INT239841

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Context Info
Confidence 0.32
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.60
Pain Relevance 0.20

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

cytosol (TNNI3) cytoplasm (TNNI3)
Anatomy Link Frequency
cardiomyocytes 2
TNNI3 (Homo sapiens)
Pain Link Frequency Relevance Heat
ischemia 11 90.28 High High
cva 15 89.04 High High
depression 2 47.32 Quite Low
cytokine 5 22.60 Low Low
Inflammation 10 17.80 Low Low
Angina 4 5.00 Very Low Very Low Very Low
Inflammatory marker 3 5.00 Very Low Very Low Very Low
chemokine 1 5.00 Very Low Very Low Very Low
Inflammatory response 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Coronary Heart Disease 13 99.40 Very High Very High Very High
Necrosis 10 90.80 High High
Cv General 4 Under Development 7 90.28 High High
Pulmonary Embolism 10 89.84 High High
Hypertension 1 76.72 Quite High
Sepsis 11 70.44 Quite High
Right Ventricular Dysfunction 2 65.92 Quite High
Natriuresis 6 58.16 Quite High
Depression 1 47.32 Quite Low
Cv General 3 Under Development 2 45.76 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It is postulated that a transient (reversible) increase in membrane permeability of the cardiomyocytes in SRMD, together with intracellular degradation of troponin I, was responsible for the increased cTn levels [78,79].
Regulation (responsible) of Protein_catabolism (degradation) of troponin I in cardiomyocytes associated with coronary heart disease
1) Confidence 0.32 Published 2008 Journal Crit Care Section Body Doc Link PMC2481437 Disease Relevance 1.60 Pain Relevance 0.20

General Comments

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