INT91815

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Context Info
Confidence 0.49
First Reported 2000
Last Reported 2007
Negated 1
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 3.79
Pain Relevance 0.75

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

peptidase activity (PRSS1) extracellular space (PRSS1) extracellular region (PRSS1)
Anatomy Link Frequency
plaque 2
parenchyma 2
PRSS1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 1 99.00 Very High Very High Very High
metalloproteinase 6 92.96 High High
Chronic pancreatitis 142 91.32 High High
Angina 1 84.12 Quite High
Inflammation 7 74.96 Quite High
fibrosis 14 5.00 Very Low Very Low Very Low
Pain 6 5.00 Very Low Very Low Very Low
Bile 6 5.00 Very Low Very Low Very Low
Pain management 3 5.00 Very Low Very Low Very Low
alcohol 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 9 99.40 Very High Very High Very High
Pancreatitis 239 98.56 Very High Very High Very High
Atherosclerotic Plaque 2 97.50 Very High Very High Very High
Hypercalcemia 35 96.56 Very High Very High Very High
Disease 41 87.00 High High
Increased Venous Pressure Under Development 3 86.00 High High
Stroke 1 85.48 High High
Myocardial Infarction 2 85.04 High High
Cv General 3 Under Development 1 84.12 Quite High
Rupture 1 81.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Transgenic expression of SPINK1 did not hinder trypsinogen activation, but reduced trypsin activity after supramaximal stimulation with cerulein.
Neg (not) Positive_regulation (hinder) of Neg (not) Positive_regulation (activation) of trypsinogen associated with targeted disruption
1) Confidence 0.49 Published 2007 Journal Orphanet J Rare Dis Section Body Doc Link PMC1774562 Disease Relevance 0.76 Pain Relevance 0.03
Studies with cathepsin B deficient mice presented evidence, that the premature and intracellular activation of trypsinogen largely depends on the presence of cathepsin B [7].
Positive_regulation (depends) of Positive_regulation (activation) of trypsinogen
2) Confidence 0.45 Published 2002 Journal BMC Gastroenterol Section Body Doc Link PMC117221 Disease Relevance 0.58 Pain Relevance 0.13
The investigation of the wild type trypsinogen molecule and three distinct mutants (i.e., N29I, N29T and R122H) found that cathepsin B mediated trypsinogen activation was not influenced by the respective mutants [8].
Positive_regulation (mediated) of Positive_regulation (activation) of trypsinogen
3) Confidence 0.45 Published 2002 Journal BMC Gastroenterol Section Body Doc Link PMC117221 Disease Relevance 0.43 Pain Relevance 0.09
Elevated serum calcium levels can lead to premature activation of trypsinogen inducing autodigestion of the pancreatic parenchyma [20].
Positive_regulation (lead) of Positive_regulation (activation) of trypsinogen in parenchyma
4) Confidence 0.45 Published 2003 Journal BMC Gastroenterol Section Body Doc Link PMC317302 Disease Relevance 1.03 Pain Relevance 0
A dramatic increase in autoactivation of cationic trypsinogen was observed in all three mutants, with D22G and K23R exhibiting the most marked increases.
Positive_regulation (increase) of Positive_regulation (increase) of trypsinogen
5) Confidence 0.43 Published 2003 Journal Mol. Biol. Evol. Section Abstract Doc Link 12832630 Disease Relevance 0.18 Pain Relevance 0.09
The increased MMP activity during atherosclerotic plaque development and instability must therefore be caused by increased cytokine and growth factor-stimulated gene transcription, elevated zymogen activation and an imbalance in the MMP:TIMP ratio.
Positive_regulation (elevated) of Positive_regulation (activation) of zymogen in plaque associated with atherosclerotic plaque and cytokine
6) Confidence 0.00 Published 2000 Journal Expert Opin Investig Drugs Section Abstract Doc Link 11060722 Disease Relevance 0.83 Pain Relevance 0.41

General Comments

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