INT102615

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Context Info
Confidence 0.44
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 7
Disease Relevance 3.93
Pain Relevance 1.17

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

extracellular space (Tgfa) extracellular region (Tgfa) plasma membrane (Tgfa)
nucleus (Tgfa)
Anatomy Link Frequency
epithelial cell 2
Tgfa (Rattus norvegicus)
Pain Link Frequency Relevance Heat
aspirin 24 100.00 Very High Very High Very High
Inflammation 23 100.00 Very High Very High Very High
qutenza 4 99.52 Very High Very High Very High
alcohol 3 64.64 Quite High
Inflammatory response 3 62.56 Quite High
cINOD 6 37.08 Quite Low
peptic ulcer disease 3 30.52 Quite Low
COX2 2 25.00 Low Low
cOX1 2 25.00 Low Low
cytokine 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ulcers 248 100.00 Very High Very High Very High
INFLAMMATION 28 100.00 Very High Very High Very High
Injury 11 100.00 Very High Very High Very High
Necrosis 4 95.32 Very High Very High Very High
Volume Depletion And Dehydration 6 95.00 High High
Infection 2 80.32 Quite High
Peptic Ulcer 85 71.36 Quite High
Parkinson's Disease 9 67.24 Quite High
Body Weight 43 64.28 Quite High
Recurrence 41 63.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Capsaicin-sensitive nerve fibres induce epithelial cell proliferation, inflammatory cell immigration and transforming growth factor-alpha expression in the rat colonic mucosa in vivo.
Positive_regulation (induce) of Gene_expression (expression) of transforming growth factor-alpha in epithelial cell associated with inflammation and qutenza
1) Confidence 0.44 Published 2002 Journal Scand. J. Gastroenterol. Section Title Doc Link 11989832 Disease Relevance 0.19 Pain Relevance 0.49
Biological molecular processes for ulcer healing are comprised of inflammation, cell migration, mitosis, and remodeling, all of which are associated with the active synthesis and release of several peptide growth factors at the site of injury such as epidermal growth factor (EGF), transforming growth factor-alpha (TGF-?)
Positive_regulation (as) of Gene_expression (synthesis) of transforming growth factor-alpha associated with inflammation, injury and ulcers
2) Confidence 0.21 Published 2008 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2386523 Disease Relevance 0.89 Pain Relevance 0.08
Immunohistochemical expression of transforming growth factor-alpha
Positive_regulation (transforming) of Gene_expression (transforming) of growth factor-alpha
3) Confidence 0.21 Published 2010 Journal Pharmacognosy Magazine Section Body Doc Link PMC2950387 Disease Relevance 0.18 Pain Relevance 0.03
Immunolocalization of transforming growth factor-alpha (TGF-?)
Positive_regulation (transforming) of Gene_expression (transforming) of growth factor-alpha
4) Confidence 0.21 Published 2010 Journal Pharmacognosy Magazine Section Body Doc Link PMC2950387 Disease Relevance 0.18 Pain Relevance 0.03
Effect of C. quadrangularis extract on transforming growth factor-alpha expression in the gastric mucosa
Positive_regulation (transforming) of Gene_expression (expression) of growth factor-alpha
5) Confidence 0.21 Published 2010 Journal Pharmacognosy Magazine Section Body Doc Link PMC2950387 Disease Relevance 0.54 Pain Relevance 0
We conclude that H. pylori antagonizes, in part, aspirin-induced delay of ulcer healing due to suppression of acid secretion, the enhancement in prostaglandin E(2) possibly derived from cyclooxygenase-2 and the overexpression of transforming growth factor alpha and vascular endothelial growth factor in the ulcer area.
Positive_regulation (overexpression) of Gene_expression (overexpression) of transforming growth factor alpha associated with aspirin and ulcers
6) Confidence 0.12 Published 2002 Journal Eur. J. Pharmacol. Section Abstract Doc Link 12231391 Disease Relevance 0.94 Pain Relevance 0.26
We conclude that H. pylori antagonizes, in part, aspirin-induced delay of ulcer healing due to suppression of acid secretion, the enhancement in prostaglandin E(2) possibly derived from cyclooxygenase-2 and the overexpression of transforming growth factor alpha and vascular endothelial growth factor in the ulcer area.
Positive_regulation (aspirin-induced) of Gene_expression (overexpression) of transforming growth factor alpha associated with aspirin and ulcers
7) Confidence 0.09 Published 2002 Journal Eur. J. Pharmacol. Section Abstract Doc Link 12231391 Disease Relevance 1.00 Pain Relevance 0.28

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