INT199335

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Context Info
Confidence 0.11
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 7
Disease Relevance 9.66
Pain Relevance 0.06

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

Golgi apparatus (Macf1) ATPase activity (Macf1) plasma membrane (Macf1)
cytoskeleton (Macf1) cytoplasm (Macf1)
Anatomy Link Frequency
colons 1
Macf1 (Mus musculus)
Pain Link Frequency Relevance Heat
anesthesia 7 58.88 Quite High
Disease Link Frequency Relevance Heat
Aberrant Crypt Foci 294 100.00 Very High Very High Very High
Targeted Disruption 560 99.44 Very High Very High Very High
Cancer 665 96.80 Very High Very High Very High
Dislocations 14 80.28 Quite High
Peripheral Arterial Disease 14 15.00 Low Low
Colon Cancer 287 5.00 Very Low Very Low Very Low
Adenoma 252 5.00 Very Low Very Low Very Low
Apoptosis 105 5.00 Very Low Very Low Very Low
Colorectal Cancer 42 5.00 Very Low Very Low Very Low
Malignant Neoplastic Disease 28 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
three AC remained constant over time, whereas the reduction in total number of ACF in both genotypes at a late stage was due to the reduced number in ACF containing one to three AC (Table 1).


Negative_regulation (number) of ACF associated with aberrant crypt foci
1) Confidence 0.11 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 1.91 Pain Relevance 0
In the late stage of carcinogenesis at 40 weeks after the first DMH application, especially in the IGF-II transgenic mice the occurrence of the ACF was found to be drastically reduced (P < 0.001) versus the earlier stage (Fig. 2B).
Negative_regulation (reduced) of ACF associated with aberrant crypt foci and targeted disruption
2) Confidence 0.09 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 1.39 Pain Relevance 0
The total number of ACF was significantly higher (P < 0.001) in the colons of IGF-II transgenic mice (47.66 ± 2.62 per 10 cm2) than in wild-type mice (26.68 ± 2.48 per 10 cm2) at 11 weeks after the first DMH application (Fig. 2B).
Negative_regulation (number) of ACF in colons associated with targeted disruption and aberrant crypt foci
3) Confidence 0.08 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 1.16 Pain Relevance 0
The number of ACF and the aberrant crypt multiplicity were determined by light microscopy at 25-fold magnification.
Negative_regulation (number) of ACF associated with aberrant crypt foci
4) Confidence 0.08 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 0.57 Pain Relevance 0.06
three AC remained constant over time, whereas the reduction in total number of ACF in both genotypes at a late stage was due to the reduced number in ACF containing one to three AC (Table 1).


Negative_regulation (reduction) of ACF associated with aberrant crypt foci
5) Confidence 0.08 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 1.83 Pain Relevance 0
Development of ACF
Negative_regulation (Development) of ACF associated with aberrant crypt foci
6) Confidence 0.08 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 1.10 Pain Relevance 0
In contrast, in the earlier stage of carcinogenesis a clear correlation between total numbers of ACF and serum IGF-II was found (Fig. 2C).
Negative_regulation (numbers) of ACF associated with aberrant crypt foci
7) Confidence 0.04 Published 2006 Journal J Carcinog Section Body Doc Link PMC1660565 Disease Relevance 1.70 Pain Relevance 0

General Comments

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