INT228394

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Context Info
Confidence 0.07
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 3
Disease Relevance 2.72
Pain Relevance 0.58

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

cytosol (Slc12a3) transport (Slc12a3) plasma membrane (Slc12a3)
transmembrane transport (Slc12a3)
Anatomy Link Frequency
ventricles 1
IB4 1
Slc12a3 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 15 96.28 Very High Very High Very High
Inflammatory response 21 94.08 High High
cytokine 6 75.52 Quite High
Central nervous system 51 63.36 Quite High
Inflammatory mediators 3 32.96 Quite Low
corticosteroid 3 5.00 Very Low Very Low Very Low
ketamine 3 5.00 Very Low Very Low Very Low
headache 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Neurocysticercosis 90 100.00 Very High Very High Very High
INFLAMMATION 39 96.28 Very High Very High Very High
Schistosomiasis 3 93.72 High High
Death 3 92.32 High High
Worm Infection 12 89.44 High High
Infection 150 86.32 High High
Disease 18 5.00 Very Low Very Low Very Low
Cestode Infection 9 5.00 Very Low Very Low Very Low
Hypersensitivity 6 5.00 Very Low Very Low Very Low
Parasitic Infection 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In parallel, a portion of GCs released during the course of NCC may enter the CSF circulation and divert immune cells to static deposits of antigens located in leptomeninges, ventricles and areas far from the parasite.
Localization (released) of NCC in ventricles associated with neurocysticercosis
1) Confidence 0.07 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 1.14 Pain Relevance 0.28
Thus, the constant release and persistence of parasite GCs during the course of NCC most likely leads to a suppressive and immunoregulatory environment that supports parasite establishment and maintenance while minimizing damaging inflammatory responses.
Localization (release) of NCC associated with inflammatory response and neurocysticercosis
2) Confidence 0.06 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 1.21 Pain Relevance 0.26
In porcine and human NCC the material bound by WGA, IB4 and ConA, but not PNA is released by the parasite, and it seems to be taken up by the cells around the metacestode (Figure 6C to 6F) resembling the pattern of release seen in murine NCC (Figure 4).
Localization (release) of NCC in IB4 associated with neurocysticercosis
3) Confidence 0.06 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.37 Pain Relevance 0.03

General Comments

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