias 4 98.00 Very High Very High Very High
Agranulocytosis 1 97.60 Very High Very High Very High
Atherosclerosis 11 97.34 Very High Very High Very High
Disease 76 96.92 Very High Very High Very High
Neutropenia 3 95.36 Very High Very High Very High
Hematological Disease 14 92.64 High High
Parkinson's Disease 3 91.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This combination of data in an animal model and in humans strongly suggests that increased enkephalinergic activity in the putamen and increased sensitivity of GABA(A) receptors in the GPi are implicated in the pathogenesis of LD-induced dyskinesias in Parkinson's disease.
Localization (sensitivity) of GPi in putamen associated with gaba, disease and dyskinesias
1) Confidence 0.73 Published 2002 Journal Parkinsonism Relat. Disord. Section Abstract Doc Link 12217634 Disease Relevance 0.89 Pain Relevance 0.22
kDa high-density lipoprotein complex composed of apolipoprotein A-I (apoA-I), haptoglobin-related protein (Hpr), apoliprotein L-I (APOL1), human cathelicidin antimicrobial peptide (hCAP18), GPI-specific phospholipase D (GPI-PLD), apolipoprotein A-II, and paraoxanase [106, 110], and (ii) TLF2, a 1000?
Localization (phospholipase D) of GPI associated with disorder of lipid metabolism
2) Confidence 0.06 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2826769 Disease Relevance 0.44 Pain Relevance 0
GPI-anchored MMPs can be released from the cells in exosomes and transferred to other cell types in a paracrine manner where they can elicit biological effects [57].
Localization (released) of GPI associated with metalloproteinase
3) Confidence 0.06 Published 2011 Journal Biochemistry Research International Section Body Doc Link PMC2989751 Disease Relevance 0 Pain Relevance 0.41
These bacteria produce phospholipase and other enzymes which can remove GPI-anchored DAF and CD59 from the corneal surface [51].
Localization (anchored) of GPI
4) Confidence 0.05 Published 2008 Journal Semin Immunopathol Section Body Doc Link PMC2315691 Disease Relevance 0.68 Pain Relevance 0.04
Finally, PNH-subclinical refers to the presence of very small GPI-deficient clones deprived of any clinical significance; in this context, the term PNH itself is misleading and should not be used, since none of the clinical manifestations of this condition are present.
Localization (presence) of GPI associated with paroxysmal nocturnal hemoglobinuria
5) Confidence 0.05 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721357 Disease Relevance 1.32 Pain Relevance 0
P and S also abrogated adherence-induced lysosomal enzyme release and FP-stimulated hexose monophosphate pathway (HMP) activity.
Localization (release) of hexose monophosphate pathway
6) Confidence 0.03 Published 1979 Journal Schweiz Med Wochenschr Section Abstract Doc Link 482916 Disease Relevance 0.53 Pain Relevance 0.18
However, on an atherosclerosis-prone Apobec-1 and LDL receptor double-knockout murine model, Egan and colleagues [23] have shown that unlike indomethacin, urinary excretion of only PGI-M (but not other major metabolites of TXA2, TXB2, or prostacyclin) was reduced by COX-2 inhibition.
Localization (excretion) of PGI-M associated with targeted disruption and atherosclerosis
7) Confidence 0.01 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860062 Disease Relevance 0.67 Pain Relevance 0

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